AFP Medical Center

History and beginning:

The V Luna General Hospital, forerunner of the AFP Medical Center was named after Colonel Victoriano
Luna, the then Chief of Medical Service and Medical Adviser of the Chief of Staff, as a fitting tribute to
his heroism during the battle of Bataan. As early as 1935, he conceptualized the idea of putting up an
Army hospital to serve the increasing needs of the Philippine Army. 

It was however, in 1937 that his dream was realized with the inauguration of the 1st Philippine Army
General Hospital. On 03 September 1946, the 1st PA General Hospital was renamed as Victoriano Luna
General Hospital (VLGH) by virtue of GO Nr 512 HPA, dated 03 September 1946. Since then,
September 3rd of every year is being observed as the Foundation Day of the hospital. The exact month
and date of the foundation of the 1st PA General Hospital have not been established by military historians
up to now because of the ravages of the last war that caused damage to life and properties. .

In an effort to establish the exact date of the hospital’s foundation, the Historical Activities Branch,
AFPMC, wrote a letter of inquiry to the National Archives and Records Service of the Military Archives
Division in Washington DC but their records failed to find a reference to the 1st PA General Hospital.

History: 

In 1937, the 1st Philippine Army General Hospital was established in Camp Murphy with an
initial capacity of 60 beds, and was first commanded by Colonel Eliseo Bringas MC. The 1st
Philippine Army General Hospital site is in the area now occupied by the Medical Dispensary at
Camp Aguinaldo. Due to the increasing number of cases among military personnel, the hospital
was expanded to accommodate 250 beds. This, being still inadequate for military needs, other
government hospitals were being availed of, especially those military units that were stationed
far from Manila. The organization, tactical employment and training of medical units were
closely patterned after those of the US Army. In 1941, the hospital was again expanded into a
500 bed capacity but unfortunately on 22 December 1941, Half of the Philippine Army General
Hospital was bombed by the Japanese. Many of the patients were killed and those seriously

1
injured were evacuated to the Quezon Institute (QI). On 24 December 1941, half of the hospital
staff was ordered by Army Headquarters to proceed to Bataan and established a General Hospital
somewhere near the base camp in Mariveles. The hospital was established in a make shift
building and tents. Together with the Base hospital Nrs 1 and 2 which were established by the
US Arrmy, the 1st Philippine Army General Hospital took care of frontline casualties until the
USAFFE forces surrendered in Bataan on April 09, 1942. 

One sad event happened in Bataan in the afternoon of 26 March 1942, while inspecting the
nearby hospital and the refugee camp in the company of Major W. McClosky and Col
Vanderboget, colonel Luna was hit by a stray bomb from a high flying Japanese palne killing
him instantly. Major McClosky died a few minutes later while Col Vanderboget was seriously
injured. 

When Bataan fell on April 09, 1942, Major Joaquin A Sanchez then commanded the hospital. He
assigned few officers to take care of the bedridden and the seriously wounded while the rest of
the staff and the ambulatory patients joined the infamous Death March to San Fernando,
Pampanga and Capas, Tarlac. From the time Bataan fell in the hands of the Japanese, the hospital
ceased exist. 

After the American Forces have liberated Manila in April 1945, most of the medical officers who
were recovered and turned over to military control were placed on duty with the presently
occupied Post Chapel. Few months later, The American Personnel of this station hospital were
deployed to Korea. They left all their equipment and supplies for the use of the Armed Forces of
the Philippines. The Commanding Officer was Colonel Gonzales Roxas, Captain Pedro M Cruz
as its Ex-O, 1st Protacio R Sotto as CO Medical Detachment, Captian Conrado B Icasiano as
Chief, Dep of Medicine, Captain Melchor Javier as Chief of Surgery, Captain Gustavo U Reyes
as Chief, Laboratory, captain Ramon Paterno as Chief X-Ray, Captain Anotniuo Santos as Chief
Dental Service and 1Lt Gregoria as Chief Nurse. 

Nine months later, the hospital was transferred to the rumbling prefabricated buildings and
Quonset huts vacated by the 331th and 312th US Army General Hospitals at the corner of High

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54 Shaw Boulevard Mandaluyung, Rizal. More equipment and supplies were requisition from
the U.S. Army Medical Depot while surgeons and nurses were sent abroad for further training.
When the Philippine USAFFE forces were turned over by the US Army to the Philippine
Government on 30 June 1946, the hospital had a bed capacity of more than 2500 beds the
patients were made to occupy the Quonset huts in the 311th hospital area while the other types of
patients were distributed all over the 310th hospital area. At about this time, the equipment and
supplies of the Orthopaedic braceshop were turned over to the Vluna General Hospital and taken
up by the ampulation and prosthetic team, pursuant to TSU SGO 9940 US Army. This newly
designated ampulation and prosthetics team was under the command of Captain Ildefonso
Gemez MC. 

It should be noted that the VGLH was the first institution in the Island to manufacture artificial
prosthesis for amputees and for many years it also served as the training ground for other
government institution. 

By virtue of General Order Nr 512 HPA, the Philippine Army General Hospital was named
Victoriano Luna General Hospital on 3 September 1946. 

In December of 1950, just when the prefabricated buildings and Quonset huts in Manduluyong
site were about to fall apart, VLGH was able to transfer to its newly established location on
Kamias Road, Quezon City, a 16 hectare lot where it still stands today. The new site included a
P800,000.00 concrete main building, ten (10) Quonset huts each worth P30,000.00 and other
facilities, which has a total value of P1,614,436.00. A kitchen, chapel, EMs barracks and
building for ARMED FORCES MEDICAL SERVICE School were added later. 

It was the time when the anti-dissident campaign was most active. The wards soon received large
number of casualties. Military personnel, Huks, as well as innocent civilians wounded in the
crossfire received equal treatment and no doubt, the solicitous care given to these dissidents was
greatly instrumental in their eventual return to the folds of law. 

While the Huks were on the run, a Muslim outlaw, Kamlon, started a new battlefront in Job. As a

3
result, the VLGH was ordered to sent surgical teams composed of doctors, nurses, and
anesthesiologist to be attached to the Constabulary Station Hospital in Jolo, Sulu to provide
much needed medical service in the area. 

Those campaigns over such widely spread brought more casualty demands on the already
overworked staff of the hospital. To cope with the problem of providing additional bed spaces,
three other wards were set up in the PC infirmary and the PC headquarters at Camp Crame. 

In 1954, when the former 10th General Hospital was vacated and turned over the Philippine
government, some of the concrete buildings and adjacent Quonset huts and officer quarters were
rehabilitated and made available for the use of VLGH. Accordingly, chronic PTB cases,
convalescent medical cases were transferred to this site. This became officially known as the
VLGH Annex. It was only in 1963 that the VLGH Annex was vacated and given to the Army
Station Hospital at Fort Bonifacio. 

V Luna General Hospital was renamed V Luna Medical Center per GO Nr 389, GHQ AFP dated
11 May 1970. 

It was redesigned Armed Forces of the Philippines Medical Center (AFPMC) effective 26 Sep 75
by virtue of GO Nr 258, GHQ dtd 09 Oct 75. 

It was evident from the above exposition of events that the AFPMC is an institution with a
glorious history ranging from pre-war days when our Armed Forces was still in its formative
years, where actual field service was rendered in the battle fields of Bataan and during the
immediate post liberation period at the height of the anti-huk campaign, the secessionist
movement in Mindanao and the upsurge on communist insurgency problems. 

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Mission

TO PROVIDE QUALITY TERTIARY HEALTH CARE SERVICES TO AFP PERSONNEL,

DEPENDENTS AND AUTHORIZED CIVILIANS. ...

 Organization Chart

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 Ward Rules and Policies

1. Only one watcher is allowed. Relatives and accompanying person should wait at the
covered place outside the ER complex.
2. Children (12 years old below) are not allowed. Except patients.
3. Watchers are not allowed to eat inside the Emergency and Observation room. Watchers
are not allowed to sit or lie on beds.
4. Keep the ER and OBS room clean and organized.
5. All patients must register and present valid military/dependent’s ID at the Triage area or
nurse’s station. Patients are required to submit Xerox copy of valid military/dependent’s
ID upon admission.
6. Non Emergency cases shall be managed at the Outpatient Department (OPD)/ specialty
clinics.
7. The extent of service to civilians is subject to the availability of medicines and medical
supplies. Medicines and medical supplies with AFPMC markings will not be allowed as
replacements.
8. All medicines and medical supplies shall be billed before the patient is discharged.
9. Please secure your valuables properly. The management will not be responsible for any
loss or damage of personal belongings.
10. Using/plugging of electrical equipment is not allowed.

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 PATIENT FLOW CHART
EMERGENCY ROOM SERVICES
AFP MEDICAL CENTER

UPON ENTRY INTO THE EMERGENCY ROOM

COMPLEX

1. Please proceed to the triage area for instructions (nurse station)

2. Enter the emergency room and proceed to
a. Medicine ER
b. Surgery ER
c. Pediatric ER
d. ENT/HNS ER
3. After the evaluation and management proceed to the admission and disposition
section for interview and issuance of cover sheet proceed to the ER nurse station for
recording and admission to the ward

If discharged please proceed to the ER Nurse station for billing and clearance

For non emergency patients please proceed to:

a. Specialty clinic – please see bulletin board for clinic schedules
b. OPD at the OPC complex

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Compilation

8
 Appendicitis

Appendicitis is a condition characterized by inflammation of the appendix. It is classified

as a medical emergency and many cases require removal of the inflamed appendix, either
by laparotomy orlaparoscopy. Untreated, mortality is high, mainly because
of peritonitis and shock. Reginald Fitz first described acute and chronic appendicitis in 1886 and
it has been recognized as one of the most common causes of
severe acute abdominal pain worldwide. A correctly diagnosed non-acute form of appendicitis is
known as "rumbling appendicitis".

Signs:

These include localized findings in the right iliac fossa. The abdominal wall becomes
very sensitive to gentle pressure (palpation). Also, there is rebound tenderness. In case of a
retrocecal appendix, however, even deep pressure in the right lower quadrant may fail to elicit
tenderness (silent appendix), the reason being that the cecum, distended with gas, prevents the
pressure exerted by the palpating hand from reaching the inflamed appendix. Similarly, if the
appendix lies entirely within the pelvis, there is usually complete absence of the abdominal
rigidity. In such cases, a digital rectal examination elicits tenderness in the rectovesical pouch.
Coughing causes point tenderness in this area (McBurney's point) and this is the least painful
way to localize the inflamed appendix. If the abdomen on palpation is also involuntarily guarded
(rigid), there should be a strong suspicion of peritonitis requiring urgent surgical intervention.

Rovsing's sign

Continuous deep palpation starting from the left iliac fossa upwards (anti clockwise along the
colon) may cause pain in the right iliac fossa, by pushing bowel contents towards the ileocaecal
valve and thus increasing pressure around the appendix. This is the Rovsing's sign.

Psoas sign

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Psoas sign or "Obraztsova's sign" is right lower-quadrant pain that is produced with the patient
extending the hip due to inflammation of the peritoneum overlying the iliopsoas muscles and
inflammation of the psoas muscles themselves. Straightening out the leg causes the pain because
it stretches the muscles, and flexing the hip into the "fetal position" relieves the pain.

Obturator sign

If an inflamed appendix is in contact with the obturator internus, spasm of the muscle can be
demonstrated by flexing and internal rotation of the hip. This maneuver will cause pain in
the hypogastrium.

Blumberg sign

Deep palpation of the viscera over the suspected inflamed appendix followed by sudden release
of the pressure causes the severe pain on the site indicating positive Blumberg's sign and
peritonitis.

Volkovich-Kocher (Kosher)'s sign

During anamnesis, the appearance of pain in the epigastric region or around the stomach at the
beginning of disease with a subsequent shift to the right iliac region.

Sitkovskiy's sign

Increased pain in the right iliac region as patient lies on his/her left side.

Bartomier-Michelson's sign

Increased pain on palpation at the right iliac region as patient lies on his/her left side compared to
when patient was on supine position.

Aure-Rozanova's sign

Increase pain on palpation with finger in right Petit triangle (can be a positive Shchetkin-

Bloomberg's sign) - typical in retroceacal position of the appendix.

Causes

On the basis of experimental evidence, acute appendicitis seems to be the end result of a
primary obstruction of the appendix lumen.[6][7] Once this obstruction occurs the appendix

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subsequently becomes filled with mucus and swells, increasing pressures within the lumen and
the walls of the appendix, resulting in thrombosis and occlusion of the small vessels, and stasis
of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the former
progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out
through the dying walls, pus forms within and around the appendix (suppuration). The end result
of this cascade is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead
to septicemia and eventually death.

Among the causative agents, such as foreign bodies, trauma, intestinal

worms, lymphadenitis, and calcified deposits known as appendicoliths,the occurrence of
an obstructing fecalith has attracted attention. The prevalence of fecaliths in patients with
appendicitis is significantly higher in developed than in developing countries, and an appendiceal
fecalith is commonly associated with complicated appendicitis. Also, fecal stasis and arrest may
play a role, as demonstrated by a significantly lower number of bowel movements per week in
patients with acute appendicitis compared with healthy controls. The occurrence of a fecalith in
the appendix seems to be attributed to a right sided fecal retention reservoir in the colon and a
prolonged transit time. From epidemiological data it has been stated that diverticular disease and
adenomatous polyps were unknown and colon cancer exceedingly rare in communities exempt
for appendicitis. Also, acute appendicitis has been shown to occur antecedent to cancer in the
colon and rectum. Several studies offer evidence that a low fiber intake is involved in the
pathogenesis of appendicitis. This is in accordance with the occurrence of a right sided fecal
reservoir and the fact that dietary fiber reduces transit time.

Management

Before surgery

The treatment begins by keeping the patient from eating or drinking in preparation for
surgery. An intravenous drip is used to hydrate the patient. Antibiotics given intravenously such
as cefuroxime andmetronidazole may be administered early to help kill bacteria and thus reduce
the spread of infection in the abdomen and postoperative complications in the abdomen or
wound. Equivocal cases may become more difficult to assess with antibiotic treatment and

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benefit from serial examinations. If the stomach is empty (no food in the past six hours) general
anaesthesia is usually used. Otherwise, spinal anaesthesia may be used.

Once the decision to perform an appendectomy has been made, the preparation procedure
takes more or less one to two hours. Meanwhile, the surgeon will explain the surgery procedure
and will present the risks that must be considered when performing an appendectomy. With all
surgeries there are certain risks that must be evaluated before performing the procedures.
However, the risks are different depending on the state of the appendix. If the appendix has not
ruptured, the complication rate is only about 3% but if the appendix has ruptured, the
complication rate rises to almost 59 The most usual complications that can occur are
pneumonia, hernia of the incision, thrombophlebitis, bleeding or adhesions.

The surgeon will also explain how long the recovery process should take. In cases of
male patients, the abdomen hair is usually removed in order to avoid complications that may
appear regarding the incision. In most of the cases patients experience nausea or vomiting which
requires specific medication before surgery. Antibiotics along with pain medication may also be
administrated prior to appendectomies.

Assessment and Diagnostic Method

·    Diagnosis is based on a complete physical examination and laboratory and radiologic tests.
·    Leukocyte count greater than 10,000/mm3; neutrophil count greater than 75%; abdominal
radiographs, ultrasound studies, and CT scans may reveal right lower quadrant density or
localized distention of the bowel.

Gerontologic Consideration

In the elderly, signs and symptoms of appendicitis may vary greatly. Signs may be very vague
and suggestive of bowel obstruction or another process; some patients may experience no
symptoms until the appendix ruptures. The incidence of perforated appendix is higher in the
elderly because many of theses people do not seek health care as quickly as younger people.

Pain management

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 Pain from appendicitis can be severe. Strong pain medications (i.e. narcotic pain
medications) are recommended for pain management prior to surgery. Morphine is generally the
standard of care in adults and children in the treatment of pain from appendicitis prior to surgery.

In the past (and in some medical textbooks that are still published today), it has been
commonly accepted that pain medication not be given until the surgeon has the chance to
evaluate the patient, so as to not "corrupt" the findings of the physical examination. This line of
practice, combined with the fact that surgeons may sometimes take hours to come to evaluate the
patient, especially if he or she is in the middle of surgery or has to drive in from home, often
leads to a situation that is ethically questionable at best. More recently, due to better
understanding of the importance of pain control in patients, it has been shown that the physical
examination is actually not that dramatically disturbed when pain medication is given prior to
medical evaluation. Individual hospitals and clinics have adapted to this new approach of pain
management of appendicitis by developing a compromise of allowing the surgeon a maximum
time to arrive for evaluation, such as 20 to 30 minutes, before active pain management is
initiated. Many surgeons also advocate this new approach of providing pain management
immediately rather than only after surgical evaluation.

Medical Management

·    Surgery is indicated if appendicitis is diagnosed and should be performed as soon as possible
to decrease risk of perforation.
·    Administer antibiotics and intravenous fluids until surgery is performed.
·    Analgesic agents can be given after diagnosis is made.

Complications of Appendectomy

·    The major complication is perforation of the appendix, which can lead to peritonitis or an
abscess.
·    Perforation generally occurs 24 hours after onset of pain (symptoms include fever (37.7°C
[100°F] or greater), toxic appearance, and continued pain or tenderness).

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Nursing Management

·    Nursing goals include relieving pain, preventing fluid volume deficit, reducing anxiety,
eliminating infection due to the potential or actual disruption of the gastrointestinal tract,
maintaining skin integrity, and attaining optimum nutrition.
·    Preoperatively, prepare patient for surgery, start intravenous line, administer antibiotic, and
insert nasogastric tube (if evidence of paralytic ileus). Do not administer an enema or laxative
(could cause perforation).
·    Postoperatively, place patient in semi-Fowler’s position, give narcotic analgesic as ordered,
administer oral fluids when tolerated, give food as desired on day of surgery (if tolerated). If
dehydrated before surgery, administer intravenous fluids.
·    If a drain is left in place at the area of the incision, monitor carefully for signs of intestinal
obstruction, secondary hemorrhage, or secondary abscesses (eg. fever, tachycardia, and increased
leukocyte count).

Promoting home and community-based care

Teaching Patients Self-Care

·    Teach patient and family to care for the wound and perform dressing changes and irrigations
as prescribed.
·    Reinforce need for follow-up appointment with surgeon.
·    Discuss incision care and activity guidelines.
·    Refer for home care nursing as indicated to assist with care and continued monitoring of
complications and wound healing.

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 Arthritis (Rheumatoid Arthritis)

Arthritis is a group of conditions where there is damage caused to the joints of the body.
Arthritis is the leading cause of disability in people over the age of 55.

There are many different forms of arthritis, each of which has a different cause. The most
common form of arthritis is Osteoarthritis (also known as degenerative joint disease) Other
forms of arthritis are rheumatoid arthritis and psoriatic arthritis, which are autoimmune
diseases in which the body is attacking itself. Septic arthritis is caused by joint infection.
Gouty arthritis is caused by deposition of uric acid crystals in the joint that results in
subsequent inflammation. Additionally, there is a less common form of gout that is caused by
the formation of rhomboidal shaped crystals of calcium pyrophosphate. This form of gout is
known as pseudogout.

History and Physical Examinaton

All arthritides feature pain. Patterns of pain differ among the arthritides and the location.
Rheumatoid arthritis is generally worse in the morning whilst Osteoarthritis is classically
worse at night or following rest. In elderly people and children, pain may not be the main
feature, and the patient simply moves less (elderly) or refuses to use the affected limb
(children).

Elements of the history of the pain (onset, number of joints and which involved, duration,
aggravating and relieving factors) all guide diagnosis. Physical examination typically
confirms diagnosis. Radiographs are often used to follow progression or assess severity in a
more quantitative manner.

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Blood tests and X-rays of the affected joints often are performed to make the diagnosis.

Screening blood tests may be indicated if certain arthritides are suspected. This may include:
rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen and specific
antibodies.

Rheumatoid Arthritis 

Rheumatoid arthritis is a chronic, inflammatory, multisystem autoimmune disorder. It is

commonly polyarticular; that is, it affects many joints. Inflammation, soft tissue swelling,
and the involvement of multiple joints are common signs and symptoms that distinguish
rheumatoid and other inflammatory arthritis from non-inflammatory arthritis such as
osteoarthritis. The joints are usually affected initially asymmetrically and then in a
symmetrical fashion as the disease progresses. The pain generally improves with use of the
affected joints, and there is usually stiffness of all joints in the morning that lasts over one
hour. Thus, the pain of rheumatoid arthritis is usually worse in the morning compared to the
classic pain of osteoarthritis where the pain worsens over the day as the joints are used.

Extra-articular manifestations also distinguish rheumatoid arthritis from osteoarthritis (hence

it is a multisystemic disease). For example, most rheumatoid athritis patients also suffer with
anemia, either as a consequence of the disease itself (anaemia of chronic disease) or as a
consequence of gastrointestinal bleeding as a side effect of drugs used in treatment,
especially NSAIDs used for analgesia. 

About 60% of patients are unable to work 10 years after the onset of their disease.

Deformities

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As the pathology progresses the inflammatory activity leads to erosion and destruction of the
joint surface, which impairs their range of movement and leads to deformity. The fingers are
typically deviated towards the little finger and can assume unnatural shapes.

Diagnosis

- Morning stiffness of >1 hour most mornings for at least 6 weeks. 

- Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups 

- Arthritis of hand joints 

- Symmetric arthritis 

- Subcutaneous nodules in specific places 

- Rheumatoid factor at a level above the 95th percentile 

- Radiological changes suggestive of joint erosion 

At least four criteria have to be met for classification as rheumatoid arthritis. 

It is important to note that these criteria are not intended for the diagnosis of patients for
routine clinical care. They were primarily intended to categorize patients, for research. For
example: one of the criteria is the presence of bone erosion on X-Ray. Prevention of bone
erosion is one of the main aims of treatment because it is generally irreversible. To wait until
all of the criteria for rheumatoid arthritis are met may sometimes result in a worse outcome
for the patient. Most patients and rheumatologists would agree that it would be better to treat
the patient as early as possible and prevent bone erosion from occurring, even if this means
treating patients who don't fulfill the criteria. 

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 The criteria are, however, very useful for categorising patients with established rheumatoid
arthritis, for example for epidemiological purposes.

A 2005 study by the Mayo Clinic noted that patients suffer a doubled risk of heart disease,
[20] independent of other risk factors such as diabetes, alcohol abuse, and elevated
cholesterol, blood pressure and body mass index. The mechanism by which the disease
causes this increased risk remains unknown; the presence of chronic inflammation has been
proposed as a contributing factor.

Causes

There is no evidence that physical and emotional effects, stress and improper diet could play
a role in the disease. Some research suggests that alcohol consumption lowers the risk of
developing the disease. In addition, a Swedish study found that the risk decreased as the
consumption of alcohol increased from light to moderate levels.

It is suspected that susceptibility to rheumatoid arthritis is an inherited trait.

Autoimmune diseases require that the affected individual have a defect in the ability to
distinguish foreign molecules from the body's own.

Thus, in theory, the sufferer requires susceptibility to the disease through genetic endowment
with specific markers and an infectious event that triggers an autoimmune response.

Nursing management

18
Pain
Help manage pain by responding immediately to complaints, providing medication as ordered by
physician, encouraging frequent rest between activities and providing distractions. Hot or cold
compresses may also provide relief.

Daily Living Activities

The patient may need help dressing, bathing, performing range of motion exercises and other
daily activities. If muscle weakness is present, the patient may be unsteady and require assistance
walking.

Emotional Support
Encourage the patient to talk about feelings and promote a sense of independence by allowing
her to perform as many tasks as possible. Monitor for signs of depression and low self-esteem.

Treatment

There is no known cure for rheumatoid arthritis. However, many different types of treatment can
be used to alleviate symptoms.

Historic treatments for this condition have included: gold salts, RICE, acupuncture, apple diet,
nutmeg, some light exercise every now and then, nettles, bee venom, copper bracelets, rhubarb
diet, rest, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electric convulsion
therapy (ECT). Cortisone therapy has offered relief to many patients in the past, but its long-term
effects have been deemed undesirable.

Anti-inflammatories and analgesics. Disease-Modifying Antirheumatic Drugs (DMARDs) have

been found to produce durable remissions and delay or halt disease progression. In particular
they prevent bone and joint damage from occurring secondary to the uncontrolled inflammation.
This is important as such damage is usually irreversible. Anti-inflammatories and analgesics
improve pain and stiffness but do not prevent joint damage or slow the disease progression.

There is an increasing recognition amongst rheumatologists that permanent damage to the joints

19
occurs at a very early stage in the disease. In the past the strategy used was to start with just an
anti-inflammatory drug, and assess progression clinically and using X-rays. If there was evidence
that joint damage was starting to occur then a more potent DMARD would be prescribed. Tools
such as ultrasound and MRI are more sensitive methods of imaging the joints and have
demonstrated that joint damage occurs much earlier and in more patients than was previously
thought. Patients with normal X-rays will often have erosions detectable by ultrasound that X ray
could not demonstrate.

There may be other reasons why starting DMARDs early is beneficial as well as prevention of
structural joint damage. In the early stage of the disease, the joints are increasingly infiltrated by
cells of the immune system that signal to one another and are thought to set up self-perpetuating
chronic inflammation. Interrupting this process as early as possible with an effective DMARD
(such as methotrexate) appears to improve the outcome from the rheumatoid arthritis for years
afterwards. Delaying therapy for as little as a few months after the onset of symptoms can result
in worse outcomes in the long term. There is therefore considerable interest in establishing the
most effective therapy in patients with early arthritis, when they are most responsive to therapy
and have the most to gain.

Treatment also includes rest and physical activity. Regular exercise is important for maintaining
joint mobility and making the joint muscles stronger. Swimming is especially good, as it allows
for exercise with a minimum of stress on the joints. Heat and cold applications are modalities
that can ease symptoms before and after exercise. Pain in the joints is sometimes alleviated by
oral acetaminophen (paracetamol). Other areas of the body, such as the eyes and lining of the
heart, are treated individually. However, there is no diet that has been shown to alleviate
rheumatoid arthritis, although fish oil may have anti-inflammatory effects.

Pain relief

Recent research indicates that cytokines, a group of chemicals that are produced by various cells
in the body, may be responsible for generating the response of chronic pain associated with
Rheumatoid Arthritis. Medications that affect the release of cytokines or block the action of

20
cytokines may reduce the response of chronic pain. Various anti-cytokine medications are now
being used to treat painful disease states such as Rheumatoid Arthritis, and Crohn's Disease. In
addition, research using the anti-cytokine medication, Thalidomide, is being evaluated for its
effect in treating chronic pain associated with Arachnoiditis. 

Food (vegetables) with higher water content should be avoided

Other therapies

Other therapies are weight loss, occupational therapy, podiatry, physiotherapy, joint injections,
and special tools to improve hard movements (e.g. special tin-openers).

Severely affected joints may require joint replacement surgery, such as knee replacement.

Prognosis

The course of the disease varies greatly from patient to patient. Some patients have mild short-
term symptoms, but in most the disease is progressive for life. 

Around 20%-30% will have subcutaneous nodules (known as rheumatoid nodules); this is
associated with a poor prognosis

Disabitity

Daily living activities are impaired in most patients. 

After 5 years of disease, approximately 33% of patients will not be working 

After 10 years, approximately half will have substantial functional disability. 

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Mortality

Estimates of the life-shortening effect of Rheumatoid Arthritis vary; most sources cite a lifespan
reduction of 5 to10 years. According to the UK's National Rheumatoid Arthritis Society, "Young
age at onset, long disease duration, the concurrent presence of other health problems (called co-
morbidity), and characteristics of a severe form of the disease – such as poor functional ability or
overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement
of organs other than the joints – have been shown to associate with higher mortality". 

Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo
Clinic noted that patients suffer a doubled risk of heart disease, independent of other risk factors
such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index.
The reason why the disease causes increased risk remains unknown; the presence of chronic
inflammation has been proposed as a contributing factor.

22
 Bronchial Asthma

Ever hear the term "bronchial asthma" and wonder what it means? When people talk about
bronchial asthma, they are really talking about asthma, a chronic inflammatory disease of the
airways that causes periodic "attacks" of coughing, wheezing, shortness of breath, and chest
tightness.

According to the CDC, more than 22 million Americans, including 6.5 million children under 18,
suffer with asthma today. Allergy clearly plays an important role in many asthma cases but not in
all. As with allergy, you can blame your family history; there's certainly a strong genetic
component for asthma.

Asthma is associated with mast cells, eosinophils, and T lymphocytes. Mast cells are the allergy-
causing cells that release chemicals like histamine. Histamine is the substance that causes nasal
stuffiness and dripping in a cold or hay fever, constriction of airways in asthma, and itchy areas
in a skin allergy. Eosinophils are a type of white blood cell associated with allergic disease. T
lymphocytes are also white blood cells associated with allergy and inflammation.

These cells, along with other inflammatory cells, are involved in the development of airway
inflammation in asthma that contributes to the airway hyperresponsiveness, airflow limitation,
respiratory symptoms, and chronic disease. In certain individuals, the inflammation results in the
feelings of chest tightness and breathlessness that's felt often at night (nocturnal asthma) or in the
early morning hours. Others only feel symptoms when they exercise (called exercise-induced
asthma). Because of the inflammation, the airway hyperresponsiveness occurs as a result of
specific triggers.

Allergies are strongly linked to bronchial asthma and to other respiratory diseases such as
chronic sinusitis, middle ear infections, and nasal polyps. Most interestingly, a recent analysis of
people with asthma showed that those who had both allergies and asthma were much more likely

23
 to have nighttime awakening due to asthma, miss work because of asthma, and require more
powerful medications to control their symptoms.

Bronchial Asthma Triggers

Bronchial asthma triggers may include:

 Tobacco smoke
 Infections such as colds, flu, or pneumonia
 Allergens such as food, pollen, mold, dust mites, and pet dander
 Exercise
 Air pollution and toxins
 Weather, especially extreme changes in temperature
 Drugs (such as aspirin, NSAID, and beta-blockers)
 Food additives (such as MSG)
 Emotional stress and anxiety
 Singing, laughing, or crying
 Smoking, perfumes, or sprays
 Acid reflux

Signs and Symptoms of Bronchial Asthma

 Shortness of breath
 Tightness of chest
 Wheezing
 Excessive coughing or a cough that keeps you awake at night

Diagnosing Bronchial Asthma

Because asthma does not always happen at the doctor's visit, it's important for you to describe
your asthma signs and symptoms to your doctor. You might also notice when the symptoms
occur such as during exercise, with a cold, or after smelling smoke. Asthma tests may include:

24
 Spirometry: A lung function test to measure your breathing capacity and how well you
breathe. You will breathe into a device called a spirometer.
 Peak Expiratory Flow (PEF): Using a device called a peak flow meter, you forcefully
exhale into the tube to measure the force of air you can expend out of your lungs. Peak flow
monitoring can allow you to monitor your how well your asthma is doing at home.
 Chest X-Ray: Your doctor may do a chest X-ray to rule out any other diseases that may
be causing similar symptoms.

NURSING CARE

1. Place patient in a room free from noise

2. Avoid visitors and noisy relatives.
3. Alleviate patient's anxiety and exhaustion.
4. Give mild sedatives as prescribed by the doctor.
5. Use supportive devices like pillows to lie on in upright position comfortably.
6. Have positive and calm approach to patient
7. Ensure the patient to sleep well without any disturbance after an attack.
8. Educate patient and relatives to keep away the patient from precipitating factors that
triggers future attack.
9. Remove patient from allergic materials.
10. Asthmatic children should provide with best available facilities for good mental and
physical hygiene, proper rest, proper nutrition and social readjustment.
11. Control secondary infections

 encourage to eat nutritious foods

 increase fruit juices that are reach in vitamin C to increase resistance against infection
 keep patient away from those infections such as cough and colds
 educate the patient that any bluish discoloration of her skin or nails is abnormal and must
report to the physician and not ignore it

PREVENTION

25
 1. Keep away patient from which material he's sensitive and allergic. i.e. pillows, mattress,
cats

Bronchiolitis

Is an inflammation of the bronchioles that causes a thick production of mucus that occludes
bronchiole tubes and small bronchi.
 Respiratory syncytial virus is a common cause of bronchiolitis.

 Respiratory syncytial virus, although not airborne, is highly communicable is usually

transferred by the hands.

ASSESSMENT
 Upper respiratory infection symptoms such as rhinorrhea and low-grade fever.

 Lethargy, poor feeding, and irritability in infants

 Tachypnea

 increased difficulty in breathing

 Nasal flaring and retractions

 expiratory wheeze and grunt

 diminished breath sounds

PATHOPHYSIOLOGY:
Inflammation; Thick respiratory secretions accumulate, plugging the bronchiolar lumen-The
narrowing of the small airways-Trapping air in the alveoli-This trapped air causes lung
hyperinflation and may lead to atelectasis.- Inadequate gas exchange results in hypoxemia and
hypercapnia

NURSING INTERVENTIONS
 maintain a patent airway

 provide cool humidified oxygen.

26
  position the child at a 30-to-40-degree angle with the neck slightly extended.

 Encourage fluids

Burn

A burn is a type of injury to the skin caused

by heat, electricity, chemicals, light, radiation or friction. Most burns only affect the skin
(epidermal tissue and dermis). Rarely deeper tissues, such asmuscle, bone, and blood vessels can
also be injured. Managing burns is important because they are common, painful and can result in
disfiguring and disabling scarring. Burns can be complicated byshock, infection, multiple organ
dysfunction syndrome, electrolyte imbalance and respiratory distress. Large burns can be fatal,
but modern treatments, developed in the last 60 years, have significantly improved the prognosis
of such burns, especially in children and young adults.

Classification of Burns

Superficial Partial Thickness

 Similar to 1st degree

 Skin pink to red

 Outer layers of skin damaged

 Painful

 Heals without grafting

Deep partial thickness

 Similar to 2nd degree

 Skin red to white

 Blisters

 Weeping surface

27
  Edema

 All epidermis and much of dermis damaged

 Painful

 Heals without grafting

Full thickness

 Similar to 3rd degree

 Charred appearance (black, brown, leathery)

 Waxy, white

 Edema

 All layers of skin destroyed

 Nerves, muscle tissue, and bone may be destroyed

Grafting preferred

Wound Treatment

 Surgical debridement

 Fasciectomy

 Escharotomy

 Autografting

 Allograft

 Xenograft

Wound Care

 Avoid

 Cross-contamination of wounds

 Wrapping dressings too tightly around extremity

 Use

 Topicals

28
  Reduce the number of bacteria only

 Silver sulfadiazine (Silvadene)

 Slow release dressings such as Acticoat, Aquacel, Silversorb, Silverlon

Basic Nursing Care

Bed:

Turning over the patient by means of the Turning

1. Advantages

The turning bed helps in the alternate exposure of the anterior, posterior and lateral parts of the
wound surface and prevents the aggravation of infection due to prolonged pressure and
formation of bed sores. The height of the turning bed is adjustable, and the patient may be sent to
the operating room and operated upon while lying on it.
The restriction of the patient's movements will cause less suffering, and will also make the
nursing care of defecation and urination easier.

2. Procedure

Patients who are mentally clear should be relieved of their anxiety and fear. They should be
informed beforehand of the therapeutic significance and procedure in order to make then
cooperative.
The upper and lower bed frames should be locked with adequate pressure between the frames,
and soft pillows should be placed between the frames to serve as cushions in those parts where
the frames cannot be closed up tightly. Two persons are needed to turn the patient over in bed.

3. Important points to note

29
Turning over the patient in bed is contraindicated in patients with respiratory tract bum, heart
failure, or severe generalized anasarea or within the first (2-3) days of the shock phase.
The time the patient is allowed to lie in the prone position should generally be restricted to 1
hour at first; this may gradually be increased according to the patient's state of adaptation.
When an extensively burned patient is turned over into the prone position for the first time,
respiration, pulse and symptoms of anoxia should be carefully considered. Instruments and
medicine for emergency treatment should be prepared beforehand. Attention should be paid
particularly to patients with burns of the head, face and neck.
The turning bed is usually narrow in width, and patients who have psychic symptoms or who are
not cooperative should be carefully fixed, especially around the. extremities. The hand and foot
supports may also be used as protection frames to prevent the patient from falling.
Bed sores may be prevented by the use of sponge pads.

Defecation and Urination in Extensively Burned Patients

The object of nursing care of defecation and urination in extensively burned patients is to prevent
contamination of the wound surfaces by urine or faeces. Bed pans and urinals of various kinds
should be used.

Defecation

When patients with bums of the buttocks or lower extremities defecate in the supine position, the
bed pan cannot be set easily and cleaning is difficult owing to the close approximation of the
anus to the bed sheet * The patient should be trained to form the habit of defecating in the prone
position, and the part above the anus should be covered with layers of sterilized toilet paper. The
anus and perianal region should be cleaned after removing the bed pan.

Urination

In children or in patients with loss of urination contrdl a condom may be used, and it is importar
watch for any edema of the penis due to tightness - the condom. The long neck urinal can also be
used.

30
 Catheterization (Urinary Catheter)

In urinary catheterization, or "cathing" for short, a plastic tube known as a

urinary catheter that is gently slid into a patient's bladder via his or her urethra. Catheterization
allows the patient's urine to drain freely from the bladder for collection, or to inject liquids used
for treatment or diagnosis of bladder conditions. The procedure of catheterization will usually be
done by a clinician, often a nurse, although self-catheterization is possible as well.

Catheter types

Catheters come in several basic designs:

 A Foley catheter (indwelling urinary catheter)is retained by means of a balloon at the tip

which is inflated with sterile water. The balloons typically come in two different sizes: 5 cc
and 30 cc. They are commonly made in silicone rubber or natural rubber.
 A Robinson catheter is a flexible catheter used for short term drainage of urine. Unlike
the Foley catheter, it has no balloon on its tip and therefore cannot stay in place unaided.
 A Coudé catheter is designed with a curved tip that makes it easier to pass through the
curvature of the prostatic urethra.
 A hematuria (or haematuria) catheter is a type of Foley catheter used for Post-TURP
hemostasis. This is useful following endoscopic surgical procedures or in the case of gross
hematuria. There are both 2-way and 3-way hematuria catheters (double and triple lumen).
 An external Texas or condom catheter is used for incontinent males and carries a lower
risk of infection than an indwelling catheter.

31
Catheter diameters are sized by the French catheter scale (F). The most common sizes are 10 F
(3.3mm) to 28 F (9.3mm). The clinician selects a size large enough to allow free flow of urine,
and large enough to control leakage of urine around the catheter. A larger size can become
necessary when the urine is thick, bloody or contains large amounts of sediment. Larger
catheters, however, are more likely to cause damage to the urethra. Some people develop
allergies or sensitivities to latex after long-term latex catheter use making it necessary to use
silicone or Teflon types. Silver alloy coated urinary catheters may reduce infections.

Sex difference

In males, the catheter tube is inserted into the urinary tract through the penis.
A condom or Texas catheter can also be used. In females, the catheter is inserted into the urethral
meatus, after a cleansing using povidone-iodine. The procedure can be complicated in females
due to varying layouts of the genitalia (due to age, obesity, Female genital cutting, childbirth, or
other factors), but a good clinician should rely on anatomical landmarks and patience when
dealing with such a patient. In the UK it is generally accepted that cleaning the area surrounding
the urethral meatus with 0.9% sodium chloride solution is sufficient for both male and female
patients as there is no reliable evidence to suggest that the use of antiseptic agents reduces the
risk of urinary tract infection.[4]

Common indications to catheterize a patient include acute or chronic urinary retention -

(which can damage the kidneys), orthopedic procedures that may limit a patient's movement, the
need for accurate monitoring of input and output (such as in anICU), benign prostatic
hyperplasia, incontinence, and the effects of various surgical interventions involving the bladder
and prostate.

For some patients the insertion and removal of a catheter causes excruciating pain, so a
topical anesthetic is used. Catheterization should be performed as a sterile medical procedure and
should only be done by trained, qualified personnel, using equipment designed for this purpose,
except in the case of intermittent self catheterization where the patient has been trained to
perform the procedure himself or herself. If correct technique is not used there may be trauma to

32
the urethra or prostate (male), urinary tract infection, or a paraphimosis in the uncircumcised
male.

Patient Education

In reviewing recently published literature, these recommendations remain

acceptable. Handwashing remains the single most important step in preventing the spread of
infection. Health care personnel should use good handwashing principles before and after direct
patient care. Patient education is very important. This should be reinforced at each encounter.

 Daily skin care isn't needed. Studies have failed to show any benefit to the application of
antibiotic ointments or betadine to the urethral meatus. Application of oil-based
lubricants should also be avoided.

 Adequate fluid intake is necessary. 30 cc/kg of body weight is currently recommended as

adequate intake. This should allow for a daily urinary output of 1,500-2,000 cc (1-4
ml/kg/24 hour) or so; unless, individual patient health care concerns dictate otherwise.
This output serves to keep urine dilute and will help decrease catheter encrustations.

 Maintain a closed system whenever possible. If the patient changes from a leg bag to a
larger overnight bag, careful handwashing must be done, and cleaning the contact ports
with an antiseptic such as alcohol is recommended.

 The care of the collection bags must be done daily with a commercially available
product, a household bleach solution diluted in a 1:10 ratio with tap water, or a vinegar
(1 part vinegar: 3 parts water) solution. When using the bleach solution, patients need to
be cautioned to wear protective gloves, thoroughly rinse the bag and allow it to air dry
before its next use. Skin burns can occur if bleach is allowed contact with skin surfaces. 

 The bag should be emptied when 1/2 to 2/3 full or every 3 to 6 hours. This helps to
prevent undue trauma/traction on the urethra related to the weight of the bag.

Nursing Considerations

 Handwashing remains the #1 infection control practice. 

33
 No evidence supports rigid timing of catheter changing. Currently the mainstay of
practice is to change chronic catheters every 4 weeks; however, the catheter should be
changed as needed. The frequency of catheter exchange should be based on clinical
symptoms: catheter encrustations, leakage, bleeding, catheter-associated UTIs, etc. This
should be individually tailored and may be needed every 3 to 6 weeks.

 The size of the catheter should be as small as possible. This reduces urethral trauma, and
allows for adequate drainage of the peri-urethral glands.

 Use sterile water for balloon inflation per manufacturer-suggested guidelines. Typically

a 5 cc balloon is inflated with 10 cc water to allow symmetrical filling of the catheter
balloon (this allows better drainage of the bladder). Do not use saline which can
crystallize and make it difficult to remove. Do not use air which can allow it to "float" in
the bladder and result in inadequate drainage. Remember, silicone catheters may lose
fluid in the balloon over time due to permeability; therefore, assessing balloon volume is
recommended every 2 weeks and as clinically indicated. Add sterile water as needed.

 Secure the catheter to either the patient's thigh or the abdomen. This helps to decrease
the risk of bleeding, trauma, meatal necrosis, and bladder spasms from pressure and
traction.

 No evidence supports the common practice of advising patients to take supplemental

vitamin C, cranberry pills, or consuming cranberry juice. The need for adequate
hydration with resultant adequate urinary output helps to decrease the encrustations of the
catheters, stone development, and catheter-associated UTIs.

 The routine collection of urine cultures is not recommended. If the patient has a catheter-
associated UTI, the old catheter should be removed and the specimen should be collected
using sterile technique when the new catheter is placed.

 Bacterial colonization of the urethra and the bladder is inevitable. This will result in
expected "urine dip" reactivity for nitrite and possibly leukocyte reactivity. Treatment of
a "UTI" is not indicated based on the "urine dip-stick" reactivity. Some studies state that

34
 unless there are > 10 WBCs/HPF or the patient is having clinical symptoms of a catheter-
associated UTI, they should not be treated.

 Routine irrigation of long-term catheters is not indicated.

CVA (Cerebrovascular accident)

Introduction:

Cerebrovascular accident is a very serious condition in which the brain is not receiving enough
oxygen to function properly. A cerebrovascular accident is also called CVA, brain
attack, cerebral infarction or stroke.

A cerebrovascular accident often results in permanent serious complications and disability and
is a common cause of death. Cerebrovascular accidents are the second leading cause
of death worldwide and the third leading cause of death in the U.S., according to the American
Heart Association.

The brain requires a steady supply of oxygen in order to pump blood effectively to all of the
body. Oxygen is supplied to the brain in the blood that flows through arteries. In a
cerebrovascular accident, one or more of these arteries becomes blocked or ruptures or begins to
leak. This deprives a portion of the brain of vital oxygen-rich blood. This damage can become
permanent within minutes and result in the death of the affected brain tissue. This is called
cerebral necrosis.

35
There are two types of cerebrovascular accidents. An ischemic cerebrovascular accident occurs
when a brain artery has been blocked. A hemorrhagic cerebrovascular accident occurs when an
artery ruptures or leaks.

There are three primary causes of cerebrovascular accidents: cerebral thrombosis, cerebral

embolism andcerebral hemorrhage.

A cerebrovascular accident caused by a cerebral thrombosis is the result of a build-up of plaque

and inflammation in the arteries, called atherosclerosis. This process narrows the brain arteries
and lowers the amount of oxygen-rich blood that reaches the brain tissue. Arteries narrowed
byatherosclerosis are more likely to develop a blood clot that completely blocks blood flow to
an area of the brain. Risk factors for atherosclerosis include having high cholesterol, diabetes,
andhypertension.

Cerebrovascular accident cause by a cerebral embolism occurs when a clot forms in another part
of the body and travels in the bloodstream to a brain artery, blocking the flow of blood to the
brain. A cerebrovascular accident caused by cerebral hemorrhage occurs when a brain artery
breaks or leaks blood into the surrounding brain tissue.

The extent of the damage done to the brain and resulting symptoms of a cerebrovascular
accident vary depending on the type, the area or areas of the brain affected, and how much time
passes before the cerebrovascular accident is treated. Complications of cerebrovascular accident
include permanent neurological damage, disability and death. For more information on key
hallmark symptoms and other complications, refer to symptoms of cerebrovascular accident.

Risk factors for a cerebrovascular accident include a having hypertension, heart

disease, diabetes,high cholesterol and obesity. Other risk factors include being of African-
American ancestry, being male, drinking excessive amounts of alcohol, smoking and having

36
a family history of heart disease or cerebrovascular accident. Having a brain aneurysm puts a
person at an extreme risk for a hemorrhagic cerebrovascular accident.
Making a diagnosis of cerebrovascular accident includes completing a complete medical
evaluation and history and physical examination, including a neurological examination. This is
often done in an emergency room.

Diagnostic testing includes imaging tests, such as a CT or MRI and cerebral angiogram of the
brain. A cerebral angiogram is an imaging test that reveals obstructed or narrowed arteries in the
brain and can show blood flow or obstruction through the arteries of the brain.

A battery of other tests are also performed to evaluate for other conditions that commonly occur
with a cerebrovascular accident, such as heart disease and cardiac arrhythmia.

It is possible that a diagnosis of cerebrovascular accident can be missed or delayed because the
symptoms may be mild and be similar to symptoms of other conditions and diseases. If caught
early, some cerebrovascular accidents can be successfully treated before the development of
permanent brain damage and complications.

Cerebrovascular accident: Occurs when the blood supply to the brain is interrupted and results
in cell injury and death.

37
The causes of stroke

An artery to the brain may be blocked by a clot (thrombosis) which typically occurs in a blood
vessel that has previously been narrowed due to atherosclerosis ("hardening of the artery").
When a blood clot or a piece of an atherosclerotic plaque (a cholesterol and calcium deposit on
the wall of the artery) breaks loose, it can travel through the circulation and lodge in an artery of
the brain, plugging it up and stopping the flow of blood; this is referred to as an embolic stroke.
A blood clot can form in a chamber of the heart when the heart beats irregularly, as in atrial
fibrillation; such clots usually stay attached to the inner lining of the heart but they may break
off, travel through the blood stream, form a plug (embolus) in a brain artery and cause a stroke.
A cerebral hemorrhage (bleeding in the brain), as from an aneurysm (a widening and weakening)
of a blood vessel in the brain, also causes stroke.

a. Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since

blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus
itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks
off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:

 Large vessel disease involves the common and internal carotids, vertebral, and the Circle

of Willis. Diseases that may form thrombi in the large vessels include (in descending
incidence): atherosclerosis, vasoconstriction (tightening of the
artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the
blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory
vasculopathy, Moyamoya disease and fibromuscular dysplasia.
 Small vessel disease involves the smaller arteries inside the brain: branches of the circle
of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral
and basilar artery. Diseases that may form thrombi in the small vessels include (in
descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as
a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these
vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).

38
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also
lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-
cell anemia.

b. Embolic stroke

An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle
or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a
thrombus, but it can also be a number of other substances including fat (e.g. from bone
marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from
infectious endocarditis).

Because an embolus arises from elsewhere, local therapy only solves the problem temporarily.
Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in
onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is
partially resorbed and moves to a different location or dissipates altogether.

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate
from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises
through an atrial or ventricular septal defect in the heart into the brain.

Cardiac causes can be distinguished between high and low-risk:

 High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of

the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the
atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction,
chronic myocardial infarction together with ejection fraction <28 percent,
symptomatic congestive heart failure with ejection fraction <30 percent, dilated
cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis,infective
endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass
graft (CABG) surgery
 Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen
ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left
ventricular aneurysm without thrombus, isolated left atrial "smoke"

39
 on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in
the ascending aorta or proximal arch
c. Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most
commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from
reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial
effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion.
Because the reduction in blood flow is global, all parts of the brain may be affected, especially
"watershed" areas - border zone regions supplied by the major cerebral arteries. A watershed
stroke refers to the condition when blood supply to these areas is compromised. Blood flow to
these areas does not necessarily stop, but instead it may lessen to the point where brain damage
can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in
irrigation the last meadow receives the least amount of water.

d. Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which
exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic
transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[9]

e. Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension,

intracranial vascular malformations (including cavernous angiomas or arteriovenous
malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has
occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug
use (e.g. amphetamines or cocaine). The hematoma enlarges until pressure from surrounding
tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or
the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality
rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly
subarachnoid hemorrhage (which, however, also may be classified as a type of stroke).

Diagnosis

40
The diagnosis of stroke involves a medical history and a physical examination. Tests are done to
search for treatable causes of a stroke and help prevent further brain damage. A CAT scan (a
special X-ray study) of the brain is often done to show bleeding into the brain; this is treated
differently than a stroke caused by lack of blood supply. A CAT scan also can rule out some
other conditions that may mimic a stroke. A soundwave of the heart (echocardiogram) may be
done to look for a source of blood clots in the heart. Narrowing of the carotid artery (the main
artery that supplies blood to each side of the brain) in the neck can be seen with a soundwave test
called a carotid ultrasound. Blood tests are done to look for signs of inflammation which can
suggest inflamed arteries. Certain blood proteins are tested that can increase the chance of stroke
by thickening the blood.

Symptoms

Symptoms of a cerebrovascular accident differ depending on a variety of factors, including the

cause and the type and size of the area of the brain that is affected. In some cases, symptoms may
be mild and only include weakness, dizziness or headache. Symptoms such as these may also be
warning symptoms of an impending cerebrovascular accident. These symptoms can also be
symptoms of a "small stroke", more accurately called a transient ischemic attack.

Cerebrovascular accidents often do occur suddenly with dramatic symptoms, such

as numbness,weakness, and paralysis  of the face, leg or arm, or entire side of the body. There
may also be a loss of consciousness, facial drooping, slurred speech,aphasia, confusion, blurred
vision, and impaired breathing or swallowing. There may also be difficulty understanding
speech, change in vision, and incoordination. Nausea and vomiting may also occur. Serious
complications of cerebrovascular accident include long-term difficulties with such activities as
walking, talking, movement of the limbs and permanent disability. Coma and death may also
occur.

Treatments

41
Early use of anticoagulants to minimize blood clotting has value in some patients. Treatment of
blood pressure that is too high or too low may be necessary. (Lowering elevated blood pressure
into the normal range is no longer recommended during the first few days following a stroke
since this may further reduce blood flow through narrowed arteries and make the stroke worse.)
The blood sugar glucose in diabetics is often quite high after a stroke; controlling the glucose
level may minimize the size of a stroke. Drugs that can dissolve blood clots may be useful in
stroke treatment. Oxygen is given as needed. New medications that can help oxygen-starved
brain cells survive while circulation is reestablished are being developed.

Rehabilitation

When a patient is no longer acutely ill after a stroke, the aim turns to maximizing the patient's
functional abilities. This can be done in an inpatient rehabilitation hospital or in a special area of
a general hospital and in a nursing facility. The rehabilitation process can involve speech therapy
to relearn talking and swallowing, occupational therapy for regaining dexterity of the arms and
hands, physical therapy for improving strength and walking, etc. The goal is for the patient to
resume as many of their pre-stroke activities as possible.

Nursing Priorities

1. Promote adequate cerebral perfusion and oxygenation

2. Prevent/maximize complications and permanent disabilities

3. Assist patient to gain independence in ADLs.

4. Support Coping process and integration of changes into self-concept

5. Provide information about disease process/prognosis and treatmen rehabilitation

Discharge Goals

1. Cerebral function improved, neurological deficits resolving/stabilized.

2. Complications prevented or maximized.

42
 3. ADL needs met by self or with assistance of others

4. Coping with situation in positive manner, planning for the future.

5. Disease process/prognosis and therapeutic regimen understood.

Cholelithiasis
Cholelithiasis (ko-le-li-THI-ah-sis) is a condition where you have gallstones (stones in
the gallbladder). The gallbladder is a pouch-like organ located just below the liver. The
gallbladder acts as a storage area for bile. Bile is a green-colored fluid made by the liver. Bile
passes through tubes called bile ducts and is released into the intestines when you eat. Bile helps
in digesting fats and other substances. Many people may have gallbladder stones but may not
know it. Pain in the abdomen (stomach) may happen when gallstones grow big and start blocking
the bile ducts.

43
What causes cholelithiasis?
Problems with the way bile is made and excreted (emptied) from the gallbladder may cause
cholelithiasis. Bile is a balanced mixture of water, cholesterol (fat), bile salts and bilirubin
(yellow pigment). Stones may be made from different bile materials. Cholesterol stones are
formed when the bile has too much cholesterol and not enough bile salts. It is thought that liver
and blood diseases, such as hepatitis and anemia, may cause pigment stones. Gallstones may also
be formed when bile does not empty from the gallbladder as fast as it should. The following may
increase the chances of having cholelithiasis:

 Being overweight.

 Certain medicines, such as estrogen, antibiotics, and cholesterol-lowering medicines.

 Diabetes or previous surgery of the small intestines.

 Fasting (going without food) or rapid weight loss.

 Having another family member with cholelithiasis.

 Pregnancy.

44
What are the signs and symptoms of cholelithiasis?
The most common symptom of cholelithiasis is a severe, steady pain felt in the right upper
abdomen. It is usually just below the right rib cage. The pain may also be felt in the right
shoulder and between the shoulder blades. There may also be nausea (feeling sick to the
stomach) and vomiting (throwing up). These symptoms may go away on their own, only to come
back later, especially after a fatty meal. Other signs and symptoms may include:

 Jaundice (yellowing of the skin or whites of the eyes).

 Feeling bloated or having too much gas in the stomach.

 Pale colored stools (bowel movements).

 Dark colored urine.

How is cholelithiasis diagnosed?

 Blood tests: You may need blood taken for tests. The blood can be taken from a blood
vessel in your hand, arm, or the bend in your elbow. It is tested to see how your body is
doing. It can give your caregivers more information about your health condition. You
may need to have blood drawn more than once.

 ERCP: ERCP is also called endoscopic retrograde cholangiopancreatography. This test is

done during an endoscopy to find stones, tumors, or other problems. Dye is put into the
endoscopy tube. The dye helps your pancreas and bile ducts show up better on x-rays.
People who are allergic to shellfish (lobster, crab, or shrimp) may be allergic to this dye.
Tell your caregiver if you are allergic to shellfish, dyes, or any medicines. If you have
stones, they may be removed during ERCP.

 Liver and gallbladder scan: This test may also be called a HIDA scan. This is a test to
look at your liver and gallbladder. You are given a small amount of radioactive dye in
your IV. Pictures are then taken by a special scanner that can "see" the dye in your body.
Caregivers look at the pictures to see if your liver and gallbladder are working normally.

45
  Oral cholecystography: Oral cholecystography is a test to look at your gallbladder and its
ducts (passages). You are given pills to swallow that have a special dye in them. Then, x-
rays are taken over time. The dye makes your gallbladder and its ducts show up on the x-
rays. This may make it easier for your caregiver to see any stones or swelling in your
gallbladder. Some people may be allergic to the kind of dye used in the pills. Tell
caregivers if you are allergic to dye or shellfish (crab, lobster, or shrimp). It is also very
important to tell your caregiver if there is any chance you could be pregnant. Your
caregiver will tell you what you can and cannot eat before the test. It is important to
follow your caregiver's instructions or the test may not work.

 Abdominal ultrasound: An abdominal ultrasound is a test that is done to see inside your
abdomen. Sound waves are used to show pictures of your abdomen on a TV-like screen.

How is cholelithiasis treated?

 Surgical treatment: Surgery is often needed to treat cholelithiasis. This may be done by

any of the following procedures:

o Open cholecystectomy: Open cholecystectomy is surgery to remove your

gallbladder through an incision (cut) under your right rib cage. Ask your caregiver
for more information about open cholecystectomy.

o Laparoscopic cholecystectomy: This procedure uses a laparoscope to take out the

gallbladder. A laparoscope is a thin, lighted tube with a camera at the tip. Small
incisions are made in the abdomen, where the laparoscope and other surgical
instruments are inserted. Ask your caregiver for more information about
laparoscopic cholecystectomy.

 Non-surgical treatment: When surgery cannot be done, you may have any of the
following treatments:

46
 o Lithotripsy: During lithotripsy, shock waves are used to break apart stones in your
gallbladder, kidney, or other areas. You may be placed in a water bath or on a
water-filled cushion. You may be given medicine to make you drowsy before the
procedure. Shock waves are sent through the water and toward the stone or
stones. The stones may break apart when the shock waves hit them. Pieces of the
stones may then pass out of your body when you use the toilet. A lithotripsy,
though seldom used, is an option that may be used in selected patients.

o Oral dissolution therapy: These are medicines that can melt small cholesterol
gallstones. Ask your caregiver for more information about using oral dissolution
therapy for cholelithiasis.

Diet:

 Eat a variety of healthy foods every day. Your diet should include fruits, vegetables,
breads, dairy products, and protein (such as chicken, fish, and beans). Eating healthy
foods may help you feel better and have more energy.

 Ask your caregiver if you should be on a special diet. You may be told to eat foods that
are low in fat or cholesterol. You may also be told to limit the amount of salt you eat.
Special cookbooks can make it easier to plan low fat and low salt meals.

 Weighing too much can make your heart work harder and can cause serious health
problems. Talk to your caregiver about a weight loss plan if you are overweight.

Exercise:

Exercising makes the heart stronger, lowers blood pressure, and helps keep you healthy. It is best
to start exercising slowly and do more as you get stronger. Talk to your caregiver before you
start exercising. Together you can plan the best exercise program for you.

47
Nursing Implication

1. Before the procedure the patient should be given an explanation of the procedure and
his/her role in it

2. Patient takes nothing my mouth for at least 8 hours before the procedure.

3. Moderate sedation is used, and the sedated patient must be monitored closely

4. The nurse observe closely for signs of respiratory and central nervous system depression,
hypotension, oversedation and vomiting.

5. During ERCP, the nurse monitors IV fluids, administers medication and positions the
patient.

6. The nurse also monitors the patient for side effects of any medication received during the
procedure and for the return of the gag reflex and cough reflex after the use of local
anesthetics.

Chronic Kidney Disease

Definition

Chronic kidney failure occurs when disease or dis- order damages the kidneys so that
they can no longer adequately remove fluids and wastes from the body or maintain proper levels
of kidney-regulated chemicals in the bloodstream.

48
Description

Chronic kidney failure, also known as chronic renal failure, affects over 250,000
Americans annually. It may be caused by a number of diseases and inherited disorders, but the
progression (end result) of chronic kidney failure is always the same. The kidneys, which serve
as the body's natural filtration system, gradually lose their ability to remove fluids and waste
products (urea) from the bloodstream. They also fail to regulate certain chemicals in the
bloodstream and allow protein to leak into the urine. Chronic kidney failure is irreversible and
eventually leads to total kidney failure, known as end-stage renal disease (ESRD). Without
treatment and intervention to remove wastes and fluids from the bloodstream, ESRD is
inevitably fatal.

Causes and symptoms

Kidney failure is caused by acquired disease or hereditary disorders in the kidneys. The four
most common causes of chronic kidney failure include:

 Diabetes. Diabetes mellitus (DM), both insulin dependant (IDDM) and non-insulin

dependant (NIDDM), occurs when the body cannot produce and/or use insulin, the
hormone necessary for the body to process glucose. Long-term diabetes may cause the
glomeruli, the filtering units located in the nephrons of the kidneys, to gradually lose
function.
 Hypertension. High blood pressure is both a cause and a result of kidney failure. The
kidneys can become stressed and ultimately sustain permanent damage
from bloodpushing through them at excessive pressures over long periods of time.
 Glomerulonephritis. Glomerulonephritis is an inflammation of the glomeruli, or filtering
units of the kidney. Certain types of glomerulonephritis are treatable, and may only cause
a temporary disruption of kidney functioning.
 Polycystic kidney disease. Polycystic kidney disease is an inherited disorder that causes
cysts to form in the kidneys. These cysts impair the regular functioning of the kidney.

49
Less common causes of chronic kidney failure include kidney cancer, obstructions such askidney
stones, pyelonephritis, reflux nephropathy, systemic lupus erythematosus, amyloidosis, sickle
cell anemia, Alport syndrome, and oxalosis.

Initially, symptoms of chronic kidney failure develop slowly. Even individuals with mild to
moderate kidney failure may have few symptoms in spite of increased urea in their blood.
Among signs and symptoms that may be present at this point are frequent urination during the
night and high blood pressure.

Most symptoms of chronic kidney failure are not apparent until kidney disease has progressed
significant- ly. Common symptoms include:

 Anemia. The kidneys are responsible for the production of erythropoietin (EPO), a
hormone that stimulates red cell production. If kidney disease causes shrinking of the
kidney, this red cell production is hampered.
 Bad breath or a bad taste in mouth. Urea in the saliva may cause an ammonia-like taste in
the mouth.
 Bone and joint problems. The kidneys produce vitamin D, which aids in the absorption
ofcalcium and keeps bones strong. In patients with kidney failure, bones may become
brittle, and in children, normal growth may be stunted. Joint pain may also occur as a
result of unchecked phosphate levels in the blood.
 Edema. Puffiness or swelling around the eyes and legs.
 Frequent urination.
 Foamy or bloody urine. Protein in the urine may cause it to foam significantly. Blood in
the urine may indicate bleeding from diseased or obstructed kidneys, bladder, or ureters.
 Headaches. High blood pressure may trigger headaches.
 Hypertension, or high blood pressure. The retention of fluids and sodium causes blood
volume to increase, which, in turn, causes blood pressure to rise.
 Increased fatigue. Toxic substances in the blood and the presence of anemia may cause
feelings of exhaustion.

50
  Itching. Phosphorus, which is typically eliminated in the urine, accumulates in the blood
of patients with kidney failure. This heightened phosphorus level may cause itching of
the skin.
 Low back pain. Pain where the kidneys are located, in the small of the back below the
ribs.
 Nausea, loss of appetite, and vomiting. Urea in the gastric juices may cause
upsetstomach. This can lead to malnutrition and weight loss.

Diagnosis

Kidney failure is typically diagnosed and treated by a nephrologist, a physician

specializing in kidney dis- ease. The patient suspected of having chronic kidney failure will
undergo an extensive blood work-up, usually performed by a laboratory technologist or
technician. Blood tests will assess the levels of creatinine, blood urea nitrogen (BUN), uric acid,
phosphate, sodium, and potassium in the blood. Urine samples will also be collected, usually
over a 24-hour period, to assess protein loss.

Uncovering the cause of kidney failure is critical to proper treatment. A full assessment
of the kidneys is necessary to determine if the underlying disease is treatable and if the kidney
failure is chronic or acute. X ray, MRI, computed tomography scan, ultrasound, renal biopsy,
and/or arteriogram of the kidneys may be employed to determine the cause of kidney failure and
level of remaining kidney function. X rays and ultrasound of the bladder and/or ureters may also
be taken. Most imaging studies are performed by radiology technicians.

Treatment

Chronic kidney failure is an irreversible condition. Hemodialysis, peritoneal dialysis, or

kidney transplantation must be employed to replace the lost function of the kidneys if the failure
progresses to ESRD. In addition, dietary changes and treatment to relieve specific symptoms
such as anemia and high blood pressure are critical to the treatment process.

Hemodialysis

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 Hemodialysis is the most frequently prescribed type of dialysis treatment in the United
States. Most hemodialysis patients require treatment three times a week, for an average of three
to four hours per dialysis "run" depending on the type of dialyzer used and their current physical
condition. The treatment involves circulating the patient's blood outside of the body through an
extracorporeal circuit (ECC), or dialysis circuit. The dialysis circuit consists of plastic blood
tubing, a two-compartment filter known as a dialyzer, or artificial kidney, and a dialysis machine
that monitors and maintains blood flow and administers dialysate, a chemical bath used to draw
waste products out of the blood. The patient's blood leaves and enters the body through two
needles inserted into the patient's vein, called an access site, and is pushed through the blood
compartment of the dialyzer. Once the patient's blood is inside the dialyzer, excess fluids and
toxins are pulled out of the bloodstream and into the dialysate compartment, where they are
carried out of the body. At the same time, electrolytes and other chemicals in the dialysate
solution move from the dialysate into the bloodstream. The purified, chemically balanced blood
is then returned to the body. Specially trained nurses and dialysis technicians supervise and
monitor patients during treatment.

Peritoneal dialysis

In peritoneal dialysis (PD), the peritoneum, (lining of the abdomen) acts as a blood filter.
A catheter is surgically inserted into the patient's abdomen. During treatment, the catheter is used
to fill the abdominal cavity with liquid dialysate. Waste products and excess fluids move from
the patient's bloodstream into the dialysate solution. After a waiting period of 6 to 24 hours,
depending on the treatment method used, the waste-filled dialysate is drained from the abdomen,
and replaced with clean dialysate. There are three types of peritoneal dialysis, which vary by
treatment time and administration method: continuous ambulatory peritoneal dialysis (CAPD),
continuous cyclic peritoneal dialysis (CCPD), and intermittent peritoneal dialysis (IPD).

Kidney transplantation

Kidney transplantation involves surgically implanting a functioning kidney, known as a

graft, from a brain dead organ donor (a cadaver transplant), or from a living donor, to a patient

52
with ESRD. Patients with chronic renal disease who need a transplant and do not have a living
donor register with UNOS (United Network for Organ Sharing), the federal organ procurement
agency. UNOS places patients on a waiting list for a cadaver kidney transplant. Kidney
availability is based on the patient's health status. When the new kidney is transplanted, the
patient's diseased kidneys may or may not be removed, depending on the circumstances
surrounding the kidney failure. A regimen of immunosuppressive (anti-rejection) medication is
required after transplantation surgery.

Dietary management

A diet low in sodium, potassium, and phosphorous, three substances that healthy kidneys
excrete, is critical in managing kidney disease. Other dietary restrictions, such as a reduction in
protein, may be prescribed depending on the cause of kidney failure and the type of dialysis
treatment employed. Patients with chronic kidney failure also need to limit their fluid intake.
Patients may receive instruction about appropriate dietary measures from registered dietitians,
nutritionists, nurses, or health educators.

Medications and dietary supplements

Kidney failure patients with hypertension typically take medication to control their high
blood pressure. Epoetin alfa, or EPO (Epogen), a hormone therapy, and intravenous or
oral ironsupplements are used to manage anemia, especially if the kidneys have been surgically
removed. A multivitamin may be prescribed to replace vitamins lost during dialysis treatments.
Vitamin D, which promotes the absorption of calcium, along with calcium supplements, may
also be prescribed.

Since 1973, Medicare has reimbursed up to 80% of ESRD treatment costs, including the

costs of dialysis and transplantation as well as the costs of some medications. To qualify for
benefits, a patient must be insured or eligible for benefits under Social Security, or be a spouse or
child of an eligible American. Private insurance and state Medicaid programs often cover the
remaining 20% of treatment costs.

53
Prognosis

Early diagnosis and treatment of kidney failure is critical to improving length and quality
of life in chronic kidney failure patients. Patient outcome varies; it depends on the cause of
chronic kidney failure and the method chosen to treat it. Overall, patients with chronic kidney
disease leading to ESRD have a shortened life span. According to the United States Renal Data
System (USRDS), the life span of an ESRD patient is 18-47% of the life span of the age-sex-race
matched general population. ESRD patients on dialysis have a life span that is 16-37% of the
general population.

The demand for kidneys to transplant continues to exceed supply. Cadaver kidney
transplants have a 50% chance of functioning nine years, and living donor kidneys that are well-
matched (have two matching antigen pairs) have a 50% chance of functioning for 24 years.
However, some transplant grafts have functioned for more than 30 years.

Health care team roles

Patients with chronic kidney failure are treated by a team that includes nephrologists,
dialysis technicians, nurses, radiology technicians, and laboratory technicians. Patients
undergoing kidney transplant are cared for by a transplant team headed by a transplant surgeon.
Registered dietitians, nutritionists, and nurses instruct patients about dietary changes to manage
their disease.

54
55
Diet for

RENAL DIET MANAGEMENT

 
The use of nutrition therapy aims to retard progression of the kidney disease. It is to afford
rest to the organ and to minimize uremic toxicity.

Diet and meal plan is computed based on the treatment plan for each patient. Allowances
for specific food and nutrient intake varies depending on the stage of the renal disease.
There are differences in the diet requirement of patients with dialysis/renal replacement
therapy (Hemodialysis and Peritoneal Dialysis), without dialysis called pre-dialysis diet
and for patients who underwent kidney transplantation.

Nutrients commonly modified in the renal diet are the daily intake of

 Protein
 Sodium and potassium
 Calcium and Phosphorus
 Fluid and water intake

NUTRITION AND RENAL DISEASE

 
 Eat just enough protein. Excess intake of protein would lead to the accumulation
of waste products like urea, creatinine and uric acid in the blood. Consumption of
white meat (chicken, fish and eggs) is better than the intake of red meat (pork and
beef). Avoid concentrated foods like organ meats, kare-kare, laing and processed
foods.
 Phosphorus level in the blood increases as kidney function declines, therefore, it is
important to avoid foods high in this nutrient, such as: 
o Excess intake of milk, cheese and other dairy products
o Legumes like beans and mongo beans
o Chocolate and cocoa
o Pinipig, peanuts and pili nuts

56
 High levels of phosphorus causes skin itchiness and disturbances in the bone and
calcium metabolism in the body. Doctors prescribe phosphate binders to correct
levels of phophorus in the blood.
 Avoid salty foods and condiments (bagoong, dried fish, salted egg, chips, soy
sauce, fish sauce, vetsin, broth cubes). Excess sodium in the diet could cause high
blood pressure and edema.
 Eat only the recommended amount of fruits and vegetables especially if you are on
hemodialysis. High levels of potassium in the blood causes irregular heartbeat,
palpitation and worse could lead to cardiac arrest.
 Drink the right amount of water or follow what is prescribed by your doctor.
Avoid excess intake of fluids especially when there is edema or oliguria.
 Eat enough carbohydrates and fats for daily energy source of the body. Fat can be
eaten in allowed amount, through frying and sautéing of foods. To avoid increases
in the blood cholesterol levels, buy and use vegetable and plant oil sources.
 Avoid eating of simple sugars and sweets (cakes, candies, chocolate bars) if you
have diabetes. These foods can increase your blood glucose level and may create
another problem.

KIDNEY TRANSPLANT DIET

 
The diet for renal transplantation is to provide adequate calories and protein to
counteract the catabolic effect of surgery during the early post transplant period
and to manage the nutritional side-effect of immunosuppressive drugs.

 Nutrition after kidney transplantation is given a well-balanced diet. This means

that it contains foods from all food groups-egg, meat, fish, chicken, milk, cheese,
fruits, vegetables, cereals, sugars. Initially, during the first month after
transplantation, the patient is advised short-term dietary management. This may
expedite wound healing, muscle growth and development and prevent drug-
induced diabetes commonly observed after transplantation. However diet-related
complication that may lead to organ rejection. Therefore, the following nutritional
guidelines are recommended.

57
Short-Term Management (During the first month after transplantation)

 Adequate protein intake to replace further protein breakdown due to high

doses of steroid. Good protein food sources are meat, fish, poultry, egg,
milk and milk products.
 Eat small amount of simple sugars: honey, jams, jelly, candy, softdrinks,
cakes and sweet desserts.
 Limit intake of salt, seasonings and processed foods to prevent increase in
blood pressure and fluid retention.

Long –Term Nutritional Management

 Lower protein intake as steroid dosage is reduced.

 Eat less fat and cholesterol to reduce the risk of developing heart disease
and increase in body weight.
 Continue limiting intake of simple sugars and salty condiments and high-
sodium containing foods.
 Mineral and vitamin supplements may be taken as allowed by the
physician

 Other renal diets commonly used in kidney disease management are:

Low Phosphorus

Foods rich in protein are also rich in phosphorus. Thus, restricting protein also
restricts phosphorus in the diet.

Foods to be avoided:

 Cheese
 Chocolate
 Cocoa

58
  Fish, dried
 Legumes
o Chick peas
o Munggo
o Sitaw
o Kadyos
 Corn
 Milk
 Oatmeal
 Meats
o Bacon
o Beef
o Chicken
o Heart
o Kidney
 Nuts-peanuts
 Pinipig
 Kalabasa
 Misua

Low Calcium Diet

 This diet is advised to patients with calcium oxalate renal stones. It is designed to
minimize the concentration of the components associated in the formation of renal
stones.

Examples of foods high in calcium: green leafy vegetables like “malunggay” and
“saluyot,” calcium-fortified fruit juices and other beverages, too much intake of
milk and dairy products, dried beans, sardines and anchovies.

59
 Low Oxalate Diet 

An oxalate-restricted diet is indicated for individuals with calcium oxalate renal

stones. The dietary modification is designed to minimize its concentration in the
urine associated with its formation. A regular or general diet is provided with
avoidance of foods known to be high in oxalate.

Examples of foods high in oxalate: Chocolate (beverages and drinks, candies and
bars), soy beans and products, strawberries, ripe tamarind, green leafy vegetables,
celery, eggplant, wheat germ/bran, cassava, sweet potato, white corn, all nuts and
products, tea and draft beer.

Low Potassium Diet 

Potassium is an essential mineral needed by the body for normal nerve

transmission and muscle contraction, including the normal beating of the heart. 

A low potassium diet is prescribed for people with renal disease, hyperkalemia or
Addison’s disease in which the potassium in the blood is high. Low level should
be less than 2 grams per day since the usual intake from foods is 2-6 grams per
day.

Foods to be avoided are the following:

 green leafy vegetables such as malunggay, spinach, talbos ng

kamote and sili
 fruits such as banana, orange, buco, siniguelas, lanzones, melon and dried
fruits
 wheat and wheat products such as oatmeal, misua and wheat bread
 crabs
 legumes and beans

60
  coconut milk
 chocolates (bars, candies, beverages)
 molasses
 cola drinks

Low Protein

This diet provides 30-40 grams protein per day only, 2/3 of the amount is derived
from intake of meat, fish and eggs (high biological value protein) and the
remaining 1/3 coming from rice, sugar, fats and vegetables (low biological value
protein). 

It aims to prevent or minimize muscle and tissue breakdown, hence sufficient

calories are provided with liberal use of carbohydrates and fats. 

Too little protein, the person develops malnutrition. Too much protein, the blood
urea rises. For people with renal insufficiency, restricting protein may help protect
the remaining nephrons.

The diet follows the regular menu selection except that intake of protein is limited.
Foods restricted are internal organs, dried fish, viands cooked with coconut milk,
beans and legumes, high sodium containing canned meats and milk in excess
amount.

Low Purine

A low purine diet restricts the amount of purine to only 150 mg per day. The low
purine diet diet is prescribed as an adjunct to drug therapy for gout, arthritis and
other disorders affecting purine metabolism. It is also recommended for people
with uric acid stone. Daily consumption of water should be increased since this
helps in eliminating uric acid. A high intake of carbohydrates also favors uric acid
secretion while a high fat intake favors its retention.

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Food to be Avoided:

 Internal organs (Pork, Chicken, Beef)

o Liver
o Lung
o Kidney
o Tongue
o Heart
o Small and large intestines
 Fishes
o Tulingan
o Tanigue
o Dilis (Anchovies)
o Alumahan
o Matang Baka
o Tamban
o Tunsoy
 Shellfish
o Halaan
o Tahong
o Talaba
 Legumes and dried beans
o Chick peas
o Lima beans
o Mungo bean
o Sitaw
o Garbanzos

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 Chronic Renal Insufficiency

What is renal insufficiency?

Renal insufficiency, also called renal failure, is when your kidneys no longer have enough
kidney function to maintain a normal state of health. Note that the term renal failure is beginning
to be replaced by renal insufficiency when in the context of chronic kidney disease. There are
two kinds.

Acute renal failure (ARF).

This is kidney failure that happens rather suddenly, where something has caused the
kidneys to shutdown. This may be due to infection, drugs (prescription, over-the-counter,
recreational), traumatic injury, major surgery, nephrotoxic poisons, etc. Emergency dialysis may
be needed until the situation resolves and the kidneys begin functioning again (this might take a
short time, or months, or it might be permanent). While more acute episodes are possible in the
case of IgAN (we often refer to them as "flare-ups"), IgA nephropathy is a condition that mainly
causes chronic renal insufficiency (CRI), not usually acute renal failure (ARF). However, some
people may experience spontaneously-reversing acute renal failure as well. The latter are cases
where serum creatinine goes up dramatically but later returns to a more normal baseline. In such
cases, dialysis may be needed until the condition improves. ARF in the context of IgAN is
usually more associated with the person developing a flare-up of HSP.

63
Chronic renal insufficiency (CRI). 

This is when a disease such as IgA nephropathy slowly and gradually destroys the
filtering capacity of the kidneys. It is sometimes referred to as progressive renal insufficiency,
chronic kidney disease or chronic renal failure (CRF). This kind of damage cannot currently be
repaired, and as such, it is irreversible. A person may have chronic renal failure for many years,
even decades, before dialysis or a kidney transplant become necessary. Chronic renal
insufficiency does not, by itself, mean complete shutdown of the kidneys, and a person with
chronic renal insufficiency may still pass urine normally, and may have more than enough
kidney function left for normal functioning of the body. Note that you cannot judge the

64
efficiency of your kidneys by the amount of urine you produce. People with quite advanced renal
insufficiency, and even people on dialysis may still produce a fair amount of urine. But this does
not mean that the kidneys are filtering waste nor regulating serum electrolyte levels efficiently.

Chronic renal insufficiency itself causes more loss of kidney function.

One important aspect of kidney disease is that, once a kidney is damaged by it to a certain
degree, it continues to deteriorate even if the underlying kidney disease can or could be cured.
This is commonly referred to as the point of no return (PNR).What happens is that the chronic
renal insufficiency (CRI) continues to progress on its own, scarring of the glomeruli continues,
and kidney function continues to gradually decline. It's possible that controlling blood pressure
with an ACE inhibitor like ramipril, or an angiotensin II receptor blocker like Cozaar or Avapro
may slow this progression of chronic renal insufficiency. There is also beginning to be some
evidence that the class of anti-cholesterol drugs called "statins" (like Lipitor, for example) may
help slow progression of CRI. The point of no return is generally considered to be when serum
creatinine reaches 2.0 mg/dl in U.S. measurements, or about 175 umol/L in international SI
measurement.

End-stage renal disease.

As chronic renal insufficiency continues and progresses, the person may eventually
reach the point where it is considered to be end-stage renal disease (ESRD).

65
 Colostomy Care

What is a colostomy?

 A colostomy is an opening that is made in the colon with surgery. After the opening is
made, the colon is brought to the surface of the abdomen to allow stools to leave your
body. The opening at the surface of the abdomen is called a stoma. The stool leaves the
colon through the stoma and drains into a flat, changeable, watertight bag or pouch. The
pouch is attached to the skin with an adhesive (substance that seals the pouch to the skin).

 A colostomy is sometimes needed for certain health conditions or diseases. Some of these
include cancer, diverticular disease, Crohn's disease and trauma or injury. A temporary
colostomy may be needed to allow the colon to rest and heal for a period of time. A
temporary colostomy may be in place for weeks, months, or years. The temporary
colostomy will eventually be closed and bowel movements will return to normal. A
permanent colostomy is usually needed when a part of the colon must be removed or
cannot be used again.

Where is the colon located?

The colon is part of the digestive system. The digestive system consists of the parts of the
body that are involved in the digestion (breakdown) of food. Food moves from your stomach to
the small intestine where food is digested and nutrients are absorbed. The food then goes to the
colon (part of the large intestine). The colon absorbs water from digested food and turns the
digested food into stool.

66
What are the different types of colostomies?

Colostomy types are related to the place on the colon where the surgery is done. The location of
the surgery depends on your health condition and the reason you need to have a colostomy.

 Ascending colostomy: This colostomy has a stoma (opening) that is located on the right
side of the abdomen. The output (stool) that drains from this stoma is in liquid form.

 Transverse colostomy: This colostomy has a stoma that is located in the upper abdomen
towards the middle or right side. The output that drains from this stoma may be loose or
soft.

 Descending or sigmoid colostomy: This colostomy has a stoma that is located on the

lower left side of the abdomen. The output that drains from this stoma is firm.

What types of products are used for colostomies?

 Pouch: There are a variety of sizes and styles of colostomy pouches. Pouches are
lightweight and odor-proof. Pouches have a special covering that prevents the pouch
from sticking to the body. Some pouches also have charcoal filters which release gas

67
 slowly and help to decrease gas odor. The following is general information about types of
colostomy pouches:

o Open-ended pouch: This type of pouch allows you to open the bottom of the
pouch to drain the output. The open end is usually closed with a clamp. The open-
ended pouch is usually used by people with ascending or transverse colostomies.
The output from these colostomies is looser and is unpredictable (does not drain
at regular times).

o Close-ended pouch: This type of pouch is removed and thrown away when the
pouch is filled. Close-ended pouches are usually used by people with a
descending or sigmoid colostomy. The output from these types of colostomies is
firm and does not need to be drained .

o One-piece: A one-piece pouch contains the pouch and adhesive skin barrier
together as one unit. The adhesive skin barrier is the part of the pouch system that
is placed around the stoma and attached to skin. When the pouch is removed and
replaced with a new one, the new pouch must be reattached to the skin.

o Two-piece: The two-piece pouch has two parts: an adhesive flange and pouch.
The adhesive flange stays in place while the pouch is removed and new pouch is
attached to the flange. The pouch does not need to be reattached to the skin each
time. The two-piece system can be helpful for patients with sensitive skin.

o Pre-cut or cut-to-fit pouches: Some pouches have pre-cut holes so you do not

have to cut the opening yourself. Other pouches can be cut to fit the size and
shape of your stoma. Cut-to-fit pouches are especially useful right after your
surgery because your stoma decreases in size for about eight weeks.
 Stoma covers and caps: Stoma caps or covers can be placed on the stoma when the stoma
is not active (draining). People with descending or sigmoid colostomies who irrigate may
use stoma covers or caps. The cover or cap is attached to the skin in the same way as a
pouch.

68
  Skin protection:

o Film: A film can be placed on the skin to protect against damage from the
adhesive material. Films are helpful for people with sensitive, dry, or oily skin.

o Pectin-based paste or paste strips/rings: These products are helpful for protecting

skin against output that contains digestive enzymes (proteins that break down
foods). Ascending or transverse colostomies can produce output that contains
digestive enzymes, which can irritate or damage the skin. The paste is also used to
create a flat pouch surface by filling in small skin creases.

Preparation

The nurse should instruct the patient and caregiver(s) about the procedure before it is performed.
Many people feel anxious and nervous when first dealing with an ostomy. Encourage the patient
to ask questions, and explain all steps as they are performed.

Aftercare

The nurse should assess the patient's tolerance of the procedure and response to teaching or
education about the appliance.

Health care team roles

Although most members of the health care team will come into contact with patients having
ostomies, it is the nurse who has the responsibility for providing ostomy care and instructing the
patient and/or caregiver how to provide care independently. An enterostomal therapy (ET) nurse
is specially educated in all aspects of ostomy care.

69
 Dehydration

Definition

Dehydration is the excessive loss of water from body tissues accompanied by an

imbalance in essential electrolytes, such as sodium, potassium, and chloride.

Description

Dehydration occurs when the body loses more fluid than it takes in. Dehydration can be
caused by illness, injury, infection, prolonged exposure to sun or high temperatures, inadequate
water intake, or overuse of diuretics or other medications that increase urination.

Water is distributed throughout three compartments in the body: inside the cells
(intracellular), in the tissue (interstitial), and in the bloodstream (intravascular). Each
compartment contains differing amounts of electrolytes that must remain in balance in order for
body organs and systems to function correctly. Dehydration upsets this delicate balance. Total
body water also varies in relation to age, gender, and amount of body fat. Adult males have
approximately 60% water content, adult females have 50%, infants have an estimated 77%, and
the elderly have 46% to 52%. An increase in body fat causes a decrease in the percent fluid
content because fat does not contain significant amounts of water.

Causes and symptoms

Different types of dehydration have different causes. When managing patients with
dehydration, the type of water loss must be determined to ensure appropriate treatment. In
addition, water and sodium levels in the body are closely related; if one is abnormal, the other
often is too.

Isotonic dehydration is an equal loss of water and sodium. Isotonic means that the
number of particles contained on one side of a permeable membrane is the same as on the other

70
side, thus there is no fluid shift in either direction. The amount of intracellular and extracellular
water remains in balance. This can be caused by a complete fast, vomiting, and diarrhea.

Hypertonic dehydration occurs when water loss is greater than sodium

loss. Blood sodium levels may be >145 mmol/l (normal range=135 to 145 mmol/l). Higher blood
sodium levels combined with decreased water in the intravascular space increases the osmotic
pressure in the bloodstream, which, in turn, pulls more fluid out of the cells. This type of
dehydration is usually caused by extended fever with limited oral rehydration. Mortality is more
likely to occur from hypertonic than from isotonic dehydration.

Hypotonic dehydration occurs when sodium loss is greater than water loss. Blood sodium
levels may be less than 135 mmol/l; and the osmotic pressure is greater inside the cells, which
pulls more fluid out of the intravascular space into the intracellular space. This type of
dehydration occurs with overuse of diuretics, which causes excessive sodium and potassium loss.
Potassium depletion affects respiration, increases nausea, and, if severe enough, may cause
respiratory arrest or central nervous system (CNS) seizures. Potassium depletion may also cause
arrhythmias (an alteration in the heartbeat). As a result, patients are told to take diuretics with
orange juice or to eat a banana, both of which are high in potassium.

Strenuous activity, excessive sweating, prolonged time in the sun, and extended vomiting
or diarrhea cause fluid loss. Elderly people who move to warm, dry climates frequently become
dehydrated because of the climate change combined with a tendency to not drink enough water.
Large amounts of fluid can also be lost from prolonged fever. Healthy people require about 1
milliliter of water for each calorie their body metabolizes; but during a fever the metabolic rate
increases by seven percent for each 1°F rise in body temperature. Fever also increases the
respiratory rate, resulting in additional water loss from the lungs. Further causes of fluid loss that
may be overlooked include caffeine and alcohol consumption, which increase urination and fluid
excretion.

Decreased oral intake of fluids is a common cause of dehydration and often occurs during
times of appetite loss from illness or after oral surgery or injury. The elderly are at high risk for
decreased intake because their thirst mechanism may no longer function or they may be

71
physically unable to get a drink. Infants, another high-risk group, are more likely to develop
dehydration than adults because they have a higher metabolic rate and their
immaturekidneys have difficulty concentrating urine. Children who do not wet their diapers for
three hours or more are dehydrated. Dehydration is also associated with disorders of the adrenal
glands, which regulate water-electrolyte balance; diabetes mellitus; eating disorders; renal
disease; and chronic lung disease.

Symptoms of dehydration at any age may include some or all of the following: cracked
lips, dry or sticky mucous membranes, sunken eyes, lethargy, and/or confusion. Urine output is
minimal and the skin loses its elasticity (turgor) and is slow to return to its normal position after
being raised off the back of the hand (tenting). The heart rate and respiratory rate may be
elevated. A dehydrated infant may not shed tears when crying and may have a depressed fontanel
(soft spot on their head), although recent studies have shown that a depressed fontanel is not an
accurate indicator of dehydration.

Diagnosis

The general diagnosis of dehydration can be made based on the patient's symptoms and
medical history. Physical examination may reveal any of the symptoms mentioned above, along
with shock, rapid heart rate, and low blood pressure. Blood tests are required to determine what
deficiency exists (or what is elevated) so that therapy for electrolyte replacement can be planned.
Blood tests to check electrolyte levels and urine tests such as urine specific gravity are used to
evaluate the severity of the fluid loss. Other laboratory tests may be ordered to determine if an
underlying condition (e.g., diabetes or an adrenal gland disorder) is the cause.

Treatment

Increased fluid intake and replacement of lost electrolytes are usually sufficient to
restorefluid balance in patients who are mildly or moderately dehydrated. For individuals who
are mildly dehydrated, just drinking plain water may be all the treatment that is needed. Adults
may replace lost electrolytes by drinking sports beverages, such as Gatorade or Recharge.
Parents should follow label instructions when giving children Pedialyte or other commercial

72
products recommended for the treatment of dehydration in children. Children who are
dehydrated should be given only clear fluids for the first 24 hours.

A child who is vomiting should sip one or two teaspoons of liquid every 10 minutes. A
child who is less than a year old and who is not vomiting should be given one tablespoon of
liquid every 20 minutes. A child who is more than one year old and who is not vomiting should
take two tablespoons of liquid every 30 minutes. A baby who is being breast-fed should be given
clear liquids for two consecutive feedings before breastfeeding is resumed. A bottle-fed baby
should be given formula diluted with water to half the formula strength for the first 24 hours
after symptoms of dehydration are identified.

To calculate fluid loss accurately, weight changes should be charted every day and a
record kept of how many times a patient vomits or has diarrhea. A record of fluid output
(including sputum or vomit) and of fluid intake or replacement should be kept for at least 24 to
48 hours to see if balance is being accomplished. Parents should note how many times a baby's
diaper must be changed. If dehydration continues, emergency department treatment or
hospitalization to receive intravenous fluids and electrolytes may be necessary.

Children and adults can gradually return to their normal diet after they have stopped
vomiting and no longer have diarrhea. Gelatin is often a welcomed substitute for additional water
and does count as fluid replacement. Bland foods should be reintroduced first, with other foods
added as the digestive system is able to tolerate them. Milk, ice cream, cheese, and butter should
not be eaten until 72 hours after symptoms have disappeared.

When treating dehydration, the underlying cause must be addressed. For example, if
dehydration is caused by vomiting or diarrhea, medications should be prescribed to resolve these
symptoms. Patients who are dehydrated due to diabetes, kidney disease, or adrenal gland
disorders must receive treatment for these conditions as well as for the resulting dehydration. If
dehydration is being caused by diuretics. a dose adjustment made by the physician or a change to
a different diuretic may be necessary.

73
Prognosis

Mild dehydration rarely results in complications. If the cause is eliminated and lost fluid
is replaced, mild dehydration can usually be resolved in 24 to 48 hours. Vomiting and diarrhea
that continue for several days without adequate fluid replacement can be fatal since more is lost
than water and sodium. Severe potassium loss may lead to cardiac arrhythmias, respiratory
distress or arrest, or convulsions (seizures). The risk of life-threatening complications is greater
for young children and the elderly. However, dehydration that is rapidly recognized and treated
has a good outcome.

Health care team roles

The nurse and the physician have the greatest responsibility in recognizing and treating
dehydration. For hospitalized patients, the physician should order appropriate fluid and
electrolyte replacement and the nurse should ensure that the correct fluids are given to the
patient. The nurse should monitor the patient for signs that the dehydration (e.g., decrease in
fever, increase in blood pressure, reduced heart rate) is resolving and should notify the physician
if it is not.

Blood tests used to diagnose dehydration are collected by specially trained nursing
assistants or by laboratory technicians. Outpatient samples in a physician's office may be taken
by the nurse or a technician. In some institutions, the nurse collects the blood sample. Usually,
urine samples are collected by the nurse, and results calculated by the laboratory technician.

Prevention

Patients who are vomiting or who have diarrhea can prevent dehydration by drinking
enough fluid to keep their urine the color of pale straw. Infants and young children with diarrhea
and vomiting can be given electrolyte solutions such as Pedialyte to help prevent dehydration, as
well as suppository medication to stop the vomiting. People who are not ill can maintain proper
fluid balance by drinking several glasses of water before going outside on a hot day. It is also a
good idea to avoid coffee and tea, which increase body temperature and water loss.

74
 Patients should ask a pharmacist whether or not any medications they are taking may
cause dehydration and what to do to prevent it other than adequate fluid intake. Prompt medical
attention should be sought to correct any underlying condition that increases the risk of
dehydration.

Dengue hemorrhagic fever

Dengue hemorrhagic fever is a severe, potentially deadly infection spread by certain

species of mosquitoes (Aedes aegypti).

Causes

Four different dengue viruses are known to cause dengue hemorrhagic fever. Dengue
hemorrhagic fever occurs when a person catches a different type dengue virus after being
infected by another one sometime before. Priorimmunity to a different dengue virus type plays
an important role in this severe disease.

Worldwide, more than 100 million cases of dengue fever occur every year. A small
number of these develop into dengue hemorrhagic fever. Most infections in the United States are
brought in from other countries. It is possible for a traveler who has returned to the United States
to pass the infection to someone who has not traveled.

Risk factors for dengue hemorrhagic fever include having antibodies to dengue virus
from prior infection and being younger than 12, female, or Caucasian.

Symptoms

Early symptoms of dengue hemorrhagic fever are similar to those of dengue fever, but
after several days the patient becomes irritable, restless, and sweaty. These symptoms are
followed by a shock -like state.

Bleeding may appear as tiny spots of blood on the skin (petechiae) and larger patches of
blood under the skin (ecchymoses). Minor injuries may cause bleeding.

75
Shock may cause death. If the patient survives, recovery begins after a one-day crisis period.

Early symptoms include:

 Decreased appetite
 Fever
 Headache
 Joint aches
 Malaise
 Muscle aches
 Vomiting

Acute phase symptoms include:

 Restlessness followed by:

o Ecchymosis
o Generalized rash
o Petechiae
o Worsening of earlier symptoms
 Shock-like state
o Cold, clammy extremities
o Sweatiness (diaphoretic)

Treatment

Because Dengue hemorrhagic fever is caused by a virus for which there is no known cure or
vaccine, the only treatment is to treat the symptoms.

 A transfusion of fresh blood or platelets can correct bleeding problems

 Intravenous (IV) fluids and electrolytes are also used to correct electrolyte imbalances
 Oxygen therapy may be needed to treat abnormally low blood oxygen
 Rehydration with intravenous (IV) fluids is often necessary to treat dehydration
 Supportive care in an intensive care unit/environment

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Possible Complications

 Encephalopathy
 Liver damage
 Residual brain damage
 Seizures
 Shock

Nursing Management

Nursing management of dengue fever is non-specific and supportive, consisting of pain

relief and oral and/or intravenous administration of fluids. Dengue patient care requires vigilant
medical monitoring for warning signs of the potentially fatal vascular permeability of dengue
hemorrhagic fever (DHF) and life-threatening circulatory failure defining dengue shock
syndrome (DSS).

Nursing management of dengue fever also requires monitoring patients for signs of
altered consciousness, confusion and other neurological implications. Watch for lethargy,
seizures, nuchal rigidity, and paresis. Neurological involvement and intense, sustained abdominal
pain with vomiting often signal development of more severe dengue hemorrhagic fever (DHF).
Relief from fever and a sudden onset of hypothermia accompanied by restlessness and mental
changes often precede onset of dengue hemorrhagic shock syndrome

77
 Diabetes Mellitus

Diabetes mellitus, often simply referred to as diabetes—is a condition in which a person has
high blood sugar, either because the body does not produce enough insulin, or because cells do
not respond to the insulin that is produced. This high blood sugar produces the classical
symptoms of polyuria (frequent urination), polydipsia (increased thirst)
and polyphagia(increased hunger).

There are three main types of diabetes:

 Type 1 diabetes: results from the body's failure to produce insulin, and presently requires
the person to inject insulin.
 Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use
insulin properly, sometimes combined with an absolute insulin deficiency.
 Gestational diabetes: is when pregnant women, who have never had diabetes before, have
a high blood glucose level during pregnancy. It may precede development of type 2 DM.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of
insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of
glucocorticoids, and several forms of monogenic diabetes.

All forms of diabetes have been treatable since insulin became available in 1921, and type 2
diabetes may be controlled with medications. Both type 1 and 2 are chronic conditions that
usually cannot be cured. Pancreas transplants have been tried with limited success in type 1
DM; gastric bypass surgery has been successful in many with morbid obesity and type 2 DM.
Gestational diabetes usually resolves after delivery. Diabetes without proper treatments can

78
cause many complications. Acute complications include hypoglycemia, diabetic ketoacidosis,
or nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular
disease, chronic renal failure, retinal damage. Adequate treatment of diabetes is thus important,
as well as blood pressure control and lifestyle factors such as smoking cessation and maintaining
a healthy body weight.

As of 2000 at least 171 million people worldwide suffer from diabetes, or 2.8% of the
population.[2] Type 2 diabetes is by far the most common, affecting 90 to 95% of the U.S.
diabetes population.[3]

Definition

The term diabetes, without qualification, usually refers to diabetes mellitus, which roughly
translates to excessive sweet urine (known as "glycosuria"). Several rare conditions are also
named diabetes. The most common of these is diabetes insipidus in which large amounts of urine
are produced (polyuria), which is not sweet (insipidus meaning "without taste" in Latin).

The term "type 1 diabetes" has replaced several former terms, including childhood-onset
diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term
"type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-
related diabetes, and non-insulin-dependent diabetes mellitus (NIDDM). Beyond these two
types, there is no agreed-upon standard nomenclature. Various sources have defined "type 3
diabetes" as: gestational diabetes, insulin-resistant type 1 diabetes (or "double diabetes"), type 2
diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of
adults (or LADA or "type 1.5" diabetes)

Classification

Type 1 diabetes

Diabetes mellitus type 1

Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets

of Langerhans in the pancreas leading to insulin deficiency. This type of diabetes can be further
classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-
mediated nature, where beta cell loss is a T-cell mediated autoimmune attack. There is no known

79
preventive measure against type 1 diabetes, which causes approximately 10% of diabetes
mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a
healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal,
especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally
termed "juvenile diabetes" because it represents a majority of the diabetes cases in children.

Type 2 diabetes

Type 2 diabetes mellitus is characterized by insulin resistance which may be combined with

relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is
believed to involve the insulin receptor. However, the specific defects are not known. Diabetes
mellitus due to a known defect are classified separately. Type 2 diabetes is the most common
type.

In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity.
At this stage hyperglycemia can be reversed by a variety of measures and medications that
improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses,
the impairment of insulin secretion occurs, and therapeutic replacement of insulin may
sometimes become necessary in certain patients.

Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a
combination of relatively inadequate insulin secretion and responsiveness. It occurs in about
2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is
fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–
50% of affected women develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus
or mother. Risks to the baby includemacrosomia (high birth weight), congenital cardiac and
central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin
may inhibit fetal surfactant production and cause respiratory distress
syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases,
perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular
impairment.Labor induction may be indicated with decreased placental function. A cesarean

80
section may be performed if there is marked fetal distress or an increased risk of injury
associated with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that more American women are entering pregnancy
with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled
in the past 6 years.[7] This is particularly problematic as diabetes raises the risk of complications
during pregnancy, as well as increasing the potential that the children of diabetic mothers will
also become diabetic in the future.

Other types

Pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher
than normal but not high enough for a diagnosis of type 2 diabetes. Many people destined to
develop type 2 diabetes spend many years in a state of pre-diabetes which has been termed
"America's largest healthcare epidemic."

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even
when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very
uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell
function. Abnormal insulin action may also have been genetically determined in some cases.
Any disease that causes extensive damage to the pancreas may lead to diabetes (for
example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion
of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the
hormone excess is removed). Many drugs impair insulin secretion and some toxins damage
pancreatic beta cells.

Signs and symptoms

The classical symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst)

and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1
diabetes while in type 2 diabetes they usually develop much more slowly and may be subtle or
absent.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of
the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually
returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes

81
diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with
type 2 change is generally more gradual, but should still be suspected.

People (usually with type 1 diabetes) may also present with diabetic ketoacidosis, a state of
metabolic dysregulation characterized by the smell of acetone; a rapid, deep breathing known
asKussmaul breathing; nausea; vomiting and abdominal pain; and an altered states of
consciousness.

A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in
type 2 diabetes and is mainly the result of dehydration. Often, the patient has been drinking
extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water
loss.

A number of skin rashes can occur in diabetes that are collectively known as diabetic
dermadromes.

Causes

The cause of diabetes depends on the type. Type 2 diabetes is due primarily to lifestyle factors
and genetics.

Type 1 diabetes is also partly inherited and then triggered by certain infections, with some
evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility
to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic
"self" identifiers relied upon by the immune system). However, even in those who have inherited
the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.

Medications

Oral medications
Insulin

Type 1 treatments usually include combinations of regular or NPH insulin, and/or synthetic
insulin analogs.

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 Nursing Management

Nurses are key educators in the fight against diabetes. Newly diagnosed patients have an
enormous amount of knowledge they must adjust to and learn to keep them healthy.
Understanding is important in regards to what the disease is and the ramifications of what
incorrect management of the disease may do for their overall health. As health care
professionals, nurses are important educational resources for patients and their families.

Understanding Diabetes

1.
Diabetes is a metabolic disorder affecting the way our bodies use food as energy. When we eat,
food is broken down and converted into glucose. As the food undergoes digestion, it flows into
the blood and is used for growth and muscular energy in the form of sugar. Glucose is unable to
enter the cells without the presence of the hormone called insulin. Insulin is made by the
pancreas and is released in response to the level of glucose found in the body to help monitor and
maintain normal blood sugar levels. A person with diabetes has too much glucose (sugar) in
their blood because the pancreas is not producing the right amount of insulin.

Monitoring Blood Glucose

2.

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 Blood glucose  monitoring is an extremely important issue for diabetic patients because
administration of medications, such as insulin, are based on the blood glucose value. Testing is
done using a blood glucose monitor and small lancets. The finger is pricked using the small
lancet, and a drop of blood is placed on a small test strip and inserted into the meter. Within a
few moments, the glucose level will display on the meter and any dosing of medications may
then take place based on that value.
Dietary Modifications

3.
A nutritionist or dietitian can help diabetic patients map and plan their dietary needs by teaching
them about the types of foods that can exacerbate and even elevate the blood glucose level and,
how food can also affect their medication usage. Many foods have an adverse effect on insulin
production, and dietary education is important for a new patient to understand how to manage
diabetes nutritionally.
Managing Insulin

4.
Insulin must be stored in a refrigerator and should be removed from the cold at least 20 minutes
before administration. Insulin dosage should be measured carefully as this hormone can have
seriously detrimental effects on the patient if given erroneously. When administering insulin, a
short small bored needle is utilized and the injection is given subcutaneously just under the skin.
The injection sites should be rotated daily to assure adequate absorption. Insulin bottles should
be labeled with the date that they were opened to make sure they are not utilized past their
expiration dates.

84
 Adjusting Blood Pressure

5.
Because high blood pressure is a risk with diabetic patients, it is important to educate patients to
monitor their blood pressure and adhere to any medication regimen prescribed by their physician.
Stressing the importance of exercise and diet as part of their blood pressure control program will
decrease their risk of strokes, heart attacks and other vascular related conditions.
Keep Eye on Eyes

6.
When blood sugar is elevated for any length of time, eye damage can occur causing diabetic
retinopathy. All newly diagnosed diabetics should have an eye screening done within three
months of the diagnosis of diabetes and every year thereafter.
Importance of Foot Care

7.
People affected by diabetes often have nerve damage or neuropathy. Neuropathy can cause the
loss of feeling in one or both of the feet, and is characterized by poor flow of blood to those feet.
Teaching the patient to have proper skin and nail care will help to avoid these conditions.

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 Dislocation of Bones

A dislocation is a separation of two bones where they meet at a joint. (Joints are areas where two
bones come together.) A dislocated bone is no longer in its normal position, which may result in
damage to ligaments, nerves, and blood vessels.

Considerations
It may be hard to tell a dislocated bone from a broken bone. Both are emergency situations and
require the same first aid treatment.

Most dislocations can be treated in a physician's office or in the emergency room. You may be
given medicine to make you sleepy. Sometimes general anesthesia in the operating room is
needed.

Most dislocations, if treated early, will not result in permanent injury.

• Injuries to the surrounding ligaments generally take 3 - 6 weeks to heal. Sometimes,

surgery to repair a torn ligament is needed.
• Injuries to nerves and blood vessels may result in more long-term or permanent problems.

Once a joint has been dislocated, it is more likely to happen again. Follow-up with an orthopedic
surgeon is recommended after a dislocation.

Causes
Dislocations are usually caused by a sudden impact to the joint. This usually occurs following a
blow, fall, or other trauma.

Symptoms
A dislocated joint may be:

• Accompanied by numbness or tingling at the joint or beyond it

• Intensely painful, especially if you try to use the joint or bear weight on it
• Limited in movement
• Swollen or bruised
• Visibly out of place, discolored, or misshapen

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Nursemaid's elbow is a partial dislocation common in toddlers. The main symptom is refusal to
use the arm. Nursemaid's elbow can be easily treated in a doctor's office.

First Aid
1. Call Emergency before you begin treating someone who may have a dislocation,
especially if the accident causing the injury may be life-threatening.
2. If there has been a serious injury, check the person's airway, breathing, and circulation. If
necessary, begin rescue breathing, CPR, or bleeding control.
3. Do not move the person if you think that the head, back, or leg has been injured. Keep the
person still. Provide reassurance.
4. If the skin is broken, take steps to prevent infection. Do not blow on the wound. Rinse the
area gently to remove obvious dirt, but do not scrub or probe. Cover the area with sterile
dressings before immobilizing the injury.
5. Splint or sling the injury in the position in which you found it. Do not move the joint. Be
sure to immobilize the area above and below the injured joint.
6. Check the person's blood circulation around the injury by pressing firmly on the skin in
the affected area. It should blanch white, then regain color within a couple of seconds.
Avoid this step if the skin has been broken, to reduce the risk of infection.
7. Apply ice packs to ease pain and swelling.
8. Take steps to prevent shock. Unless there is a head, leg, or back injury, lay the victim flat,
elevate the feet about 12 inches, and cover the person with a coat or blanket.

DO NOT
• Do NOT move the person unless the injury has been completely immobilized.
• Do NOT move a person with an injured hip, pelvis, or upper leg unless it is absolutely
necessary. If you are the only rescuer and the person must be moved, drag him or her by
the clothing.
• Do NOT attempt to straighten a misshapen bone or joint or to change its position.
• Do NOT test a misshapen bone or joint for loss of function.
• Do NOT give the person anything by mouth.

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Prevention
Preventing injuries in children:

• Create a safe environment around your home.

• Pay careful attention to preventing falls by gating stairways and keeping windows closed
and locked.
• Supervise children carefully. There is no substitute for close supervision no matter how
safe the environment or situation appears to be.
• Teach children how to be safe and look out for themselves.

Preventing dislocations in adults:

• Avoid falls by not standing on chairs, countertops, or other unstable objects.

• Eliminate throw rugs, especially for the elderly.
• Wear protective gear when participating in contact sports.

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 Edema

Edema, is swelling caused by fluid retention - excess fluid is trapped in the body's tissues. In the
UK/Ireland/Australasia and some other countries the word is spelled oedema. Swelling caused
by edema commonly occurs in the hands, arms, ankles, legs and feet. It is usually linked to the
venous or lymphatic systems. Edema was formerly known as dropsy or hydropsy.

Edema may be generalized or local. It can appear suddenly, but usually develops subtly - the
patient may first gain weight, or wake up with puffy eyes. Many patients wait until symptoms are
well advanced before seeking medical help.

The English word "edema" comes from the Greek wordoidema, meaning "a swelling tumor",
which is derived from the Greek verb oidein meaning "to swell". 

It is estimated that approximately 4.4 million people in USA have edema. 

There are many types of edema. The most common ones are:

 Peripheral edema - in the feet (pedal edema), ankles, legs, hands and arms.
 Cerebral edema - in and around the brain (cerebral edema).
 Eye edema - in and around the eyes, e.g. macular edema, corneal edema, periorbital
edema (puffiness around the eys. Macular edema is a serious complication of diabetic
retinopathy. The CDC (Centers for Disease Control and Prevention) estimates that the number
of cases of diabetic retinopathy will triple from 5.5 million in 2005 to 16 million in 2050.

What causes edema?

If the capillaries (tiny blood vessels) leak fluid into the surrounding tissue the area will start to
swell. This could be due to capillary damage or increased pressure. 

Leaking capillaries will cause the kidneys to accumulate higher than normal quantities of sodium
(salt) and water in order to compensate for the capillary fluid loss. This results in more blood
circulating in the body, which in turn causes even more capillary leakage into the surrounding

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 tissue, which produces additional swelling - a vicious cycle. 

Edema is most commonly caused by:

 Physical inactivity - edema is more prevalent among people who do not exercise at all, and
walk very little.
 Standing or sitting still for long - if you stand or sit still for a long time there is a much higher
chance of swelling.
 Genes - researchers in Spain identified the genes that cause blindness produced by corneal
edema.
 Surgery - there is usually some swelling after a surgical procedure.
 High altitudes - especially when combined with physical exertion. Acute mountain sickness
can lead to high altitude pulmonary edema or high altitude cerebral edema.
 Heat - especially when combined with physical exertion. During high temperatures the body
is less efficient at removing fluid from tissues, especially around the ankles.
 Burns - the skin reacts to a burn by retaining fluid, causing localized swelling.
 Pregnancy - during pregnancy the woman releases hormones which encourage the body to
retain fluids. Pregnant women tend to retain much more sodium and water than women who
are not pregnant. When a woman is pregnant her face will typically swell, as will her hands,
lower limbs and feet. 

When the woman is resting in a reclined position the enlarged uterus occasionally compresses
the inferior vena cava, causing obstruction of both femoral veins, leading to edema. 

A pregnant woman's blood is hypercoaguble (clots more easily), raising the risk of deep
venous thrombosis (DVT), a cause of edema. Eclampsia, which results from pregnancy-
induced hypertension (high blood pressure), can also cause edema.
 Menstruation and pre-menstruation - hormone levels fluctuate during the menstrual cycle.
During the days before menstrual bleeding there will be a reduction in the levels of the
hormone progesterone, which may cause fluid retention.

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 The contraceptive pill - any medication that includes estrogen can cause fluid retention. It is
not uncommon for women to put on weight when they first go on the pill.
 Menopause - around the period of the menopause as well as after it, hormone fluctuations can
cause fluid retention. Hormone replacement therapy after the menopause can also cause
edema.
 Certain medications - such as vasodilators (drugs that open blood vessels), calcium channel
blockers, NSAIDs (non-steroidal anti-inflammatory drugs), estrogens, several chemotherapy
drugs, and some diabetes drugs, such as thiazolidinediones. 
 Excessive salt intake - this is especially the case for people who are susceptible to developing
edema.
 Malnutrition and/or bad diet - dietitians say low consumption of thiamine (vitamin B1), as
well as insufficient vitamins B6 and B5 may contribute toward fluid retention. Low levels of
albumin levels may also play a part - low albumin levels can also be caused by kidney disease.

Edema can also be caused by the following diseases:

 Kidney disease/damage - patients with kidney disease may not be able to eliminate
enough fluid and sodium from the blood. This results in more pressure on the blood vessels,
which causes some of the liquid to leak out. Kidney disease patients with edema will generally
have swelling around their legs and eyes. 

Damage to the capillaries in the kidneys (glomeruli) that filter waste and excess fluids from
the blood can result in nephrotic syndrome. Among the many symptoms of nephrotic
syndrome is an insufficient level of blood albumin, which leads to edema.
 Heart failure - this is when the heart cannot pump blood properly to all parts of the body.
If one or both of the lower chambers of the heart lose the ability to pump blood effectively, the
blood can accumulate in the limbs, causing edema.
 Chronic lung disease - this includes many lung diseases, such as asthma, chronic
bronchitis, COPD, emphysema, pulmonary fibrosis and sarcoidosis. Some patients may
experience an accumulation of fluids in the lungs - pulmonary edema.

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 Liver disease - such as cirrhosis, which causes scarring of the liver. This affects liver
function, which causes the secretion of hormones and fluid-regulating chemicals to change.
People with cirrhosis of the liver also have increased pressure within the portal vein - a large
vein that carries blood from the intestines, spleen and pancreas into the liver. The problems
can lead to fluid retention in the legs and ascites (abdominal cavity).
 Diabetes - a patient with diabetes may have edema for several different reasons, including
cardiovascular disease and its complications, acute renal failure, acute liver failure, protein
losing enteropathy (disease of the intestine causing protein loss), and some medications.
Diabetic macular edema is the swelling of the retina in diabetes.
 Allergies - some foods and insect bites may cause edema in susceptible people.
 Arthritis - people with arthritis most commonly have swelling in the ankles, feet, legs,
and calves - peripheral edema. Arthritis may cause swelling for many reasons, for example,
sporadic ankle swelling in rheumatoid arthritis is common and occurs mainly as a result of
active inflammatory synovitis (inflammation of the synovial membrane, the lining of the
joint).
 Thyroid disease - people with a disorder of the thyroid gland commonly experience
edema.
 Brain tumor - a brain tumor will accumulate water around itself, especially as it builds
new blood vessels.
 Head injury - a blow to the head may result in an accumulation of fluids in the brain or
between the brain and the skull.

Edema in the leg is most commonly caused by:

 A blood clot - any blockage, such as a clot in one of the veins can impede the flow of
blood. This causes an increase in pressure in the vein, which may result in leakage of fluids
into the surrounding tissue, causing edema.
 Varicose veins - these often accompany symptoms of edema. Varicose veins usually
occur because valves become damaged; static pressure increases, resulting in the bulging
veins. The static pressure also increases the risk of leakage of fluids into the surrounding
tissue.

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 Infection/inflammation - the lymph nodes may swell in response to infection.
 A cyst/growth/tumor - edema can causes cysts, which can then cause more edema. Any
lump can cause edema for a number of reasons. The lump may press against a vein causing a
build-up of pressure in that vein, which may result in fluids leaking into surrounding tissue.
The lymph nodes may react to a tumor and swell.
 Lymphedema - the lymphatic system helps get rid of excess fluid from tissues. If this
system is damaged the lymph nodes and lymph vessels which continually drain an area may
not work as they should, it could result in edema. 

If the damage is due to lymphedema it is called primary lymphedema, if it is caused by a

disease or medical condition, such as an infection or cancer, it is caused secondary
lymphedema.

What are the symptoms of edema?

Symptoms will mainly depend on the underlying cause. The following refer to generalized
edema:

 Swelling of the skin.

 Skin may be stretched and shiny.
 The skin may retain a dimple after being pressed for about ten seconds.
 Puffiness of the ankles, face or eyes.
 Aching body parts.
 Stiff joints.
 Weight gain.
 Weight loss.
 Hand and neck veins are fuller.
 Raised pulse rate.
 Hypertension - raised blood pressure.
 Ascites - increased abdominal size.

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 What is the diagnosis of edema?

 Medical history.
 Current state of health.
 How long the signs and symptoms have existed.
 How permanent or intermittent the signs and symptoms are.
 Whether the patient has had edema before.

 A chest X-ray
 Blood tests
 Urine tests
 Liver function tests
 Heart function tests

What is the treatment for edema?

 Diuretics
These are drugs that raise the rate of urination, providing a means of forced dieresis. Diuresis
is the increased production of urine by the kidney. There are several types of diuretics - they
increase the excretion of water from the body in various different ways. Diuretics are not
suitable if the patient is pregnant, or has chronic venous insufficiency (weakened valves in the
veins of the legs). 

Many medications appear to cause pedal edema (foot edema), especially estrogens,
vasodilators, NSAIDS, and calcium channel blockers. Most edemas caused by medications are
the types that are caused by high blood pressure in the capillaries. For these patients diuretics
are not an effective treatment. Physicians report that angiotensin-converting enzyme inhibitors
and angiotensin-receptor blockers give better results.
 Antiangiogenesis therapy (controlling blood vessel growth)
The beneficial effects of anti-angiogenesis drugs in the treatment of the glioblastomas (deadly

94
 brain tumors) appear to result primarily from reduction of edema, researchers at the
Massachusetts General Hospital reported.
 Oxygen therapy

Oxygen delivered through the nose may improve poor vision caused by diabetic macular
edema, say researchers at Johns Hopkins.

The following self-care techniques which may help resolve the fluid retention problem:

 Cut down salt consumption.

 If the patient is overweight, to lose weight.
 Do regular exercise.
 Raise the legs several times per day to improve circulation.
 Wear supporting stockings.
 Not to sit/stand still for too long.
 Get up and walk about regularly when travelling by car, train, boat or plane.
 Avoid extremes of temperature, such as hot baths, showers, and saunas. Dress warmly if
it is cold.
 Massage - if the affected area is stroked firmly in the direction of the heart it may help
move the fluid. It is important that the hand movements do not cause pain. A qualified
masseuse or physical therapist will know how to do this more effectively.

What are the complications of edema?

Edema is usually caused by an underlying disease or condition. If that condition is not treated,
the health consequences could be serious. Untreated edema can cause:

 Painful swelling. The pain can gradually get worse.

 Walking difficulty.
 Stiffness.
 Awkward gait.
 Skin can become stretched, itchy and bothersome.

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 The swollen area is more likely to become infected.
 Scarring may occur between the layers of tissue.
 Poor blood circulation.
 Arteries, veins, and joints may lose their elasticity.
 Ulcerations of the skin.

Goiter

I. Epidemiology
A. Endemic in areas distant from sea (eg. mountains)
1. Common sites: Alps, Andes, and Himalayas
2. Related to deficient iodine intake
3. Often occurs before puberty
B. Sporadic form much more common in women (8:1)
1. Adolescent girls
2. Pregnant, Lactating or Menopausal women

II. Criteria
A. Diffuse Thyroid enlargement without nodularity
B. Euthyroid function

III. Causes
A. Idiopathic (Sporadic)
B. Iodine Deficiency (Endemic Goiter)
C. Goitrogens (Thyroid Suppressants)
1. Calcium and fluorides in water

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 2. Cabbage
3. Cassava
4. Cauliflower
5. Brussels sprouts
6. Turnips

IV. Symptoms
A. Often asymptomatic
B. Thyroid sensitive to touch
C. Dyspnea
D. Dysphagia
E. Cough with large glands

V. Signs
A. Palpable diffuse Thyroid Enlargement
B. No Thyroid Nodularity

VI. Management
A. Early Goiter
1. Iodine replacement results in goiter regression
B. Late Goiter
1. Thyroid Replacement Required

VII. Prevention
A. Iodized salt in diet

VIII. Prevention
A. If untreated, develops into Multinodular Goiter

Multinodular Goiter

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I. Causes
A. Simple Goiter develops into multinodular Goiter

II. Types
A. Non-Toxic multinodular Goiter
B. Toxic Multinodular Goiter (50%)
1. Results in Thyrotoxicosis

III. Differential Diagnosis

A. Thyroid Cancer

IV. Symptoms
A. Dysphagia
B. Choking Sensation

V. Signs
A. Markedly enlarged nodular Thyroid
B. Stridor

VI. Complications
A. Toxic multinodular Goiter (Thyrotoxicosis)
1. Cardiovascular complications
a. Artirial Fibrillation
b. Tachycardia
c. Congestive Heart Failure
2. No Opthalmopathy (Proptosis and stare)
3. No Dermopathy
B. Both Toxic and Non-Toxic multinodular Goiter
1. Superior Vena Cava Syndrome
a. Results from throracic outlet obstruction

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Nursing management for goiter and multinodular goiter

1. Assist the client and his family in exploring treatment options

2. Promote adequate rest. Encourage a calm environment conductive to rest and

relaxation. Minimize client’s energy expenditure by assisting with activities as
necessary and encouraging the client to alternate periods of activity with rest.

3. Promote adequate nutrition. Monitor nutritional status. Provide increased

calories and other nutritional support needed.

4. Prevent injury. Assess the client’s mental status and decision-making ability;
intervene as needed to ensure safety. Provide eye protection for a client with
exophthalmos: patches, drops, and artificial tears. Instruct the client regarding
the use of these items.

5. Maintain normothermia. Reduce the client’s body temperature with cooling

mattress and acetaminophen. Avoid aspirin, which may displace thyroid
hormone from its carrier protein and increase hormone levels. Supply
sufficient fluids to offset losses from diaphoresis. Provide appropriate comfort
measures for the febrile client.

6. Provide client and family teachings

7. Provide post-operative care.

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 IgA Nephropathy

What is IgA nephropathy?

IgA nephropathy is a kidney disorder that occurs when IgA—a protein that helps the
body fight infections—settles in the kidneys. After many years, the IgA deposits may cause the
kidneys to leak blood and sometimes protein in the urine.

Many people with IgA nephropathy leak blood in the urine, but this leakage does not
mean they will have long-term problems. Others leak both blood and protein in the urine. If too
much protein leaks into the urine, the hands and feet can swell. After 10 to 20 years with IgA
nephropathy, the kidneys may show signs of damage. About 25 percent of adults with IgA
nephropathy develop total kidney failure. Only 5 to 10 percent of children develop total kidney
failure. Symptoms of kidney failure include swelling in the hands and feet, nausea, fatigue,
headaches, and sleep problems. By the time these symptoms occur, total kidney failure is near.
Total kidney failure means the kidney damage is permanent. People with kidney failure need
dialysis or a kidney transplant.

How do people know that they have IgA nephropathy?

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 In the early stages, IgA nephropathy has no symptoms. This disease can be silent for
years, even decades. The first sign of IgA nephropathy may be blood in the urine. The blood may
appear during a cold, sore throat, or other infection. At times, blood in the urine can only be
detected by a doctor or nurse using special tests. If the amount of blood increases, urine may turn
pink or the color of tea or cola. People who have blood in their urine should see a doctor or
nurse, but the condition is not always a sign of a serious disease. For example, heavy exercise
can cause blood in the urine.

Who is at risk for IgA nephropathy?

IgA nephropathy can occur at any age, even in childhood. More men are affected than
women. Although found all over the world, IgA nephropathy is more common among
Caucasians and Asians. It is one of the most common diseases of the kidney, other than those
caused by diabetes or high blood pressure.

What causes IgA nephropathy?

Scientists do not know what causes IgA deposits to form in the kidneys. IgA nephropathy
may run in families or be related to respiratory infections. No consistent trigger for the disease
has been found.

How is IgA nephropathy diagnosed?

A urine test called urinalysis usually provides the first clues. In a urinalysis, the doctor or
nurse dips a special strip with chemicals into the urine sample. The strip changes color when
blood or protein is present in the urine. If the test strip is positive, the urine will then be
examined with a microscope to look for red blood cells. The red blood cells may be clumped
together to form little tubes. These tubes are called casts because they are formed or molded
inside the kidneys’ tiny draining structures. If casts are found, it usually means the kidney filters
are damaged.

Blood tests measure the waste products in the blood that the kidneys usually get rid of. Two
examples are creatinine and blood urea nitrogen (BUN). If the BUN and creatinine levels are

101
high, it means the kidneys are not working well. If the creatinine level is high at the time of
diagnosis, the patient is more likely to develop kidney failure.

If there is kidney damage, the doctor will probably recommend a kidney biopsy. In this
procedure, a needle is used to retrieve a small piece of kidney tissue for examination with
different microscopes. Only a biopsy can show the IgA deposits in the kidney filters. The biopsy
can also tell how much kidney damage has already occurred. The biopsy results can help the
doctor determine the best treatment. Once a diagnosis of IgA nephropathy is established, a
person should have regular blood tests to monitor kidney function.

How is IgA nephropathy treated?

Kidney disease usually cannot be cured. When the kidneys are damaged, they cannot be
repaired. Treatment focuses on slowing the disease and preventing complications.

One complication is high blood pressure, also called hypertension. Hypertension damages the
kidneys. Two types of blood pressure medicines called angiotensin-converting enzyme (ACE)
inhibitors and angiotensin receptor blockers (ARBs) protect kidney function. These medicines
not only lower blood pressure but also decrease the loss of protein into the urine. Because of this
effect, they are often used in IgA nephropathy to protect the kidneys. They are good medicines
but have certain side effects. Pregnant women should not take ACE inhibitors or ARBs because
they can damage the unborn baby.

People with IgA nephropathy may develop high cholesterol. By watching their diet and taking
medicine, they can help lower their cholesterol level. Lowering cholesterol may help slow
kidney damage.

Medicines such as prednisone may help treat IgA nephropathy. Prednisone belongs to a class of
medicines called corticosteroids, which can have harmful side effects. In research studies, fish oil
supplements containing omega 3 fatty acids also slowed kidney damage in some patients.

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 Vitamin E may help lower protein in the urine but not blood. One of the newer
immunosuppressive agents called mycophenolate mofetil (MMF) is also being tested in treating
IgA nephropathy

Management of chronic renal failure related to IgA nephropathy

 Erythropoietin agonists - for management of anaemia associated with chronic renal

failure
 Phosphate binders - for management of hyperphosphatemia in chronic renal failure
 Calcium supplements - for hypocalcaemia associated with chronic renal failure
 Calcitriol and other Vitamin D supplements - for hypocalcaemia and
hyperparathyroidism associated with chronic renal failure
 Sodium bicarbonate - for acid-base disturbance
 Diuretics - may be used in situation of volume overload
 Renal dialysis - used when there are manifestations of uraemia and the GFR is <
10mL/min

Head Injury

I. Pathophysiology
A. Intracranial Pressure (ICP) association with injury
1. Note measurements are in mmHg, not cmH2O
2. Normal: 10 mmHg ICP
3. Abnormal: 20 mmHg ICP
4. Severe: 40 mmHg ICP
5. Herniation: 50 mmHg ICP
B. Crushing’s Response
1. Hypertensive response in face of increased ICP
2. Helps maintain cerebral perfusion
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 3. Do not use antihypertensives to lower Blood Pressure
a. Result in decreased brain perfusion

II. Assessment
A. Glasgow Coma Scale
B. Pupil Exam
C. Neurologic Exam
D. Alcohol or drug intake history
E. Hypotension seen in pediatric closed head injury
F. Signs Skull Fracture
1. Vault skull Fracture
2. Basilar skull Fracture
a. CSF Rhinorrhea or Otorrhea
b. Hemotympanum
c. Post-auricular Bruising (Battle’s Sign)
d. Orbital Bruising (Raccoon’s Eyes)
e. CN VII palsy (Bell’s Palsy)
G. Signs Intracranial Injury
1. Focal
a. Epidural Hemorrhage
b. Subdural Hemorrhage
c. Intracerebral Hemorrhage
2. Diffuse
a. Mild Concussion
b. Classic Concussion
c. Diffuse axonal injury

III. Causes
A. Idiopathic (Sporadic)
B. Iodine Deficiency (Endemic Goiter)
C. Goitrogens (Thyroid Suppressants)

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 1. Calcium and fluorides in water
2. Cabbage
3. Cassava
4. Cauliflower
5. Brussels sprouts

Nursing Management

1. Assest neurologic and respiratory status to monitor for sign of increased ICP and
respiratory distress
2. Monitor and record vital sign and intake and output, hemodynamic variables, ICP,
cerebral perfusion pressure, specific gravity, laboratory studies, and pulse oximetry to
detect early sign of compromise.
3. Observe for sign of increasing ICP to avoid treatment delay and prevent neurologic
compromise
4. Assess for CSF leak as evidenced by otorhea or rinorrhea. CSF leak could leave the
patient at risk for infection
5. Assess for pain. Pain may cause anxiety and increase ICP
6. Check cough and gag reflex to prevent aspiration
7. Check for sign of diabetes insipidus (low urine specific gravity, high urine output) to
maintain hydration
8. Administer I.V fluids to maintain hydration
9. Administer Oxygen to maintain position and patency of endotracheal tube if present, to
maintain airway and hyperventilate the patient and to lower ICP
10. Provide suctioning; if patient is able, assist with turning, coughing, and deep breating to
prevent pooling of secretions
11. Maintain postion, patency and low suction of NGT to prevent vomiting
12. Maintain seizure precautions to maintain patient safety
13. Administer medication as prescription to decrease ICP and pain
14. Allow a rest period between nursing activities to avoid increase in ICP
15. Encourage the patient to express feeling about changes in body image ot allay anxiety

105
 16. Provide appropriate sensory input and stimuli with frequent reorientation to foster
awarness of the environtment
17. Provide means of communication, such as a communcation board to prevent anxiety
18. Provide eye, skin, and mouth care to prevent tissue damage
19. Turn the patient every 2 hours or maintain in a rotating bed if condition allows to prevent
skin breakdown.

Hemophilia

A. Definition:

1. Hemophilia is a group of hereditary bleeding disorder characterized by a deficiency

in a blood-clotting factor.
2. The two most common forms are factor VIII deficiency (classic hemophilia,
hemophilia A) and factor IX deficiency (Christmas disease, hemophilia B). The
classic form is the most common.
3. Hemophilia is classified as mild, moderate or severe depending on the level of
factor produced by the body.

B. History:
1. In 1803, Dr. John Conrad Otto, a Philadelphia physician, wrote an account about “a
hemorrhagic disposition existing in certain families.”
2. He recognized that the disorder was hereditary and that it affected males and rarely
females.
3. The first usage of the term “hemophilia” appears in a description of the
conditionwritten by Hopff at the University of Zurich in 1828.
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 4. Pavlosky, a doctor from Buenos Aires, found Hemophilia A and Hemophilia B to
be separate diseases by doing a lab test.

C. Etiology:

1. Hemphilia is an X-linked recessive disorder transmitted by females and found

predominantly in males. It may also caused by gene mutation.

107
108
D. Pathophysiology:

1. In hemophilia A, there is a deficiency of, or a defect in, factor VIII (antihemophilic
factor [AHF]), which is necessary for the formation of thromboplastin.
2. In hemophilia B, there is a defect or deficiency of factor IX.
3. Clotting factor malfunction causes abnormal bleeding owing to impaired ability to
form a fibrin clot.

E. Assessment findings:

1. Clinical Manifestations
a. Hemophilia is suspected in a newborn with excessive bleeding from the
umbilical cord or after circumcision.
b. In mild hemophilia, characterized by a factor level of 5% to
50%,children have prolonged bleeding only when they have been
injured.
c. In moderate hemophilia, characterized by a factor level of 1% to 5%,
prolonged bleeding occurs with trauma or surgery, but there may be
episode of spontaneous bleeding as well.
d. In severe hemophilia, characterized by a factor level under 1%, prolonged
bleeding occurs spontaneously without injury.
e. Common manifestations can include:
1. Easy bruising
2. Prolonged bleeding from wounds
3. Spontaneous hematuria
4. Epistaxis
5. Hemarthrosis (hemorrhages in the joints causing pain, swelling and
limited movement)
f. Complications may include:
1. Bone changes, osteoporosis and muscle atrophy, resulting in
crippling deformities as a consequence of hemarthrosis

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 2. Intracranial bleeding
3. Gastrointestinal hemorrhage, leading to intestinal obstruction
4. Hematomas in the spinal cord, resulting in paralysis
5. Airway obstruction due to bleeding into the neck, mouth or thorax

2. Laboratory and diagnostic study findings

a. Coagulation studies will reveal normal prothrombin and bleeding times,
normal fibrinogen levels, low factor VIII in hemophilia A, low factor IX
in hemophilia B, and a prolonged partial thromboplastin time.
b. CBC will reveal a normal plate count.
c. DNA testing for hemophilia A will detect carriers of the disease
d. Amniocentesis will diagnose hemophilia prenatally.

F. Nursing Management:

1. Assess for acute or chronic bleeding

a. The skin, joints and muscles are assessment priorities
b. Check vision, hearing, and neurologic development.
c. Check for hematuria and bleeding from the mouth, lips, gums and rectum.
2. Administer the missing clotting factor (ie factor VIII or factor IX concentrate)
a. Due to recombinant DNA technology, the risk of transmitting human
immunodeficiency virus (HIV), hepatitis, and other viruses has been
eliminated because recombinant factor VIII is not derived from human
plasma.
b. Recombinant factor IX will soon be available.
3. Administer DDAVP (desmopressin) to children with mild to moderate hemophilia
A.
a. DDAVP promotes the release of factor VIII.
b. It is not used in hemophilia B.
4. Prevent or minimize bleeding

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 a. Assess home safety and teach about injury prevention. Consider the
child’s developmental level to ask specific safety questions.
b. Recommend using a soft toothbrush and point out the need for regular
dental checkups:
c. Major bleeding requires hospitalization with nursing management.
1. Monitor for bleeding and its consequences.
2. Provide joint care (exercise).
d. Control bleeding by applying pressure and cold to the injury site and by
elevating and immobilizing the injured area.
e. Observe for swelling and tenderness in the joints, and prevent
contractures. Prevent crippling effects of joint degeneration by
implementing a physical therapy program.
f. Monitor for signs of hypovolemia.
5. Provide Support
a. Foster the child’s self-esteem by encouraging him or her to express
concerns and feelings and by promoting a positive self-image.
b. Encourage family members to verbalize their feelings, especially about
any guilt they may have due to the genetic nature of the disorder. Assist
their coping efforts by providing information about the diseaseand its
management.
c. Refer to the child and family to support groups such as the national
hemophilia Foundation.
6. Provide the child and family teaching.
a. Explain how to care for, administer, store and reconstitute the
replacement factor.
b. Inform the child and family that superficial injuries are treated with ice
and pressure.
c. Identify signs of hemarthrosis and teach parents how to immobilize the
joint, pack it in ice, and administer replacement factor.

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 d. Assist the child and parents to recognize signs of major bleeding (central
nervous system manifestations such as headache, blurred vision,
vomiting, lethargy, confusion and seizures)
e. Explain the possible side effects of therapy.
f. Demonstrate passive ROM exercises.
g. Emphasize avoidance of aspirin and aspirin-containing compounds.
h. Provide diet information because weight increase can impose further
stress on joints.
G. Treatment:
1. The main treatment for
hemophilia is
“replacement therapy” —
giving or replacing the
clotting factor that is too
low or missing.
2. Concentrates of the clotting factor are infused, or injected, directly into the
bloodstream. The specific factors used to treat hemophilia are: Factor VIII for
hemophilia A – Factor IX for hemophilia B
3. Replacement therapy can be used:
a. To prevent bleeding (prophylactic or preventive therapy)
b. To stop bleeding when it occurs, on an as-needed basis (demand therapy)
4. The type of treatment you receive depends on several things, including whether
you have mild, moderate or severe hemophilia.
a. Mild hemophilia. Replacement therapy is usually not needed for mild
hemophilia; however, a medicine called desmopressin (DDAVP) is
sometimes given to raise the body’s levels of factor VIII. Since the
effect wears off with chronic use, it is applied only in certain situations
(for example, prior to dental work or participation in sports) to prevent
or reduce bleeding. Desmopressin does not help in hemophilia B.
b. Moderate hemophilia. You may need treatment only when bleeding
occurs. You will need to learn to recognize signs and symptoms of

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 bleeding so that you can get treatment as quickly as possible. You also
may have treatment to prevent bleeding that could occur when
participating in some activity.
c. Severe hemophilia. You usually need long-term or shorter term
preventive therapy to prevent bleeding that could cause permanent
damage to your joints, muscles or other parts of the body. Some people
with severe hemophilia receive treatment only when bleeding occurs,
however.

Hepatitis C

Hepatitis C is an infection of the liver caused by the hepatitis C virus (HCV). It is

difficult for the human immune system to eliminate the virus from the body, and infection with
HCV usually becomes chronic. Over decades, chronic infection with HCV damages the liver and
can cause liver failure in some people. In the U.S., the number of new cases of infection with
HCV has declined over the last 10 years from a peak of some 200,000 annually to about 19,000
in 2006. When the virus first enters the body, there usually are no symptoms, so these numbers
are estimates. Up to 85% of newly infected people fail to clear the virus and become chronically
infected. In the U.S., more than three million people are chronically infected with HCV.
Infection is most common among people who are 40 to 60 years of age, reflecting the high rates
of infection in the 1970s and 1980s. There are 8,000 to 10,000 deaths each year in the U.S.
related to HCV. HCV is the leading cause of liver transplantation in the U.S and is a risk factor
for liver cancer.

How is hepatitis C virus spread and how can transmission be prevented

HCV is spread (transmitted) most efficiently through inadvertent exposure to infected blood.

 The most common route of transmission is needles shared among users of illicit drugs. 

 Accidental needle-sticks in healthcare workers also have transmitted the virus.

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 The average risk of getting HCV from a stick with a contaminated needle is 1.8% (range
0% to 10%). 

 Prior to 1992, some people acquired the infection from transfusions of blood or blood
products. Since 1992, all blood products are screened for HCV, and cases of HCV due
to blood transfusionnow are extremely rare. 

 HCV also can be passed from mother to unborn child. Approximately 4 of every 100
infants born to HCV-infected mothers become infected with the virus.

 A small number of cases are transmitted through sexual intercourse. The risk of
transmission of HCV from an infected individual to a non-infected spouse or partner without
the use ofcondoms over a lifetime has been estimated to be 1% to 4% 

 Finally, there have been some outbreaks of HCV when instruments or sharp tool have
been re-used without appropriate cleaning between patients.

Transmission of HCV can be prevented in several ways.

 Programs have been aimed at avoiding needle sharing among drug addicts. Needle
exchange programs and educational interventions have reduced high-risk behaviors. However,
the population of drug addicts is a difficult population to reach, and rates of HCV remain high
among addicts (30% of younger users). 

 Among healthcare workers, safe needle-usage techniques have been developed to reduce
accidental needle-sticks. Newer syringes have self-capping needle systems that avoid the need
to manually replace a cap after drawing blood and reduce the risk of needle-sticks. 

 There is no clear way to prevent transmission of the HCV from mother to child. 

 Persons with multiple sexual partners should use barrier precautions such as condoms to
limit the risk of HCV as well as other sexually-transmitted diseases. 

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 Monogamous couples should consider the low risk of transmission when deciding
whether to use condoms during intercourse. Some couples may decide to use them and some
may not. 

 Screening tests for blood products have almost eliminated the risk of transmission
through transfusion, estimated by the CDC to be less than one in two million transfused blood
products. 

 People with HCV should not share razors or toothbrushes with others. 

 It is critical that physicians and clinics follow manufacturer's directions for

sterilizing/cleaning instruments and that disposable sharp instruments be discarded properly.

It is important to realize that HCV is not spread by casual contact. Thus, shaking hands, kissing,
and hugging are not behaviors that increase the risk of transmission. There is no need to use
special isolation procedures when dealing with infected patients.

Symptoms of hepatitis C infection

About 75% of people have no symptoms when they first acquire HCV infection. The remaining
25% may complain of fatigue, loss of appetite, muscle aches or fever. Yellowing of the skin or
eyes (jaundice) is rare at this early stage of infection.

Over time, the liver in people with chronic infection may begin to experience the effects of the
persistent inflammation caused by the immune reaction to the virus. Blood tests may show
elevated levels of liver enzymes, a sign of liver damage, which is often the first suggestion that
the infection may be present. Patients may become easily fatigued or complain of nonspecific
symptoms.

As cirrhosis develops, symptoms increase and may include :

 weakness, 

 loss of appetite, 

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 weight loss, 

 breast enlargement in men, 

 a rash on the palms, 

 difficulty with the clotting of blood, and 

 spider-like blood vessels on the skin.

In patients with advanced cirrhosis, the liver begins to fail. This is a life-threatening
problem. Confusion and even coma(encephalopathy) may result from the inability of the liver to
process certain toxic substances.

Increased pressure in the blood vessels of the liver (portal hypertension) may cause fluid to build
up in the abdominal cavity (ascites) and result in engorged veins in theswallowing
tube (esophageal varices) that tear easily and can bleed suddenly and massively. Portal
hypertension also can cause kidney failure or an enlarged spleenresulting in a decrease of blood
cells and the development of anemia, increased risk of infection and bleeding.

In advanced cirrhosis, liver failure causes decreased production of clotting factors. Patients with
advanced cirrhosis often develop jaundice because the damaged liver is unable to eliminate a
yellow compound, called bilirubin that is formed from thehemoglobin of old red blood cells.

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Nursing Responsibilities in Patients With Hepatitis C

Hepatitis C causes inflammation of the liver. Caused by the hepatitis C virus, this disease spreads
through sexual contact with an infected person; using dirty needles for tattooing, piercing and
drug use; or using the personal hygiene products of someone with the disease. Nurses have
specific responsibilities in caring for hepatitis C patients. These responsibilities help patients
better manage the disease and improve their quality of life.

Patient Education
Nurses play an important role in patient education. They explain hepatitis C to infected patients,
tell them how the disease usually progresses and advise them on when to contact a doctor.

Nutrition Management
Since nutrition affects the overall health of the body, nurses discuss the importance of nutrition
with hepatitis C patients, and counsel them about how to improve their nutrition habits. Since
some herbal supplements can harm the liver, nurses also discuss the importance of checking
supplement labels and avoiding supplements that cause liver damage.

Medication Management
Nebraska Health & Human Services reports that nurses review prescriptions, determine if
patients take all of their medications appropriately, ask patients which over-the-counter
medications they use and determine if any of the drugs have the potential to cause liver damage.
If any of the medications pose a risk to the liver, nurses work to identify safer alternatives.

Risk Identification
Since people infected with hepatitis C can spread the disease to other people, nurses work with
infected patients to identify risky behaviors. During an assessment, a nurse should ask if the
person shares needles, has unprotected sex or shares personal hygiene products with others. If the
patient reports that he engages in any of these behaviors, the nurse should provide counseling

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and educate the patient about how these behaviors increase the risk of transmitting the disease to
others.

Patient Monitoring
Hospital and clinic nurses monitor hepatitis patients to determine if the medical team should
make any changes in their treatment plans. Nurses review laboratory results, identify signs of
advancing hepatitis and determine how well each patient responds to treatment.

Nephrotic Syndrome

Nephrotic syndrome is characterized by the following symptoms that result from changes that
occur to the small, functional structures in the kidneys, such as:

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  very high levels of protein in the urine
 low levels of protein in the blood due to its loss in the urine
 tissue swelling all over the body (edema) especially in the abdomen (ascites)
 high cholesterol levels in the blood

Different types of nephrotic syndrome

The type of nephrotic syndrome that is most common in children is called idiopathic nephrotic
syndrome. Idiopathic means that a disease occurs with no known cause. The most common type
of idiopathic nephrotic syndrome is called minimal-change nephrotic syndrome (MCNS).
Idiopathic nephrotic syndrome is more common in boys than girls.

With MCNS, the child usually has relapses of the illness, but the disease can usually be managed
and prognosis is good. In rare cases, a child may develop kidney failure that requires dialysis.

There is a rare nephrotic syndrome present in the first week of life called "congenital nephrotic
syndrome." Congenital nephrotic syndrome is inherited by an autosomal recessive gene, which
means that males and females are equally affected, and the child inherited one copy of the gene
from each parent, who are carriers. The chance for carrier parents to have a child with congenital
nephrotic syndrome is one in four, or 25 percent, with each pregnancy. The outcome for this type
of nephrotic syndrome is extremely poor.

Symptoms of nephrotic syndrome

The following are the most common symptoms of nephrotic syndrome. However, each child may
experience symptoms differently. Symptoms may include:

 fatigue and malaise

 decreased appetite
 weight gain and facial swelling
 abdominal swelling or pain
 foamy urine
 fluid accumulation in the body spaces (edema)

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  pale fingernail beds
 dull hair
 ears cartilage may feel less firm
 food intolerances or allergies

The symptoms of nephrotic syndrome may resemble other conditions and medical problems.
Always consult your child's physician for a diagnosis.

How is nephrotic syndrome diagnosed?

In addition to a thorough physical examination and complete medical history, your child's
physician may recommend the following diagnostic tests:

 urine tests (to check for protein)

 blood tests (to check the levels of cholesterol and a special blood protein called albumin)
 renal ultrasound - a non-invasive test in which a transducer is passed over the kidney
producing sound waves which bounce off of the kidney, transmitting a picture of the
organ on a video screen. The test is used to determine the size and shape of the kidney
and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities.
 renal biopsy - a procedure where a small sample of tissue is taken from the kidney
through a needle. The tissue is sent for special testing to determine the specific disease.

Treatment for nephrotic syndrome:

Specific treatment for nephrotic syndrome will be determined by your child's physician based on:

 your child's age, overall health, and medical history

 the extent of the disease
 your child's tolerance for specific medications, procedures, or therapies
 expectations for the course of the disease
 your opinion or preference

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During the initial episode of nephrotic syndrome, your child may require hospitalization. He/She
may need to be monitored if the edema is severe or if he/she has blood pressure and/or breathing
problems.

Medications may be required to treat initial symptoms and during relapses, including:

 corticosteroids
 immunosuppressive drug therapy
 diuretics (to reduce the edema)
 intravenous (IV) albumin - a blood protein that can be administered to replace the low
levels
 a special diet that restricts salt and has other specifications

The medications used to treat nephrotic syndrome weaken the immune system so your child
should not receive live vaccines. If your child has been exposed to chickenpox and has not
already had the vaccine, the vaccine may be recommended.

Nursing interventions 

 Assessment and Document the location and character of the patient's edema.

 Measure blood pressure with the patient lying down and standing. Immediately report a
decrease in systolic or diastolic pressure exceeding 20 mm Hg.

 If the patients receive a renal biopsy, watch for bleeding and signs of shock.

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  Monitor intake and output and weigh the patient each morning after he voids and before
he eats. Make sure he's wearing the same amount of clothing each time you weigh him.

 Ask the dietitian to plan a low-sodium diet with moderate amounts of protein.

 Frequently check urine for protein.

 Monitor plasma albumin and transferrin concentrations to evaluate overall nutritional

status.

 Provide meticulous skin care to combat the edema that usually occurs withnephrotic
syndrome.

 Use a reduced-pressure mattress or padding to help prevent pressure ulcers.

 To prevent the occurrence of thrombophlebitis, encourage activity and exercise, and

provide antiembolism stockings as ordered.

 Give the patient and family reassurance and support, especially during the acute phase,
when edema is severe and the patient's body image changes

Patient teaching and home health care guide for Nephrotic Syndrome

 If the patients receive immunosuppressants, teach him and family members to report even
mild signs of infection.

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  If the patients receive long-term corticosteroid therapy, teach him and family members to
report muscle weakness and mental changes.

 To prevent GI complications, suggest to the patient that he take steroids with an antacid
or with cimetidine or ranitidine. Explain that the adverse effects of steroids subside when
therapy stops, but warn the patient not to discontinue the drug abruptly or without a
physician's consent.

 Stress the importance of adhering to the special diet.

 If the physician prescribes antiembolism stockings for home use, show the patient how to
safely apply and remove them.

Pneumonia

Pneumonia is an inflammation of your lungs, usually caused by infection. Bacteria,

viruses, fungi or parasites can cause pneumonia. Pneumonia is a particular concern if you're
older than 65 or have a chronic illness or impaired immune system. It can also occur in young,
healthy people.

Pneumonia can range in seriousness from mild to life-threatening. Pneumonia often is a

complication of another condition, such as the flu. Antibiotics can treat most common forms of
bacterial pneumonias, but antibiotic-resistant strains are a growing problem. The best approach is
to try to prevent infection.

Symptoms
Pneumonia symptoms can vary greatly, depending on any underlying conditions you may have
and the type of organism causing the infection. Pneumonia often mimics the flu, beginning with
a cough and a fever, so you may not realize you have a more serious condition.

Common signs and symptoms of pneumonia may include:

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 Fever

 Cough

 Shortness of breath

 Sweating

 Shaking chills

 Chest pain that fluctuates with breathing (pleurisy)

 Headache

 Muscle pain

 Fatigue

Ironically, people in high-risk groups such as older adults and people with chronic illnesses or
weakened immune systems may have fewer or milder symptoms than less vulnerable people do.
And instead of having the high fever that often characterizes pneumonia, older adults may even
have a lower than normal temperature.

Classifications of pneumonia 
Pneumonia is sometimes classified according to the cause of pneumonia:

 Community-acquired pneumonia. This refers to pneumonia you acquire in the course of

your daily life — at school, work or the gym, for instance. The most common cause is the
bacterium Streptococcus pneumoniae. Another, less common cause is Mycoplasma pneumoniae,
a tiny organism that typically produces milder signs and symptoms than other types of
pneumonia. Walking pneumonia, a term used to describe pneumonia that isn't severe enough to
require bed rest, may result from Mycoplasma pneumoniae.

 Hospital-acquired (nosocomial) pneumonia. If you're hospitalized, you're at a higher risk

of pneumonia, especially if you're breathing with the help of a mechanical ventilator, in an
intensive care unit or have a weakened immune system. This type of pneumonia can be

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 extremely serious, especially for older adults, young children and people with chronic
obstructive pulmonary diseases (COPD) or HIV/AIDS.

Hospital-acquired pneumonia develops at least 48 hours after you're admitted to the hospital.
This category includes post-operative pneumonia — most common in people older than age 70
who have abdominal or chest surgery — and health-care associated pneumonia — acquired in
chronic care facilities, centers where drugs are given by intravenous drip (infusion) and kidney
dialysis centers.

A common predisposing factor for this type of pneumonia is gastroesophageal reflux disease
(GERD). This occurs when some of the contents of your stomach flow back into the upper
esophagus. From there, the gastroesophageal contents can be inhaled (aspirated) into your
windpipe and then into your lower airways. Even small amounts of gastroesophageal reflux can
lead to pneumonia in people who are hospitalized.

 Aspiration pneumonia. This type of pneumonia occurs when you aspirate foreign matter
into your lungs — most often when the contents of your stomach enter your lungs after you
vomit. This commonly happens when a brain injury or other condition affects your normal gag
reflex.

Another cause of aspiration pneumonia is consuming too much alcohol. Aspiration occurs when
the inebriated person passes out and then vomits due to the effects of alcohol on the stomach. If
someone's unconscious, it's possible to aspirate the liquid contents and possibly solid food from
the stomach into the lungs, causing aspiration pneumonia.

Difficulty swallowing, which occurs with diseases such as amyotrophic lateral sclerosis (ALS),
Parkinson's disease and strokes, may also lead to aspiration pneumonia.

 Pneumonia caused by opportunistic organisms. This type of pneumonia strikes people

with weakened immune systems. Organisms that aren't harmful for healthy people can be
dangerous for people with AIDS and other conditions that impair the immune system, as well as

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 people who have had an organ transplant. Medications that suppress your immune system, such
as corticosteroids or chemotherapy, also can put you at risk of opportunistic pneumonia.

 Other pathogens. Outbreaks of the H5N1 influenza (bird flu) virus and severe acute
respiratory syndrome (SARS) have caused serious, sometimes deadly pneumonia infections,
even in otherwise healthy people. Although rare, anthrax, plague and tularemia also may cause
pneumonia. Some forms of fungi, when inhaled can cause pneumonia. Tuberculosis in the lung
also can cause pneumonia.

Risk factors
Factors associated with an increased risk of pneumonia include:

 Age. If you're age 65 or older, particularly if you have other conditions that make you
more prone to developing pneumonia, you're at increased risk of pneumonia. Very young
children, whose immune systems aren't fully developed, also are at increased risk of pneumonia.

 Certain diseases. These include immune deficiency diseases such as HIV/AIDS and

chronic illnesses such as cardiovascular disease, emphysema and other lung diseases, and
diabetes. You're also at increased risk if your immune system has been impaired by
chemotherapy or long-term use of immunosuppressant drugs.

 Smoking, alcohol abuse. Millions of microscopic hairs (cilia) cover the surface of the
cells lining your bronchial tubes. The hairs beat in a wave-like fashion to clear your airways of
normal secretions, but irritants such as tobacco smoke paralyze the cilia, causing secretions to
accumulate. If these secretions contain bacteria, they can develop into pneumonia. Alcohol
interferes with your normal gag reflex as well as with the action of the white blood cells that
fight infection.

 Hospitalization in an intensive care unit. Pneumonia acquired in the hospital tends to be

more serious than other types of pneumonia. People who need mechanical ventilation are
particularly at risk because the breathing tube bypasses the normal defenses of the upper
respiratory tract, prevents coughing, may allow the stomach's contents to back up into the

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 esophagus where they can be inhaled (aspirated), and can harbor bacteria and other harmful
organisms.

 Having COPD and using inhaled corticosteroids for more than 24 weeks. Research
indicates that this greatly increases your risk of developing pneumonia, possibly serious
pneumonia.

 Exposure to certain chemicals or pollutants. Your risk of developing some uncommon

types of pneumonia may be increased if you work in agriculture, in construction or around
certain industrial chemicals or animals. Exposure to air pollution or toxic fumes can also
contribute to lung inflammation, which makes it harder for the lungs to clear themselves.

 Surgery or traumatic injury. People who've had surgery or who are immobilized from a
traumatic injury have a higher risk of pneumonia because surgery or serious injuries may make
coughing — which helps clear your lungs — more difficult, and lying flat can allow mucus to
collect in your lungs, providing a breeding ground for bacteria.

 Ethnicity. If you're a Native Alaskan or from certain Native American tribes, you're at
greater risk for contracting pneumonia.

Pneumonia complications may include:

 Bacteria in your bloodstream. Pneumonia can be life-threatening when inflammation

from the disease fills the air sacs in your lungs and interferes with your ability to breathe. In
some cases the infection may invade your bloodstream (bacteremia). It can then spread quickly
to other organs.

 Fluid accumulation and infection around your lungs.Sometimes fluid accumulates

between the thin, transparent membrane (pleura) covering your lungs and the membrane that
lines the inner surface of your chest wall — a condition known as pleural effusion. Normally, the
pleurae are smooth, allowing your lungs to slide easily along your chest wall when you breathe
in and out. But when the pleurae around your lungs become inflamed (pleurisy) — often as a
result of pneumonia — fluid can accumulate and may become infected (empyema).

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 Lung abscess. A cavity containing pus (abscess) that forms within the area affected by
pneumonia is another potential complication.

 Acute respiratory distress syndrome (ARDS). The pneumonia involves most areas of both
lungs, making breathing difficult and depriving your body of oxygen. Underlying lung disease of
any kind, but especially COPD, makes you more susceptible to ARDS.

Nursing Management

1. Administer prescribed medications which may include antibiotics, mucolytics,

expectorants, or antitussive agents.
2. Promote infection-control measures, especially droplet precaution as indication
3. Prevent aspiration pneumonia in a client receiving tube feedings. Keep client in an
upright position during feedings and for 30 minutes afterwards.
4. Improve breathing patters. By encouraging upright position at least 30-45 degrees.
5. Promote gas exchange.
6. Encourage effective coughing
7. Encourage the client to eliminate or minimize exposure to all pulmonary irritants
8. Encourage client to alternate rest with activity to prevent overexertion that may
exacerbate symptoms and to increase activity gradually.
9. Promote coping and minimize anxiety
10.Provide client and family teaching

Tracheostomy Care

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Definition

A tracheostomy is a surgically created opening in the trachea. A tracheostomy tube is placed in

the incision to secure an airway and to prevent it from closing. Tracheostomy care is generally
done every eight hours and involves cleaning around the incision, as well as replacing the inner
cannula of the tracheostomy tube. After the site heals, the entire tracheostomy tube is replaced
once or twice per week, depending on the physician's order.

Purpose

The goals of tracheostomy care are to maintain the patency of the airway, prevent breakdown of
the skin surrounding the site, and prevent infection. Sterile technique should be used during the
procedure.

Precautions

Extra precautions should be taken when performing site care during the first few days after the
tracheostomy is surgically created. The site is prone to bleeding and is sensitive to movement of
the tracheostomy tube. It is recommended that another health care professional securely hold the
tube while site care is performed. Tracheostomy care should not be done while the patient is
restless or agitated, since this increases the chance that the tube may be pulled out and the airway
lost.

Description

Tracheostomy care starts with suctioning the patient's airway, both via the tracheostomy and
orally. Sterile technique must be used when suctioning the tracheostomy. The gauze dressing is
removed from the tracheostomy site, and the amount and color of drainage should be noted.
Using sterile technique, the skin and external portion of the tube are cleaned with hydrogen
peroxide. Cotton-tipped applicators should be used to clean closely around the stoma. The
condition of the skin and stoma should be noted. The area is then wiped with gauze dampened in
0.9% sodium chloride and a new tracheostomy dressing is applied.

If the patient has a disposable inner cannula, the old cannula can simply be removed and
discarded. A new cannula is inserted using sterile technique. If the inner cannula is not
disposable, it must be cleaned with hydrogen peroxide, rinsed with 0.9% sodium chloride, and
reinserted. Sterile technique must be used, and the cannula should be tapped against the side of

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the sterile container to remove excess fluid. It should not be completely dried, as the film of
saline facilitates reinsertion.

Preparation

All supplies needed for tracheostomy care should be at the bedside prior to beginning the
procedure. There are prepackaged tracheostomy care kits available that contain gauze pads,
cotton-tipped applicators, a tracheostomy dressing, and hydrogen peroxide. In addition, a
container of 0.9% sodium chloride solution, a suction kit, and sterile gloves are needed. The
velcro strap that holds the tracheostomy tube in place may be soiled and need to be replaced as
well.

The patient should be preoxygenated with 100% oxygen prior to suctioning. If the patient is
agitated, a sedative should be given or the procedure should be rescheduled for a later time when
the patient is calm. Pain medication may be offered, especially during the first few days after
surgery when manipulating the incision can cause discomfort.

Aftercare

After tracheostomy care is finished, the soiled dressing and supplies should be discarded, either
in the garbage or in a biohazard container if there is a large amount of blood. The patient may
need to be suctioned again, and his or her respiratory status should be reassessed. Again, pain
medication should be offered as appropriate.

Complications

Tracheostomy care is a relatively benign procedure. The greatest risk is that the tube may be
inadvertently removed and the airway lost.

Results

The anticipated outcomes of tracheostomy care include continual patency of the airway,
prevention of skin breakdown around the stoma, and prevention of infection.

Health care team roles

The nurse has the primary role in tracheostomy care, as he or she is responsible for doing it in the
acute care setting. The respiratory therapist may assist the nurse during the procedure and during
respiratory assessment. Some patients may be sent home with a tracheostomy. In this case, the

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 nurse and respiratory therapist are both responsible for teaching the patient and the family how to
perform site care at home.

Tonsilitis
Tonsillitisis inflammation of the tonsils, two oval-shaped pads of tissue at the back of the throat
— one tonsil on each side. Signs and symptoms of tonsillitis include swollen tonsils, sore throat
and difficulty swallowing.

Most cases of tonsillitis are caused by infection with a common virus, but a bacterial infection
also may cause tonsillitis.

Because appropriate treatment for tonsillitis depends on the cause, it's important to get a prompt
and accurate diagnosis. Surgery to remove tonsils, once a common procedure to treat tonsillitis,
is usually performed only when tonsillitis occurs frequently, doesn't respond to other treatments
or causes serious complications.

Symptoms

Tonsillitis most commonly affects children between preschool ages and the mid-teenage years.
Common signs and symptoms of tonsillitis include:

 Red, swollen tonsils

 White or yellow coating or patches on the tonsils

 Sore throat

 Difficult or painful swallowing

 Fever

 Enlarged, tender glands (lymph nodes) in the neck

 A scratchy, muffled or throaty voice

 Bad breath

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 Stomachache, particularly in younger children

 Stiff neck

 Headache

In young children who are unable to describe how they feel, signs of tonsillitis may include:

 Drooling due to difficult or painful swallowing

 Refusal to eat

 Unusual fussiness

Causes

Tonsillitis is most often caused by a common cold virus, but other viral and bacterial infections
can also be the cause.

The most common bacterium causing tonsillitis is Streptococcus pyogenes, or group A

streptococcus, the bacterium that causes most cases of strep throat.

Why do tonsils get infected?

Tonsils produce certain types of disease-fighting white blood cells. So the tonsils are believed to
act as the immune system's first line of defense against bacteria and viruses that enter your
mouth.

This function may make the tonsils particularly vulnerable to infection and inflammation.
However, the tonsil's immune system function declines after puberty — a factor that may
account for the rare cases of tonsillitis in adults.

Risk factors for tonsillitis include:

 Young age. Tonsillitis is most common from the preschool years to the mid-teenage
years.

 Frequent exposure to germs. School-age children are in close contact with their peers and
frequently exposed to viruses or bacteria that can cause tonsillitis.

Complications

Inflammation or swelling of the tonsils from frequent or ongoing (chronic) tonsillitis can cause
complications such as:

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 Difficulty breathing

 Disrupted breathing during sleep (obstructive sleep apnea)

 Infection that spreads deep into surrounding tissue (tonsillar cellulitis)

 Infection that results in a collection of pus behind a tonsil (tonsillar abscess)

Strep infection 
If tonsillitis caused by group A streptococcus or another strain of streptococcal bacteria isn't
treated or if antibiotic treatment is incomplete, your child has an increased risk of rare disorders
such as:

 Rheumatic fever, an inflammatory disorder that affects the heart, joints and other tissues

 Post-streptococcal glomerulonephritis, an inflammatory disorder of the kidneys that

results in inadequate removal of waste and excess fluids from blood

NURSING MEASURES:

 warm saline gargles

 soft diet if pain upon swallowing

Self-Care at Home

 Throat pain and fever may be improved withover-the-counter pain relievers such

asibuprofen (Advil, for example) oracetaminophen (Tylenol).

 Ease sore throat pain by gargling frequently with warm salt water (8 ounces of warm
water mixed with 1 teaspoon salt).

 Drink plenty of clear liquids to avoiddehydration.

Ureterolithiasis or Kidney stone.

Ureterolithiasis is the condition of having a calculus in the ureter, the tube connecting the
kidneys and the bladder. The term bladder stones usually applies to urolithiasis of the bladder in
non-human animals such as dogs and cats.

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 Kidney stones typically leave the body by passage in the urine stream, and many stones
are formed and passed without causing symptoms. If stones grow to sufficient size before
passage on the order of at least 2-3 millimeters they can cause obstruction of the ureter. The
resulting obstruction causes dilation or stretching of the upper ureter and renal pelvis (the part of
the kidney where the urine collects before entering the ureter) as well as muscle spasm of the
ureter, trying to move the stone. This leads to pain, most commonly felt in the flank, lower
abdomen and groin (a condition called renal colic). Renal colic can be associated with nausea
and vomiting. There can be blood in the urine, visible with the naked eye or under the
microscope (macroscopic or microscopic hematuria) due to damage to the lining of the urinary
tract.

There are several types of kidney stones based on the type of crystals of which they
consist. The majority are calcium oxalate stones, followed by calcium phosphate stones. More
rarely, struvite stones are produced by urea-splitting bacteria in people with urinary tract
infections, and people with certain metabolic abnormalities may produce uric acid stones or
cystine stones.

The diagnosis of a kidney stone can be confirmed by radiological studies and or

ultrasound examination; urine tests and blood tests are also commonly performed. When a stone
causes no symptoms, watchful waiting is a valid option. In other cases, pain control is the first
measure, using for example non-steroidal anti-inflammatory drugs or opioids. Using
soundwaves, some stones can be shattered into smaller fragments (this is called extracorporeal
shock wave lithotripsy). Sometimes a procedure is required, which can be through a tube into the
urethra, bladder and ureter (ureteroscopy), or a keyhole or open surgical approach from the
kidney's side. Sometimes, a tube may be left in the ureter (a ureteric stent) to prevent the
recurrence of pain. Preventive and structive measures are often advised such as drinking
sufficient amounts of water and milk although the effect of many dietary interventions has not
been rigorously studied.

Signs and symptoms

Symptoms of kidney stones include:

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Localization of kidney stone pain

 Colicky pain: "loin to groin". Often described as "the worst pain [...] ever experienced".
This can also occur in the lower back.
 Nausea/vomiting: embryological link with intestine– stimulates the vomiting center.
 Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter
and/or urethra.
 Pyuria: pus in the urine.
 Dysuria: burning on urination when passing stones (rare). More typical of infection.
 Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra by
stone, or extremely rarely, simultaneous obstruction of both ureters by a stone.
 Postrenal azotemia: the blockage of urine flow through a ureter.
 Hydronephrosis: the distension and dilation of the renal pelvis and calyces.

Causes

Kidney stones or calcium oxalate crystals in kidney can be due to underlying metabolic
conditions, such as renal tubular acidosis, Dent's disease, hyperparathyroidism, primary
hyperoxaluria and medullary sponge kidney. Kidney stones are also more common in patients
with Crohn's disease. Patients with recurrent kidney stones should be screened for these

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disorders. This is typically done with a 24 hour urine collection that is chemically analyzed for
deficiencies and excesses that promote stone formation.

There has been some evidence that water fluoridation may increase the risk of kidney stone
formation. In one study, patients with symptoms of skeletal fluorosis were 4.6 times as likely to
develop kidney stones.

Diagnosis

Clinical diagnosis is usually made on the basis of the location and severity of the pain, which is
typically colicky in nature (comes and goes in spasmodic waves). Pain in the back occurs when
calculi produce an obstruction in the kidney.

Imaging is used to confirm the diagnosis and a number of other tests can be undertaken to help
establish both the possible cause and consequences of the stone.

X-rays

The relatively dense calcium renders these stones radio-opaque and they can be detected by a
traditional X-ray of the abdomen that includes the kidneys, ureters and bladder—KUB. This may
be followed by an IVP (intravenous pyelogram—intravenous urogram (IVU) is the same test by
another name) which requires about 50 ml of a special dye to be injected into the bloodstream
that is excreted by the kidneys and by its density helps outline any stone on a repeated X-ray.
These can also be detected by a retrograde pyelogram where similar "dye" is injected directly
into the ureteral opening in the bladder by a surgeon, usually a urologist.

About 10% of stones do not have enough calcium to be seen on standard X-rays (radiolucent
stones).

Computed tomography

Computed tomography without contrast is considered the gold standard diagnostic test for the
detection of kidney stones. All stones are detectable by CT except very rare stones composed of
certain drug residues in the urine. If positive for stones, a single standard X-ray of the abdomen

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(KUB) is recommended. This gives a clearer idea of the exact size and shape of the stone as well
as its surgical orientation. Further, it makes it simple to follow the progress of the stone by doing
another X-ray in the future.

Drawbacks of CT scans include radiation exposure and cost.

Ultrasound

Ultrasound imaging is useful as it gives details about the presence of hydronephrosis (swelling of
the kidney—suggesting the stone is blocking the outflow of urine). It can also be used to detect
stones during pregnancy when x-rays or CT are discouraged. Radiolucent stones may show up
on ultrasound however they are also typically seen on CT scans.

Some recommend that US be used as the primary diagnostic technique with CT being reserved
for those with negative US result and continued suspicion of a kidney stone. This is due to its
lesser cost and avoidance of radiation.

Other

Other investigations typically carried out include:

 Microscopic study of urine, which may show proteins, red blood cells, bacteria, cellular
casts and crystals.
 Culture of a urine sample to exclude urine infection (either as a differential cause of the
patient's pain, or secondary to the presence of a stone)
 Blood tests: Full blood count for the presence of a raised white cell count (Neutrophilia)
suggestive of infection, a check of renal function and to look for abnormally high blood
calcium blood levels (hypercalcaemia).
 24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric
acid, calcium, citrate, oxalate and phosphate.
 Catching of passed stones at home (usually by urinating through a tea strainer or
stonescreen) for later examination and evaluation by a doctor.

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Nursing Care

 Monitor intake of fluid amount and urinary output.

 Medicate for pain as prescribed.
 Continue antibiotic therapy as prescribed.
 Correct diet to include reduced protein and calcium content.

Wound Care

PART 1: Wound Healing

EXTERNAL WOUNDS

A wound is a damaged area of the body. Because this course, addresses external
wounds—damage that includes the skin—we begin with a review of the anatomy of
skin.

The Structure of Skin

Skin varies in thickness from less than one millimeter in the eyelids to greater than
four millimeters on the soles of the feet, but everywhere, skin is composed of two
layers, the epidermis and the dermis, underlain by a sheet of subcutaneous tissue
(Figure 1) (Habif, 2004).

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Figure 1. The skin has two layers, the epidermis and the dermis, below which lies
subcutaneous tissue. (National Cancer Institute, n.d.)

EPIDERMIS

The outer layer of the skin is the epidermis. The deepest part of the epidermis is a row
of germinative cells. Germinative cells are specialized stem cells that continually
divide to give offkeratinocytes, the main cells in the remainder of the epidermis. As
they age, the new keratinocytes fill with keratin (a tough fibrous protein) and are
pushed to the surface, where they die; thus, the outermost layer of the epidermis is
made of flat, dead keratinocytes. The epidermis also contains melanocytes (pigment-
containing cells) and immune system cells. The epidermis, a protective layer that is
normally impermeable to water, does not have sufficient strength to hold sutures or
staples.

There are no blood vessels in the epidermis, and it receives its oxygen and nutrients
by diffusion from blood circulating in the underlying dermis. Hair, nails, sweat
glands, and sebaceous glands are sunken epidermal appendages that lie in deep
valleys in the dermis surrounded by a row of germinative epidermal cells.

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During normal healing, the epidermis re-grows from germinative cells left in the skin
at the edges of the wound. The growing cells are called epithelial cells, and the
regrowth of the epidermis is calledre-epithelialization.

Some wounds, such as surface abrasions (scrapes), are confined mostly to the
epidermis. Inepidermal wounds, a new epidermis grows from the germinative cells
that surround the bottoms of epidermal appendages deep in the dermis. Epidermal
wounds usually heal quickly with little or no scarring.

Partial-thickness wounds, such as deep abrasions, destroy or remove the epidermis

and the upper portion of the dermis. When there are still some germinative cells left
in the remaining dermis, they will re-grow a new epidermis. Partial-thickness wounds
usually heal with scarring.

DERMIS

The layer of skin directly beneath the epidermis is the dermis. A basement membrane
separates these two layers. The dermis is mainly connective tissue and is therefore
much stronger than the epidermis. The dermis varies in thickness across the surface of
the body, but everywhere it is significantly thicker than the overlying epidermis.

The connective tissue of the dermis contains small blood vessels, lymph vessels,
nerves, nerve endings, and in a few places, muscles. The dermis is also populated by
a variety of individual cells including macrophages, fibroblasts (which synthesize the
extracellular connective tissue components such as collagen), and mast cells (which
release histamine and other molecules that increase inflammation).

The dermis is loosely stratified. The upper (most superficial) layer contains capillaries
and sensory endings of nerves. The deepest layer has thick interlacing collagen and
elastic fibers arranged in parallel rows. The extracellular fibers in the deep dermis are
responsible for the strength and toughness of the skin. When closing a wound with
sutures, they must be anchored in the strong connective tissue of the lower layer of
the dermis.

Wounds that penetrate the dermis are true breaks in the skin. For the skin to regain its
strength, new fibrous connective tissue must bridge these wounds; however, the new

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fibrous tissue—the scar—is never as strong as the original dermis. In full-thickness
wounds, both the epidermis and the dermis are destroyed or removed. These wounds
always heal with a scar.

SUBCUTANEOUS TISSUE

Beneath the dermis is a layer of subcutaneous tissue containing fat. The thickness of
the subcutaneous layer varies throughout the body. It is thickest along the anterior
thigh and thinnest on the back of the hands.

Besides fat cells, subcutaneous tissue contains blood vessels, lymph vessels, and
nerves. The subcutaneous layer is held together by a continuous sheet of fibrous
membrane that runs parallel to the surface of the skin. This membrane is called
the superficial fascia.

Beneath the subcutaneous tissue layer, structures (such as muscles and organs) are
enclosed in their own separate connective tissue sheaths. The generic name for these
sheaths is deep fasciae. Deep fasciae generally look off-white in fresh wounds. When
treating a wound, tears in the deep fasciae are repaired whenever possible.

The subcutaneous tissue is a loosely organized compartment. When skin wounds

extend deeper than the dermis, dirt is easily pushed into and spread within the
subcutaneous tissue. When cleansing a wound that has penetrated deeper than the
dermis, remove any loose fat and wash out the subcutaneous compartment thoroughly
to reduce the risk of infection.

Types of Wounds

External wounds are named by the type of force that caused them. There are seven
basic wound types: abrasions, lacerations, crushes or contusions, punctures,
avulsions, burns, and ulcers. A traumatic wound is often a mixture of types.

 Abrasions are scrapes. Mild abrasions remove epidermis; serious abrasions

also remove the dermis and, sometimes, subcutaneous tissue. An abrasion is
usually a broad, shallow wound with irregular edges.

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  Lacerations are cuts. When made by a knife-like object, a laceration is a
narrow, deep wound with sharp edges. When made by a blunt object, a
laceration is a rip with jagged edges.
 Crushes or contusions are compression wounds. A crush wound bruises and
damages the skin and the underlying tissue, although the skin can remain
closed in some crush wounds.
 Punctures are narrow, deep wounds. Typically, punctures have small
openings with sharp edges. Puncture wounds have a relatively high risk of
infection.
 Avulsions are wounds in which tissue has been torn out. Sometimes, the
avulsed tissue remains partly connected to its normal surroundings.
 Burns are wounds made by external destructive energy (eg, heat) or by
external chemicals (eg, acid). First-degree burns are superficial and red.
Second-degree wounds include damage to the dermis and produce blisters
(see photograph of second-degree wound below). Third-degree wounds go
deeper than the dermis and produce dry, dead tissue.
 Ulcers are usually made by innate destructive processes, such as ischemia.
Ulcers often have destruction of tissue in a broad, roughly circular area (Shai
& Maibach, 2005). (See the photograph of an inflamed diabetic foot ulcer
below.)

Scars

Many parts of the human body can heal after being wounded, but few wounds heal
seamlessly. The new seam, or patch, is called a scar. Scars are mainly connective
tissue and cannot replicate the specialized functions of the original injured tissue. In
the skin, scars are covered by a layer of epidermis (Habif, 2004).

NORMAL SCARS

Scars are imperfect replacements for damaged tissue, but scars are a natural result of
healthy healing. Large wounds, wounds that heal slowly, and wounds involving
extensive destruction of the surrounding tissues heal with large scars; nonetheless,
these scars are not necessarily abnormal.

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PROBLEM SCARS

Normal scars can lead to problems. Even under the best healing conditions, some
normal scars may end up interfering with the movement of the skin and the
underlying tissue. In addition, some normal scars are unsightly.

When the healing situation is not ideal, however, scars are more likely to become
problems. After poor healing, some scars become unnecessarily large or
unnecessarily weak. For example, infections, tissue necrosis, sebaceous skin, and
wounds perpendicular to natural lines of minimal skin tension will all lead to scars
that are larger than normal. If a wound separates (process of dehiscence*) before it is
effectively sealed, the scar will be wider and, usually, weaker. If too few capillaries
grow into the forming scar tissue, leading to ischemia, the scar will be very weak and
may develop into an ulcer.

* Dehiscence is the spontaneous re-opening of a closed wound before it has fully

healed.

At the other end of the spectrum, the wound patching process may go overboard and
generate too many new cells or, more commonly, too much collagen in the scar. Such
scars will enlarge and bulge from the wound. Scars built of too many cells (mainly
fibroblasts) are called desmoids, oraggressive fibromatoses. Scars built from too
much collagen are either hypertrophic scars or keloids. When excessive scars form
tight ridges along the skin and permanently interfere with normal movement (such as
bending a joint), they are called contractures.

HYPERTROPHIC SCARS

Hypertrophic scars are caused by excess deposition of collagen fibers in a healing

wound. This overactive scar-making process is usually triggered by a prolonged
regrowth (proliferative) phase during healing. This happens in burns, infected
wounds, and wounds healing under tension. In hypertrophic scars, the excessive
formation of collagen usually stops within a few weeks. The result is a scar that is
thicker than normal and is raised above the plane of the skin, but unlike a keloid, a
hypertrophic scar does not expand out beyond the actual wound. Hypertrophic scars,
which usually get smaller spontaneously, can occur anywhere on the body.

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KELOIDS

Keloids are also caused by the excess deposition of collagen in a healing

wound. Keloids, however, are benign tumors, and the tendency to develop keloids is
inherited, African Americans being particularly susceptible. Unlike hypertrophic
scars, keloids develop late in the healing process; they can show up months or even
years after the injury. Keloids bulge out beyond the edges of the wound, and some
keloids can get sizeable. Keloids, which do not regress spontaneously, are usually
found on the upper half of the body.

Figure 3. A keloid scar that developed from a skin wound along the edge of the jaw.
The tendency to develop keloids is a genetic trait. (Courtesy of Leonard C. Sperling,
MD.)

CONTRACTURES

All scars go through a process of shrinking or contracting. Enlarged scars, however,

sometimes contract excessively, becoming disabling or disfiguring ridges of
connective tissue called contractures (Tomasek et al., 2002). When contractures form
over joints, the scars can make bending difficult or impossible. Disabling contractures
most commonly form across finger joints, along the neck, across the axilla, and across
the antecubital fossa.

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 A contracture is a permanent fixture of the skin, and it cannot be repaired by
stretching, massaging, or applying ointments, lotions, or creams. The most successful
treatment for a contracture is to have it excised surgically.

PHASES IN NORMAL WOUND HEALING

Most tissues in the body heal by going through the three R's: Reaction, Regrowth,
andRemodeling. These steps produce a patch or a scar in the place of a wound (Habif,
2004; Baum & Arpey, 2005; Shai & Maibach, 2005). In a small clean wound such as
a surgical incision, most of the healing processes are quick and take only a few days.
In complex wounds, healing can take weeks. In all wounds, the scar matures and
becomes stronger over the course of weeks, months, or even years.

Reaction Phase

The first set of events in wound healing is the reaction, reactive, or inflammatory
phase. In this phase, blood clots seal the wound and a normal inflammatory reaction
begins to remove bits of dirt and debris.

The reaction phase begins immediately after an injury, as blood vessels constrict
temporarily and blood clotting begins. Soon, the local capillaries become excessively
permeable, fluid flows out, and the tissues swell, producing edema. The blood
coagulation process releases chemical activators from inside entrapped blood
platelets; these activators increase the capillary permeability and attract wandering
tissue cells (macrophages) and white blood cells.

The first white blood cells on the scene—polymorphonuclear cells, also called
neutrophils—chew up debris and release chemicals that attract more white blood
cells. The various biologically active molecules being released into the wound also
hypersensitize the endings of local pain nerves, making them react to smaller amounts
of chemical and mechanical irritation, making the wound site tender. Together, the
processes in the reaction phase produce local inflammation.

Large wounds, such as ulcerative pressure sores or burns, do not seal during this
phase. Instead, the accumulating fluid, cells, and clotting materials form a pale

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yellowish viscous exudate, aneschar. As they age, the coagulant proteins of the
exudate link together and dry, making the wound bed crusty.

During the reaction phase, neutrophils remove bacteria and debris. If the wound does
not become colonized with bacteria, neutrophils stop entering the wound by about
day 2 following the injury. Neutrophils live for less than 24 hours, so in a healthy
wound most neutrophils are gone by about day 3. In infected wounds, however,
neutrophils continue to pour in and, as they die, they accumulate to form pus.

Under healthy conditions, most of the new cells entering the wound after day 2 are
mononuclear cells (monocytes), which are the second wave of white blood cells to
migrate into a wound. Monocytes transform into macrophages. Macrophages are
scavengers that continue to debride the wound biologically by removing dead and
dying bits of tissue, dirt, and bacteria. Macrophages also release growth factors,
chemicals that stimulate the growth of fibroblasts, endothelial cells, and epithelial
cells, all of which are players in the next phase of wound healing.

Regrowth Phase

The second set of events in wound healing is the regrowth, reparative, or proliferative
phase. In this phase, new cells grow into the wound and begin to lay down the
collagen and other extracellular fibers that will give strength to the scar. At the same
time, new blood vessels are growing into the wound. Together, the newly forming
cells, blood vessels, and loose extracellular matrix are called granulation tissue.
Granulation tissue fills the base of an open wound (eg, a pressure ulcer) during the
regrowth phase of wound healing.

The phases of wound healing overlap. Even as white blood cells are cleansing the
wound area in the reaction phase, epithelial cells are moving over the granulation
tissue from the cut edges of the wound to begin the regrowth phase. These epithelial
cells come from germinative cells in the adjacent skin, and the new epithelial cells
will eventually give rise to the epidermis covering the scar.

If the granulation tissue is moist, the epithelial cells can move quickly. In contrast, if
the granulation tissue is covered with a dry, scabby exudate, the epithelial cells

146
migrate slowly. For this reason, wounds that are kept moist heal more quickly than
those that dry out.

When the wound area is not too large, epithelial cells repopulate the entire surface
and generate a new epidermal covering; this process is called re-epithelialization. A
healthy wound that has been closed (eg, with sutures) has only a small area to be
covered with epidermis, and it will re-epithelialize in less than two days.

When a wound has been re-covered with epithelium, it is impermeable to water. Over
the next few days, the new epithelium continues to deepen and differentiate, and
eventually, it becomes a typical epidermal layer. In the process, the new epithelium
grows along the top of the granulation tissue but it grows under the crust from the
wound exudate and under any remaining blood clots. This dried matter forms the
scab, and as the underlying epithelium turns into an epidermis, it loosens the scab,
which eventually crumbles off the top of the scar.

Underneath the growing epithelial layer, the granulation tissue is thickening and
solidifying. Within 48 hours after the injury, fibroblasts are filling the granulation
tissue and laying down collagen and elastin fibers. Collagen is the principal structural
protein of the body, and healthy tissue repair requires that new collagen be
synthesized, deposited, and cross-linked (ie, strengthened). Besides making collagen,
fibroblasts also secrete sticky amorphous extracellular matrix molecules,
the glycoproteins.

In a healthy wound, fibroblasts begin to fill the wound during days 2 to 4 after an
injury. Fibroblasts grow especially well in the low oxygen/high lactate environment
of a healing wound, when it is still covered by an exudate or a scab.

Remodeling Phase

The final set of events in wound healing is the remodeling, or maturational, phase. In
this phase, the number of fibroblasts in the new scar decreases and the temporary
dense capillary network thins. The scar tissue contracts, edema disappears, and the
wounded region continues to strengthen and to adjust to the tensions applied during
day-to-day life. This remodeling continues for 6 to 12 months.

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 As the wound heals, a special class of cells, the myofibroblasts, begins to pull the
edges of the wound toward one another. Myofibroblasts are modified fibroblasts.
Like fibroblasts, myofibroblasts secrete extracellular molecules. Unlike fibroblasts,
however, myofibroblasts can contract like smooth muscle cells. Over a period of 3 to
4 days, the myofibroblasts in the scar contract and slowly shrink the wound (Tomasek
et al., 2002).

Wound contraction usually begins after about a week of healing. The contraction is
not only a surface phenomenon: the whole thickness of the wound edge is gradually
pulled toward the center of the wound. Significant contraction occurs mainly in large
wounds, such as ulcers, that are not yet entirely covered by a regrown epithelium.

The new scar is weak for the first five days. Its strength increases markedly over the
next month, as new collagen is laid down and then cross-linked. Nonetheless, most
scars will never be as strong as the original tissues they replace. Scar strengthening
and remodeling taper off after about a year.

IMPEDIMENTS TO WOUND HEALING

The steps in the formation of a normal scar offer many opportunities for the process
of wound healing to become sidetracked (Habif, 2004; Baum & Arpey, 2005; Shai &
Maibach, 2005). Even when all the steps do eventually occur, delays can cause
abnormal healing.

Large wounds and wounds in which much tissue has been lost heal slowly and
produce larger scars. Wounds containing dirt and debris have more problems healing
than cleaner wounds. Poor blood supply to the injured area can slow or even stop the
healing process. Of all problems, however, infection is the most common impediment
to wound healing.

Infection

Infections always obstruct wound healing. Wounds that have been contaminated with
significant numbers of bacteria and other foreign material are at risk for developing
infections, because such wounds are not easily cleansed by the natural scavenging
processes of the reaction (inflammatory) phase of healing.

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Figure 4. A sutured laceration (on the knee) that became infected. (Courtesy of
Antonio M. de Gordon, MD.)

Within hours of an injury, neutrophils and macrophages migrate into the wound and
begin removing debris. Large amounts of bacteria, however, cannot be removed
within the normal reaction phase. When contamination persists, the influx of white
cells continues too. Neutrophils die after 24 hours, and when they are continuing to
infiltrate the wound because of persistent contamination, the dead neutrophils pile up
and begin to clog the wound in the form of pus. Pus slows the formation of
granulation tissue and the re-epithelialization of the wound, giving bacteria still more
time to multiply. Furthermore, many bacteria secrete toxins that add to the tissue
damage in the wound when it has become infected.

When bacteria are given enough time, they will build to the level of an infection. It is
not always easy to recognize an infected wound in the early stages: to the untrained
eye, normal healing can look like a pathologic process. To complicate matters,
different types of wounds can show different clusters of signs when they are infected
(Cutting & White, 2004). Nonetheless, all infected wounds will show at least some of
the following signs:

 Fever
 Pus
 Abscess
 Abnormal smell
 Cellulitis
 Persistent inflammation with an exudate

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  Warmth and redness
 Delayed healing
 Continued or increasing pain
 Edema
 Weak, crumbly granulation tissue that bleeds easily

Operationally, the dirtier the wound, the more it must be rigorously cleansed to avoid
infection.

Re-Injury

Re-injury can slow or stop wound healing. A new scar is weaker than the adjacent
tissue, and the newest scars are the weakest. Pushes and pulls that would have no
effect on healthy parts of the body can reopen a healing wound, even when it is
protected by a well-made dressing. Similarly, if there is significant skin tension
surrounding the wound (eg, over a bent knee), the healing wound will not be able to
seal tightly.

Ischemia/Hypoxia

During normal healing, the granulation tissue develops a temporary dense capillary
bed to provide sufficient fluid, nutrients, and oxygen to the growing cells. After the
reaction (inflammatory) phase, oxygen is especially important for strengthening (ie,
cross-linking) the collagen in the developing connective tissue (Habif, 2004; Baum &
Arpey; 2005, Shai & Maibach, 2005). Anything that decreases the effectiveness of
the local circulation will impede wound healing and weaken the scar.

Ischemia of a wound can arise from too much physical tension across the wound,
ineffective oxygenation of the blood (anemia, lung problems, smoking), or reduced
circulation (atherosclerosis, heart failure, kidney failure, vasoconstriction, too much
pressure on the wound). Differences in the available blood supplies account, in part,
for the fact that facial wounds tend to heal better than foot wounds. The importance of
local circulation to wound healing is reflected in the healthcare maxim "Wounds that
don't bleed don't heal."

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Local Skin Tension

Skin and its underlying tissues are normally under tension. Skin tension is negligible
along skin creases, moderate over relaxed joints and muscles, and high over bent
joints (knees and elbows) and over the skull. During a cutting, ripping, or puncturing
injury, the tension from the adjacent intact skin pulls the free edges of the wound
apart. In places where the wounded skin is under greater tension, the wound gapes
more widely and heals more slowly, and the resulting scar is relatively large.

Figure 5. Lines of least skin tension on the body. The drawing also indicates the areas
of the body where skin wounds have the highest risk of infection. (Courtesy of Scott
Moses, MD.)

Patient Factors

DISEASES

Certain diseases are noted for causing poor wound healing. The most common of the
problem diseases is diabetes mellitus. Scars formed by diabetics have less collagen,
and the collagen that is laid down is more brittle than normal.

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Diabetes also damages blood vessels and makes the skin more prone to ischemia. The
reduced circulation is especially notable in the feet, and foot wounds are notorious for
not healing well in diabetic patients. (See photograph of diabetic foot ulcer below.)

To make matters worse, diabetes leads to peripheral neuropathy. Diabetic patients

lose sensation in their fingers and toes, so diabetic injuries tend to go unnoticed in the
extremities. Finally, diabetics have a weakened inflammatory response, and they are
more susceptible than other people to developing tissue infections.

MALNUTRITION

Malnourished people begin to break down their proteins as a source of energy, and
this slows healing. Specific vitamin deficiencies also lead to poor wound healing.
Vitamin A deficiency impedes the transformation of monocytes into macrophages,
which can slow or halt healing. Vitamin C deficiency leads to weak collagen, which
is the basis of scurvy. Vitamin K deficiency impairs blood clotting.

OLD AGE

As people age, they heal more slowly. In older people, scars form with less and
poorer-quality collagen, and older adults are more likely than the young to have
wounds reopen (dehiscence).

SMOKING

Patients who smoke have poor wounding healing—in addition to suffering a number
of other skin problems that include wrinkling, premature skin aging, higher risks of
squamous cell carcinoma, psoriasis, and hair loss (Freiman et al., 2004).

Healthcare Impediments

Medical care of wounds is an attempt to overcome obstacles to natural healing. In the

course of managing a wound, we reduce the amount of contamination, minimize the
area that must be filled by new tissue, keep the granulation tissue moist, and protect
the healing area. However, our efforts at facilitating wound healing sometimes
introduce new impediments.

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WOUND CLOSURE MISSTEPS

Wounds must be clean before they can safely seal themselves. In an attempt to close
wounds quickly, doctors sometimes suture together insufficiently cleansed tissues.
This leads to an infection and then the dehiscence of the closure.

Another problem in wound closure is the use of suture material that is too thin and
subsequently breaks. In addition, sutures that are too thin or that are tied too tightly
can tear through the weakened skin at the edges of the wound.

Finally, if sutures, staples, or tapes are removed too early, the wound edges will not
have developed sufficient adhesion and the wound will reopen.

PROBLEMATIC DRUGS, SOLUTIONS, AND OINTMENTS

Certain drugs, solutions, and ointments slow wound healing. Doxorubicin

(Adriamycin) given preoperatively inhibits postoperative wound healing.
Glucocorticoids (eg, prednisone) limit the proliferation of fibroblasts and the
production of collagen, and thus steroids make scars relatively weak. Some antiseptic
solutions (eg, 10% povidone-iodine, 3% hydrogen peroxide, 0.5% chlorhexidine) can
slow wound healing. Hemostatic solutions (e.g., ferric subsulfate, 30% aluminum
chloride, silver nitrate) slow the healing of large wounds.

Some topical ointments also slow wound healing; these include triamcinolone
acetonide ointment (0.1%), Furacin, and USP petrolatum. In contrast, other ointments
speed wound healing; these include Neosporin ointment, Silvadene cream, Benoxyl
peroxide preparations, and Eucerin.

X-RAYS

Ionizing radiation damages actively dividing cells. In wounds, the regrowing

epithelium, the newly growing blood vessels, and the fibroblasts that form new
connective tissue are likely to be damaged by a large dose of ionizing radiation.
Normal x-ray imaging is usually not a problem. Cancer therapies, however, give
relatively high doses of ionizing radiation and, in areas of the body exposed to
radiation therapy, wounds heal poorly and infections are more common.

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PART 2: Primary Wound Care

PROTECTION OF CAREGIVERS

People who take care of patients, especially patients with open wounds, should not be
allowed to pose a risk of infecting the patients. At the same time, caregivers should be
protected from acquiring infections from patients. Both goals can be met through the
same set of precautions.

General Precautions

Healthcare workers who will have contact with patients should be screened for
infectious diseases when they are hired. They should be up to date on
their immunizations; this includes vaccination against measles, rubella, varicella, and
hepatitis B, and ongoing yearly influenza immunizations.

A health clinic, office, or hospital will have written safety rules and procedures for
controlling infections, and these should be reviewed regularly with staff. The rules
should include a list of steps to be taken by healthcare workers who inadvertently
come in direct contact with a patient's blood or body fluids—for example, by an
accidental needle stick.

Specific Precautions

Any patient can potentially carry the human immunodeficiency virus (HIV). Medical

staffers working on the first stage of wound care—inspecting, cleansing, closing, and
covering—should wear protective eyewear, a surgical mask, and gloves that are not
easily ripped. Although they will be wearing face masks, medical personnel who have
upper respiratory infections should further protect their patients by not talking or
coughing while leaning over wounds.

PATIENT CARE

Primary wound care means acute wound care—managing a wound the first time it is

presented to a healthcare professional. Currently, we do not have the technology to
repair a wound. Nonetheless, we can remove many obstacles that inhibit the body's
innate wound repair mechanisms.

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Before modern medicine, many wounds did not heal. These wounds may have been
too big, have involved too great a loss of blood, or have became infected. Today, we
can give natural healing mechanisms a much better chance of success because we
have the technology to stop serious bleeding, to cleanse the wound well, and to close
surgically (or otherwise effectively protect) large wounds. The elements of modern
wound care are inspecting, cleansing, closing, and covering.

Basic Plan

Before going into the details of how to inspect, cleanse, close, and cover a wound,
here is the basic plan for treating acute wounds (Auerbach, 2001; Kroot & Hurst,
2004; Simon & Hern, 2004; Lammers, 2006b).

STABILIZE THE PATIENT

Wounds can be dramatic, but treat any life-threatening conditions first. After the
patient has been stabilized, take an inventory of his injuries and plan the order in
which they are to be treated.

TAKE A HISTORY

Follow the order of your treatment plan. When it is time to treat an external
wound, get a historyof the cause of the wound and get a description of the
environment in which it occurred. Also, find out the patient's chronic illnesses,
medical conditions, current medicines, and allergies. Ask about the immunization
history for tetanus. While taking the history, explain to the patient what to expect
during the wound care procedures.

EXAMINE AND ANESTHETIZE THE INJURY

Inspect the wound. Estimate its depth, the degree of contamination, and the internal
tissues that are injured, if any. When there are injuries to internal structures (nerves,
tendons, bones, muscles, ducts, organs), call in a surgical specialist.

Check for significant neural or vascular damage. Caring for a wound will cause the
patient pain; nevertheless, before giving an anesthetic you must check to see if major

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nerves or blood vessels have been injured. Test the injured area and the more distal
areas of the body:

 Is there full sensation?

 Can all muscles be moved?
 Is there adequate circulation?

If you suspect major neural or vascular problems, call in a surgical specialist.

Now, anesthetize the injured area and create a bloodless field. You will already have
stopped any major bleeding. At this point, stop any continuing bleeding. For wounds
on the extremities, consider using an inflated blood pressure cuff as a controllable
tourniquet proximal to the wound.

CLEANSE THE WOUND

Prepare the wound field by cleansing the area surrounding the wound, clipping any
interfering hair, and washing all the adjacent regions with an antiseptic solution.
Drape the areas surrounding the wound.

With instruments (not gloved fingers), remove visible debris. If there is a possibility

that you have missed contaminants or pieces of broken bone, have the wound imaged
to search for debris.Debride the wound, removing devitalized or shredded tissue.
Then, irrigate the wound with a cleansing solution at high pressure

CLOSE THE WOUND

Stop any bleeding that the cleansing process has restarted. If you are going to close
the wound immediately, now suture, staple, tape, or glue the edges of the wound
together.

COVER THE WOUND

Apply topical antibiotics or ointments if appropriate. If the wound is complex, large,

or highly contaminated, you may decide to delay wound closure, instead packing the
wound with saline-moistened sterile gauze. Whether open or closed, cover the wound
with a dressing. Immobilize the injured part of the body as needed.

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MEDICATIONS AND CARE INSTRUCTIONS

Give tetanus prophylaxis, rabies prophylaxis, or systemic antibiotics as needed. If you

are sending the patient home, give wound care instructions. Describe the signs and
symptoms of infection. Schedule a follow-up visit for a wound inspection and/or
suture or staple removal.

Detailed Plan

This section spells out the details for carrying out the basic primary treatment of an
external body wound (Auerbach, 2001; Kroot & Hurst, 2004; Simon & Hern, 2004;
Lammers, 2006b).

STABILIZE THE PATIENT

A bleeding wound will grab your attention, but you must always assess the whole
patient first and immediately begin treating any life-threatening problems. Check the
patient's breathing and heart function. Look for signs of shock, for neck, back, or
skull injuries, and for indications of internal bleeding.

In the beginning, establish the ABCs of trauma care: Airway, Breathing,

and Circulation. Of prime importance is a clear airway; if necessary, intubate or
perform a tracheotomy. If the patient is not breathing spontaneously, the lungs must
be artificially inflated at regular intervals. If the heart is not beating, perform cardiac
resuscitation immediately.

At the same time, serious bleeding must be stopped by pressure or clamping, and
hypovolemic shock needs to be treated with replacement fluids. All these procedures
should be carried out without moving the patient's head or cervical spine until it is
clear that there are no injuries that threaten the spinal cord.

TAKE A HISTORY

After ensuring the stability of the patient and assessing his overall condition, take a
history. Find out the cause of the injury (eg, "hit with a hammer," "fell down the
steps"). The cause can warn you of internal damage, as happens, for example, in
crush injuries. The cause will also alert you to the possibility of hidden internal

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debris, such as bullet fragments, glass, metal shards, gravel, or wood chips. Finally,
the cause will be a guide to prophylaxis, especially if there is the possibility of tetanus
or rabies infection.

Ascertain the time of the injury. The longer a wound remains unclean, the more likely
it is to be infected. A wound that is 12 or more hours old may need to be observed for
a few days before it is directly closed. Determine the environment in which the injury
occurred (eg, "on my back lawn," "in my car"). The surroundings at the time of injury
can suggest the degree to which the wound may be contaminated.

Has the patient had a recent tetanus immunization? What are the patient's
current diseases and medications? For example, does the patient have diabetes or
other diseases such as anemia or atherosclerosis that may compromise the
effectiveness of local circulation? Does the patient have clotting disorders, drug
allergies, or heart disease? Is the patient taking anti-coagulants, immunosuppressive
drugs, or glucocorticoids?

Next, explain the procedures and assure the patient that you will be keeping pain to a
minimum. Your calmness will reduce the patient's fear and stress.

If the patient wants emotional support, limit the friends or family to one person. Warn
this person that there will be needles, scalpels, and blood, and to sit during the
procedures. Then, have the patient lie supine because fainting is common. Wound
care for children requires special patient and family preparation.

EXAMINE AND ANESTHETIZE THE INJURY

While talking to the patient, completely expose and examine the wound area. Remove
jewelry and constricting clothing both proximal and distal to the wound area. Wound
inspection and physical examination are important, but they must be done carefully to
avoid worsening the injuries.

Try to determine the depth of the wound, the degree of contamination, and the
internal tissues (if any) that have been injured. When nerves, tendons, bones, joints,
muscles, ducts, or organs have been injured, call in the appropriate surgical specialist.
If there is the possibility of a fracture, get x-rays.

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Before administering anesthetics, you must determine any significant nerve, blood
vessel, or tendon damage. Test the sensory perception and muscle movements in the
wound area and more distally. Check that there is appropriate perfusion distal to the
wound area. When the wound area involves joints or tendons, be certain that there is
still full range of motion. If there are any deficits, get the advice of a surgeon of the
appropriate specialty.

At this point, the patient should be stable and lying on the back (supine). Bleeding
should be minimal, and you should know whether any major arteries or nerves have
been damaged. You should also have a medical history of the injury and of the
patient.

Your goal, now, is to cleanse the wound of bacteria, dirt, and debris. This can be
painful for the patient, so first provide anesthesia. In an outpatient setting, you will be
using a local anesthetic. Most anesthetics used for wound care are synthetic relatives
of cocaine; they include:

 Benzocaine (Americaine)
 Bupivacaine (Marcaine)
 Chloroprocaine (Nesacaine)
 Dibucaine (Nupercaine)
 Lidocaine (Xylocaine)
 Mepivacaine (Carbocaine)
 Prilocaine (Citanest)
 Procaine (Novocain)
 Ropivacaine (Naropin)
 Tetracaine (Pontocaine) (Strichartz & Berde, 2005)

Local anesthetics can be applied topically, infiltrated locally, or injected at a distance

from the wound to produce a regional block. Anesthetics applied directly to the
wound may slow the healing process, and injections in or near the wound site will
temporarily distort the anatomy. For these reasons, regional anesthesia is often
preferable to local anesthesia, but regional nerve blocks require a trained operator,
such as an anesthesiologist, surgeon, or experienced trauma specialist (Strichartz &
Berde, 2005).

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Various topical anesthetic solutions are used for shallow wounds. Common solutions
include:

 EMLA (lidocaine-adrenaline-prilocaine)
 LAT (lidocaine-adrenaline-tetracaine)
 TAC (tetracaine-adrenaline-cocaine) (TAC is not used for highly
contaminated wounds or wounds in or near mucous membranes.)

Note that adrenaline is commonly known today as epinephrine.

Topical anesthetics are applied by holding cotton balls or sterile gauze soaked in the
drug against the wound for between 10 and 60 minutes, depending on the drug and
the wound.

Local infiltration anesthetics are safe and fast-acting. The commonly used anesthetics
differ mainly in their duration of action. Duration of numbness produced by three
common infiltration anesthetics is:

 Procaine (Novocaine) 20–30 minutes

 Lidocaine (Xylocaine) 30–60 minutes
 Bupivacaine (Marcaine) 120–240 minutes

The dose and concentration of the local anesthetic depends upon the weight of the
patient and the area that needs to be anesthetized.

To infiltrate a local anesthetic, begin injecting at the periphery of the wound. Make
successive small injections moving toward the center of the wound, with each needle
stick in an area that is already becoming numb.

Infiltrating the skin with an anesthetic produces a sharp pain. This pain can be
reduced by using a small (25- to 30-gauge) needle, inserting the needle perpendicular
to the skin rather than at an angle, and injecting the anesthetic slowly. To further
minimize the pain, the anesthetic should be warm and buffered with sodium
bicarbonate.

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Figure 6. Lidocaine (Xylocaine) is a local anesthetic commonly used to infiltrate an
injury in preparation for debridement and washing. (Courtesy of John L. Bezzant,
MD.)

Injecting a local anesthetic proximal to the wound and alongside the appropriate
nerve produces anesthesia in the entire sensory region of the nerve. This is effective,
and especially useful for wounds in the extremities. In such a regional block, the
onset of anesthesia takes longer (typically, 10–20 min) but it lasts 3 to 4 times longer
than when the same drug is used locally (Thomson & Lalonde, 2006). Administering
a regional nerve block requires special training and a detailed knowledge of anatomy.

Before proceeding, it is important to create a bloodless field. Direct pressure is an

effective way to reduce rapid bleeding. Using gauze sponges, sterile packing material,
a pressure dressing, or simply a gloved hand, press down on the wound and maintain
the pressure for at least 10 minutes. A simple compression dressing can be made by
putting a stack of absorptive sponges on the bleed and then wrapping the stack (not
too tightly) with elastic tape or an elastic wrap.

If the wound is in a limb, elevate it above the level of the heart. If direct elevation and
sustained pressure for 15 to 20 minutes are not sufficient to slow the bleeding in an
extremity, temporarily inflate a blood pressure cuff around the limb proximal to (on
the heart side of) the wound; the cuff should left on no longer than 45 minutes.

When wounds continue to bleed, severed small vessels can be clamped and then
ligated individually with absorbable suture material. (Arteries can be tied off, but
veins need to be sutured.) There is an art to clamping vessels while avoiding adjacent
structures such as nerves. Electrocautery at minimum power can be used for the tinier

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vessels. Closing large vessels is a job for a vascular surgeon. Controlling bleeding in
highly vascularized areas, such as the scalp, may require other specialized techniques.

CLEANSE THE WOUND

Traumatic wounds must be cleared of dirt and debris. Before cleansing, debridement,
and wound closure, the wound area must be prepared and draped. When hair hangs
into the wound or makes it hard to cleanse the regions around a wound, it is better to
cut the hair rather than to shave it with a razor. Shaved wounds have a higher rate of
infection.

Put on rip-resistant gloves, protective eyewear, and a surgical mask. Begin by

cleansing the surfaces of skin adjacent to the wound, but avoid getting antiseptic into
the wound itself. Wipe off all the particulate matter, and then scrub the skin with 10%
povidone-iodine (Betadine scrub), which effectively reduces viruses, fungi, and gram-
positive and gram-negative bacteria. Chlorhexidine gluconate (Hibiclens) solution is a
commonly used and effective alternative skin antiseptic.

After cleansing a wide area, paint the antiseptic broadly around the wound. Cover the
painted areas with drapes, leaving an open window over the wound. When the
wounded area is on a hand, paint the hand with an antiseptic. Then, put the hand in a
sterile glove, and cut a window in the glove over the wound.

After draping the area, put on clean, rip-resistant gloves to protect both you and the
patient. The gloves need not be sterile, but if they have any talc or powder, then they
should be rinsed before you touch the wound. Be sure to wear eye protection and a
face mask.

Foreign material increases the risk for infection, so examine the wound for debris.
Use good lighting and try to create a bloodless field. With a metal probe look
methodically through the whole wound – do not use your fingers, because sharp
wood, bone, glass, or metal can rip your glove, cut your skin, and inoculate you with
the patient's blood. With a hemostat or forceps, remove all visible debris.

Sometimes it is necessary to extend the wound by separating or even removing

tissues to explore the injured area thoroughly. Fatty tissues are especially difficult to

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search. If there is any question that you may have missed debris, then use imaging
studies (x-rays, ultrasound, CT scan) to survey the wound.

After carefully picking visible foreign material from a wound, you must remove
tissue that is seriously injured or that is contaminated by bacteria and other debris.
Contaminated and dying tissues provide an ideal growth environment for bacteria,
and thorough debridement (removing seriously damaged and contaminated tissue)
will dramatically decrease the risk of infection.

Debride the wound with forceps and scalpel or scissors. (This is called sharp or
surgical debridement.) Sharp debridement is one of the arts of trauma management,
and it is best left to an experienced physician, but the following are some of the
principles of debridement.

In a few special cases, an entire wound area can be excised. In this way, an irregular,
contaminated wound can be converted into a clean, smooth-edged surgical wound.
This can sometimes be done for small wounds when (a) there are no vital structures—
eg, major blood vessels, nerves, tendons—in the wound, and (b) the skin tension in
the area is not too great. Complete excision is an ideal way to deal with highly
contaminated wounds, such as animal bites, and with certain puncture wounds, from
which debris can be difficult to remove.

Surgical debridement is known as sharp debridement when it is done in an office,

clinic, or emergency room. In most cases, the entire wound cannot be excised.
Instead, through use of a scalpel or scissors, the wound is examined inch by inch,
cutting off bits of devitalized and contaminated tissue and attempting to smooth
extremely ragged or shredded edges. The severely injured or necrotic tissue is
grasped with a forceps or a small hemostat and cut out along the healthy edge. The art
of sharp debridement is in distinguishing viable and nonviable areas of the tissue
(Shai & Maibach, 2005).

When a wound is contaminated, all the exposed fat should be removed during
debridement. Care must be taken not to spread contamination deeper into the wound.
Structural tissues, such as fascia, tendons, and bones, are cleansed and left in place.
Nerves, too, are very gently cleansed and left in place.

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For the protection of healthcare workers and other patients, wounds should be treated
as if they contain contagious bacteria and viruses. Therefore, debrided material must
be put in decontamination containers. Sharp debridement is done with an eye to the
geometry of the eventual wound closure. On the face and the hands, sharp
debridement is an especially challenging task. Wounds should be washed both before
and after debridement.

You have stabilized the patient, assessed and anesthetized the injured area, cleansed
and draped the adjacent skin surfaces, and debrided the wound. The clock is still
ticking, however, because the longer you wait before cleansing the wound, the greater
the chance that bacterial growth will reach infective levels.

Wounds are cleansed by irrigation, and when irrigation is insufficient, wounds are
directly scrubbed and then re-irrigated. Soaking a wound (in saline or in an antiseptic
solution) is not an effective substitute for irrigation.

Irrigation means continuously pressure-washing a wound. When done with sufficient

force, irrigation effectively removes bacteria and debris from the wound and from the
crevices extending into the edges and bottom of the wound. Proper irrigation reduces
wound infection rates dramatically.

Pressure-washing is critical – simply flooding the wound or rinsing it by pouring on

cleansing solution will not reduce the chance of infection. Effective irrigation requires
that the washing solution be squirted into the wound at pressures greater than 7
pounds per square inch (psi). Commercial irrigating machines, such as Water Pik,
Canyons Wound Irrigation System, Irrijet, and the Travenol Pressure Irrigation Set,
all deliver irrigating solution at effective pressures. A 19-gauge needle attached to a
35-ml syringe will also squirt solution at sufficiently high pressures if you push the
plunger with both hands (Auerbach, 2001).

When washing a small wound, try to irrigate it with at least 1/3 liter of cleansing
solution. When irrigating larger wounds (or if you are using lower than optimal
pressure), flush with more than 1/3 liter of solution. Let the continuous drainage of
solution run off into a basin. Be sure to carry out the irrigation behind a protective
cover or splash shield to keep droplets of the patient's blood from spraying the

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surroundings. ZeroWet Inc. makes a protective device (ZeroWet Splashshield) that
fits on the end of a syringe to contain splashes from the wound.

Scrubbing a wound by hand is called mechanical scrubbing. Mechanical scrubbing

with an antiseptic sponge is effective at removing bacteria and debris, but it is also
damaging to the wound tissues. When a wound is highly contaminated, mechanical
scrubbing may be the only way to fully cleanse the wound. In this case, you minimize
the abrasive damage by using a nonionic detergent solution and a fine-pore sponge
(eg, Optipore sponges). Irrigate the wound after the mechanical scrubbing.

Many cleansing solutions are available for wound irrigation. One of the best is plain
tap water, which is safe, inexpensive, and as good as or better than sterile saline
(Anglen, 2005; Beam, 2006). In the past, sterile 0.9% saline was the standard
irrigating solution. Another commonly used solution is 1% povidone-iodine (Betadine
preparation, not the 10% Betadine scrub), which is then followed by flushing with
sterile 0.9% saline solution. In addition, nonionic detergents, such as Poloxamer 188
(Pluronic F-68, Shur-Clens, Pharma Clens), are safe for wound irrigation.

Other cleansing solutions are not recommended for irrigation. For example, some
antiseptic solutions [eg, 5%, 7.5%, or 10% povidone-iodine; chlorhexidine gluconate
(Hibiclens); 3% hydrogen peroxide; hexachlorophene (pHisoHex); alcohols] that are
very effective on intact skin can be too harsh for wounds when used in a pressure
irrigator. Antibiotics are not needed in the irrigation solution, even for deep or
complex wounds (Anglen, 2005).

CLOSE THE WOUND

After washing the wound, gently pat it dry with a sterile pad and then wipe the skin
around the edges. Now, decide whether to close the wound directly and, if so, what
method to use. Your decision can minimize the risk of infection and will also
determine the size of the scar.

When deciding about wound closure, take into account the local skin tensions in the
area of the wound (Habif, 2004). Most skin in the body is being stretched, at least
slightly, by the adjacent skin and the underlying structures, but the actual tension at
any one location varies along the surface of the body. Movement changes skin

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tension: bending a joint stretches the overlying skin, while contracting a muscle tends
to reduce tension in the overlying skin. Skin creases and skin wrinkles are indications
of lines of least tension; on the face, the lines of facial expression are also lines of
least tension. As a rule, the lines of least skin tension are perpendicular to the long
axis of underlying muscles.

In areas of high skin tension (eg, on the scalp, along the front of the tibia) the edges of
a wound are pulled apart, and the wound gaps in the direction of the greatest tension
(perpendicular to the lines of least tension). Skin tension will strain a healing wound
and it will widen the final scar. To achieve the thinnest scars, surgeons make elective
incisions in or parallel to skin creases and perpendicular to underlying muscles. If you
decide to close the wound that you have just cleansed, try to make the long axis of the
wound seam parallel to skin creases, perpendicular to underlying muscles, and along
the local line of least skin tension.

There are three general plans for wound closures: immediate direct closure, indirect
closure, and delayed direct closure (Lammers, 2006a).

 Immediate direct closure (by suturing, stapling, gluing, or taping) is

called healing by first intention or primary wound repair. The wound closure
at the end of a typical surgical operation is an immediate direct closure.
 Indirect closure allows the wound to contract and to re-epithelialize on its
own. This is called healing by second intention or secondary wound repair.
Indirect closures tend to leave a larger scar, but they avoid protecting
bacteria inside a warm moist tissue environment. For highly contaminated
wounds, indirect closure significantly reduces the risk of infection.

Figure 7. A pressure sore healing by indirect closure. Periosteum of bone is visible in
the top picture. Healthy granulation tissue covers the wound in the two middle
pictures. Healing took several months. (Courtesy of Charlie Goldberg, MD.
Copyright © Regents of the University of California.)

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  Delayed direct closure lets the wound remain open initially and later closes it
with sutures or staples. This two-part closure plan is called healing by third
intention ortertiary wound repair. Delayed direct closure is used for highly
contaminated wounds, which may need repeated debridement or may need to
be treated with antibiotics before being closed.

Choosing among the three closure plans is a balance between protection, risk of
infection, and size of the eventual scar. The immediate direct closure of a well-
cleansed wound protects it from new contamination and allows the most control over
the size and appearance of the final scar. In addition, immediate direct closure
protects from drying any exposed deep tissues and structures, such as nerves, blood
vessels, tendons, or bones.

On the other hand, immediate direct closure of an unclean wound encourages the
development of infection. Besides providing a protected environment for bacteria,
wounds closed with sutures add new foci for infection, namely, the suture holes, the
sutures themselves, and the tissue damaged by the sutures. Clean unsutured wounds
are less likely to become infected than clean sutured wounds.

Indirect closures heal more slowly than direct closures. A healthy indirect closure
provides a longer reaction (inflammatory) phase and a more thorough natural
debridement. Moreover, if infection does develop in an indirect closure, you have
direct access to the inside of the wound, so you can debride, irrigate, and apply
antibiotic. Indirect closure (ie, helping a wound to grow closed naturally) is also
called open wound management.

Open wound management should always be considered for wounds that are:

 Already infected
 Very dirty (especially when contaminated by organic matter)
 Made by animal or human bites
 Many hours old at the time of treatment
 Made by crushes, explosions, or other forces causing extensive tissue
damage
 On the bottom of a foot, especially wounds made when stepping in organic
matter, such as found in fields, woods, streams, or garbage

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While managing an open wound, you usually have the option of closing the wound
directly during the first five days. Delayed direct closure is sometimes the best
compromise between immediately suturing a wound to prevent a large scar and
leaving the wound open to prevent the development of infection. Waiting and
watching is often the wisest course.

In wounds with exposed or injured internal structures, such as nerves, joints, or

bones, consult a surgical specialist before deciding on a closure plan.

When you decide on indirect closure, pack the wound and cover it with a dressing. It
is usually unnecessary to apply antibiotics. The packing material should be sterile
fine-mesh gauze moistened with sterile 0.9% saline. The cover dressing should be a
dry, thick absorbent sterile pad or pack of gauze pads. When the wound is near a
joint, the joint should be splinted to keep the injured area immobile.

From this point on, open wound management can often be an outpatient procedure.
The patient, a household member, or a visiting nurse is enlisted to repack the wound
with saline-moistened sterile gauze and to re-cover it with a dry dressing once each
day. (See instructions below.) Although doctors frequently send a patient home with
oral antibiotics, this is usually not necessary.

The wound should be evaluated professionally in 3 to 4 days, which is approximately

the time when the healing process in an open wound is making the transition from the
reaction (inflammatory) phase to the regrowth (proliferative) phase. If there is no
evidence of infection and if the edges of the wound can be pulled together without too
much tension, you can suture the wound closed.

The delay will have allowed time for nonviable tissue to become apparent, and you
should debride the wound and irrigate it again before closing it. A direct closure that
has been delayed only a few days will produce a scar not much larger than if the
wound had been directly closed immediately.

If a hematoma forms in a closed wound, it will push the edges apart, slow the healing
processes, and increase the chance of infection. Even though you stopped the
bleeding earlier, the subsequent debridement and cleansing may restart it; therefore,
before you directly close a wound, make certain that all bleeding is stopped.

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To hold the edges of a wound together in a direct closure, your arsenal includes
sutures, staples, tape, and adhesives. Sutures are the best choice for wounds that are
being pulled apart by tension from the surrounding tissues and for wounds that
require detailed matching of the opposing edges.

Suturing is probably the most widely used direct closure technique, but stapling and
gluing are better methods for closing wounds in the field, away from a medical
facility (Auerbach, 2001). When closing a wound with sutures, you can align the
edges of the wound carefully and hold them together strongly. The detailed nature of
each wound dictates its particular suturing requirements.

Suturing takes skill and experience. In broad terms, the first step is closing the major
deep tissues. When closing an acute traumatic wound, you typically use an absorbable
suture, such as chromic gut or polyglactin (eg, Vicryl) for the deep tissues.

The second step is closing the skin. Typically, you use nonabsorbable sutures, such as
nylon (eg, Ethilon) or polypropylene (e.g., Prolene) for the skin. To close the skin,
push the needle perpendicularly through the full skin so that when you pull the edges
together they will be everted. Carefully match jagged wound edges as long as the skin
along the edges is still viable. The goal is to align the upper surface of the skin along
the scar, so try to insert the needle through equal depths of the opposing edges of the
wound. Tighten each stitch gently so that the edges are everted and touching but are
not crushed together.

After closure, there should be minimal tension across the wound. Semi-permeable
tape strips (e.g., SteriStrips, Clearon Skin Closures) can help to further reduce tension
across a sutured wound. Leave spaces between the strips of tape so fluid and exudate
can escape and be absorbed by the overlying dressing. When the wound is large,
tension across the sutured edges can be reduced by first stitching together individual
deeper layers of tissue or by carefully undercutting and removing some of the deeper
tissue. Undercutting wound edges should be left to an experienced clinician.

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Figure 8. Staplers crimp together the edges of a wound. (Courtesy of Incisive
Surgical.)

Staples hold a wound together more strongly than sutures. Staples are also quicker.
Moreover, metal staples are nonreactive and they produce less inflammation and
shorter healing times than sutures. On the other hand, metal staples are less
comfortable for the patient, and they tend to leave a patterned scar. Metal staples
should not be used on facial wounds or other areas where appearance is important.

Figure 9. Metal staples are less reactive than sutures but they leave a patterned scar.
Staples can also be made of absorbable suture-like material that is less scarring.
(Courtesy of Incisive Surgical.)

For small superficial wounds, tape is often better than staples or sutures. Tape can be
applied quickly and without additional anesthesia, it poses very little added risk of

170
infection, and it is inexpensive. The best tapes for wound closure are nonwoven,
unreinforced, and microporous. Tape is not as strong as staples or sutures, and it does
not work well for gaping wounds or for wounds that will be under tension, such as
those across joints.

To tape a wound closed, first stop all the bleeding and dry the edges of the wound. If
the skin is oily or sweaty, wipe it thoroughly; you can even use a solvent such as
acetone to wipe the adjacent skin. Closely crop any hair around the wound.

When the adjacent skin is clean and dry, increase its adhesiveness by painting tincture
of benzoin, Matisol, or cyanoacrylate glue on the skin alongside the wound. (Let the
benzoin or Matisol become tacky before putting on the tape. Glue can be taped when
it is still wet.)

Use a pre-cut tape (eg, SteriStrips) or cut a piece of sterile adhesive tape to a width of
1/4 inch (0.5 cm). Each strip should be long enough to extend beyond the wound
about 1 inch (2.5 cm) on either side. Fix an end of each tape strip onto the skin at one
side of the wound. Use your fingers to hold the edges of the wound closed, and fix the
other end of the tape strip to the skin along the opposed edge of the wound. Put the
tape strips in parallel, like railroad ties, along the wound. Space the strips 1/8 inch
(0.3 cm) apart to allow for wound drainage. After putting strips across the full length
of the wound, lay a single long thin strip of tape along the ends of the cross strips on
either side of the wound, like a railroad track on railroad ties. The long strips will help
to keep the cross strips from peeling off the skin.

Tissue glues—butyl-2-cyanoacrylate (Histoacryl) or octyl-2-cyanoacrylate

(Dermabond), which is the stronger of the two—are good for closing shallow, sharp-
edged wounds. Like tape, tissue glue can be applied quickly and easily without
additional anesthesia. Glues not only pose no additional infection risk, they actually
decrease the rate of wound infections. Tissue glues are ideal for closing small
lacerations in the field, away from medical facilities (Auerbach, 2001). Glues,
however, are not as strong as sutures or staples.

When closing a wound with tissue glue, first stop the bleeding. Then cleanse and dry
the skin along the edges of the wound. Hold the wound edges together with your
fingers, and paint a thin layer of glue along the cut. Allow the glue to dry
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(approximately 2 minutes), and paint on another layer. Repeat the process until there
are 3 or 4 layers of glue coating the wound.

Glued wounds need extra care: they cannot be immersed in water, and they can only
be rubbed gently. Glues are also disrupted by petroleum-based ointments and salves,
which should not be used on glued wounds. Sometimes tissue glues cause a mild
local inflammatory reaction.

Tissue glues slough off spontaneously after about 4 days, by which time the wound
has usually healed sufficiently to remain sealed without the glue.

COVER THE WOUND

After closing the wound, gently cleanse the surface with moistened gauze, and cover
the wound—typically with an ointment, a dressing, and a protective bandage.

Ointments help to keep wounds moist, and they reduce the crust that can form on the
surface. Ointments also keep dressings from sticking to the wound. On the other
hand, ointments will dissolve tissue glues, so ointments should not be put on wounds
that have been closed with adhesives. For any wound, do not apply ointments
containing corticosteroids, which impede wound healing.

Triple antibiotic ointments with neomycin, bacitracin, and polymyxin are commonly
used on open wounds. Most wound ointments contain antibiotics, but it is currently
unclear whether the antimicrobial action plays any useful role in the healing of
uninfected wounds. Neosporin ointment and Silvadene cream have been shown to
improve wound healing.

Dressings keep a healing wound warm and protected. They also keep the wound from
drying out, while at the same time absorbing excess fluid and exudate, both of which
can slow healing. On the other hand, once a wound is infected, a thick dressing will
encourage bacterial growth; therefore, thick or impermeable dressings are not put
over infected wounds.

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A wound dressing usually has two layers. The primary dressing is put directly on the
wound surface, and it is used to keep the wound moist. The secondary dressing is the
outer layer, and it is used to absorb excess drainage and to protect the wound.

Ideally, the full dressing should protect the wound from bacteria and dirt while
allowing oxygen to diffuse into and water vapor to diffuse away from the wound. The
ideal dressing should keep the wound moist and it should absorb excess fluid. In
addition, in most cases, the primary layer of the dressing should not stick to the
healing surfaces.

A simple traditional dressing begins with a primary layer of petrolatum gauze

(Adaptic, Aquaflo, Betadine, Xeroform) applied to an ointment-covered wound. Over
this, there is a secondary layer of thick, dry gauze. The whole dressing is held in place
by tape (Auerbach, 2001).

Today, a wide variety of primary dressings is available beyond petrolatum gauze. If

you have a choice, tailor the primary dressing to the amount of drainage you expect
from the wound. A non-draining wound can be covered with an occlusive
(impermeable) or semi-occlusive (semi-permeable) dressing such as a wound film.
(See the illustration below of wound film applied to a burn.) A wound draining 1 to 2
ml fluid/day needs a semi-occlusive or an absorbent (nonadherent) dressing. A wound
draining >3 ml fluid/day should have a very absorbent dressing.

In general, changing a dressing daily is frequent enough to avoid infections.

Therefore, wounds with significant drainage should have secondary dressings
sufficiently absorbent to soak up a day's worth of wound fluid. This may require extra
gauze pads, sponges, or cotton.

A wide variety of primary dressings is available, and in a well-stocked clinic or

hospital you can tailor the primary dressing to the specific needs of each particular
wound. Briefly, the major types of specialty primary dressings include (Shai &
Maibach, 2005):

 Nonocclusive dressings
o Activated charcoal—absorbent (Carboflex, Carbonet, Kaltocarb)

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 o Alginate dressings—very absorbent (Algiderm, Curasorb,
Hyperion, Kaltostat, Maxorb, Nu-derm alginate, Nutrastat, Orisorb,
Seasorb, Tegagen alginate)
o Dextranomer hydrophilic granules—very absorbent (Debrisan,
Iodosorb)
 Occlusive dressings
o Water-retentive foams—absorbent (3M Foam, Biatain, Curafoam
plus, Hydrasorb, Lyofoam, Orifoam, Sof-foam, Tielle, Vigifoam)
o Hydrocolloids—absorbent (Comfeel, Dermacol, DuoDerm,
Exuderm, Granuflex, Hydrocol, Nu-derm, Oriderm, Tegasorb,
Ultec)
o Hydrogel—nonabsorbent, moistening (Aquaflo, Curafil,
Dermagran hydrogel zinc-saline, Duoderm hydroactive gel,
Granugel, Hydrosorb, Purilon gel, Vigilon)
o Thin films—nonabsorbent (Bioclusive, Blisterfilm transparent,
Dermafilm, Epiview, Opsite, Orifilm, Polyskin, Tegaderm)

A bandage—an outer layer of dressing—is used to mechanically protect a wound.

Bandages help hold the wound closure in place and can reduce tension across the
healing scar. In addition, the compression provided by a bandage will reduce the open
space (dead space) in a wound and thus discourage hematomas and edema. Bandages
also protect against injuries to the healing wound by providing an additional layer of
padding and by reducing the mobility of the wound area.

Bandages can be made of pads or of cotton overlaid with tape. On the limbs,
bandages can be made using an elastic wrap. All bandages should be smooth and
unwrinkled and should apply pressure equally across a wound. Fix the bandage in
place with tape, and make sure it feels firm, but do not make the bandage so tight that
it impedes circulation.

Repeatedly moving a wound by contracting nearby muscles will slow wound healing
and increase the size of the eventual scar, so immobilize any nontrivial wound that is
in a part of the body near a joint. On the extremities, you can immobilize an injured
area by splinting the nearby joints. Plastic or aluminum splints can sometimes be
added to the outer bandages of a wound. Otherwise, put a separate splint along the
joint. At times, a plaster cast may be needed.

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Give any necessary prophylactic medications. For nonsurgical wounds, you must
always consider protection against tetanus. For wounds caused by mammal bites,
rabies is a consideration. In addition, certain, but not all, wounds should be treated
prophylactically with systemic antibiotics.

Tetanus is a neurologic disease resulting from the poison produced by Clostridium

tetani bacteria. This toxin causes uncontrollable, continuous muscle contractions.
Even in the best hospital settings, tetanus has a fatality rate of 10% or more (Bleck,
2005).

In the United States there are approximately 50 cases of tetanus reported each year,
mainly in older adults. Even this small number could be reduced by a more
comprehensive immunization program. For adults, the CDC recommends a routine
booster dose of tetanus toxoid–containing vaccine every 10 years. For adults who do
not know if they have had a primary set of vaccinations, the CDC recommends that
they begin with a three-dose primary series. Detailed up-to-date recommendations for
wound prophylaxis can be found at http://www.cdc.gov/mmwr/preview/mmwrhtml/.

Adults who have completed the three-dose primary tetanus vaccination series and
who have received a tetanus toxoid-containing vaccine <5 years ago are protected
against tetanus and do not require tetanus prophylaxis as part of their wound care. For
other injured patients, the treatment recommendations depend on the known history
of tetanus vaccinations and the category of the wound.

For tetanus prophylaxis, wounds are divided into two categories: clean-minor
wounds, and major and/or tetanus-prone wounds. Clean-minor wounds are small open
lacerations made by clean objects in clean environments (eg, an accidental cut with a
clean scalpel). Major and/or tetanus-prone wounds include:

 Wounds contaminated with dirt, saliva, or feces

 Wounds untreated for >6 hours
 Puncture wounds (including nonsterile injections)
 Bullet wounds
 Burns
 Frostbite
 Avulsions
 Crushes

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TETANUS PROPHYLAXIS DURING WOUND CARE (adults aged 19–64 years)

If the patient has had a three-dose primary series of tetanus immunizations and has had:

 A booster within the last 5 years—no tetanus prophylaxis is needed for any wound.
 A booster within the last 10 years—tetanus toxoid–containing vaccine should be
given only for major and tetanus-prone wounds.
 No booster within the last 10 years—tetanus toxoid–containing vaccine should be
given for all wounds.

If the patient has NOT had a complete three-dose primary series of tetanus immunizations (or
if primary immunization status is unknown):

 Tetanus toxoid–containing vaccine should be given for clean wounds.

 Tetanus toxoid–containing vaccine and tetanus immune globulin should be given for
major and tetanus-prone wounds.

All bites by mammals should be considered for rabies prophylaxis. Rabies is a viral

disease with a typical incubation period of 1 to 3 months. Once symptoms appear, the
disease is almost 100% fatal; therefore, prophylactic treatment of bites from
potentially rabid animals is essential (Bleck & Rupprecht, 2005).

Rabies is most common in bats, raccoons, and skunks, and the disease is transmitted
in saliva. Most human cases of rabies have come from bat bites. Some increased risk
factors:

 Bites on bare skin are more likely to develop rabies than bites through
clothes.
 Multiple bites are more likely to lead to rabies than a single bite.
 Bites on the face are more likely to transmit rabies than bites on the
extremities.
 Unprovoked animal bites are more likely to develop rabies than bites from
animals biting because were disturbed or frightened.

The decision to begin rabies prophylaxis depends mainly on the type of animal that
caused the bite. Most patients will be able to tell you what bit them and why, and by
contacting your local public health officials or the CDC 24-hour rabies hotline (404-
332-4555), you will be advised about the risk in your location of the biting animal
having rabies. Your public health officials will also try to find the animal if there is

176
any chance that it might be rabid. Rabies prophylaxis can be begun after the wound
has been cared for, so there is time to consult and to make a well-informed decision.

A few general rules can help you in your initial decisions:

 All mammals can potentially be infected with rabies.

 Rabies virus is inactivated by drying and by ultraviolet irradiation.
 Rabies is transmitted only in saliva, but saliva can get into existing cuts or
abrasions even when the animal does not bite a person.
 Blood, urine, and feces will not transmit rabies.
 Petting a rabid animal will not transmit rabies.

The risk for developing rabies from an animal bite depends on the prevalence of the
disease in your locale. The following table presents some general guidelines on
prophylactic treatment for a variety of mammal bites.

People who may have been infected with rabies virus need both active and passive
immunization. Active immunization comes from a five-dose course of rabies vaccine
injections; the effect begins within 7 to 10 days and lasts at least two years. Passive
(direct) immunization comes from an injection of anti-rabies immune globulin; the
effect begins immediately and lasts for a few weeks (Rupprecht, 2004). Before
administering rabies prophylaxis, consult with local public officials and review the
latest CDC recommendations.

Err on the side of caution. If prophylaxis has been started and subsequent tests find
that the offending animal did not have rabies, the treatment regimen can always be
stopped safely.

Although systemic antibiotics are often given to patients with acute wounds, most

clinicians argue that antibiotics should only be given with a specific purpose in mind.

Surgically, all open, fresh, accidental, or penetrating wounds are considered to be

potentially contaminated wounds, and some physicians use this as a reason for giving
anti–skin flora antibiotics such as Cefazolin.

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On the other hand, emergency department physicians usually flag only certain
wounds for systemic antibiotic prophylaxis (Kroot & Hurst, 2004; Simon & Hern,
2004; Lammers 2006b). These wounds include:

 Bite wounds
 Overwhelmingly contaminated wounds
 Sutured intraoral lacerations
 Orocutaneous wounds (mouth wounds that open out into the skin)
 Crush wounds
 Wounds involving tendons, bones, or joints
 Delayed-treatment wounds
 Wounds in people at risk for developing infections

Systemic antibiotics are best given as early as possible during wound treatment, and
the first dose should be administered intravenously or intramuscularly. There is no
one standard antibiotic regimen for wounds at high risk of infection, and there is no
universal agreement on how long the antibiotic prophylaxis should last.

For minimizing the risk of infection, systemic antibiotics cannot replace debridement
and irrigation. Remember that when a wound needs systemic antibiotic prophylaxis it
probably also needs indirect or delayed direct wound closure.

Specific Types of Acute Wounds

The basic wound care techniques detailed above need to be tailored to the particulars
of each individual wound. Here are some cautions, changes, and additional techniques
for specific types of wounds (Auerbach 2001, Kroot & Hurst 2004, Simon & Hern
2004, Lammers 2006b).

MINOR BURNS

Serious burns require treatment in a specialized burn center. The following discussion
is about the treatment of minor burns (Kumar et al., 2004; Edlich et al., 2006). To be
considered a minor burn, the area injured must be a single small patch of the body
outside of the hands, face, feet, armpits, popliteal region, or perineum. The burn
cannot be across a major joint, and it cannot be in a band extending around any part
of the body. Chemical and electrical burns should be treated in a burn center. Infants,

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older adults, and patients with major medical problems may need to be hospitalized
for burns that would otherwise seem minor.

Minor burns are limited to first- and second-degree burns. First-degree burns, such as
sunburns, are called epidermal burns because the damage is mainly to the outermost
layer of the skin. Epidermal burns are red and painful but they do not blister. After
about 2 days, the injured epidermis in a first-degree burn sloughs off ("peels") as new
epithelium grows underneath the damaged tissue.

Second-degree burns are called partial-thickness burns because they involve injury to
the epidermis and part of the dermis. Partial-thickness burns form blisters, usually
beginning a few hours after the injury. The tissue under these blisters is moist and
pink, and it is extremely sensitive; even air currents can be painful. Superficial
partial-thickness burns will heal in 2 to 3 weeks, leaving minor scarring with a lighter
pigmentation than the surrounding skin. Deep partial-thickness burns will heal in 3 to
6 weeks and will leave significant scars.

Full-thickness burns are third-degree burns. They go all the way through the dermis,
and they require treatment in a specialized burn center. In the emergency room, it can
be difficult to distinguish between partial-thickness burns and full-thickness burns.
Here are some general rules (Alsbjorn, 2007):

 Partial-thickness burns look red, white, or pink, and they tend to be wet,
painful, and blistering.
 Full-thickness burns look grey, white, or brownish, and they tend to be dry,
painless, and without blisters. Full-thickness burns can give the appearance
of intact skin, but burn areas lack sensation.

Removing Debris and Debriding

In second-degree wounds, collapsed burn blisters can turn into protected areas of
infection. The decision to drain burn blisters or to leave them intact is a matter of
experience. Small burn blisters and burn blisters on the palms or soles are usually left
intact. Large burn blisters and those over mobile joints are usually opened, and the
blister roof is entirely removed. The open surface is then re-irrigated.

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Cleansed

A new burn should be cleansed immediately with cold tap water. A strong stream of
cold water will irrigate the injury, reduce the pain, minimize edema, and slow some
of the developing damage. Do not use ice or ice water, however (Alsbjorn 2007).

Closing and Covering

Dressings for burns should keep the wound moist and absorb excess exuded fluids.
When the dressing is of a type that must be changed regularly, the dressing should not
be allowed to stick to the wound.

First-degree wounds are irrigated and then overlaid with a nonadherent dressing, such
as petrolatum-impregnated gauze. Second-degree wounds are covered in one of three
ways:

 Bulky gauze dressing. Strips of sterile fine-mesh (type 1) gauze are soaked in
sterile saline and laid over the wound. Fluffed coarse-mesh (type 6) gauze
pads are layered over the strips and are held in place with an inelastic roller-
gauze bandage.
 Synthetic occlusive dressing. For uncontaminated burns on flat body areas,
synthetic membranes (Biobrane, DuoDerm, Epi-lock, Opsite, Tegaderm) are
put directly on the wound as a temporary artificial skin. The synthetic
membrane is then protected with gauze pads.

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Figure 10. This second-degree burn on the back of the hand has been debrided,
washed, and covered with a synthetic occlusive dressing (DuoDerm). (Courtesy of
Ross Bailey.)

 Artificial skin. Laboratory-grown skin and skin substitutes are already being

used to cover and protect burn wounds (Kumar et al., 2004). These
engineered preparations will be more widely available in the near future.

Medications and Follow-Up

Provide tetanus prophylaxis if necessary. Systemic antibiotics are not recommended

for most minor burns. Second-degree burns remain painful, and oral analgesics (eg,
codeine, oxycodone) should be prescribed. Schedule a re-examination in 1 to 2 days.
In the interim, when the burn is on an extremity, advise the patient to keep the
extremity elevated to minimize edema. Describe the signs and symptoms of infection
to the patient and advise to report any problems immediately.

At the re-examination, remove the outer coverings (using sterile techniques) and
inspect the innermost dressing. If the primary dressing is adherent to a fairly dry, pink
wound bed, leave the primary dressing in place. Put a new secondary dressing over
the primary, and schedule another wound check in 5 to 7 days.

If the primary dressing is no longer sticking, if the wound is draining fluid, or if the
wound looks infected, then remove the entire dressing, irrigate and debride the
wound, and treat the specific wound problem. Patients with infected wounds need
systemic antibiotics (Kroot & Hurst, 2004; Simon & Hern, 2004; Lammers, 2006b).

When first- or second-degree burns have healed, the patient should moisturize the
burn area once or twice daily with lotions, creams, or ointments. The patient should
also be advised to try to keep the burn area shaded when he is outdoors and to apply
sunscreen of >25 SPF before exposing the burn area to sunlight.

BITES

All animal bites pose a risk of infection (Rupprecht, 2004; Taplitz, 2004). The most
critical piece of information about a bite wound is the type of animal that inflicted it.
This will guide your choice of prophylactic medicines.

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Bites by adult humans are some of the most serious. Human bites can transmit HIV
and hepatitis along with a variety of necrotizing bacteria. In addition, human bites are
both crushing and tearing and are often made to the hand, where they injure tendons
and joints.

Anesthetizing and Examining

When examining a bite wound, look for underlying fractures and damage to tendons,
ligaments, or joints. Also search for tooth fragments.

Patients do not always get immediate medical care for bites. Those who present after
a delay often do so because they already have signs and symptoms of infection. If an
old bite wound shows evidence of a necrotizing infection—signs such as progressing
redness, blistering, or blackened dying tissue—the patient should be hospitalized for
extensive debridement and IV antibiotics.

Removing Debris and Debriding

Dog bites are typically a mix of lacerations and crushes, producing significant
destruction to the tissues. These bites can require sharp debridement, ideally within a
few hours of the injury.

Cleansing

The best way to prevent infection in bite wounds is aggressive cleansing. Cleanse,
debride, and irrigate the wound thoroughly.

Closing and Covering

Whether to suture a bite wound is frequently a judgment call. Other than human and
monkey bites, most bite wounds are minor, and of these, only about 10% will need
suturing.

Of the serious bites, those with a high risk of infection should be left open, packed,
and watched. Human, monkey, and cat bites are always cleansed and left open. Dog
bites to the hands, dog bite puncture wounds, and dog bites that crush tissues are
usually left open. All bite wounds older than 6 to 12 hours are left open. In addition,

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bites to the hand, ear, or other areas in which tendon, joints, or cartilage are likely to
have been injured are left open.

Other large bites should be cleansed vigorously and sutured to prevent new microbes
from invading the deeper tissues.

Medications and Follow-Up

For a bite wound, always consider tetanus prophylaxis. For mammalian bites, also
consider rabies prophylaxis.

For a human bite, victims should be considered for prophylactic treatments for HIV
and for viral hepatitis if there is a chance the attacker was a carrier. Human bites do
not transmit HIV through saliva alone—blood inoculation is necessary. Details of
recent CDC recommendations for HIV prophylaxis may be found at
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5402a1.htm.

Hepatitis B has been transmitted by a human bite, possibly through infected saliva.
For details of recent CDC recommendations for hepatitis B prophylaxis, go to
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5516a3.htm.

Consult an infectious disease specialist to decide on the proper prophylaxis for your
specific case.

As to prophylaxis for other microbes, systemic antibiotics are recommended for bite
wounds that are not medically treated until 6 or more hours after the injury, for bites
to the face, and for bites that have injured deep tissues such as tendons, joints, and
bones. Antimicrobial prophylaxis is also recommended for all human bites. Bites by
cats are deep puncture wounds and carry an especially high risk of infection;
therefore, antimicrobial prophylaxis is recommended for most cat bites. Dog bites to
the hands, dog bite puncture wounds, and dog bites that have crushed tissue are also
given prophylactic antibiotics.

A culture of the wound (unless it is already infected) will not identify an incipient
wound infection. The best way to choose the appropriate antibiotic is by the type of
animal that made the bite. Many bites will include various species of staphylococcus,

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streptococcus, and corynebacterium. Dog bites are also associated
with Capnocytophaga canimorsus, cat bites with Bartonella henselae and Pasteurella
multocida, and rat bites with Streptobacillus moniliformis and Spirillum minus. A
recent discussion of systemic antibiotic prophylaxis for various animal bites may be
found in Taplitz (2004). If possible, consult an infectious disease specialist when
choosing the antibiotics for your specific case.

Patients who present with an infected bite wound, especially when there is a
necrotizing infection, need to be hospitalized for treatment, which should include
parenteral antibiotics. Likewise, bite wounds that include tendon, joint, cartilage, or
bone injuries should be treated in a hospital.

If a bite wound victim is treated and sent home, the patient should be told to keep the
injured part elevated and immobilized, and to monitor the wound for signs of
infection. The wound should be professionally examined daily for the first 3 days and
then every second day for two more visits.

PUNCTURE WOUNDS

Puncture wounds, especially of the foot, are commonly seen in emergency

departments. Puncture wounds are difficult to cleanse and are prone to infection
(Auerbach, 2001).

Anesthetizing and Examining

Begin by infiltrating the tissue with 1% lidocaine.

Removing Debris and Debridement

It is usually not possible to cleanse a deep puncture wound fully. Use a forceps to
probe gently and then remove debris. Puncture wounds in the hands, wrists, feet, or
ankles can be near critical tendons, nerves, or muscles; to avoid damaging these
structures, do not probe the wounds extensively. In other parts of the body, you can
sometimes carefully open the top of ("unroof") the wound to cleanse it more
thoroughly. If the history suggests there may be internal debris, such as shattered
glass or bits of metal, order radiologic images to identify foreign objects.

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Coring out (excising) or other forms of major debridement are only used when a
puncture wound has a great deal of contamination or an existing infection.

Cleansing

Irrigate the wound under low pressure. Too much direct pressure will force
contamination deeper into the tissues.

Closing and Covering

If the wound is wide enough (eg, if it has been unroofed) pack it open with moist
sterile gauze. Otherwise, simply put on a protective dressing. In all cases, plan to have
the wound professionally re-examined in 2 to 3 days.

Medications and Follow-Up

Be sure the patient is up-to-date with tetanus immunizations. (Tetanus prophylaxis is

discussed in more detail in the Basic Wound Care section above.)

Even medically treated puncture wounds have a high rate of bacterial infection,
frequently by pseudomonas species. For this reason, anti-pseudomonas
cephalosporins, such as ceftazidime (intramuscular) or ciprofloxacin (oral), are often
prescribed prophylactically.

It is hard to predict how well a puncture wound will heal, so schedule a professional
examination of the wound in 2 to 3 days. Give the patient a list of the signs and
symptoms of infection and instruct to report to a medical professional if any problems
develop.

The patient should keep wounded extremities elevated and should not put pressure on
the wound (e.g., walking on an injured foot) until after the first follow-up
examination.

If you find tenderness or infection in a puncture wound during a follow-up visit,

consider cellulitis, septic arthritis, abscess, and osteomyelitis. Imaging, including
local bone scans, may be needed for a proper diagnosis of an infected puncture
wound, and consulting a specialist is the best course of action.

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GUNSHOTS

High-velocity military weapons and shotguns produce severe blast injuries and
extensive tissue damage. Such wounds require surgical debridement, irrigation, and
sometimes fracture treatment. These patients need to be hospitalized and given at
least 24 to 48 hours of IV antibiotics. On the other hand, low-velocity minor gunshot
wounds can often be treated as outpatient cases, even when the wound includes minor
fractures and retained bullet fragments (Hollerman & Fackler, 2004). In general,
minor gunshot wounds are treated as puncture wounds.

Anesthetizing and Examining

Infiltrate the tissue with 1% lidocaine, and image the wound for bullet fragments and
for evidence of internal structural damage.

Removing Debris and Debridement

Debride the surface tissue of powder burns. Unless radiographic images show bullet
fragments that are easily accessible, do not explore the wound deeply for debris. Be
especially careful exploring wounds in the hands, wrists, feet, or ankles. Excising the
wound is rarely a good plan for gunshot injuries.

Cleansing

When a gunshot wound creates a complete tunnel through the body, irrigate the
wound with high pressure. If the wound does not have an exit, irrigate the wound
under low pressure; too much direct pressure can force contamination deeper into the
tissues.

Closing and Covering

If the wound includes bone fractures, consult an orthopedic surgeon. Otherwise, pack
the wound, and leave it open under a protective dressing.

Medications and Follow-Up

Unlike other types of puncture wounds, minor gunshot wounds have a low infection
rate. In general, antibiotic prophylaxis is not needed.

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The patient should keep a wounded extremity elevated and should not put pressure on
the wound (eg, walking on an injured foot) until after the first follow-up examination.
Give the patient a list of the signs and symptoms of infection and instruct to report to
a medical professional if any problems develop. Schedule a professional examination
of the wound in 1 to 2 days.

ORAL WOUNDS

Small wounds of the tongue and the mucosa of the mouth heal quickly. Larger
wounds may require the attention of an oral surgeon.

Anesthetizing and Examining

Be sure to examine the teeth near the wound because they may be loose or fractured.

Closing and Covering

Small lacerations will probably not need closing. Large wounds and wounds
involving underlying structures need to be repaired. After thorough irrigation with
saline, re-approximate muscles with absorbable sutures (eg, 5-0 Vicryl). Then, with a
minimum number of absorbable sutures, close the overlying mucosa. For wounds
with extensive damage, consult an oral surgeon.

Medications and Follow-Up

Wounds limited to the inside of the mouth are slightly more likely to become infected
than similar external wounds. When the wound penetrates through to the outside skin,
however, the infection rate doubles. Prophylactic antibiotics, such as penicillin, are
recommended for large or complex wounds inside the mouth and for penetrating
(through-and-through) wounds.

Have the patient rinse the wound with warm salt water 2 to 3 times daily.

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PART 3: Secondary Wound Care

After their primary treatment, most patients with external wounds can be sent home.
At that point secondary wound care begins, and its success depends on the
cooperation of the patient.

Instructions to Patient

Be sure to take time and explain what the patient can expect over the next few days
and what things the patient should do.

FOLLOW-UP SCHEDULE

Any serious or infection-prone wound must be re-examined professionally in a few

days. Schedule the follow-up examination before discharging the patient.

For Wound Examination

If a wound is complex or prone to infection (such as a bite wound), have it re-

examined by a professional in 1 or 2 days. Wounds that have been left open and that
are being considered for a delayed closure should be re-examined in 4 to 5 days.
Otherwise, schedule a return visit for suture, staple, or tape removal, and have the
patient monitor the wound and report any signs of infection, any re-injury, or any
other problems to a professional.

You will be giving the patient specific guidelines for recognizing an infected wound,
but not all patients will be able use your guidelines effectively. If you suspect that
your patient may not recognize an infected wound, schedule a re-examination in 2 to
3 days.

For Suture Removal

The proper time to remove wound sutures is decided case by case. A general
timetable is:

 Face at 3 to 5 days
 Scalp or trunk at 7 to 10 days
 Arms or legs at 7 to 14 days

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  Joints at 14 days

Staples can usually be removed somewhat earlier than sutures.

PATIENT TEACHING

Your patient should be told what to expect during and after wound healing. Some
helpful information to give a patient includes:

 The wound area may tingle, feel strange, or itch. By pressing on the skin or
by lightly rubbing it, the feelings can usually be toned down. These feelings
may show up for many months, but they should be gone within a year.
 Deeper wounds may have injured some sensory nerves, so the patient may
have numbness or lessened sensation distal to the wound. This problem
usually improves on its own within a year.
 All wounds, no matter how artfully repaired, leave a scar. Typical scars get
darker and redder before they eventually fade. It can be a year or more
before they reach their final appearance.
 Currently, there is not enough scientific support to recommend any of the
creams or lotions that claim to limit scar formation.

HOME CARE INSTRUCTIONS

Write down a set of instructions telling the patient how to care for the healing wound.

Check for Signs of Infection

Include a written list of the basic signs and symptoms of infection. Tell patients that if
they are worried about something seen or felt in the wound or if they develop any of
the signs and symptoms of an infection, they should report it to a healthcare
professional. Be sure to tell your patient whom to contact.

Signs and symptoms of an infected wound

 Pus or yellow, greenish, or think whitish fluid in the wound

 Increased redness in the wound

 Redness radiating out into the skin around the wound

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  Red lines progressing up an extremity

 Increasing pain or tenderness (uninfected sutures do not cause pain)

 Swelling

 Wound getting warmer than normal skin

 Fever

Elevate the Wound

Elevating the injured area will minimize swelling, reduce any throbbing pain, and
speed up healing. If the wound is on an arm or a leg, tell the patient to try to keep the
injured area elevated during the first 2 days. For injuries to the hand or forearm, the
patient should consider wearing a sling.

Protect the Wound

Tell the patient:

 When it is healing normally, most wounds that have been directly closed will
become impermeable to bacteria and water within two days.
 The edges of a directly closed healing wound are held together only weakly
for the first 5 days; therefore, be especially careful with the wound for the
first week. The new scar will then strengthen rapidly over the next month.
 A wound that has been splinted should remain immobilized until the sutures
or staples have been removed.
 There is no general reason that most healing wounds need to be kept dry.
After day 2, patients with sutured or stapled wounds can bathe and shower.
Swimming in uncontaminated water is usually safe after the wound begins to
strengthen (i.e., after about 5 days).

Cleanse the Wound

You will probably send all wounds home with a protective dressing. Minor wounds
and many sutured or stapled wounds will not need these coverings after a day. The
coverings can then be discarded and the wound left uncovered.

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In most cases, you can tell your patient that, when treating the wound, cleanliness is
needed but sterility is not.

A sutured or stapled wound without a dressing can be cleansed gently twice a day
with soap and water, beginning 1 day after the suturing or stapling. A major goal of
these washings is to remove the crusting that develops from the wound exudate. Such
a wound can remain uncovered from day 2 on.

When the wound is inside the mouth, have the patient rinse the injured area at least
three times daily with warm salt water.

For wounds that need continued covering, for the first 2 days, the patient should keep
the wound dressing clean and dry, and change the dressing only if it gets dirty or
becomes saturated with exudate. Beginning on day 2, the wound can be cleansed and
the dressing changed daily. After a week, most wounds can be left uncovered.

To change a dressing:

 Gently remove the dressings.

 Wash the wound with soap and tap water (Anglen, 2005)
 Pat the wound dry.
 Apply a moistening ointment, such as a triple antibiotic ointment.
 Put on a fresh dressing.

Medicines to Avoid

In the early healing stages, patients should not take aspirin, because it decreases the
strength of the scar and it increases the risk of developing a hematoma. Patients
should also not drink alcohol during the hours after the initial wound treatment.

Professional Care

For serious, infected, and nonhealing wounds, a professional should handle the
secondary care.

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DRESSING CHANGES AND WOUND CLEANSING

As a general rule, wait 48 hours before the first dressing change, unless the dressing
becomes saturated with wound exudate. After the first dressing change, change the
dressing only when it becomes dirty or saturated with wound drainage or other fluid.
When a dressing becomes filled with fluid, microbes can diffuse through it and into
the underlying wound. Therefore, any wound coverings that become saturated with
drainage need to be changed. Dressings over heavily draining wounds may have to be
changed frequently. Sometimes, you can reduce the number of dressing changes by
aspirating the fluid (eg, with a sterile needle and syringe) from the dressing.

A dressing change includes gently removing the dressings, washing the wound with
soap and tap water, patting the wound dry, applying a moistening ointment, and
putting on a fresh dressing. If the dressing sticks to the wound during removal,
replace it with a less adherent type of primary dressing.

EXCESS GRANULATION TISSUE

Granulation tissue is the loose collection of fibroblasts, inflammatory cells, and new
blood vessels that forms in the base of open wounds during the regrowth
(proliferative) phase of healing. Epithelial cells use granulation tissue as a surface to
move along as they re-cover the wound.

When wounds are left open to heal by indirect closure, the regrowth phase is
prolonged. Sometimes, the granulation tissue has sufficient time to overgrow the top
of the wound and become a barrier to the growing epithelial cells. Excess granulation
tissue (also called exuberant granulation tissue) forms most often in scalp, temple,
and lower leg wounds.

For a wound to heal properly, excess granulation tissue should be removed. To clear
the wound, scrape out the granulation tissue down to the base of the wound. Then,
irrigate the wound. Regrowth of the granulation tissue can be inhibited by treating the
wound base with silver nitrate or by covering the wound base with Scarlet Red–
impregnated gauze (Scarlet Red Ointment Dressing). Finally, protect the wound with
sterile gauze (Habif, 2004).

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INFLAMED WOUNDS

Infected wounds become red, warm, tender, and swollen; they may ooze pus and have
a disagreeable smell (Cutting & White, 2004). If a closed wound becomes infected,
remove the sutures, staples, tape, or glue. Re-examine the wound for debris, then
debride, irrigate, and pack the wound with moist sterile gauze. Apply warm
compresses over the packing, and give the appropriate antibiotics. Re-cleanse and
repack the wound at least once daily, and plan to let the wound heal by secondary
intention, without closure. If patients develops sepsis, they must be hospitalized.

Some wounds that have been sutured closed over extensive subcutaneous tissue
dissection and debridement can develop a temporary inflammatory reaction in which
they become red and edematous, although they are not infected. If you suspect this
problem, remove one or two stitches to lessen the tension, and apply warm
compresses. Then, cleanse the wound daily with soap and water. This type of
inflammatory reaction will decrease within 48 hours.

CHRONIC NONHEALING WOUNDS

Chronic wounds are those that fail to heal when expected. Large wounds heal slowly,
but you would expect even large wounds to be healing within 3 to 4 months.

Figure 11. A chronic nonhealing wound—an inflamed ulcer on the foot of a diabetic
patient. (Courtesy of Frank DiMauro.)

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Treat the Whole Person

Wounds do not heal well if they are infected, edematous, or ischemic. In chronic
nonhealing wounds, these problems are often secondary to broader health disorders,
such as diabetes, venous blockage, arterial insufficiency, malnutrition, cigarette
smoking, or excess alcohol consumption. Therefore, when dealing with a chronic
wound, begin by assessing the entire person, and try to improve overall health.
Meanwhile, find and work on the specific direct impediments to the healing of the
wound (Shai & Maibach, 2005; Kravitz et al., 2007).

Debride, Irrigate, Pack, and Leave Open

All open wounds contain some bacteria, but ulcers and other chronic wounds
frequently have an excess bacterial burden, even when the surrounding tissue has not
developed overt infection (cellulitis). Moreover, given sufficient time, chronic wound
bacteria become coated with polysaccharides that form a biofilm that keeps
antibiotics at bay. Therefore, many chronic wounds need a new debridement followed
by thorough irrigation (Falanga, 2006; Shai & Maibach, 2005).

Debridement appears to help any chronic wound that has not produced much
granulation tissue (Sherman, 2002; Williams et al., 2005), and the classic treatment
for most chronic wounds is debride, irrigate, pack with moist gauze, and leave open
for natural (indirect) closure.

Pressure Ulcers

Pressure ulcers (formerly, decubitus ulcers) are the most common type of chronic
wound (Shai & Maibach, 2005). In a pressure ulcer, the injury has been caused by
local ischemia from the continuous compression of capillary beds. Often, this
compression happens when a patient lies unmoving on a hard mattress.

A pressure ulcer is usually worse than it appears from the surface. Skin is more
resistant to ischemia than is underlying tissue, and in a pressure ulcer a small skin
wound can be the top of a larger injury in the subcutaneous tissue and muscle below.
As the deeper tissues break down hidden pockets form, and these spaces will shelter
bacteria from superficial cleansings (Diegelmann, 2003).

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Pressure ulcers usually need debridement, irrigation, and packing with moist gauze.
As with other ischemic wounds, pressure ulcers can benefit from treatment with
hyperbaric oxygen (Mathieu et al., 2006; Niinikoski, 2006).

Negative-Pressure Dressings

Some chronic wounds became stalled in the reaction (inflammatory) phase of healing
(Shai & Maibach, 2005). Typically, these wounds exude fluid that is low in
constructive molecules, such as growth factors, and high in destructive molecules,
such as proteases (Diegelmann, 2003). The destructive factors constantly impede the
construction of the extracellular matrix that is the foundation of healthy granulation
tissue. To get healing back on track, the excess fluid produced by these wounds must
be wicked away.

Negative-pressure dressings (also called vacuum-assisted closure devices or sub-

atmospheric pressure dressings) are labor-saving devices for removing excess fluid
from wounds (Wolvos, 2004; Shirakawa & Isseroff, 2005; Segre et al., 2006). A
negative-pressure dressing is made of an absorbent pad fitted into the wound and
covered by a plastic film. A suction tube is buried in the pad, and when vacuum is
applied to the tube it continuously sucks fluid from the wound. The vacuum also pulls
the plastic film tightly over the top of the wound, sealing the wound from the
environment. In addition to removing excess wound fluid, a negative-pressure
dressing dilates capillary beds around the wound and increases local circulation. For
complex wounds, it may be necessary to apply a negative-pressure dressing
continuously for as long as 3 weeks (Herscovici et al., 2003).

Negative-pressure dressings remove fluid while maintaining moisture in the wound.

This is important, because drying a wound will slow its healing.

Culture and Biopsy

Wounds that refuse to heal after special care may have unusual infections such as
fungi, or have developed destructive processes such as carcinomas. When a wound
resists healing, consider having it cultured and biopsied (Shai & Maibach, 2005).

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Future Aids

Skin grafts, even when they are not permanent, can help some recalcitrant wounds to
heal. In the near future, artificial skin, laboratory-grown skin, and skin substitutes will
be more commonly available to cover and protect wounds that are not able to
epithelialize themselves (Clark et al., 2007). In addition, the application of
constructive biochemical molecules, such as growth factors, has proved useful in
inducing healing in chronic wounds (Cianfarani et al., 2006; Faler et al., 2006;
Inokuma et al., 2006; Deshane et al., 2007). Solutions of these molecules will be
more widely available in the future.

Suture and Staple Removal

The edges of a closed wound must be held together long enough for a strong natural
seal to form. If sutures or staples are removed too early, the wound will reopen
(dehisce) and the final scar will be unnecessarily wide. When planning to remove
staples or sutures, first remove one or two and check the strength of the developing
seal between the skin edges. If the seal seems too weak to stay closed without help,
replace the removed sutures or staples with tape strips.

When preparing to remove sutures or staples:

1. Wash the wound and gently remove crust around the sutures or staples.
2. Wipe the skin with an alcohol swab.

To remove sutures:

3. Cut the stitches one by one with the tip of a scissors (or a No. 11 scalpel blade)
close to the skin on one side of the wound. Then grasp the suture near the skin
on the opposite side of the wound and pull the suture out through the wound.
4. After removing sutures from the face or from wounds that may be weak, replace
the sutures with tape strips (eg, SteriStrips) to ease the tension on the wound.

If sutures have been left in place too long (usually >10 days), they will leave holes
(epithelial tracts) that can become infected and that may heal with an unsightly
pattern of scars. If small abscesses develop in the epithelial tracts, apply warm moist
compresses after the sutures have been removed. The abscesses should clear quickly
and antibiotics are rarely needed.
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When the suturing has been complicated—such as when nonabsorbable subcuticular
sutures have been used or when there are special cosmetic requirements—an
experienced professional should decide on the removal schedule and should then
carry out the removal.

Staples can usually be removed somewhat sooner than sutures. When staples are
removed from any part of the body, they are often replaced with tape strips to
continue protecting the healing seam.

Minimizing Scars

Scars are the natural patches produced in a healing wound. In the skin, scars are made
of unspecialized fibrous tissue covered by a layer of epidermis (Habif, 2004).

In the first few days after an injury, closed skin wounds are being knit weakly
together by the forming scar tissue. By about day 5, the basic architecture of the
wound patch has been established, and from then on, the healing process consists
largely of strengthening and remodeling the scar.

Scars can take 6 to 9 months to mature. New scars tend to be red and thick for a
month or two before gradually become less vascular (i.e., paler), less bulky, and flat.
It can take as long as 5 years for a scar to reach its final color.

The width of the scar can be minimized by thorough debridement, by careful suturing
(avoiding inversion of the skin edges), by removing excess granulation tissue, by
good secondary wound care (especially by keeping the wound from becoming
infected), and by removing sutures promptly.

Some maturing scars manufacture too much collagen. These scars are either keloids
or hypertrophic scars. Keloids are benign tumors that grow beyond the bounds of the
wound and do not regress. The tendency to form keloids is genetic, and there are, at
present, no preventive measures. (See earlier photograph of a keloid scar.)

In contrast, hypertrophic scars, which are thick but do not grow outside the edges of
the wound, usually get smaller spontaneously. Hypertrophic scars are produced in
wounds that are under tension, such as those parallel to underlying muscles. By

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reducing the tension on a wound, hypertrophic scars can often be prevented or
minimized.

Hypertrophic scars are also produced in wounds that have a long reaction
(inflammatory) healing phase, where re-epithelialization has been delayed, such as is
the case in many burn wounds. For burn patients, continuous pressure (constant
pressure lasting 6 to 12 months) can help to reshape and flatten hypertrophic scars.

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