Life-Threatening Conditions and General

Interventions
Diabetic Ketoacidosis

DEFINITION

Diabetic ketoacidosis (DKA) is a life-threatening complication in patients with untreated

diabetes mellitus (chronic high blood sugar or hyperglycemia). Near complete deficiency
of insulin and elevated levels of certain stress hormones combine to cause DKA. DKA is
more common among Type I diabetics, but may also occur in Type II diabetics generally
when physiologically stressed, such as during an infection. Patients with new,
undiagnosed Type I diabetes frequently present to hospitals with DKA. DKA can also
occur in a known diabetic who fails to take prescribed insulin. DKA was a major cause of
death in Type I diabetics before insulin injections were available; untreated DKA has a
high mortality rate.

PATHOPHYSIOLOGY

DKA is characterized by hyperglycemia, acidosis, and high levels of circulating ketone

bodies. The pathogenesis of DKA is mainly due to acidosis. Excessive production of
ketone bodies lowers the pH of the blood; a blood pH below 6.7 is incompatible with life.
Onset of DKA may be fairly rapid, often within 24 hours.
A key component of DKA is that there is no or very little circulating insulin so it occurs
mainly (but not exclusively) in type 1 diabetes (because type 1 diabetes is characterized
by a lack of insulin production in the pancreas). It is much less common in type 2
diabetes because that is closely related to cell insensitivity to insulin, not shortage or
absence of insulin. Some type 2 diabetics have lost their own insulin production and must
take external insulin; they have some susceptibility to DKA.

Symptoms and Signs

• Sluggish, extreme tiredness.

• Extreme thirst, despite large fluid intake.
• Constant urination
• Fruity smell to breath, similar to nail polish remover or peardrops.
• Hyperventilation, at first rapid and shallow, then progressively deeper and less
rapid.
• Extreme weight-loss.
• Oral Thrush may be present, or/ yeast infections that fail to go away, this is
because the normal fungal/flora present in oral cavity/cervix in women, the balance is
upset and bacterial began to feast on the high sugar from urine output/ dry mouth from
extreme thirst.
• Muscle wasting.
• Agitation / Irritation / Aggression / Confusion
Complications

People with diabetic ketoacidosis need close and frequent monitoring for complications.
Surprisingly, the most common complications of DKA are related to the treatment:
• Hypokalemia and often, potassium depletion
• Cerebral edema
• Hyperglycemia
• Ketoacidemia
• Fluid and electrolyte depletion
• Aspiration
• Unrecognized renal tubular necrosis
• Pulmonary edema
• Myocardial Infarction

Treatment

Treatment consists of hydration to lower the osmolality of the blood, replacement of lost
electrolytes, insulin to force glucose and potassium into the cells, and eventually glucose
simultaneously with insulin in order to correct other metabolic abnormalities, such as
lowered blood potassium (hypokalemia) and elevated ketone levels. Many patients
require admission to a step-down unit or an intensive care unit (ICU) so that vital signs,
urine output, and blood tests can be monitored frequently. Brain edema is not rare, and so
this may suggest intensive monitoring as well. In patients with severe alteration of mental
status, intubation and mechanical ventilation may be required. Survival is dependent on
how badly-deranged the metabolism is at presentation to a hospital, but the process is
only occasionally fatal.

Hepatic encephalopathy (HE)

DEFINITION

Hepatic encephalopathy (HE), also known as Porto systemic encephalopathy or PSE, is

defined as mental or neuromotor dysfunction in a patient with acute or chronic liver
disease. Several forms of HE have been described the acute form of HE is often
associated with fulminant hepatic failure and may rapidly progress to seizures, coma,
decerebrate posturing and death. In patients with cirrhosis, acute encephalopathy is most
commonly associated with a precipitating factor such as electrolyte disturbance,
medications, gastrointestinal hemorrhage, or infection. Recurrent HE may occur with or
without a precipitating factor and is usually easily reversible. Persistent HE is rare, and is
defined as the persistence of neuropsychiatric symptoms despite aggressive medical and
dietary therapy. The most frequent form of HE is not always clinically apparent: a patient
with sub clinical HE has only mild cognitive deficits or subtle personality changes.
Specific neuropsychological or neurophysiologic testing is required to secure the
diagnosis.
PREVALENCE

By definition, all patients with fulminant hepatic failure have some degree of hepatic
encephalopathy. Because there is no definitive test for HE, the prevalence in other
patients is difficult to describe. Clinical findings may be apparent in as many as one third
of cirrhotic patients; if rigorously tested, up to two thirds have some degree of mild or
sub clinical hepatic encephalopathy.

PATHOPHYSIOLOGY

HE remains a complex clinical problem, the precise mechanism of which is unknown.

The premise of most pathophysiologic theories is that ammonia accumulates in the
central nervous system producing alterations of neurotransmission that affect
consciousness and behavior. These "ammonia toxicity" theories have been supported by
studies demonstrating increased ammonia levels in patients with both fulminant hepatic
failure and chronic liver disease. The lack of strong correlation between serum ammonia
levels and stage or degree of encephalopathy has been used in the argument that
hyperammonemia may not be the sole factor in HE pathogenesis.

SIGNS AND SYMPTOMS

In patients with progressive HE, there is a gradual decrease in level of consciousness,

intellectual capacity, and logical behavior along with development of specific neurologic
deficits. Two staging systems have been described. (1) Numerous studies have employed
the West Haven criteria of altered mental status in patients with HE.

DIAGNOSIS

HE is a diagnosis of exclusion. Similar neuropsychiatric symptoms are seen in a variety

of metabolic disorders, toxic ingestions, or intracranial processes in certain patients, brain
imaging or electroencephalography may be indicated to exclude an intracranial
abnormality. Lumbar puncture with cerebrospinal fluid analysis may also be required in
patients with unexplained fever, leukocytosis, or symptoms suggestive of meningeal
irritation. Knowledge of the existence of acute or chronic liver disease and/or the history
of HE are often helpful in heightening clinical suspicion and/or securing the diagnosis.

Precipitating Factors In Hepatic Encephalopathy

• Anemia
• Azotemia/uremia
• Constipation
• Dehydration
• Excessive dietary protein
• Gastrointestinal bleeding
• Hepatoma
• Hypokalemia, metabolic alkalosis
• Hypoglycemia
• Hypothyroidism
• Hypoxia
• Infection (urinary tract, ascites, etc.)
• Medications (narcotics, sedatives, etc.)
• Vascular occlusion

TREATMENT

The main objectives in the treatment of HE are fourfold: (1) provide supportive care, (2)
correct any precipitating factors, (3) reduce the nitrogen load in the gastrointestinal tract,
and (4) assess the need for long-term therapy. Each of these objectives will be discussed
separately here.

Standard supportive care is required for all hospitalized patients with HE. Patient safety
and frequent monitoring of mental status is crucial. This may require additional
personnel. In the case of comatose patients, admission to the intensive care unit and/or
endotracheal intubation may be necessary. Patients with HE should also avoid prolonged
periods of fasting. Although the restriction of dietary protein at the time of acute HE is
often a cornerstone of therapy, protracted nitrogen restriction can lead to malnutrition.
Therefore, appropriate enteral nutrition, either by mouth or nasogastric feeding tube,
should be administered as soon as feasible.

KIDNEY FAILURE / END STAGE RENAL DISEASE

DEFINITION

Renal failure or kidney failure is a situation in which the kidneys fail to function
adequately. It is divided in acute and chronic forms; either form may be due to a large
number of other medical problems.
Biochemical, it is typically detected by an elevated serum creatinine. In the science of
physiology, renal failure is described as a decrease in the glomerular filtration rate. When
the kidneys malfunction, problems frequently encountered are abnormal fluid levels in
the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate,
hematuria (blood in the urine) and (in the longer term) anemia. Long-term kidney
problems have significant repercussions on other diseases, such as cardiovascular disease.

Classification
Renal failure can broadly be divided into two categories: acute renal failure and chronic
kidney disease.
The type of renal failure (acute vs. chronic) is determined by the trend in the serum
creatinine. Other factors which may help differentiate acute and chronic kidney disease
include the presence of anemia and the kidney size on ultrasound. Long-standing, i.e.
chronic, kidney disease generally leads to anemia and small kidney size.
Causes
Unlike acute renal failure, chronic renal failure slowly gets worse. It most often results
from any disease that causes gradual loss of kidney function. It can range from mild
dysfunction to severe kidney failure. The disease may lead to end-stage renal disease
(ESRD).
Chronic renal failure usually occurs over a number of years as the internal structures of
the kidney are slowly damaged. In the early stages, there may be no symptoms. In fact,
progression may be so slow that symptoms do not occur until kidney function is less than
one-tenth of normal.
Chronic renal failure and ESRD affect more than 2 out of 1,000 people in the United
States. Diabetes and high blood pressure are the two most common causes and account
for most cases. Other major causes include:
• Alport syndrome
• Analgesic nephropathy
• Glomerulonephritis of any type (one of the most common causes)
• Kidney stones and infection
• Obstructive uropathy
• Polycystic kidney disease
• Reflux nephropathy

Symptoms

Initial symptoms may include the following:

• Fatigue
• Frequent hiccups
• General ill feeling
• Generalized itching (pruritus)
• Headache
• Nausea, vomiting
• Unintentional weight loss

Exams and Tests

There may be mild to severe high blood pressure. A neurologic examination may show
polyneuropathy. Abnormal heart or lung sounds may be heard with a stethoscope.
A urinalysis may show protein or other abnormalities. An abnormal urinalysis may occur
6 months to 10 or more years before symptoms appear.
• Creatinine levels progressively increase.
• BUN is progressively increased.
• Creatinine clearance progressively decreases.
• Potassium test may show elevated levels.
• Arterial blood gas and blood chemistry analysis may show metabolic acidosis.
Than normal, may be seen on: Signs of chronic renal failure, including both kidneys
being smaller
• Abdominal CT scan
• Abdominal MRI
• Abdominal ultrasound
• X-rays of the kidneys and abdomen

Treatment

The goal of treatment is to control symptoms, reduce complications, and slow the
progression of the disease.
Diseases that cause or result from chronic kidney failure must be controlled and treated as
appropriate.
Blood transfusions or medications such as iron and erythropoietin supplements may be
needed to control anemia.
Fluids may be restricted, often to an amount equal to the volume of urine produced.
Restricting the amount of protein in the diet may slow the build up of wastes in the blood
and control associated symptoms such as nausea and vomiting.
Salt, potassium, phosphorus, and other electrolytes may be restricted.
Dialysis or kidney transplant may eventually be needed.

Possible Complications

• Anemia
• Cardiac tamponade
• Changes in blood sugar metabolism
• Congestive heart failure
• Decreased functioning of white blood cells
• Decreased immune response
• Decreased libido, impotence
• Dementia
• Electrolyte abnormalities including hyperkalemia
• Encephalopathy
• End-stage renal disease
• Fractures
• Hemorrhage
• High blood pressure
• Increased infections
• Joint disorders
• Liver inflammation (hepatitis B or hepatitis C)
• Liver failure
• Loss of blood from the gastrointestinal tract
• Menstrual irregularities,mscarriage, infertility
• Nerve damage
• Pericarditis
• Peripheral neuropathy
• Platelet dysfunction
• Ulcers
• Seizures
• Skin dryness, itching /scratching with resultant skin infection
• Weakening of the bones
Prevention

Treatment of the underlying disorders may help prevent or delay development of chronic
renal failure. Diabetics should control blood sugar and blood pressure closely and should
refrain from smoking.

Respiratory Distress Syndrome

Adult respiratory distress syndrome (ARDS) is a diffuse pulmonary parenchymal injury

associated with noncardiogenic pulmonary edema and resulting in severe respiratory
distress and hypoxemic respiratory failure.

The pathologic hallmark is diffuse alveolar damage (DAD), but lung tissue rarely is
available for a pathologic diagnosis.

Pathophysiology

DAD results in loss of the integrity of the alveolar-capillary barrier, transudation of

protein-rich fluid across the barrier, pulmonary edema, and hypoxemia from
intrapulmonary shunting. ARDS has a diversity of predisposing conditions, including
direct pulmonary injury (eg, pulmonary infection or aspiration) and indirect injury (eg,
sepsis, pancreatitis, multiple trauma). Frequently, ARDS develops in association with
other organ dysfunction, in which case it is part of the multiple organ dysfunction
syndrome (MODS).

The exact mechanism by which the predisposing condition results in DAD is not known
fully, but most likely it is mediated, at least in part, by reactive oxygen radicals and
proteolytic enzymes from neutrophils. Other mechanisms mediated by cytokines,
complement, or endotoxin also may be involved.

The following 3 phases in the pathogenesis of ARDS have been described:

• Exudative phase is the initial phase, with injury to the endothelium and
epithelium, inflammation, and fluid exudation.
• Fibroproliferative phase follows the exudative phase and is characterized by the
influx and proliferation of fibroblasts and other cellular elements. In this phase,
injury may begin to resolve or become persistent.
• In those who recover, the fibrosis phase of healing is marked by resolution of
inflammation and development of varying degrees of pulmonary fibrosis.

Clinical Manifestations:

Findings on physical examination are not specific for ARDS and can be found in
pulmonary edema of any cause.
• Labored breathing and tachypnea (almost universally present)
• Cyanosis and moist skin
• Tachycardia
• Hyperventilation
• Scattered crackles
• Increased work of breathing
• Agitation
• Lethargy followed by obtundation

Causes

• Many conditions have been found to precipitate ARDS. In some cases a

predisposing condition cannot be identified. The following is a partial list of the most
common predisposing conditions:
•
o Infection - Pneumonia of any etiology (especially viral) and systemic sepsis
(especially gram negative)
o Shock - Any type, particularly septic and traumatic shock
o Aspiration - Gastric contents, near drowning, and toxic inhalation
o Trauma - Pulmonary contusion, fat embolization, and multiple trauma
o Other - Systemic inflammatory response syndrome, pancreatitis,
postcardiopulmonary bypass, massive blood transfusion, drug ingestion (eg, heroin,
methadone, barbiturates, salicylates)
Imaging Studies
• The chest radiograph reveals characteristic diffuse alveolar-interstitial infiltrates
in all lung fields.
•
o In early cases, the radiographic findings may not be fully developed.
o Additional localized pulmonary findings may be present if the predisposing
condition involves a pulmonary process.
• Chest CT may be helpful in advanced cases but is not necessary for diagnosis.
• Echocardiography may be helpful to exclude a cardiogenic etiology for
pulmonary edema.

Procedures

• Sputum should be collected for Gram stain and cultures (eg, bacterial, fungal,
viral) if a pulmonary infection is present. These are best obtained from the lower
respiratory tract shortly after endotracheal (ET) intubation.
• Bronchoscopy with bronchoalveolar lavage may be helpful to identify occult
pulmonary infection but is usually performed in the ICU.
• A pulmonary artery catheter may be helpful to exclude cardiogenic causes but
usually is placed in the ICU.

Medications:

As of yet, no medication has been shown to affect the pulmonary inflammatory process
of ARDS directly. Late cases with a persistent fibroproliferative phase may respond to
steroids, but these cases are not seen in the ED. Administer antibiotics following
appropriate cultures in cases of pulmonary or extrapulmonary infection leading to ARDS.
The mainstays of therapy are cardiopulmonary support and treatment/eradication of the
underlying or predisposing conditions. Cardiovascular instability despite fluid
administration is managed with catecholamines, such as dopamine and/or dobutamine.

ASTHMA

Description

Asthma is a chronic inflammatory disease of the airways. Asthma commonly is caused by

physical and chemical irritants such as foods, pollens, dust mites, cockroaches, smoke,
animal dander, temperature changes, respiratory infection, activity and stress. The allergic
reaction in the airways can cause an immediate reaction, with obstruction occurring, and
it can precipitate a late bronchial obstructive reaction several hours after the initial
exposure. A common symptom is coughing in the absence of respiratory infection,
especially at night.

Status Asthmaticus

a. Child displays respiratory distress despite vigorous treatment measures.

b. Status asthmaticus is a medical emergency that can result in respiratory failure and
death if left untreated.

Assessment

Client has episodes of wheezing, breathlessness, dyspnea, chest tightness and cough,
particularly at night and/or in the early morning.

Client has itching localized at the front of the neck or over the upper part of the back.

Exacerbations are episodes of progressively worsening shortness of breath, cough,

wheezing, chest tightness, decreases in expiratory airflow because of bronchospasm,
mucosal edema, and mucus plugging; air is trapped behind occluded or narrow airways,
and hypoxemia can occur.

Asthmatic Episode

a. The episode begins with irritability, restlessness, headache, feeling tired, or chest
tightness.
b. Respiratory symptoms include a hacking, irritable, nonproductive cough caused by
bronchial edema.
c. Accumulated secretions stimulate the cough, and the cough becomes rattling and
productive of frothy, clear, gelatinous sputum.
d. Child mat be pale or flushed, and the lips may have a deep, dark red color that may
progress to cyanosis observed in the nailbeds and skin, especially around the mouth.
e. Restlessness, apprehension, and diaphoresis occur.
f. Younger children assume the tripod sitting position; older children sit upright with the
shoulders in a hunched-over position, with the hands on the bed or a chair, and arms
braced to facilitate the use of accessory muscles of breathing (child refuses to lie
down).
g. Child speaks in short, broken phrases.
h. Child experiences reactions.
i. Hyperresonance or percussion of the chest is noted.
j. Breath sounds are coarse and loud, with crackles and coarse rhonchi and inspiratory
and expiratory wheezing; expiration is prolonged.
k. Exercise-induced bronchospasm: cough, shortness of breath, chest pain or tightness,
wheezing, and endurance problems during exercise.
l. Severe spasm or obstruction: breath sounds and crackles may become inaudible, and
the cough is ineffective (represents a lack of air movement).
m. Ventilatory failure and asphyxia: shortness of breath, with air movement in the chest
restricted to the point of absent breath sounds accompanied by a sudden rise in the
respiratory rate.

Interventions: Acute Episode

A. Assess airway patency
B. Administer humidified oxygen by nasal prongs or face mask

C. Administer quick-relief (rescue) medications

D. Continuously monitor respiratory status, pulse oximetry, and color; be alert to
decreased wheezing or silent chest, which may signal the inability to move air.
E. Initiate an intravenous line, and prepare to correct dehydration, acidosis, or electrolyte
imbalances.
F. Prepare the child for a chest radiograph.
G. Prepare to obtain samples for determining arterial blood gases and serum electrolytes.

Medications

A. Quick-relief (rescue medications): to treat symptoms and exacerbations

B. Long-term control (preventer medications): to achieve and maintain control of
inflammation
C. Nebulizer, metered-dose inhaler or peak expiratory flow meters.
• There devices deliver many of medications used to treat asthma.
• If the child has difficulty using the metered0dose inhaler, medication can be
administered by nebulization (medication is mixed with saline and then
nebulized with compressed air by a machine).

D. Chest Physiotherapy
• Chest physiotherapy includes breathing exercises and physical training.
• Chest physiotherapy is not recommended during an acute exacerbation.

E. Allergen Control
 • Prevention and reduction of exposure to airborne and environmental allergens.
• Skin testing to identify allergens; immunotherapy (hyposensitization) is not
recommended for allergens that can be eliminated effectively.
•
F. Home Care Measures
• Instruct the client in measures to eliminate allergens.
• Avoid extremes of environmental temperature; in cold temperatures, instruct
the child to breathe through the nose, not the mouth, and to cover the nose and
mouth with a scarf.
• Avoid exposure to individuals with a viral respiratory infection.
• Instruct the child in how to recognize early symptoms of an asthma attack.
• Instruct the child in the administration of medications of an asthma attack.
• Instruct the child in the use of nebulizer, metered-dose inhaler, or peak
expiratory flow meter.
• Instruct the child about the importance of home monitoring of peak expiratory
flow rate; decrease in rate may indicate impending infection or exacerbation.
• Instruct the child in the cleaning of devices used for inhaled medications (oral
candidiasis can occur with the use of aerosolized steroids).
• Encourage adequate rest, sleep, and a well-balanced diet.
• Instruct the child in the importance of adequate fluid intake to liquefy
secretions.
• Assist in developing an exercise program.
• Instruct the child in the procedure for respiratory treatments and exercises as
prescribed.
• Encourage the child to cough effectively.
• Encourage the parents to keep immunizations up to date; annual influenza
vaccinations are recommended.
• Inform other health care providers and school personnel of the asthma
condition.
• Allow the child to take control of self-care measures based on age
appropriateness.

PULMONARY EMBOLISM

A. Description

1. Pulmonary embolism occurs when a thrombus that forms in a deep vein

detaches and travels to the right side of the heart and then lodges in a
branch of the pulmonary artery.
2. Clients prone to pulmonary embolism are those at risk for deep vein
thrombosis, including those with prolonged immobilization, surgery,
obesity, pregnancy, congestive heart failure, advanced age, or history of
thromboembolism.
 3. Fat emboli can occur as complication following a fracture of a flat long
bone.
4. Treatment is aimed at preventing venous status and includes range of
motion exercises and early ambulation following surgery, the use of
antiembolism or pneumatic compression stockings, and preventing
pressure under the popliteal space.

B. Assessment

1. Blood-tinged sputum
2. Chest pain
3. Cough
4. Cyanosis
5. Distended neck veins
6. Dyspnea accompanied by anginal pleuritic pain, exacerbated by
inspiration
7. Hypotension
8. Wheezes on auscultation
9. Shallow respiration
10. Tachypnea and tachycardia

C. Interventions

1. Administer oxygen as prescribed

2. Position client in high Fowler’s position
3. Monitor lung sounds
4. Maintain bed rest and active and passive range of motion exercises as
prescribed.
5. Encourage use of incentive spirometry as prescribed
6. Monitor pulse oximetry
7. Prepare for intubation and mechanical ventilation for severe hypoxemia
8. Administer anticoagulation therapy intravenously with heparin sodium
(bolus), followed by continuous infusion during the acute phase.
9. Administer warfarin (Coumadin) orally, as prescribed, when heparin
infusion is discontinued.
10. Monitor prothrombin time and partial thromboplastin time closely.
11. Prepare the client the embolectomy, vein ligation, or insertion of an
umbrella filter, as prescribed.

PNEUMOTHORAX

• Occurs when the parietal or visceral pleura is breached and the pleural space is
exposed to positive atmospheric pressure.
• Normally the pressure in the pleural space is negative or subatmospheric; this
negative pressure is required to maintain lung inflation.
 • When either pleura is breached, air enters the pleural space, and the lung or a
portion of it collapses.

Types

• Types of pneumothorax include simple, traumatic, and tension pneumothorax.

SIMPLE PNEUMOTHORAX

• A simple, or spontaneous, pneumothorax occurs when air enters the pleural space
through a breach of either the parietal or visceral pleura.
• Most commonly this occurs as air enters the pleural space through the rupture of a
bleb or a bronchopleural fistula.
• A spontaneous pneumothorax may occur in an apparently healthy person in the
absence of trauma due to rupture of an air-filled bleb, or blister, on the surface of
the lung, allowing air from the airways to enter the pleural cavity.
• It may be associated with diffuse interstitial lung disease and sever emphysema.

TRAUMATIC PNEUMOTHORAX

• Occurs when air escapes from a laceration in the lung itself and enters the
pleural space or enters the pleural space through a wound in the chest wall.
• It may result from blunt trauma (eg, rib fractures), penetrating chest or
abdominal trauma (eg, stab wounds or gun shot wounds), or diaphragmatic
tears.
• May occur during invasive thoracic procedures (ie, thoracentesis,
transbronchial lung biopsy, insertion of a subclavian line) in which the pleura
is inadvertently punctured, or with barotraumas from mechanical ventilation.

TENSION PNEUMOTHORAX

• Occurs when air is drawn into the pleural space from a lacerated lung or
through a small opening or wound in the chest wall.
• It may be a complication of other types of pneumothorax.
• In contrast to open pneumothorax, the air that enters the chest cavity with each
inspiration is trapped; it cannot be expelled during expiration through the air
passages or the opening in the chest wall.
• In effect, a one way valve or ball valve mechanism occurs where air enters the
pleural space but cannot escape.
• With each breath, tension (positive pressure) is increased within the affected
pleural space.
 • This cause the lung to collapse and the heart, the great vessels, and the trachea
to shift toward the unaffected side of the chest (mediastinal shift).
• Both respiration and circulatory function are compromised because of the
increased intrathoracic pressure, which decreases venous return to the heart,
causing decreased cardiac output and impairment of peripheral circulation.
• In extreme cases, the pulse may be undetectable—this is known as pulseless
electrical activity.

NURSING ALERT!

Relief of tension pneumothorax is considered an emergency measure.

Assessment findings

1. Sudden sharp pain in the chest, dyspnea, diminished or absent breath sounds on
affected side, tracheal shift to the opposite side (tension pneumothorax accompanied
by mediastinal shift)
2. Weak, rapid pulse; anxiety; diaphoresis
3. Diagnostic tests
a. Chest x-ray reveals area and degree of pneumothorax
b. pCO2 elevated
c. pH decreased

Implementation

- Apply a dressing over an open chest wound

- Administer oxygen as prescribed
- Position the client in high fowler’s position
- Prepare for chest tube placement
- Monitor chest tube drainage system

Nursing interventions

1. Provide nursing care for the client with an endotracheal tube: suction secretions,
vomitus, blood from nose, mouth, throat, or via endotracheal tube; monitor mechanical
ventilation.
2. Restore/promote adequate respiratory function.
a. Assist with thoracentesis and provide appropriate nursing care.
b. Assist with insertion of a chest tube to water- seal drainage and provide appropriate
nursing care.
c. Continuously evaluate respiratory patterns and report any changes.
3. Provide relief/control of pain.
a. Administer narcotics/analgesics/sedatives as ordered and monitor effects.
b. Position client in high-Fowler’s position.

POISONING
 • A poison is any substance that when ingested, inhaled, absorbed, applied to the
skin, or produced within the body in relatively small amounts of injuries in the
body by its chemical action.
• Poisoning from inhalation and ingestion of toxic materials, both intentional and
unintentional, constitutes a major health hazard and an emergency situation.

Emergency treatment is initiated with the following goals:

• To remove or inactivate the poison before it is absorbed

• To provide supportive care in maintaining vital organ system
• To administer a specific antidote to neutralize a specific poison
• To implement treatment that hastens the elimination of the absorbed poison

INGESTED (SWALLOWED) POISONS

• may be corrosive
• Corrosive poisons include alkaline and acid agents that can cause tissue
destruction after coming in contact with mucous membranes

Alkaline products:

• Lye
• Drain cleaners
• Toilet bowl cleaners
• Bleach
• Nonphosphate detergents
• Oven cleaners
• Button batteries (batteries used to power watches, calculators, or cameras)

Acid products:

• Toilet bowl cleaners

• Pool cleaners
• Metal cleaners
• Rust removers
• Battery acids

Signs and Symptoms

• Pain or burning sensations

• Any evidence of redness or burn in the mouth or throat
 • Pain on swallowing or an inability to swallow
• Vomiting or drooling
• Age and weight of the patient
• Pertinent health history

NURSING ALERT!

The area poison control center should be called if an unknown toxic agent
has been taken or if it is necessary to identify an antidote for a known toxic
agent.

The following gastric emptying procedures may be used as prescribed:

• Syrup of ipecac to induce vomiting in the alert patient (never use with
corrosive poisons)
• Gastric lavage for the obtunded patient. Gastric aspirate is saved and sent to
the laboratory for testing (toxicology screens).
• Activated charcoal administration if the poison is one that is absorbed by
charcoal
• Cathartic, when appropriate

Management

• Control the airway, ventilation and oxygenation

• Managing respiratory and its circulation in the absence of cerebral or renal
damage
• Stabilized cardiovascular and other body functions
• Monitoring closely for changes in ECG, vital signs, neurologist status
• Insert an indwelling urinary catheter to monitor renal function
• Test for concentration of drugs or poison obtained by blood specimen
• Determining what substance was taken, the amount, the time of ingestion
• Give water or milk to drink for dilution for patient who ingested corrosive
poison
• Doing gastric emptying procedure as prescribed such as: syrup of ipecac,
gastric lavage, gastric aspirate
• Administer the specific chemical antagonist or physiologic antagonist to
reverse or diminish the effects of the toxin
• Administering multiple doses of charcoal or diuresis, dialysis and
hemoperfusiion

CARBON MONOXIDE POISONING

• Inhaled poisons.
 • may occur as a result of industrial or household incidents or attempted suicide.
• It is implicated in more deaths than any other toxin except alcohol.
• carbon monoxide exerts its toxic effect by binding to circulating hemoglobin and
thereby reducing the oxygen-carrying capacity of the blood.
• Hemoglobin absorbs carbon monoxide 200 times more readily than it absorbs
oxygen.
• carboxyhemoglobin is called carbon monoxide-bound hemoglobin which does
not transport oxygen.

Clinical manifestation

• Because the CNS has critical need for oxygen, CNS symptoms predominate
with carbon monoxide toxicity.
• A person with carbon monoxide poisoning may appear intoxicated (from
cerebral hypoxia).
• Other signs and symptoms include headache, muscular weakness, palpitation,
dizziness, and confusion, which can progress rapidly to coma.
• Skin color (range from pink or cherry red to cyanotic and pale is not a reliable
sign.
• Pulse oximetry is also not valid, because the hemoglobin is well saturated.
• It is not saturated with oxygen, but the pulse oximeter only reads whether or
not the hemoglobin is saturated; in this case, it is saturated with carbon
monoxide rather than oxygen.
• Signs of permanent CNS damage: Psychoses, Spastic paralysis, Ataxia, Visual
disturbances and Deterioration of personality.

Management

• Exposure to carbon monoxide requires immediate treatment.

• Goals of management are to reverse cerebral and myocardial hypoxia and to
hasten carbon monoxide elimination.

Whenever a patient inhales a poison, the following general measures apply:

• Carry the patient to fresh air immediately; open all doors and windows
• Loosen all tight clothing
• Initiate CPR if required; administer 100% oxygen
• Prevent chilling; wrap the patient in blankets
• Keep the patient as quite as possible
• Do not give alcohol in any form or permit the patient to smoke

SKIN CONTAMINATION POISONING (CHEMICAL BURNS)

 • Skin contamination injuries from exposure to chemicals with large number of
offending agents diverse action and metabolic effects
• the severity of chemical burn is determined by the mechanism of action,
penetrating strength and concentration and the amount and duration of exposure
of the skin to the chemical
• the skin should be drenched immediately with running water from a shower, hose,
or faucet, except in the case of lye and white phosphorus, which should be
brushed off the skin, dry.
• The skin should be flushed with a constant stream of water as the patient’s
clothing is removed.
• The skin of health care personnel assisting the patient should be appropriately
protected if the burn is extensive or if the agent is significantly toxic or is still
present.
• Prolonged lavage with generous amounts of tepid water is important.
• In the meantime, attempts to determine the identity and characteristics of the
chemical agent are necessary for future treatment.
• The standard burn treatment appropriate for the size and location of the wound
(antimicrobial treatment, debridement, tetanus prophylaxis as prescribed) is
instituted.
• The patient may require plastic surgery for further wound management.
• The patient is instructed to have the affected area reexamined at 24 and 48 hours
and in 7 days because of the risk of underestimating the extent and depth of these
types of injuries.

NURSING ALERT!

Water should not be applied to burns from lye or white phosphorus

because of the potential for an explosion or for deepening of the burn. All
evidence of these chemicals should be brushed off the patient before any flushing
occurs.

Management

• The skin should be drenched immediately with running water from shower,
hose, or faucet
• Water should not be applied to burns from lye or white phosphorus because of
the potential for an explosion or deepening the burn
• A constant stream of water should continue as the patient’s clothing is being
removed
• Prolonged lavage with generous amounts of tepid water is important
• Identify and characteristics of the chemical agent for future treatment
• Antimicrobial treatment
• Debridement
• Tetanus prophylaxis as prescribed
 • Plastic surgery if required for further wound management
• Reexamined the affected area at 24 and 72 hours and in 7 days due to the risk
for understanding the extent and depth of these types of injuries

FOOD POISONING

• is a sudden, explosive illness that may occur after ingestion of contaminated food
or drink
• Botulism is a serious form of food poisoning that requires continual surveillance.
• The key treatment is determining the source and type of food poisoning. If
possible, the suspected food should be brought to the medical facility and a
history obtained from the patient or family.
• Food, gastric contents, vomitus, serum, and feces are collected for examination.
• The patient’s respirations, blood pressure, level of consciousness, CVP (if
indicated), and muscular activity are monitored closely.
• Measures are instituted to support the respiratory system.
• Death from respiratory paralysis can occur with botulism, fish poisoning, and
other food poisonings.

Signs and Symptoms

• Fluid and electrolyte imbalances

• Lethargy
• Rapid pulse rate
• Fever
• Oliguria
• Anuria
• Hypotension
• Delirium
• Hypovolemic shock

Assessment questions for Food Poisoning

• How soon after eating did the symptoms occur? (Immediate onset suggests
chemical, plant, or animal poisoning.)
• What was eaten in the previous meal? Did the food have an unusual odor or taste?
(Most foods causing bacterial poisoning do not have unusual odor or taste.)
• Did anyone else become ill from eating the same food?
• Did vomiting occur? What was the appearance of the vomitus?
• Did diarrhea occur? (Diarrhea is usually absent with botulism and with shellfish
or other fish poisoning.)
 • Are any neurologic symptoms present? (These occur in botulism and in chemical,
plant, and animal poisoning.)
• Does the patient have a fever? (Fever is characteristic in salmonella, ingestion of
fava beans, and some fish poisoning.)
• What is the patient’s appearance?

Management

• The key treatment is to determining the source and type of food poisoning
• The suspected food should be brought to the medical facility and a history
obtained from the patient or family
• Food, gastric contents, vomitus, serum, and feces are collected for examination
• Monitoring the patient’s respiration, blood pressure, sensorium, CVP( if
indicated) and muscular activity
• Measure to control nausea are also important to prevent vomiting
• Anti emetic medication is administered parenterally as prescribed if the patient
cannot tolerate fluids or medication orally
• For mild nausea, the patient takes a sips of weak tea, carbonated drinks, or tap
water
• After 12 to 42 hours if nausea and vomiting subsides the diet gradually progress
to a low-residue, blant diet

SUBSTANCE ABUSE

• Is the misuse of specific substances to alter mood or behavior.

• Drug and alcohol abuse are two examples of substance abuse.
• DRUG ABUSE is the use of drugs for other than legitimate medical purposes
• People who abuse drugs often take a variety of drugs simultaneously (such as
alcohol, barbiturates, opioids, and tranquilizers), and the combination may have
additive and addictive effects.

CLINICAL MANIFESTATION

• Vary with the substance used, but the underlying principles of management are
essentially the same.

TREATMENT GOALS FOR A PATIENT WITH A DRUG OVERDOSE

• To support the respiratory and cardiovascular functions

• To enhance clearance of the agent
• To provide for safety of the patient and staff

ACUTE ALCOHOL INTOXICATION

 • Alcohol is psychotropic drug that affects mood, judgment behavior, concentration,
and consciousness.
• Many heavy drinkers are young adults or people older than 60 years.
• There is a high prevalence of alcoholism among ED patients.
• Patients who abuse alcohol return frequency to the ED, they often frustrate and
tax the patience of the health care professionals who care for them.
• Their management requires patience and thoughtful accurate, long-term treatment.
• Alcohol, or ethanol, is a multi system toxin and CNS depressant that causes
drowsiness, impaired coordination, slurring of speech, sudden mood changes,
aggression, belligerence, grandiosity, and uninhibited behavior.
• In excess, it also can cause stupor, coma, and death.
• Increasingly, underage minors and college students arrive at the ED with alcohol
poisoning from binge drinking.
• Frequently, the result is death.

Management

• Treatment involves detoxification of the acute poisoning, recovery, and

rehabilitation
• The nurse should approach the patient in a nonjudgmental manner, using a firm,
consistent accepting, and reasonable attitude.
• Speaking in calm and slow manner is helpful because alcohol interferes with
thought processes.
• If the patient appears intoxicated, hypoxia, hypovolemia and neurologic
impairment must be ruled out before it is assumed that the patient is intoxicated.
• Typically, a blood specimen is obtained for analysis of the blood alcohol level.
• If drowsy, the patient should be allowed to sleep off the state of alcoholic
intoxication
• During this time, maintenance of a patent airway and observation for symptoms
of CNS depression are essential.
• The patient should be undressed and kept warm with blankets.
• On the other hand, if the patient is noisy or belligerent, sedation may be
necessary, if sedation is used, the patient should be monitored carefully for
hypotension and decreased level of consciousness.
• Additionally, the patient is examined for alcohol withdrawal and delirium and also
for injuries and organic dse, such as head injury, seizures, pulmonary infections,
hypoglycemia and nutritional deficiencies, that may be masked by alcoholic
intoxication.

ALCOHOL WITHRAWAL SYNDROME/ DELIIUM TREMENS

 • Alcohol withdrawal syndrome (AWS) is an acute toxic state that occurs as a result
of sudden cessation of alcohol intake after a bout of heavy drinking or, more
usually, after prolonged intake of alcohol.
• Severity of symptoms depends on how much alcohol was ingested and for how
long.
• Delirium tremens may be precipitated by acute injury or infection (pneumonia,
pancreatitis, hepatitis) and is the most severe form of alcohol withdrawal
syndrome.

SIGNS

• Anxiety
• Uncontrollable fear
• Tremor
• Irritability
• Agitation
• Insomnia
• Incontinence
• Talkative and preoccupied
• Experience visual, tactile, olfactory, and auditory hallucinations that often
are terrifying
• Autonomic over activity occurs and is evidenced by tachycardia, dilated
pupils, and profuse perspiration
• Usually, all V/S are elevated in the alcohol toxic state
• Delirium tremens is a life-threatening condition and carries a high
mortality rate.

Management

• The goals of management are to give adequate sedation and support to allow the
patient to rest and recover without any danger of injury or peripheral vascular
collapse.
• A physical examination is performed to identify pre existing or contributing
illnesses or injuries,
• A drug history is obtained to elicit information that may facilitate adjustment of
any sedative requirements.
• Baseline blood pressure is determined, because the patient’s subsequent treatment
may depend on blood pressure changes.
• Usually, the patient is sedated as direct with a sufficient dosage of
benzodiazepines to establish and maintain sedation, which reduce agitation
prevents exhaustion, prevents seizures, and promotes sleep
• .The patient should be calm, able to respond, and able to maintain an airway
safely on his or her own.
 • A variety of medication and combinations of medications are used (for example
chlerdiazepoxide [Librium], lorazepam and clonidine).
• Haloperidol or droperidol may be administered for severe acute AWS dosages are
adjusted according to the patient’s symptoms and blood pressure response.
• The patient is placed in a calm, nonstressful environment and observed closely.
The room remains lighted to minimize the potential for illusions and
hallucinations.
• Closet and bathroom doors are closed to eliminate shadows. Some one is
designated to stay with the patient as much as possible.
• The presence of another person has reassuring and calming effect, which helps the
patient maintain contact with reality.
• Any visual misrepresentations (illusions) are explained to orient the patient to
reality.
• Oral or intravenous route is used to restore fluid and electrolyte balance.
• Phenytoin (dilantin) or other antiseizure medications may be prescribed to prevent
or control repeated withdrawal seizures.
• Parenteral dextrose may be prescribed if the liver glycogen level is depleted
• Orange juice Gatorade or other forms of carbohydrates are given to stabilized the
blood glucose level and counteract tremulousness.
• Supplemental vitamin therapy and high protein diet are provided as prescribed to
counteract vitamin deficiency.
• The patient should be referred to an alcoholic treatment center for follow up care
and rehabilitation.

EMERGENCY MANAGEMENT OF DRUGABUSE PATIENTS AND DRUG

OVERDOSE PATIENTS

Narcotics
Cocaine – intranasally ( “snorting”) inhaled into nostrils through straws.

Clinical manifestations
• Cocaine is a central nervous system stimulant that can increase heart rate
and blood pressure and hyperpyrexia, seizures, and ventricular
dysrhythmias.
• It produces intense euphoria then anxiety, sadness, insomnia and sexual
indifference; cocaine hallucinations with delusions; psychosis with
extreme paranoia and ideas of persecution and hypervigilance.

Therapeutic management.

• ensure airway and ventilation.

• control seizures.
 • monitor cardiovascular effects
• treat for hyperthermia.
• if cocaine was ingested, use charcoal to treat.
• refer for psychiatric evaluation and treatment in an inpatient unit that eliminates
access to the drug. Include drug rehabilitation counseling.

Heroin
Opium or paregoric
Morphine, codeine, oxycontin. Fentanyl

Clinical manifestations

• Pinpoint pupils (may be dilated with sever hypoxia); decreased blood pressure.
• Marked respiratory depression
• stupor to coma fresh needle marks along course of any superficial vein; skin
abscesses.

Therapeutic management

• Support respiratory and cardiovascular functions.

• Establish an intravenous IV line; obtain blood for chemical and toxicologic
analysis. Patient may be given bolus of glucose to eliminate possibility of
hypoglycemia.
• Give narcotic antagonist (naloxone hydrochloride) as prescribed to reverse severe
respiratory depression and coma.
• Continue to monitor level of responsiveness and respirations, pulse and blood
pressure. Duration of action of naloxone hydrochloride is shorter than that of
heroin; repeated dosages may be necessary.
• Send urine for analysis
• Obtain an ECG
• Do not leave patient unattended; he or she may lapse back into coma rapidly.
Clinical status may change from minute to minute. Hemodialysis may be
indicated for sever drug intoxication
• Monitor for pulmonary edema, Which is frequently seen in patients who abuse/
overdose on narcotics.
• Refer patient for psychiatric and drug rehabilitation evaluation before discharge

Barbiturates

Pentobarbital (nebutal)
Secoobarbital (seconal)
Amobarbital (amytal)

Clinical manifestations
 • Actue intoxication (may mimic alcohol intoxication);
 respiratory depression
 flushed face
 decreased pulse rate; decreased blood pressure
 increasinf nystagmus
 depressed deep tendon reflex
 decreasing mental alertness
 difficulty in speaking
 poor motor coordination
 coma, death

Therapeutic Management

• Maintain airway and provide respiratory support.

• Endotracheal intubation or tracheostomy is considered if there is any doubt about
the adequacy of airway exchange.
• Check airway frequently.
• Perform suctioning as necessary.
• Support cardiovascular and respiratory functions; most deaths result from
respiratory depression or shock.
• Start infusion through large-gauge needle or IV catheter to support blood
pressure;
• Coma and dehydration result in hypotension and respond to infusion of
intravenous fluids with elevation of blood pressure. Sodium bicarbonate may be
prescribed to alkalinize urine; it promotes excretion of barbiturates/
• Evacuate stomach contents or lavage as soon doses of activated charcoal may be
administered.
• Assist with hemodialysis for severely overdose patient.
• Maintain neurologic and vital sign flow sheet.
• Patient awakening from overdose may demonstrate combative behavior.
• Refer for psychiatric and drug rehabilitation consultation/rehabilitation to evaluate
suicide potential and drug abuse.

Amphetamine Type Drugs

Ampethamine (benzadrine)
Destroamphetamine (Dexedrine)
Methamphetamine (Desoxyn)
MDMA (exstasy, adam)
MDEA (eve)
MDA

Clinical manifestations
 • Nausea, vomiting, anorexia, palpitations, tachycardia, increased blood pressure,
tachypnea, anxiety, nervousness, diaphoresis, mydriasis.
• Repetitive or stereotyped behavior
• Irritability, insomnia, agitation
• Visual misperceptions, auditory hallucinations
• Fearful anxiety
• Hyperactivity, rapid speech, euphoria
• Seizures, coma, hyperthermia, cardiovascular collapse rhabdomyolysis

Therapeutic Management.

• Provide airway support, ventilation, cardiac monitoring; insert IV line.

• Employ gastrointestinal GI decontamination in cases of oral overdose
• Keep in calm, cool quiet environment
• Use small doses of diazepam IV or haloperidol as prescribed for CNS muscular
hyperactivity.
• Administer appropriate pharmacologic therapy as prescribed for sever
hypertension and ventricular dysrhythmias.
• Treat seizures wit benzodiazepines.
• Treat sympathetic stimulation with beta blocker agents.
• Try to communicate with patient if delusions or hallucinations are present
• Place in a protective environment
• Refer psychiatric and drug rehabilitation evaluation.

Hallucinogens or Psychedelic- type of drugs

Lysergic acid dietjylamide (LSD)
Phencyclidine HCL (PCP_
Mescaline, Psiclocybin
Cannabinoids (marijuana)

Clinical manifestations

• nystagmus
• mild hypertension
• marked confused or bordering panic
• incoherence hyperactivity
• withdrawn
• combative behavior
• hallucinations
• hypertension
• flashback
Therapeutic Management

• evaluate and maintain patient’s airway

• determine by urine or serum drug screen
• try to communicate with and reassure the patient
• sedate the patient as prescribed if hyperactivity cannot be controlled; diazepam or
a barbiturate may be prescribed.
• search for evidence for trauma
• manage seizures
• observe patient closely
• monitor for hypertensive crisis
• place patient in a protected environment

Drugs Producing sedation, intoxication or Psychological and physical dependence

Diazepam (valiums)
Chlordiazepoxide (libriun)
Oxazepam (serax)
Lorazepam (ativan)
Midazilam (versed)

Clinical manifestations

• seizures, coma, circulatory collapse, death.

• acute intoxication

Therapeutic management.

• endotracheal tube is inserted as a precaution

• assess for hypotension
• evacuate stomach contents; emesis lavage; activated charcoal; cathartic
• Start ECG monitoring
• administer flumazenil
• refer patient for psychiatric evaluation

Salicylate Poisoning
Aspirin

Clinical manifestations

• restlessness
• tinnitus
• deafness
 • blurring of vision
• hyperpnea
• hyperpyrexia
• sweating
• epigastric pain
• vomiting
• dehydration
• respiratory and metabolic acidosis

Therapeutic management

• Treat respiratory depression.

• Induce gastric emptying by lavage.
• Give activated charcoal to absorb aspirin
• Support patient with IV infusion as prescribed to establish hydration and correct
electrolyte imbalances.
• Enhance elimination of salicylates as directed by forces diuresis, alkalinization of
urine, peritoneal dialysis, or hemodialysis, according to severity of intoxication.
• Monitor serum salicylate level for efficacy of treatment.
• Administer specific prescribed pharmacologic agent for bleeding and other
problems.
• Refer patient for psychiatric evaluation.

Acetaminophen (present in prescription and non prescription analgesics, anti pyretics

and cold remedies)

Clinical manifestations:

• Lethargy to encephalopathy and death

• GI upset diaphoresis Right upper quadrant pain
• Abnormal Liver function test, prolonged prothrombin time, increased blilirubin.
• Hepatomegaly.

Therapeutic Management:

• Maintain airway.
• Obtain ecetaminophen level. Levels greater than or equal to 140 mg/kg are toxic.
• Laboratory studies- liver function test, prothrombin time/ partial thromboplastin
time, complete blood count, blood urea nitrogen, creatinine.
• Administer syrup of ipecac and follow emesis with activated charcoal.
• Prepare for possible hemodialysis, which clears acetaminophen but does not halt
liver damage.
• Administer N-acetylcysteine (NAC, mucomyst) as soon as possible.
 • Refer patient for psychiatric evaluation.

Tricyclic Antidepressants
Amitritipyline
Doxepin
Norttiptyline
Imitpramine

Clinical Manifestations:

• Dysrhythmia: Ventricular fibrillation/tachycardia.

• Hypotension
• Pulmonary edema, hypoxemia, acidosis
• Confusion, agitation, coma
• Visual hallucinations
• Clonus, hyperactive reflexes, nystagmus, myoclonic jerking
• seizures
• Blurred vision, Flushing, Hyperthermia.

Therapeutic Management:

• Provide airway support

• If within 1 hr. after overdose, insert a nasogastric tube and instill activated
charcoal with sorbitol every 4hr X3.
• Administer sodium bicarbonate drip to decrease dysrhythmias; the alkaline
environment increases the protein binding of the metabolite.
• Administer vasopressors.
• Use only class IB antiarrhythmics, as some other types of antiarrhythmics have
the same effect as TCA.
• Manage seizure activity.
• Refer patient for psychiatric evaluation for potential suicide intent and evaluation.