PROBLEM 4A

GROUP 13
 GROUP 13
• Tutor : dr. Enny
• Leader : Felicia Faustine Faraday (405100070)
• Secretary : Khairunnisa Nugrahenni (405100210)
• Scriber : Andy Halim (405100193)
• Members :
- Renata C.F Tjieputri (405080137)
- Mieliani (405080191)
- Feny Chandra Dewi (405090208)
- Charlie (405100005)
- I Putu Mana Nitia (405100103)
- Adhitia Mahardika (405100124)
- Boe, Obet Agung Sanjaya (405100125)
- Eva Fauziah (405100132)
- Rahma Marini Sulwan (405100200)
 PROBLEM 4A
• A 50-year old man comes to the emergency room with a complaint
of progressive abdominal pain. Complaint accompanied by
abdominal bloating, vomiting, and constipation since 3 days ago.
There was a history of intermittent pain since 3 months ago. There
was a 5-kilograms weight loss in 3 months. The patient had
undergone an appendectomy 1 year ago
• On physical examination: heart rate 112x/minute, temperature
38,2⁰C, respiratory rate 24x/minute. Abdominal examination: there
is abdominal distension, increased bowel sounds. Laboratory
examination: leucocytes 15.000/μL (normal: 5000-10.000/μL),
potassium level 2,5 mEq/dL(normal: 3,5-5,5 mEq/dL). Imaging
studies: supine and upright plain abdominal films reveal a ladder-
like pattern of dilated small bowel loops with air fluid level.
• What can you learn from the problem?
 UNFAMILIAR TERMS
• Appendectomy : Surgical treatment of
appendicitis.
 LEARNING OBJECTIVE
1. Able to explain Acute abdomen (appendicitis, ileus,
ascaris ball, peritonitis, perforation, adhesions, hernia,
intussusception, malrotation):
- Definition
- Etiology
- Epidemiology
- Patophysiology
- Sign & Symptom
- Diagnosis
- Management
- Complication
- Prognosis
Acute Abdomen
 Definition

• The acute abdomen can be defined generally as an intra-

abdominal process causing severe pain and often requiring
surgical intervention. It is a condition that requires a fairly
immediate judgement or decision as to management.

• Is an abdominal distress may occur due to surgical and non

surgical problems are usually accompanied by abdominal pain
that occurs arrived - arrived and lasted less than 24 hours

http://www.ece.ncsu.edu/
Etiology
 ETIOLOGY
(ACCORDING TO AGE)
Neonatal causes of Abdominal
Pain
– Colic
– Milk Protein Allergy
– Gastroesophageal reflux
– Malrotation or Midgut volvulus
– Necrotizing Enterocolitis
– Hirschprung's Enterocolitis
Infant causes of Abdominal Pain
– Intussusception
– Infantile colic
– Bowel Obstructionn
• Pyloric stenosis
• Incarcerated Herniaa
• Internal hernia
• Omphalomesenteric band
• Hirschprung's Diseasee
– Battered Infant
• Jejunum perforation
• Duodenal hematoma
– Gastroenteritis
– Constipation
– Urinary Tract Infection
 ETIOLOGY
(ACCORDING TO AGE)
Child causes of Abdominal Pain Adolescent
– Constipation – Appendicitis
– Lactose Intolerance – Gastroenteritis
– Lead Poisoning
– Constipation
– Helicobacte pylori
– Urinary Tract Infection – Gynecologic cause
– Pneumonia • Pregnancy (or Ectopic Pregnancy)
– Pancreatitis • Mittelschmerz
– Appendicitis • Dysmenorrhea
– Mesenteric Lymphadenitis • Pelvic Inflammatory Disease
– Gastroenteritis • Ovarian torsion
– Intussusception or Volvulus (children – Testicular Torsion
under age 6) – Drug and Alcohol use
– Abdominal trauma
– Sexual abuse
– Pharyngitis (e.g. Strep Throat)
– Sickle Cell Crisis – Gallbladder disease
– Henoch-Schonlein Purpura – Neoplasm
– Inflammatory Bowel Disease
 ETIOLOGY/CAUSES/DIFFERENTIAL DIAGNOSIS
OF ACUTE ABDOMEN
• Gastrointestinal
– Appendisitis
– Perforated peptic ulcer
– Intestinal ischemia
– Diverticulitis
– Inflammatory bowel disease
– Meckel’s diverticulitis
• Pancreaticobiliary tract, liver,
spleen
– Acute pancreatitis
– Calculous cholecystitis
– Acalculous cholecystitis
– Acute cholangitis
– Hepatic abscess
– Ruptured hepatic tumor
– Splenic rupture
• Urinary tract
– Renal/ureteral stone
• Gynecologic
– Ectopic pregnancy
– Tuboovarian abscess
– Ovarian torsion
– Uterine rupture
– Ruptured ovarian cyst or follicle
• Retroperitoneum
– Abdominal aortic aneurysm
• Supradiaphragmatic
– Pneumothorax
– Pulmonary embolus
– Acute pericarditis
– Empyema
 Pathophysiology
• Mechanisms of Pain Originating in the
Abdomen
– Inflammation of the Parietal Peritoneum
– Obstruction of Hollow Viscera
– Vascular Disturbances
– Abdominal Wall
 Inflammation of the parietal
peritoneum
• The pain of parietal peritoneal inflammation is
steady and aching in character and is located
directly over the inflamed area
• The intensity of the pain is dependent on the
type and amount of material to which the
peritoneal surfaces are exposed in a given
time period
 Obstruction of hollow viscera
• The pain of obstruction of hollow abdominal
viscera is classically described as intermittent,
or colicky
• Yet the lack of a truly cramping character
should not be misleading, because distention
of a hollow viscus may produce steady pain
with only very occasional exacerbations
 Vascular disturbance
• absence of tenderness and rigidity in the
presence of continuous, diffuse pain in a
patient likely to have vascular disease is quite
characteristic of occlusion of the superior
mesenteric artery
• Abdominal pain with radiation to the sacral
region, flank, or genitalia should always signal
the possible presence of a rupturing
abdominal aortic aneurysm.
 Abdominal Wall
• Pain arising from the abdominal wall is usually
constant and aching
• Movement, prolonged standing, and pressure
accentuate the discomfort and muscle spasm
Location of abdominal pain and possible causes.
Possible Causes of Pain by Location
Location of Pain Associated Diseases
Right upper quadrant Acute cholecystitis, biliary colic, acute hepatitis,
(liver, kidney, gallbladder) duodenal ulcer, right lower lobe pneumonia
Right lower quadrant Appendicitis, cecal diverticulitis, ectopic pregnancy,
(ascending colon, appendix, ovary, fallopian tube) tubo-ovarian abcess, ruptured ovarian cyst, ovarian
torsion
Left upper quadrant Gastritis, acute pancreatitis, splenic pathology, left
(pancreas, spleen, kidney) lower lobe pneumonia
Left lower quadrant Diverticulitis, ectopic pregnancy, tubo-ovarian
(sigmoid and descending colon, ovary, fallopian tube) abcess, ruptured ovarian cyst, ovarian torsion

Midline or periumbilical Appendicitis (early), gastroenteritis, mesenteric

lymphadenitis, myocardial ischemia or infarction,
pacreatitis
Flank Abdominal aortic aneurysm, renal colic,
pyelonephritis
Front to back Acute pancreatitis, ruptured abdominal aortic
aneurysm, retrocecal appendicitis, posterior
duodenal ulcer
Suprapubic or lower abdominal Ectopic pregnancy, mittelschmerz, ruptured ovarian
cyst, pelvic inflammatory disease, endometriosis,
urinary tract infection
 Acute Abdomen
• Anamnesis
– Past history
appendectomy, cholecystectomy, and so forth
– Medication
corticosteroid, anticoagulants, cocaine
– Age
– Patients position
– Menstrual history
 Examination of Acute Abdomen
• Inspection
– Looking for scars, hernias, masses.
– Contour of the abdomen is scaphoid, flat or distended.
– Abdominal distended can mean intestinal obstruction,
ileus or acites.
• Auscultation
– Inform the presence or absence of bowel sound
– Hyperactive bowel sound may occur in bowel obstruction
– Hypoactive bowel sound may occur in paralytic
obstruction.
 Examination of Acute Abdomen
• Percussion
– Hyperresonance mean gaseous distention of the intestine.
– Shifting dullness mean acites.
• Palpation
– The examiner should asses the patient’s facial expression
for sign of pain.
– Should begin in an area away from the pain site.
– Tenderness and rebound tenderness indicates
inflammation in peritoneum
– Deep palpation can detect abdominal masses.
Appendicitis
 Definition
• Acute appendicitis is a common cause of abdominal pain
requiring surgery, particulary in the West, where there is
low roughage diet
• Inflammation & obstruction of the vermiform appendix
 EPYDEMIOLOGY
• Peak incidence : ages 10 – 30 years
• Most common acute surgical condition of
abdomen
• 250.000 cases / year in USA
 Etiology
Appendicitis is believed to occur as a result of appendiceal luminal
obstruction. Obstruction is most commonly caused by:

• Fecalith, which results from accumulation and inspissation of fecal

matter around vegetable fibers.

• Enlarged lymphoid follicles associated with viral infections (e.g.,

measles), inspissated barium,

• Worms (e.g., pinworms, Ascaris, and Taenia),

• Tumors (e.g., carcinoid or carcinoma) may also obstruct the lumen.

Pathogenesis
Obstruction

Mucous can’t be drained

Edema

Increase intraluminal pressure

Bacterial diapedesis

Mucosal Ulceration

Epigastric pain

Appendicitis acute focal

 Mucous >>

Intraluminal pressure >>

Bacterial invasion of the

appendix wall

Vein obstruction

Peritonitis

Pain in RLQ

Appendicitis supurative acute

 Bad arterial flow

Gangren

Appendicitic gangrenosa

Infark

Appendicitis perforation
 Acute appendicitis
• Tipikal
– First, the pain is located in periumbilcal / epigastric and
then, the pain relocated in fossa illiaca dexter (RLQ)  it is
because the pain localitation by visceral nerve is bad.
– Nausea, vomit, anorexia
– Fever
• Atipikal
– The pain is located in fossa iliaca dexter (RLQ)
– Could cause constipation and diarhhea.
– Increasing of urinary frequency
– tenessmus
SIGN AND SYMPTOM
http://www.aafp.org/afp/991101ap/2027.html
Sign Description Diagnosis/condition
Aaron sign Pain or pressure in Aute appendicitis
epigastrium or anterior
chest with persistent firm
pressure applied to
McBurney’s point
Bassler sign Sharp pain created by Chronic appendicitis
compresing appendix
between abdominal wall
and iliacus
Blumberg’s sign Transient abdominal wall Peritoneal inflammation
rebound tenderness
Iliopsoas sign Elevation and extension Appendicitis with
of leg againts resistance retrocecal abcess
creates pain
Rovsing’s sign Pain at McBurney’s point Acute appendicitis
when compressing the
left lower abdomen
Ten Horn sign Pain caused ny gentle Acute appendicitis
traction of righttesticle
ILIOPSOAS SIGN
PSOAS SIGN
OBTURATOR SIGN
 Acute Appendicitis
• Appendicitis is believed to occur as a result of
appendiceal luminal obstruction
• commonly caused by a fecalith, which results
from accumulation and inspissation of fecal
matter around vegetable fibers
• Luminal bacteria multiply and invade the
appendiceal wall as venous engorgement and
subsequent arterial compromise result from the
high intraluminal pressures. Finally, gangrene and
perforation occur
 Examination
• Simple critical inspection of the patient
– facies, position in bed, and respiratory activity
• Gentle percussion of the abdomen (rebound
tenderness on a miniature scale), a maneuver
that can be far more precise and localizing
• Abdominal signs may be virtually or totally absent
in cases of pelvic peritonitis
• Auscultation of the abdomen
– strangulating small intestinal obstruction or
perforated appendicitis  normal peristaltic sounds
– proximal part of the intestine above an obstruction
becomes markedly distended and edematous  weak
or absent even when peritonitis is not present
– Severe chemical peritonitis  truly silent abdomen
 Laboratory examination
• White blood cell count
– >20,000/L may be observed  perforation of a viscus, but
pancreatitis, acute cholecystitis, pelvic inflammatory
disease, and intestinal infarction
– Normal count is not rare in cases of perforation of
abdominal viscera
• Urinalysis
– state of hydration or rule out severe renal disease,
diabetes, or urinary infection
– Serum amylase levels may be increased by many diseases
other than pancreatitis, e.g., perforated ulcer,
strangulating intestinal obstruction, and acute cholecystitis
• Plain & upright or lateral decubitus
radiographs of the abdomen
– Intestinal obstruction, perforated ulcer, and a
variety of other conditions
 Clinical Manifestations
• The sequence of abdominal discomfort and
anorexia associated with acute appendicitis is
pathognomonic
• Pain located in the periumbilical region
initially and then migrating to the right lower
quadrant
• The diagnosis cannot be established unless
tenderness can be elicited
• Typically, tenderness to palpation will often
occur at McBurney's point, anatomically
located on a line one-third of the way
between the anterior iliac spine and the
umbilicus
• The temperature is usually normal or slightly
elevated [37.2°–38°C (99°–100.5°F)], but a
temperature >38.3°C (101°F) should suggest
perforation.
• Rigidity and tenderness become more marked
as the disease progresses to perforation and
localized or diffuse peritonitis
• Leukocytosis of >20,000 cells/L suggests
probable perforation
• Anemia and blood in the stool suggest a
primary diagnosis of carcinoma of the cecum,
especially in elderly individuals
• The diagnosis is best made with ultrasound,
which has an 80% accuracy; however, if
perforation has already occurred, the accuracy
of ultrasound decreases to 30%
• Ultrasound is most useful to exclude ovarian
cysts, ectopic pregnancy, or tuboovarian
abscess
 • Clinical diagnostic scores
CHARACTERISTIC SCORE

M = Migration of pain to the

1
RLQ

A = Anorexia 1

N = Nausea and vomiting 1

T = Tenderness in RLQ 2

R = Rebound pain 1 SCORING :

E = Elevated temperature
L = Leukocytosis
S = Shift of WBC to the left
Total
• score of 3 or lower had a 3.6%
1
incidence of appendicitis
2 •scores of 4-6 had a 32%
1
incidence of appendicitis
• scores of 7-10 had a 78%
10 incidence of appendicitis.
 TREATMENT
PHARMACOLOGY
• Antibiotik
– Metronidazole
– Gentamisin
– Cefotetan
– Cefoxitin
– Meropenem
– Piperacillin dan tazobactam natrium
– Ampicillin dan sulbactam
• Analgesik
– Morfin sulfat (Astramorph, Duramorph, MS CONTIN,
MSIR, Oramorph)
Appendectomy
 DIFFERENTIAL DIAGNOSES
 Meckel's diverticulitis.
 A Meckel's diverticulum :small outpouching of the small intestine which
usually is located in the right lower abdomen near the appendix
 The diverticulum may become inflamed or even perforate  surgically.
 Pelvic inflammatory disease.
 The right fallopian tube and ovary lie near the appendix
 Sexually active women may contract infectious diseases that involve the
tube and ovary.
 Usually, antibiotic therapy is sufficient treatment, and surgical removal of
the tube and ovary are not necessary.
 Inflammatory diseases of the right upper abdomen
 Fluids from the right upper abdomen may drain into the lower abdomen
where they stimulate inflammation and mimic appendicitis
 Such fluids come from a perforated duodenal ulcer, gallbladder disease, or
inflammatory diseases of the liver (liver abscess)
• Right-sided diverticulitis
– When a right-sided diverticulum ruptures it
can provoke inflammation they mimics
appendicitis.
• Kidney diseases.
– The right kidney is close enough to the
appendix that inflammatory problems in the
kidney-for example, an abscess-can mimic
appendicitis.
 Complication
• Intra-abdominal abscess
• Fecal fistula
• Intestinal obstruction
• Incisional hernia
• Peritonitis
• Death
 PROGNOSIS APENDICITIS
• If the appendix has not ruptured, recovery is usually quick,
and children usually leave the hospital one or two days after
surgery.
• Most children can usually return to normal activities in two to
three weeks. If rupture occurs, the recovery process can be
more complicated.
Mechanical Obstruction
 Overview
• A mechanical bowel obstruction is a partial or complete
blockage in the intestine, which is also called the bowel.
• Blockages can occur at any point along the small or large
bowel.
• They are more common in the small bowel.
• When the bowel is blocked, food and liquid cannot pass
through.
• Over time, food, liquid, and gas build up in the area above the
blockage.
• This can cause abdominal pain and swelling.
 Classification
• Speed of onset : acute, chronic, acute on chronic
• Site : high or low
• Nature : simple versus strangulating
• Aetiology
 Speed of Onset
• In acute obstruction, the onset rapid and the
symptoms severe.
• In chronic obstruction, the symptoms are insidious
and slowly progressive (ex: carcinoma of the large
bowel).
• A chronic obstruction may develop acute symptoms
as the obstruction suddenly becomes complete (ex:
when a narrowed lumen becomes totally occluded
by inspissated bowel contents).
 Site
• The site of the obstruction is classified into
high or low, which is roughly synonymous with
amall or large bowel obstruction.
Nature
• Simple Obstruction : occurs when the bowel is
occluded without damage to its blood supply.
• Strangulating Obstruction : when the blood
supply of the involved segment of intestine is
cut off.
 Aetiology
• In the lumen : faecal impaction, gallstone
‘illeus’, food bolus, parasite (ex: ascariasis),
intussespection.
• In the wall : congenital atresia, crohn disease,
tumours, diverticulitis of the colon.
• Outside the wall : strangulated hernia,
volvulus, and obstruction due to adhesions or
bands.
 Pathology
• Proximal dilatation occurs above obstructing lesion.
• Results in the accumulation of gas and fluid and reduced
reabsorption.
• Dilation of the gut wall produced mucosal oedema.
• This impairs venous and then arterial blood flow.
• Intestinal ischaemia eventually results in infarction and
perforation of that segment of bowel.
• Ischaemia also results in bacterial and endotoxin
translocation.
• The overall effect is progressive dehydration, electrolyte
imbalance and systemic toxicity.
 Clinical Feature
• Colicky central abdominal pain
• Vomiting - early in high obstruction
• Abdominal distension - extent depends on level of
obstruction
• Absolute constipation - late feature of small bowel
obstruction
• Dehydration associated with tachycardia, hypotension
and oliguria
• Features of peritonism indicate strangulation or
perforation
 Clinical Feature
• Palpation reveals generalized abdominal tenderness.

• While listening to the abdomen with a stethoscope,

may hear high-pitched bowel sounds .

• If the obstruction has persisted for too long or the

bowel has been significantly damaged, bowel sounds
decrease, eventually becoming silent.

• Early paralytic ileus is marked by decreased or absent

bowel sounds.
 Strangulating Obstruction
• Toxic apperance, with a rapid pulse and aome
elevation of temperature.
• Colicky pain, becoming continous as peritonitis
develops.
• Tenderness and abdominal rigidity more marked.
• Bowel sound becoming reduced or absent,
reflecting peritonism.
• Raised white cell count, mostly neutrophils,
which is usual with infarcted bowel.
 Radiological Investigations
• An abdominal x-ray taken in a supine or
standing position is the first investigation in
patients with suspected small bowel
obstruction to document the dilated loops of
bowel, air-fluid interfaces, or both.

• Contrast radiography can help to evaluate

dysmotility, partial obstruction, and to define
the site and extent of the obstruction.
 Radiological Investigations
• Retrograde transrectal radiographic contrast
studies can be used to diagnose isolated or
concomitant obstruction of the large bowel.

• An abdominal computed tomography scan is

useful for evaluating the global extent of disease,
to perform staging, and to assist in the choice of
surgical, endoscopic, or pharmacological
intervention for the management of the
obstruction.
 Management
• Adequate resuscitation prior to surgery is vital
• May require more than 5 litres of intravenous crystalloid
• Adequacy of resuscitation should be judged by urine output or
central venous pressure
• Surgery in under resuscitated patient is associated with
increased mortality
• If obstruction presumed to be due to adhesions and there are no
features of peritonism
– Conservative management for up to 48 hours is often safe
– Requires regular clinical review
• If features of peritonism or systemic toxicity present
– Need to consider early operation
– Exact procedure will depend on underlying cause
Paralytic Ileus
 Definition
• Paralytic ileus is a condition in which the intestine failed / not
able to perform the contraction peristaltic to distribute its
content.

• Paralytic ileus is not a primary disease but rather a result of

various intestinal primary disease, surgery is associated with
abdominal cavities, toxins and drugs that can affect intestinal
smooth muscle contraction
 Etiology
• Neurogenic : • Drugs :
– post-surgery – Narcotics, anticholinergic,
– spinal cord damage catecholamines, fenotoazin,
– lead poisoning antihistamines
– ureteric colic • Infections :
– spanknikus neural irritation – Pneumonia, empyema,
urosepsis, peritonitis, other
– pancreatitis severe systemic infection
• Metabolic : • Colon ischemia
– Electrolyte balance
disturbances (especially
hypokalemia)
– Uremia
– diabetic complications
– systemic diseases such as SLE
– multiple sclerosis
 Pathophysiology

Acummulation and swallowed air static

There is no peristaltic And intraluminal fluid
in gaster and intestine

Bowel sounds Nausea, bloating,

minimal and abdomen distention
• Clinical manifestations:
– abdominal distension,
– anorexia,
– nausea,
– obstipasi,
– vomiting may exist may not

• Physical examination:
– Tympanic percussion with a weak bowel sounds may not sound
even at all
– Palpation: the patient simply stating the uneasy feeling in his
stomach
– Not found any tenderness and rebound tenderness

• Investigations:
– Plain abdominal: Air fluid level in the form of a picture line-up
(alignment).
 Management
• Management of paralytic ileus are conservative and supportive:

– Actions in the form of decompression with nasogastric tube

installation,

– Fluid and electrolyte balance, treating the primary disease and the
provision of adequate nutrition.

– Drugs:

• Sisaprid useful for postoperative paralytic ileus

• Klonidin reported to be useful to overcome the paralytic ileus due

to drugs
The Difference between Paralytic Ileus and
Obstructive Ileus

Paralytic Ileus Obstructive Ileus

• Bowel sounds minimal • Bowel sounds hyperactive

• Air Fluid level provides • Air fluid level provides a

line up stepladder

• Not accompanied by a • Accompanied by a

paroxysmal colicky paroxysmal colicky
abdominal pain abdominal pain
Bolus Ascariasis
 Ascaris lumbricoides
• Morphology :
– Adult worm :
• large size, smooth finely striated cuticle, terminal
mouth with 3 oval lips with sensory papillae; paired
reproductive organs in posterior two thirds of female
and single long tortuous tubule in male.
– The eggs
• There is an outer, coarsely mammilated, albuminous
covering
• The egg proper has a thick, transparent, hyaline shell
and a delicate vitelline, lipoidal, inner membrane that
is highly impermeable.
 Pathophysiological Mechanism
 Adult worms move throughout the GI tract and may become incarcerated, leading
to obstructive pathology.

 The worms may die → leading to inflammation, necrosis, infection, and abscess
formation.

 If they migrate through an existing perforation in the bowel wall → secondary to

tuberculosis or typhoid → cause a granulomatous peritonitis.

 Larvae during migration → may be deposited in the brain, spinal cord, kidney, or
other organs → leading to granuloma formation, inflammation, or infection.

 They may become entwined in a bolus and obstruct the small bowel; this is most
common in the terminal ileum, although other, more proximal, sites have been
rarely reported.
 Risk Factors
• Preschool age or younger
• Eating unsanitary food
• Drinking unclean water
 Symptoms
• Small burdens of worms in the intestine may cause no
symptoms
• The patient may have symptoms of pneumonitis with cough,
dyspnea, wheezing, chest pain and low grade fever during the
migration of the larvae through the liver and lungs.
• In heavy worm burdens the adult worms actively migrate in the
intestine resulting in intestinal blockage, vomiting,
abdominal pain, colic, nausea, anorexia, and intermittent
diarrhea
• A heavy worm burden in children may lead to severe
nutritional impairment and retardation in growth.
• Worms exiting through the nose or mouth
 Treatment
• Albendazole
– 400 mg PO once, for all ages
• Mebendazole
– 100 mg bid PO for 3 days or 500 mg PO once for all
ages
• Piperazine citrate
– 150 mg/kg PO initially, followed by 6 doses of 65 mg/kg
at 12 hr intervals PO, which causes neuromuscular
paralysis of the parasite (the treatment of choice for
intestinal or biliary obstruction)
 Treatment
• Pyrantel pamoate
– 11 mg/kg PO once, maximum 1 g
• Nitazoxanide
– 100 mg bid PO for 3 days for children 1-3 yrs of age,
– 200 mg bid PO for 3 days for children 4-11 yr
– 500 mg bid PO for 3 days for adolescents and adults
produces cure rates comparable with single-dose
albendazole.
• Surgery may be required for cases with severe
obstruction
Operatif Bolus Ascaris
 Complications
• Intestinal obstruction - 63%
• Bile duct obstruction - 23%
• Perforation, peritonitis, or both - 3.2%
• Volvulus - 2.7%
• Hepatitic abscess - 2.1%
• Appendicitis - 2.1%
• Pancreatitis - 1%
• Cerebral encephalitis - 1%
• Intussusception - 0.5%
• Other sites of pathology (<0.5%) include Meckel diverticulum, the gallbladder, ears,
eyes, nose, lungs, kidneys, vagina, urethra, heart, placenta, spleen, thoracic cavity,
and umbilicus.
• In endemic regions, ascariasis is a significant part of the differential diagnosis for
intestinal obstruction, appendicitis, biliary tract disease, pancreatitis, intussusception,
and volvulus.
Peritonitis
• Inflammation of the peritoneum, the thin membrane that lines the
abdominal wall and covers the organs inside.
• The inflammation is caused by a bacterial or fungal infection of this
membrane. There are two major types of peritonitis. Primary
peritonitis is caused by the spread of an infection from the blood
and lymph nodes to the peritoneum. This type of peritonitis is rare -
- less than 1% of all cases of peritonitis.
• The more common type of peritonitis, called secondary peritonitis,
happens when the infection comes into the peritoneum from the
gastrointestinal or biliary tract. Both cases of peritonitis are very
serious and can be life threatening if not treated quickly.
•
: http://www.umm.edu/altmed/articles/peritonitis-
000127.htm#ixzz26MKIOz84
 Etiology
• Bacteria enetr peritoneal cavity via four portal:
1. Exterior : penetrating wound, infection at laparotomy,
peritoneal dialysis
2. Intraabdominal viscera :
- Gangrene of viscus: acute apendisitis and
cholecystitis, diverticulitis or infarction of intestine
- Perforation of a viscus : perforated duodenale ulcer
and appendicitis, ruptur intestine from trauma
- Postoperative leakage
3. Via blood stream
4. Via the female genital tract
 Pathology
• Mixed fecal flora : E.coli, streptococcus
faecalis, pseudomonas, klebsiela and proteus,
anaerobic(clostridium and bacteroides)
• Gynecological infections : clamydial,
gonococcal or streptococcal
• Blood borne :streptococcal, pneumococcal,
staphilococcal or tuberculous
 Pathological effect of peritonitis
• Widespread absorption of toxin from the
large, inflamed surface
• Associated paralytic ileus : loos fluid,
electrolyte, protein
• Abdominal distension with elevation
diafhragm, which produces a liability to lung
collaps and pneumonia
 Primary (spontaneous) bacterial
peritonitis
• Usually caused by single organism
• Etiology
– Occurs most commonly in conjunction with cirrhosis
of the liver (frequently the result of alcoholism)
– Metastatic malignant disease
– postnecrotic cirrhosis
– chronic active hepatitis & acute viral hepatitis
– congestive heart failure
– systemic lupus erythematosus
– lymphedema
• Clinical manifestation
– Fever (80%)
– Acites  predates infection
– Abdominal pain, an acute onset of
symptoms, and peritoneal irritation
(physical examination)
– Nonlocalizing symptoms  malaise, fatigue,
or encephalopathy
• Other examination
– >250 PMNs/L is diagnostic for PBP
– Blood culture
• enteric gram-negative bacilli (Escherichia coli)  most
commonly encountered
• gram-positive organisms (streptococci, enterococci, or
even pneumococci)  sometimes found
• Aerobic bacteria
– Contrast-enhanced CT  intraabdominal source for
infection
– Chest & abdominal radiography  to exclude free air
• Treatment
– Third-generation cephalosporins (cefotaxime 2 g q8h,
administered IV)  initial coverage in moderately ill patients
– Broad-spectrum antibiotics, such as penicillin/β-lactamase
inhibitor combinations (piperacillin/tazobactam 3.375 g q6h IV
for adults with normal renal function); ceftriaxone (2 g q24h IV)
• Prevention
– Up to 70% of patients experience a recurrence within 1 year
– Antibiotic prophylaxis reduces this rate to <20%
– Prophylaxis agents
• fluoroquinolones (ciprofloxacin, 750 mg weekly; norfloxacin, 400
mg/d)
• trimethoprim-sulfamethoxazole (one double-strength tablet daily)
 Secondary peritonitis
• Develops when bacteria contaminate the peritoneum
as a result of spillage from an intraabdominal viscus 
chemical irritation and/or bacterial contamination
• Found almost always constitute a mixed flora in which
– facultative gram-negative bacilli
– anaerobes predominate, especially when the
contaminating source is colonic
• Early death in this  gram-negative bacillary sepsis
and to potent endotoxins circulating in the
bloodstream
– E. coli, are common bloodstream isolates, but Bacteroides
fragilis bacteremia also occurs
• Clinical manifestation
– local symptoms may occur in secondary peritonitis, ex:
• Epigastric pain from a ruptured gastric ulcer
• Appendicitis  vague, with periumbilical discomfort and nausea;
number of hours  pain localized right lower quadrant
– lie motionless
– knees drawn up to avoid stretching the nerve fibers of the
peritoneal cavity
– Coughing and sneezing  increase pressure within the
peritoneal cavity  sharp pain
• Physical examination
– voluntary and involuntary guarding of the anterior abdominal
musculature
– tenderness, especially rebound tenderness
• Treatment
– antibiotics aimed particularly at aerobic gram-negative
bacilli and anaerobes
– penicillin/β-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q4–6h IV); cefoxitin (2 g q4–6h
IV)
– Patients in the intensive care unit  imipenem (500 mg
q6h IV), meropenem (1 g q8h IV), or combinations of
drugs, such as ampicillin plus metronidazole plus
ciprofloxacin
– Surgical intervention + antibiotics (bacteremia) 
decrease incidence of abscess formation & wound
infection; prevent distant spread of infection
Peritonitis Etiologic Organisms Antibiotic Therapy
(Type) Class Type of Organism
Primary Gram- E coli (40%) Third-generation
negative K pneumoniae (7%) cephalosporin
Pseudomonas species (5%)
Proteus species (5%)
Streptococcus species
(15%)
Staphylococcus species
(3%)
Anaerobic species ( <5%)
Secondary Gram- E coli Second-generation
negative Enterobacter species cephalosporin
Klebsiella species Third-generation
Proteus species cephalosporin
Gram-positive Streptococcus species Penicillins with
Enterococcus species anaerobic activity
Quinolones with
Anaerobic Bacteroides fragilis anaerobic activity
Other Bacteroides species Quinolone and
Eubacterium species metronidazole
Clostridium species Aminoglycoside and
Anaerobic Streptococcus metronidazole
species
Perforation
 Perforation
Definition
• Gastrointestinal perforation is a hole that develops through the
entire wall of the stomach, small intestine, large bowel, or
gallbladder. This condition is a medical emergency.

Etiology
• Gastrointestinal perforation can be caused by a variety of illnesses,
including appendicitis, diverticulitis, ulcer disease, gallstones or
gallbladder infection, and less commonly, inflammatory bowel
disease, including Crohn's disease and ulcerative colitis.
• It may also be caused by abdominal surgery.
 Perforation
Symptoms
 Perforation of the intestine leads to leakage of intestinal
contents into the abdominal cavity. This causes
inflammation called peritonitis.

 Symptoms may include:

 Abdominal pain - severe
 Chills
 Fever
 Nausea
 Vomiting
 Perforation
Examinations
• X-rays of the chest or abdomen may show air in the
abdominal cavity (not in the stomach or intestines),
suggesting a perforation.
• CT scan of the abdomen often shows the location of the
perforation.
• The white blood cell (WBC) count is often higher than
normal.
 Perforation
Treatments
• Treatment usually involves surgery to repair the hole
(perforation). Occasionally, a small part of the intestine
must be removed. A temporary colostomy or ileostomy
may be needed.

• In rare cases, antibiotics alone can be used to treat patients

whose perforations have closed. This can be confirmed by a
physical exam, blood tests, CT scan, and x-rays.
 Perforation
Prognosis
 Surgery is usually successful, but depends on the severity of the
perforation and the length of time to treatment.

Complications
 Bleeding
 Infection ( including a widespread infection called sepsis, which can lead
to death )
 Intra-abdominal abscess

Preventions
 Prevention depends on the cause. Diseases that may lead to intestinal
perforation should be treated appropriately.
Adhesive Obstruction
 Overview
• Intraabdominal adhesions develop after abdominal
surgery as part of the normal healing processes that
occur after damage to the peritoneum.
• Treatment is initially conservative, with nasogastric
suction and intavenous fluid replacement.
• However, clinical features of strangulation,
peritonitis or failure to respond to the conservative
regimen are indications for urgent laparotomy.
 Biological events involved in peritoneal tissue repair and adhesion formation.

PAI-1 = plasminogen activator inhibitors group 1; tPA = tissue plasminogen activator;

uPA= urokinase-like plasminogen activator.
Intussusception
 Intussusception
• Intussusception occurs when one part of the
intestine invaginates into the lumen of the
adjoining bowel
• The mesentery is dragged along with the
prolapsed bowel, causing venous
compression, swelling, and edema of the
bowel wall
• If untreated, the edema eventually will cause
arterial obstruction, ischemia, and perforation
 Epidemiology
• Incidence varies from 1 to 4 per 1000 live
births, with a male preponderance of 3:2
• Common between 2 months to 5 years of age,
with a peak incidence at 4 to 10 months
 Intussusception
• Etiology
– Small bowel polyp
– Meckel diverticulum
– Omphalomesenteric remnant
– Henoch-Schonlein purpura
– Lymphoma
– Lipoma
– Parasites
– Foreign bodies
– Viral enteritis with hypertrophy of Peyer patches
 Intussusception
• Clinical findings
Infant 3-12 months
– Recurring paroxysms of abdominal pain
– Screaming
– Drawing up of the knees
– Vomiting and diarrhea (occur soon)
– Bloody bowel movement with mucus (next 12 hours)
Child
– Lethargic between paroxysms and febrile (+)
– Abdomen is tender and often distended
– A sausage-shaped mass may be palpated (usually in the upper mid
abdomen)
• Abdominal radiograph shows small bowel
dilatation and paucity of gas in the right lower
and upper quadrants.
• Air contrast enema • Barium enema shows
shows intussusception intussusception in the
in the cecum. descending colon
• Abdominal • Laparoscopic view of a
ultrasonography reveals jejuno-jejunal
the classic target sign of intussusception
an intussusceptum
inside an
intussuscipiens.
 Intussusception
• Treatment
– Barium enema and air enema
• Barium enema should not be attempted if signs of
strangulated bowel, perforation, or toxicity are present
– Surgery
• Extremely ill patients
• Patients with evidence of bowel perforation
• Patients whom hydrostatic or pneumatic reduction has
been unsuccessful
 Intussusception
• Prognosis
– Relates directly to the duration of intussusception
before reduction
– Mortality rate with treatment is 1-2 %
Malrotation
 Malrotation
• Malrotation of the intestines results when the
intestinal rotation and fixation that occurs during
pregnancy fails to occur.
• This normally happens in the 4th and 12th weeks
of fetal life.
• In the 4th fetal week, the entire bowel is basically
a straight tube with the superior mesenteric
artery (SMA).
• During the course of pregnancy, the bowel
rotates in place to the left of the SMA at the
ligament of Treitz.
Normal fixation of the
bowel in place looks Malrotation of the bowel may look like this:
like this:
• In normal rotation and fixation of the intestines,
the bowel has plenty of room to function
normally.
• In malrotation, the primary concern becomes
volvulus, or twisting of the intestine that causes
obstruction and death to that part of the gut
(pictured below).
• Accidental bodily movements, unusual effort,
abnormal peristaltic movement (digestive
wavelike motion of the intestines) or distention of
the intestine can bring on this volvulus.
• Diagrams showing how volvulus occurs in a case
of malrotation.
• The first diagram shows the non-fixed terminal
ileum and cecum.
• The second diagram shows early volvulus as this
area begins to twist on itself.
• The twisting continues until, as shown in the third
diagram (late volvulus), the intestines are
obstructed and the blood supply to this area is
constricted (shut-off)
 Symptoms
• The major symptoms of malrotation are
– bilious vomiting
– abdominal pain and abdominal distention.
– All of these are signs of the intestinal
obstruction that has occurred.
• The bowel twists causing pain; becomes
distended (enlarged) because of the pressure
and the child will vomit the bile that is
released for normal digestion.
 Diagnose
• X-rays of the abdomen will show air in the
stomach and lower in the intestine past the
obstruction without air being present anywhere
else.
• Further testing that can occur is a barium swallow
that will show the barium coming to a stop at the
point of the obstruction.
• A barium enema will show the location of
obstruction and, more clearly, the malrotation as
the colon is visualized.
 Treatment
• A child with volvulus is usually dehydrated and has a rapid heart rate. IV
fluids will be needed immediately with antibiotics.
• A nasogastric tube will be placed through the child’s nose into the
stomach to decompress or allow the fluids backing up into the stomach to
empty.
• An exploratory laparotomy (surgery) will be performed to take a look at
the bowel. The bowel will be detorsed (unwound) and checked carefully
(see pictures).
• The bowel that turns pink (showing returned circulation) after torsion is
good bowel. If all bowel turns pink, a Ladd’s procedure will be performed
to put the bowel in place to prevent another volvulus.
• An appendectomy is usually done since the appendix will not be located
in the normal area in the abdomen. This could lead to confusion and delay
in diagnosing appendicitis in the future.
• If there is a question about the bowel’s viability, the abdomen will be left
open and a second-look procedure will be planned within 24 to 48 hours.
• If there is a section of necrotic (dead) bowel a colostomy may be needed
temporarily. The ostomy nurse will consult with you on ostomy care.
• The operation done to repair malrotation is called Ladd's
procedure.
• In Ladd's procedure, the abdomen is opened (Diagram
A).The small intestines are seen first and appear to hide the
colon.
• The entire intestinal mass is delivered out of the abdomen
(Diagram B).
• The intestinal mass is rotated to reduce the volvulus
(Diagram C).
• The intestines are re-positioned in the abdomen (Diagram
D).
• Diagram E shows the appearance of the intestines at the
end of surgery.
Hernia
 Definition
• A hernia is an abnormal protrusion, or bulging
out, of part of an organ through the tissues
that normally contain it.
• In this condition, a weak spot or opening in a
body wall, often due to laxity of the muscles,
allows part of the organ to protrude.
• A hernia may develop in almost any part of
the body; however, the muscles of the
abdominal wall are most commonly affected.
 Description of Hernia
• Hernias cause pain and reduce general
mobility.
• They never cure themselves, even though
some can be cured (at least temporarily) by
external manual manipulation.
• Depending on the nature of the protruding
organ and the solidity of the structure through
which it is protruding, a hernia may cause
complications that are medically dangerous.
 Description of Hernia
• One major danger of a hernia is that if bowel
is contained within the protruding loop it may
hinder or stop the flow through the intestine
(occlusion).
 Description of Hernia
• More serious still, if the loop itself becomes twisted
outside its containing structure, or compressed at
the point where it breaks through that structure (a
strangulated hernia), the blood supply to the loop
will also cease and the entire hernia will undergo
tissue death (necrosis).
• This requires immediate emergency surgery.
 Types Of Hernia
• Abdominal wall hernia
• Indirect inguinal hernia
• Direct inguinal hernia
• Femoral hernia
• Umbilical hernia
• Hiatal hernia
• Incisional hernia
 Abdominal wall hernia
• Also called an epigastric or ventral hernia;
affects 1 person in 100 nationwide.
• Technically, this group also includes inguinal
hernias and umbilical hernias.
 Indirect inguinal hernia
• This affects men only.
• A loop of intestine passes down the canal
from where a testis descends early in
childhood into the scrotum.
• If neglected, this type of hernia tends to
increase progressively in size (a "sliding
hernia") causing the scrotum to expand
grossly.
 Direct inguinal hernia
• This affects both sexes. The intestinal loop
forms a swelling in the inner part of the fold of
the groin.
 Femoral hernia
• This affects both sexes, although most often
women.
• An intestinal loop passes down the canal
containing the major blood vessels to and
from the leg, between the abdomen and the
thigh, causing a bulge in the groin and another
at the top of the inner thigh.
 Umbilical hernia
• This affects both sexes.
• An intestinal loop protrudes through
a weakness in the abdominal wall at the navel
(but remains beneath the skin).
 Hiatal hernia
• This affects both sexes.
• A loop of the stomach when particularly full
protrudes upward through the small opening in the
diaphragm through which the esophagus passes,
thus leaving the abdominal cavity and entering the
chest.
 Incisional hernia
• This is a hernia that occurs at the site of a
surgical incision.
• This is due to strain on the healing tissues due
to excessive muscular effort, lifting, coughing,
or extreme pressure.
 Causes and Risk Factors of Hernia
• Umbilical hernias can be present from birth, but
most happen later due to pressure on openings or
weaknesses in the abdominal cavity or wall.
• Hernias tend to run in families, and can be caused
by such things as straining during elimination, lifting
heavy objects, accumulation of fluid in the
abdominal cavity, and obesity, Chronic lung
disease can also cause a hernia.
 Symptoms of Hernia
• Symptoms of hernias vary, depending on the
cause and the structures involved.
• Most begin as small, hardly noticeable
breakthroughs.
• At first, they may be soft lumps under the skin, a
little larger than a marble; there usually is no
pain.
• Gradually, the pressure of the internal contents
against the weak wall increases, and the size of
the lump increases.
 Symptoms of Hernia
• Early on, the hernia may be reducible - the
protruding structures can be pushed back
gently into their normal places.
• If those structures, however, cannot be
returned to their normal locations through
manipulation, the hernia is said to be
irreducible, or incarcerated.
 Treatment of Hernia
• For small, non-strangulated and non-
incarcerated hernias, various supports and
trusses may offer
temporary, symptomatic relief.
• However, the best treatment is herniorrhaphy
(surgical closure or repair of the muscle wall
through which the hernia protrudes).
 CONCLUSION
• We had studied learning objective:
1. Acute abdomen (appendicitis, ileus, ascaris ball, peritonitis,
perforation, adhesions, hernia, intussusception, malrotation):
- Definition
- Etiology
- Epidemiology
- Patophysiology
- Sign & Symptom
- Diagnosis
- Management
- Complication
- Prognosis
 SUGGESTION
• Rehydration
• Further examination
• Surgery if needed
 REFERENCES
• Evers BM. Small intestine. In: Townsend CM,
Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston
Textbook of Surgery. 18th ed. St. Louis, Mo: WB
Saunders; 2008
• http://www.surgical-tutor.org.uk
• http://www.umm.edu
• http://emedicine.medscape.com
• http://www.cdc.gov
• http://www.nlm.nih.gov