Group 17 - Gastrointestinal system block

Faculty of Medicine
Tarumanagara University

PROBLEM 4B (CHILD)
Jesly Charlies
405100171
LEARNING OBJECTIVES:
1. Acute Abdomen
a. Ileus
b. Appendicitis
c. Peritonitis
d. Perforation
e. Intussusception
f. Malrotation
g. Hernia
h. Adhesion
i. Ascaris ball
ACUTE ABDOMEN
DEFINITION
Acute abdomen sign and symptoms of abdominal
pain and tenderness, a clinical presentation that often
requires emergency surgical therapy.
NONSURGICAL CAUSES OF
ACUTE ABDOMEN
Endocrine and Metabolic Causes
Uremia
Diabetic crisis
Addisonian crisis
Acute intermittent porphyria
Hereditary Mediterranean fever
Hematologic Causes
Sickle cell crisis
Acute leukemia
Other blood dyscrasias
Toxins and Drugs
Lead poisoning
Other heavy metal poisoning
Narcotic withdrawal
Black widow spider poisoning
SURGICAL ACUTE ABDOMINAL
CONDITIONS
Hemorrhage
Solid organ trauma
Leaking or ruptured arterial aneurysm
Ruptured ectopic pregnancy
Bleeding gastrointestinal deiverticulum
Arteriovenous malformation of gastrointestinal tract
Intestinal ulceration
Aortoduodenal fistula after aortic vascular graft
Hemorrhagic pancreatitis
Mallory Weiss syndrome
Spontaneous rupture of spleen
Infection
Appendicitis
Cholecystitis
Meckels diverticulitis
Hepatic abscess
Diverticular abscess
Psoas abscess
Perforation
Perforated gastrointestinal ulcer
Perforated gastrointestinal cancer
Boerhaaves syndrome
Perforated diverticulum
Obstruction
Adhesion related small or large bowel obstruction
Sigmoid volvulus
Cecal volvulus
Incarcerated hernias
Inflammatory bowel disease
Gastrointestinal malignancy
Intussusception
Ischemia
Buergers disease
Mesenteric thrombosis or embolism
Ovarian torsion
Ischemic colitis
Testicular torsion
Strangulated hernias
CLASSIFICATION

Visceral
pain
Abdominal Parietal
Pain pain
Reffered
pain
CLASSIFICATION
Visceral pain
Tends to be vague, poorly localized to the epigastrium,
periumbilical region, or hypogastrium
Depending on its origin from the primitive foregut, midgut,
or hindgut
Mediated by autonomic nerves (sympathetic and
parasympathetic)

Parietal pain
Coorresponds to the segmental nerve roots innervating the
peritoneum
Tends to be sharper and better localized
 Referred pain
Perceived at a site that is distant from the sourced of
stimulus
For example irritation of the diaphragm may produce pain
in the shoulder

Locations of Reffered Pain and Its Causes

Right Shoulder
Liver
Gallbladder
Right hemidiaphragm
Left Shoulder
Heart
Tail of pancreas
Spleen
Left hemidiaphragm
Scrotum and Testicles
Ureter
SOME MECHANISMS OF PAIN ORIGINATING
IN ABDOMEN
Inflammation of the parietal peritoneum
Pain of parietal peritoneal inflammation is steady and aching
in character and is located directly over the inflamed area
transmitted by somatic nerves supplying the parietal
peritoneum
Pain intensity type and amount of material to which the
peritoneal surfaces are exposed in a given time period
The pain of peritoneal inflammation is invariably accentuated
by pressure or changes in tension of the peritoneum
Produced by palpation or by movement, as in coughing or sneezing
Lies quietly in bed, preferring to avoid motion,

In contrast to the patient with colic, who may writhe incessantly

Tonic reflex spasm of the abdominal musculature, localized

to the involved body segment
 Obstruction of hollow viscera
Intermittent, or colicky
Distention of a hollow viscus steady pain + very occasional
exacerbations
The colicky pain of obstruction of the small intestine
periumbilical or supraumbilical, poorly localized
Acute distention of the gallbladder pain in the right upper
quadrant with radiation to right posterior region of the thorax / to
the tip of the right scapula
Distention of the common bile duct pain in the epigastrium
radiating to the upper part of the lumbar region
Obstruction of the urinary bladder dull suprapubic pain, usually
low in intensity
In contrast, acute obstruction of the intravesicular portion of the
ureter severe suprapubic and flank pain radiates to penis,
scrotum, or inner aspect of the upper thigh
 Vascular Disturbances
Pain associated with intraabdominal vascular disturbances is
sudden and catastrophic in nature
Embolism or thrombosis of the superior mesenteric artery
Severe & diffuse; only mild continuous diffuse pain for 2 or 3 days
before vascular collapse or findings of peritoneal inflammation
appear
Impending rupture of an abdominal aortic aneurysm
Abdominal pain with radiation to the sacral region, flank, or genitalia;
persist over a period of several days before rupture and collapse
occur
Abdominal wall
Pain from the abdominal wall constant & aching
e/ Movement, prolonged standing, and pressure accentuate the
discomfort and muscle spasm
Ex: hematoma of the rectus sheath
APPROACH TO THE PATIENT
Only those patients with exsanguinating intraabdominal
hemorrhage (e.g., ruptured aneurysm) operate
But in such instances only a few minutes are required to
assess the critical nature of the problem

Orderly, pains takingly detailed history

Even though a reasonably accurate diagnosis can be
made on the basis of the history alone in the majority of
cases
DIFFERENTIAL DIAGNOSE
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
ILEUS
ILEUS
Ileus is the failure of intestinal peristalsis without
evidence of mechanical obstruction.
Lack of normal gut motility interferes with abnormal
movement of intestinal contents and in children is most
often associated with abdominal surgery or infection
(pneumonia, gastroenteritis, peritonitis).
Ileus also accompanies metabolic abnormalities, such as
uremia, hypokalemia, or acidosis, and occurs with
administration of certain drugs, such as opiates and
vincristine.
Ileus may also occur when antimotility drugs such as
loperamide are used during episodes of gastroenteritis.
 Clinical features
Increasing abdominal distention and initially minimal pain
Pain increases with increasing distention
Examination
Bowel sounds are minimal or absent, in contrast to early
mechanical obstruction, when they are hyperactive.
Radiographs
Plain abdominal many air-fluid levels throughout the
abdomen.
Serial do not show progressive distention as they do in
mechanical obstruction.
Contrast slow movement of the barium through a patent
lumen.
 Treatment
Correction of underlying abnormality.
Nasogastric decompression is used if abdominal distention is
associated with pain or to relieve recurrent vomiting.
Ileus after abdominal surgical procedures usually results in
return of normal intestinal motility within 24-72 hr.
Prokinetic agents such as metoclopramide or erythromycin
may stimulate the return of normal bowel motility and be of
assistance to children with prolonged ileus.
Oral administration of drugs that block gastrointestinal
opiate receptors but do not block central nervous system
opiate action may reduce the ileus in postoperative patients
receiving narcotics.
ACUTE APPENDICITIS
ACUTE APPENDICITIS
Acute appendicitis is the most common condition
requiring emergency abdominal operation in childhood.
Diagnosis is difficult in young children, a factor
contributing to perforation rates of 30-60%.
50% of children with perforated appendicitis have been
seen by a physician before the diagnosis.
The risk of perforation is greatest in 1- to 4-yr-old
children (70-75%) and is lowest in the adolescent age
group (30-40%), which has the highest age-specific
incidence of appendicitis in childhood.
 Epidemiology
Approximately 80,000 children experience appendicitis in the
United States annually
A rate of 4/1,000 children younger than age 14 yr.
Rare in developing countries, where diets are high in fiber.
However, no causal relationship has been established between lack
of dietary fiber and appendicitis.
The incidence of appendicitis increases with age, peaking in
adolescence and rarely occurring in children younger than 1
yr old.
A familial predilection to appendicitis has been reported.
Cases occur more often in males.
Cases occur more often in the autumn and spring.
 Pathogenesis
occur as a result of appendiceal luminal obstruction
Obstruction is most commonly caused by a fecalith
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)

appendiceal ulceration
Infection with Yersinia organisms may cause the disease
Luminal bacteria multiply and invade the appendiceal wall
venous engorgement and subsequent arterial compromise
gangrene and perforation occur
slow: terminal ileum, cecum, and omentum (localized abscess);
rapid: perforation with free access to the peritoneal cavity
 Clinical manifestations
abdominal discomfort and anorexia
The pain is described as being located in the periumbilical
region initially and then migrating to the right lower
quadrant
resulting from distention of the appendiceal lumen; pain is carried
on slow-conducting C fibers and is usually poorly localized in the
periumbilical or epigastric region
In general, this visceral pain is mild, often cramping and
usually lasting 46 h
As inflammation spreads to the parietal peritoneal surfaces
pain becomes somatic, steady, and more severe and
aggravated by motion or cough
Nausea and vomiting occur in 5060% of cases
DIFFERENTIAL DIAGNOSIS
 Physical findings
tenderness to palpation will often occur at McBurney's point
Abdominal tenderness may be completely absent if a
retrocecal or pelvic appendix is present tenderness in the
flank or on rectal or pelvic examination
Referred rebound tenderness is often present and is most likely to
be absent early in the illness
Flexion of the right hip and guarded movement by the
patient are due to parietal peritoneal involvement
The temperature is usually normal or slightly elevated
[37.238C (99100.5F)], >38.3C (101F) perforation
Rigidity and tenderness more marked as the disease
progresses to perforation and localized or diffuse peritonitis
Perforation is rare before 24 h after onset of symptoms, but
the rate may be as high as 80% after 48 h
 Any infant or child with diarrhea, vomiting, and abdominal
pain is highly suspect
Fever is much more common in this age group
abdominal distention is often the only physical finding

In the elderly, pain and tenderness are often blunted

the diagnosis is also frequently delayed and leads to a 30%
incidence of perforation in patients over 70
often present initially with a slightly painful mass (a primary
appendiceal abscess) or with adhesive intestinal obstruction
5 or 6 days after a previously undetected perforated
appendix
 Laboratorium findings
moderate leukocytosis of 10,00018,000 cells/microL is
frequent
Leukocytosis of >20,000 cells/microL perforation
Anemia and blood in the stool suggest a primary diagnosis of
carcinoma of the cecum, especially in elderly individuals
urine may contain a few white or red blood cells without
bacteria if the appendix lies close to the right ureter or
bladder
Urinalysis is most useful in excluding genitourinary
conditions that may mimic acute appendicitis
 Radiographs
opaque fecalith (5% of patients) is observed in the right
lower quadrant (especially in children)
intestinal obstruction or ureteral calculus may be present
Ultrasound an enlarged and thick-walled appendix
CT will include a thickened appendix with periappendiceal
stranding and often the presence of a fecalith
 Treatment
early operation and appendectomy as soon as the patient
can be prepared
A different approach is indicated if a palpable mass is found
35 days after the onset of symptoms phlegmon / abscess
broad-spectrum antibiotics, drainage of abscesses >3 cm, parenteral
fluids, and bowel rest usually show resolution of symptoms within 1
week
Interval appendectomy can be performed safely 612 weeks later

antibiotics alone can effectively treat acute, nonperforated

appendicitis in 86% of male patients (higher recurrence rate)
PERITONITIS
PERITONITIS
Peritonitis is an inflammation of the peritoneum; it may
be localized or diffuse in location, acute or chronic in
natural history, infectious or aseptic in pathogenesis.
Acute peritonitis is most often infectious and is usually
related to a perforated viscus (and called secondary
peritonitis).
When no intraabdominal source is identified, infectious
peritonitis is called primary or spontaneous.
 Acute peritonitis is associated with decreased intestinal
motor activity, resulting in distention of the intestinal
lumen with gas and fluid. The accumulation of fluid in
the bowel together with the lack of oral intake leads to
rapid intravascular volume depletion with effects on
cardiac, renal, and other systems.

The cardinal manifestations of peritonitis are acute

abdominal pain and tenderness, usually with fever.
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/-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/-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q46h IV); cefoxitin (2 g q46h
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 IN PATIENTS UNDERGOING
CAPD
CAPD (continuous ambulatory peritoneal dialysis)
CAPD-associated peritonitis usually involves skin
organisms
Pathogenesis
skin organisms migrate along the catheter serves as an
entry point and exerts the effects of a foreign body
usually caused by a single organism
 Clinical presentation
diffuse pain and peritoneal signs are common

dialysate is usually cloudy and contains >100 WBCs/L, >50%

of which are neutrophils
Organisms:
most common organisms are Staphylococcus spp
Gram-negative bacilli and fungi such as Candida spp. are also found

Vancomycin-resistant enterococci and vancomycin-intermediate S.

Aureus
 Treatment
should be directed at S. aureus, coagulase-negative
Staphylococcus, and gram-negative bacilli until the results of
cultures are available
first-generation cephalosporin such as cefazolin (for gram-
positive bacteria)
fluoroquinolone or a third-generation cephalosporin such as
ceftazidime (for gram-negative bacteria)
MRSA vancomysin
If the patient is severely ill, IV antibiotics should be added at
doses appropriate for the patient's degree of renal failure
if the patient has not responded after 48 h of treatment,
catheter removal should be considered
PERFORATION
PERFORATION
Perforated Ulcer
Perforated gastric/duodenal ulcer requires immediate
operative therapy
Anterior gastric perforations cause peritonitis
Posterior gastric and duodenal perforations may not cause
peritonitis, and after the acute episode of pain, the leak may
wall off, giving the impression that the patient is improving
Free air (80% of perforated ulcers)
ETIOLOGY
Helicobacter Pylori
Smoking

NSAIDs
PATOPHYSIOLOGY
TREATMENT
Immediate surgery
For a perforated duodenal ulcer,may include:
a highly selective vagotomy, a truncal vagotomy and
pyloroplasty, or vagotomy and antrectomy.
For a perforated gastric ulcerdepends on the patient's
condition:
If the patient is moribund, the ulcer is best excised by
grasping it with multiple Allis clamps and using a GIA-60
linear stapler. Or,can be excised with electrocautery
In a stable patient, the ulcer is excised and sent for frozen
section analysis to exclude malignancy
INTUSSUSCEPTION
INTUSSUSCEPTION
Intussusception occurs when a portion of the alimentary
tract is telescoped into an adjacent segment.
It is the most common cause of intestinal obstruction
between 3 mo and 6 yr of age.
60% younger than 1 yr, and 80% before 24 mo; it is rare
in neonates.
The incidence varies from 1-4 in 1,000 live births;

The male : female ratio is 4:1

A few intussusceptions reduce spontaneously, but if left

untreated, most will lead to peritonitis, perforation, and
death.
 Etiology & Risk factors
The etiology is unknown correlation with adenovirus &
rotavirus
Risk factors Meckel diverticulum, intestinal polyp,
neurofibroma, intestinal duplication, hemangioma, or
malignant conditions such as lymphoma, cystic fibrosis
Postoperative intussusception is ileoileal occurs within 5
days of an abdominal operation
Lead points are more common in children older than 2 yr of age
 Pathology
Most often ileocolic and ileoileocolic, less commonly
cecocolic
Engorgement of the intussusceptum follows, with edema &
bleeding from the mucosa bloody stool, sometimes
containing mucus
The apex of the intussusception may extend into the
transverse, descending, or sigmoid colon
Most intussusceptions do not strangulate the bowel within
the first 24 hr, but may later eventuate in intestinal gangrene
and shock
 Clinical manifestations
Sudden onset, in a previously well child severe paroxysmal
colicky pain that recurs at frequent intervals and is
accompanied by straining efforts with legs and knees flexed
and loud cries
The infant may initially be comfortable and play normally between
the paroxysms of pain; but if the intussusception is not reduced, the
infant becomes progressively weaker and lethargic.
Eventually a shocklike state may develop with fever
The pulse becomes weak and thready
The respirations become shallow and grunting
The pain may be manifested only by moaning sounds
Vomiting occurs in most cases and is usually more frequent
early
In the later phase, the vomitus becomes bile stained
 After the first few hours fecal excretions are small or more
often do not occur and little or no flatus is passed
Blood generally is passed in the first 12 hr but at times not
for 1-2 days and infrequently not at all; 60% of infants pass a
stool containing red blood and mucus, the currant jelly stool
Some patients have only irritability and alternating or
progressive lethargy
 Examination
Palpation a slightly tender sausage-shaped mass,
sometimes ill defined, increase in size and firmness during a
paroxysm of pain and is most often in the right upper
abdomen
30% of patients do not have a palpable mass
Presence of bloody mucus on the finger as it is withdrawn
after rectal examination supports the diagnosis
Abdominal distention and tenderness develop as intestinal
obstruction becomes more acute
 Diagnosis
The clinical history and physical findings
Plain abdominal radiographs may show a density in the
area of the intussusception
Barium enema filling defect or cupping in the head of
barium where its advance is obstructed by the
intussusceptum
USG sensitive diagnostic tool in the diagnosis of
intussusception
 Treatment
Reduction of an acute intussusception is an emergency
procedure and performed immediately after diagnosis in
preparation for possible surgery
If the patient have signs of shock, peritoneal irritation, intestinal
perforation, or pneumatosis intestinalis, reduction should not be
attempted
Radiologic reduction under fluoroscopic or ultrasonic
guidance
50% if symptoms are present longer than 48 hr; 70-90% if reduction
is done within the first 48 hr
Barium and hydrostatic (saline) reductions
Bowel perforations occur in 0.5-2.5%
 Prognosis
Untreated intussusception in infants is almost always fatal
Most infants recover if the intussusception is reduced within
the first 24 hr, but the mortality rate rises rapidly after this
time, especially after the 2nd day
The recurrence rate after barium enema reduction of
intussusceptions is about 10%, and after surgical reduction it
is 2-5%
Administration of dexamethasone has been reported to
reduce the frequency of recurrent intussusception
MALROTATION
MALROTATION
Malrotation is incomplete rotation of the intestine during
fetal development.
The gut starts as a straight tube from stomach to rectum.
The midbowel (distal duodenum to midtransverse colon)
begins to elongate and progressively protrudes into the
umbilical cord until it lies totally outside the confines of the
abdominal cavity.
As the developing bowel rotates in and out of the abdominal
cavity, the superior mesenteric artery, which supplies blood
to this section of gut, acts as an axis.
The duodenum, on re-entering the abdominal cavity, moves
to the region of the ligament of Treitz, and the colon that
follows is directed to the left upper quadrant.
 The cecum subsequently rotates counterclockwise within the
abdominal cavity and comes to lie in the right lower
quadrant.
The duodenum becomes fixed to the posterior abdominal
wall before the colon is completely rotated.
After rotation, the right and left colon and the mesenteric
root become fixed to the posterior abdomen.
These attachments provide a broad base of support to the
mesentery and the superior mesenteric artery, thus
preventing twisting of the mesenteric root and kinking of the
vascular supply.
Abdominal rotation and attachment are completed by 3 mo
gestation.
 Nonrotation occurs when the bowel fails to rotate after
it returns to the abdominal cavity.
The first and second portions of the duodenum are in
their normal position, but the remainder of the
duodenum, jejunum, and ileum occupy the right side of
the abdomen while the colon is located on the left.
Malrotation and nonrotation are associated with
abdominal heterotaxia and the asplenia-polysplenia
congenital heart malformation syndrome anomalad.
Normal fixation of the
Malrotation of the bowel:
bowel:
 The most common type of malrotation failure of the
cecum to move into the right lower quadrant.
The mesentery including the superior mesenteric artery
is tethered by a narrow stalk, which may twist around
itself, producing a midgut volvulus.
Bands of tissue (Ladd bands) may extend from the
cecum to the right upper quadrant, crossing and
possibly obstructing the duodenum.
The mechanism of
intestinal obstruction
with incomplete
rotation of the midgut
(malrotation).
The dotted lines show
the course the cecum
should have taken.
Failure to rotate has
left obstructing bands
across the duodenum
and a narrow pedicle
for the midgut loop,
making it susceptible
to volvulus.
 Clinical manifestation
The majority, within the 1st yr of life symptoms of acute
or chronic obstruction.
Infants often present within the 1st wk of life bilious
emesis and acute bowel obstruction.
Older infants episodes of recurrent abdominal pain that
may mimic colic.
Older children recurrent episodes of vomiting, abdominal
pain, or both.
Patients occasionally present with malabsorption or protein-
losing enteropathy associated with bacterial overgrowth.
 Symptoms are caused by intermittent volvulus or duodenal
compression by Ladd bands or other adhesive bands
affecting the small and large bowel.
25-50% of adolescents with malrotation asymptomatic.
Adolescents, symptomatic acute intestinal obstruction or
history of recurrent episodes of abdominal pain with less
frequent vomiting and diarrhea.
Patients of any age with a rotational anomaly can develop
volvulus without pre-existing symptoms.
 Complication
Volvulus associated with malrotation life threatening
Diagnosis
Ultrasound inversion of the superior mesenteric artery and vein
Contrast radiographic studies (Barium enema) malposition of the
cecum (may be normal in 10% of patients)
The abdominal plain film is usually nonspecific duodenal
obstruction double-bubble sign
Upper gastrointestinal series malposition of the ligament of
Treitz
Treatment
Surgical intervention, regardless of age
Persistent symptoms after repair of malrotation should suggest a
pseudo-obstruction-like motility disorder
 HOW VOLVULUS OCCURS IN A CASE
OF MALROTATION

Malrotation Early volvulus Late volvulus

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).
HERNIA
HERNIA
Hernia is the protrusion of an organ or part of an organ
through a defect in the wall of the cavity containing it,
into an abnormal position.
Abdominal wall hernia
Inguinal (direct or indirect)
Femoral
Umbilical & para-umbilical
Incisional
Ventral & epigastric
 Etiology
Weakness in the abdominal wall
Occur at the site of penetration of structures through the
abdominal wall
The layers of the abdominal wall may be weakened following a
surgical incision
Poor healing as a result of infection, hematoma formation
Damage to the nerve paralysis of abdominal muscles
Increase of intra-abdominal pressure
Chronic cough
Constipation
Urinary obstruction
Pregnancy
Abdominal distention with ascites
Weak abdominal muscles
 Varieties
Reducible hernia
Can be replaced completely into the peritoneal cavity
Presents as a lump that may disappear on lying down, not painful
Examination: reveals a reducible lump with cough impulse
Irreducible hernia
Adhesions of its contents to the inner wall of the sac
Painless, absence of cough impulse
Strangulated hernia
The hernia constricted on the neck of the sac circulation is cut off
perforation & gangrene
Severe pain of sudden onset, colicky pain, vomitting, distention,
absolute constipation
Examination: tender, tense hernia, overlying skin become inflamed,
noisy bowel sound
(femoral, indirect inguinal, umbilical)
INGUINAL HERNIA
Indirect inguinal hernia
Passes through the internal ring, along the canal in front of the
spermatic cord ; if large enough emerges through the external
ring into scrotum
Features
Hernia doesnt reach its full size until patient has been up & around a
little time; doesnt reduce immediately when lies down
Distinct tendency to strangulate
Examination
Can be felt in the mid-inguinal point
Direct inguinal hernia
Pushes its way directly forward through the posterior wall of the
inguinal canal
Features
Appears immediately on standing; disappearing at once when lies down
 Treatment
Herniotomy
Patent processus vaginalis is ligated & hernial sac excised at the age
of about 1 year and adult
Shouldice repair
Excision of the sac & repair of the weakened inguinal canal by
plicating the transversalis fascia in the posterior wall by nylon suture
Lichtenstein repair
Reinforcing the posterior wall with a nylon or polypropylene mesh
FEMORAL HERNIA
Hernia passes through the femoral canal
Clinical features
Commonly in women (wider female pelvis)
A non strangulated globular swelling below & lateral to
the pubic tubercle; it enlarged on standing, coughing,
disappear when lies down
Hernia enlargement passes through the saphenous
opening in the deep fascia penetration of the great
saphenous vein
RICHTERS HERNIA
Occur in femoral sac, only part of the wall of small
intestine herniates through the defect strangulated
Knuckle of bowel can become necrotic perforate
acute peritonitis
Treatment
Repaired with excision of the sac & closure of the femoral
canal because the danger of strangulation
UMBILICAL HERNIA
Exomphalos
Failure of all part of the midgut to return to the abdominal cavity in
fetal life
Bowel is contained within a translucent sac through a defective
anterior wall
Untreated rupture fatal peritonitis (rupture may occur during
delivery)
Treatment
Surgical repair immediately
Congenital umbilical hernia
Result from failure of complete clossure of the umbilical cicatrix
Common in black children
Treatment
Not surgical repair (unless the hernia persist when the child is 2 yo
PARA-UMBILICAL HERNIA
Acquired hernia that occurs just above or below
umbilicus
Occurs in obese, multiparous, middle-aged women

Neck is narrow, prone to become irreducible or

strangulated
Treatment
Sac is excised and the edges of the rectus sheath are
overlapped above and below the hernia (Mayos operation)
VENTRAL, EPIGASTRIC, INCISIONAL
HERNIA
Ventral hernia
Exist as an elongated gap between the recti
No treatment is required
Epigastric hernia
Consists of one or more small protursions through the defects in
the linea alba above umbilicus
Contain only extraperitoneal fat, often surprisingly painful
Treatment
Suturing the defect
Incisional hernia
Occurs through a defect in the scar of a previous abdominal
operation
Wide neck, strangulation is rare
Treatment
Dissecting out and suturing the individual layers of abdominal wall
If operation is inadviseable abdominal belt
ADHESIONS
ADHESIONS
Adhesions are fibrous bands of tissue that are a
common cause of postoperative small bowel obstruction
after abdominal surgery.
The risk of forming an adhesion that causes obstructive
symptoms in childhood has not been well studied but
seems to occur in 2-3% of patients after abdominal
surgery.
The majority of obstructions are associated with single
adhesions and can occur at any time after the 2nd
postoperative week.
 Diagnostic
Abdominal pain, constipation, emesis, and a history of
intraperitoneal surgery
Nausea and vomiting quickly follow the development of pain
Bowel sounds initially are hyperactive, and the abdomen is flat
The bowel subsequently dilates abdominal distention bowel
sounds disappear
Fever and leukocytosis are suggestive of necrotic bowel and
peritonitis
Plain radiographs obstructive features; contrast studies may
be needed to define the cause
Treatment
Nasogastric decompression, intravenous fluid resuscitation, and
broad-spectrum antibiotics in anticipation of surgery
Nonoperative intervention is contraindicated unless a patient is
stable with clear evidence of clinical improvement.
ASCARIS BALL