Fifth Stage
Pediatric Surgery
Dr. Moayed – Lecture 3
J. Intussusception
Although intussusception can occur at any age, the greatest incidence occurs in
infants between 4-10 months of age. Over half of the cases are in the first year of life.
Frequently occurs after a recent upper respiratory infection, by Adenovirus type 3 that
causes a reactive lymphoid hyperplasia that act as lead point (of Peyer's patch).
A definite lead point is identified in about 5% of patients. These include: Meckel's
diverticulum, polyps, Henoch's Sch?nlein purpura, hematoma, lymphoma, foreign bodies,
and duplications. Most children have no lead point and it is felt that enlarged mesenteric
nodes or swollen Peyer's patches may be the cause. The baby has intermittent periods of
severe discomfort with screaming, stiffening and drawing up of the legs, followed by
periods of rest. Vomiting may occur and bloody, mucoid (currant jelly) stool may be
passed. The baby may become dehydrated and appear acutely ill. Frequently, lethargy
may be an early sign. The diagnosis is made by water soluble contrast colon enema.
Hydrostatic reduction of the intussusception with the contrast material is successful in
approximately 50% of cases. To be successful, the water soluble material must reflux into
the terminal ileum. The surgeon should be notified before an attempt at hydrostatic
reduction. Recently the use of gas enema reduction has been successful in patients with:
(1) symptoms less than 12 hours, (2) no rectal bleeding, (3) absence of small bowel
obstruction, and (4) normally hydrated. Ultrasonography can be used as a rapid sensitive
screening procedure in the initial diagnosis of intussusception. Previous adverse clinical
features that precluded barium reduction can be replaced during gas reduction. Predictors
of failure of reduction are: (1) ileocolic intussusception, (2) long duration of symptoms, (3)
rectal bleeding, and (4) failed reduction at another institution. Air reduction
(pneumocolon) is a very effective alternative method since it brings less radiation (shorter
fluoroscopy time), less costs and less morbidity in cases of perforations.
Failure of hydrostatic reduction requires urgent operation through a right lower
quadrant horizontal incision. The intussusception is reduced by pushing on the distal
bowel like a tube of toothpaste rather than pulling the proximal bowel and appendectomy
is added as cecopexy and avoidance of future diagnostic problems of a RLQ incision. Most
cases are ileo-colic intussusception, and a few are jejuno-jejunal or ileo-ileal
intussusception.
K. Appendicitis
Included in this group because is caused by obstruction of the appendiceal lumen,
most commonly by fecaliths. When obstruction occurs, secretions from the appendix
accumulate and acutely distend the lumen. The pressure eventually produces arterial
obstruction leading to infarction. Bacteria initially invade the mucosa and produce
intramural infection. Other causes include pinworm infestation, carcinoids and lymphoid
hyperplasia.
Initially periumbilical pain secondary to distension of the lumen of the appendix
occurs. Pain impulses from the wall of the distended appendix are carried by visceral
afferent sympathetic fibers through the celiac ganglion to T10 and then referred to the
umbilical area in the tenth dermatome. Later the pain shifts to the right lower quadrant
of the abdomen, where it localizes. The shift in location is an important diagnostic sign
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and indicates the formation of irritating exudate around the inflamed appendix that
stimulates the pain receptors of the peritoneum locally. Anorexia, nausea and vomiting
follow the onset of abdominal pain.
Physical findings include an obviously ill-appearing child who usually will walk slowly
and bent over. Motion, heel tap, or bouncing on the heels will elicit pain in the right lower
quadrant. Point tenderness in the right lower quadrant (or the persistence of right lower
quadrant pain) is the most reliable physical finding. There is usually rebound and referred
pain to the right lower quadrant, indicating peritoneal inflammation. Fever is usually
present. Laboratory findings are an elevated white blood cell count in most instances.
Very high WBC's > 18,000 may indicate perforation. Urinalysis is generally clear, but
occasionally RBC's or WBC's may be associated with the inflamed appendix adjacent to
the bladder or ureter. Radiographic findings may include ileus, appendicolith
(pathognomonic finding), splinting, abdominal wall edema, and only very rarely, free air.
Initial treatment is rehydration to establish adequate urinary output. Any evidence
of possible perforation should mandate the use of appropriate antibiotics. Once adequate
then surgical intervention proceeds quickly. Most patients are approached through a right
lower quadrant horizontal muscle splitting incision. Removal of the appendix, irrigation
and, when localized abscesses are identified, institution of drainage.
Appendicitis is usually diagnosed from signs, symptoms and results of simple
laboratory tests a/o simple abdominal films. After simple abdominal films an appendicolith
(coprolith, fecalith, retained barium or foreign body) is sometimes found in the
symptomatic child with right lower quadrant pain or less commonly in an asymptomatic
situation. In the child WITH SYMPTOMS of low abdominal pain this finding should be
followed by appendectomy. Appendiceal fecaliths and calculi play a role in the
pathogenesis of appendicitis and are associated with perforation and gangrene. In the
ASYMPTOMATIC situation a prophylactic appendectomy is NOT justified when an
appendicolith, retained barium or another foreign body within the lumen of the appendix
is identified. A normal appendix will expel the appendicolith or barium in a variable period.
The parents should be informed that appendicitis may develop and that the child should
seek a physician if abdominal symptoms develop. A note should appear in the record
explaining this conversation.
In the event of right lower abdominal pain caused by appendicitis, almost 15% of
children will present with a right lower quadrant mass effect. The mass can be a phlegmon
with a central inflamed appendix which appears after four to five days from the onset of
abdominal pain accounting for 50% of appendiceal masses. Almost 20% of these masses
will contain a frank abscess cavity. Periappendiceal masses are the result of perforated
appendicitis. Due to the increase use of abdominal CT in the setting of abdominal pain
more cases of periappendiceal phlegmon/abscess are discovered with this diagnostic
modality. CT is reliable in distinguishing periappendiceal abscesses from phegmons and
its use can be extended into percutaneously draining the abscess cavity. US with color
Doppler demonstrate a hyperemic periappendiceal or pelvic fluid collection and
periappendiceal soft-tissue hyperemia. Management of a periappendiceal abscess
depends on the clinical condition of the child. Nontoxic patient with mild peritoneal signs
warrants non-operative management with intravenous fluids and antibiotics until the
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acute process subsides. Rising heart rate, continued spiking fever, worsening peritoneal
signs, intestinal obstruction or enlargement of the mass may require urgent surgery.
Patients undergoing initial nonoperative management have a lower rate of complications.
Six to eight weeks after resolution of the inflammatory process interval appendectomy is
recommended to avoid recurrent abdominal pain. Laparoscopic appendectomy can be
performed safely and effectively in such interval cases.
Mesenteric lymphadenitis is the condition most commonly mimicking acute
appendicitis resulting in a high rate of negative appendectomies in children. Mesenteric
adenitis is frequently associated with an upper respiratory infection. Clinical presentation
includes fever, leukocytosis and low abdominal pain. Mesenteric adenitis can be the result
of a viral or bacterial infection. Viruses implicated include Epstein-Barr; Adenovirus type
3, influenza B and Coxsackie B. Bacteria associated with mesenteric adenitis includes
hemolytic streptococci, Yersinia and Salmonella species. The diagnosis of mesenteric
adenitis is principally one of exclusion. CT-Scan can help decide whether the child has
mesenteric adenitis when the lymph nodes aggregates can be clearly seen. Otherwise,
since it can be very difficult to distinguish appendicitis from mesenteric adenitis the
diagnosis is establish at surgery. Laparoscopy can also be useful to differentiate
appendicitis from mesenteric adenitis. After surgery the postoperative course of children
with mesenteric adenitis is usually uneventful and recovery is rapid.
L. Chronic Intestinal Pseudo-Obstruction
Chronic Intestinal Pseudo-Obstruction is a rare disorder of intestinal motility in
infants and children characterized by recurrent attacks of abdominal pain, distension,
vomiting, constipation and weight loss in the absence of obvious mechanical lesions. The
disease can be familial or sporadic. Suggested etiology is degeneration of enteric nervous
or smooth muscle cells. The diagnosis is based on history, physical exam, radiographies
and motility studies. X-Ray hallmarks are: absent strictures, absent, decreased or
disorganized intestinal motility, and dilated small/large bowel loops. Associated conditions
identified in 10-30% of patients are bladder dysfunction (megacystis) and neurological
problems. Histologic pattern portrayed: myenteric plexus hyperplasia, glial cell
hyperplasia, and small ganglion cells (hypoganglionosis). Management is primary
supportive: intestinal decompression (NG), long-term TPN and antibiotic prophylaxis.
Motility agents are unsuccessful. Venting gastrostomy with home parenteral nutrition has
shortened the high hospitalization rate associated to this disease process. A similar
condition can be seen in early fed prematures due to immaturity of intestinal motility.
M. Bezoars
Bezoars are rare foreign body concretions formed in the stomach and small bowel
composed mainly of hair (tricho), vegetable matter (phyto) or milk curds (lacto). Most
cases are females’ children, 6-10 years old, with bizarre appetite (trichophagia) and
emotional disturbances. Originally the mass forms in the stomach and can move to the
small bowel by fragmentation, extension or total translocation. Diagnosis can be
confirmed by UGIS, CT-Scan or endoscopy. The child can develop an asymptomatic
palpable abdominal mass, pain, obstruction or perforation. Other children will reduce
intake and develop weight loss. Predisposing conditions to bezoar formations are: gastric
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dysmotility and decreased acidity. Management can consist of mechanical or pulsating jet
of water fragmentation via the endoscope, operative extraction, shock-wave lithotripsy
(ESWL) with subsequent evacuation, or dissolution by oral ingestion of proteolytic
enzymes (papain, acetylcysteine, and cellulase). With ESWL the shock wave pressure
needed is less than half used for urolithiasis cases.
N. Carcinoids
This argentaffin cell tumor causes interest because of its diverse presentation,
hormonal secretion, and malignant potential. The carcinoid is the most common neoplasm
of the GI tract in childhood and may occur at any site along the alimentary tract. Above
the diaphragm is commonly identified in the bronchus, and below the diaphragm in the
appendix. Female predominates, the tumor is seldom life-threatening, and children rarely
develop hormonal hypersecretion of 5-hydroxy indole acetic acid (Carcinoid syndrome).
Carcinoids are usually discovered as an incidental finding during surgery done for other
reasons. The appendix tumor arises from subepithelial endocrine cells with exclusive
growth in the lamina propria beneath the epithelial crypts. Most tumors are found in the
tip of the appendix. Simple appendectomy is curative in most cases. Tumors larger than
2 cm invading neighboring structures may need right hemicolectomy. Long term follow-
up is imperative.
The carcinoid syndrome (fascial flushing, diarrhea, tricuspid regurgitation, pulmonic
stenosis, valvular fibrosis and wheezing) is the result of serotonin overproduction by a
carcinoid tumor. Carcinoid tumors arise from enterochromaffin cells (APUD cells from the
neural crests), occur in virtually every organ, could be multiple, metastatic and associated
with a second malignancy. Patients are diagnosed biochemically from increased urinary
excretion of 5-hydroxyindoleacetic acid (5-HIAA). Platelet serotonin levels are more
sensitive for detecting carcinoids that secrete small amounts of serotonin. Jejunum-ileum,
bronchus and appendix are the most common sites of origin. Carcinoid of the appendix is
the most common neoplasm of the GI tract in childhood. Metastasis to liver of midgut
carcinoids produces the syndrome. Tumors greater than 2 cm are more prone to
metastasis needing aggressive surgical management. Octreotide scan and I-131 MIBG are
useful in determination of location and extent of some carcinoid tumors, particularly those
of midgut origin. A positive scan may predict the ability of Octreotide therapy to control
symptoms of hormonal hypersecretion. Scans provide localization of the primary tumor
that should be widely excised including lymph nodes. Higher survival rates are found for
patients with midgut lesions who undergo intra abdominal debulking procedures
excluding the liver. For single liver lesion resection is justified, otherwise with multiple
diffuse disease hepatic artery ligation or embolization has been tried. Symptomatic
metastasis should be managed with Octreotide. Prognosis is associated with the presence
of liver metastasis, syndrome development and level of tumor markers (chromogranin A).
O. Meconium-related Disease
1. Meconium Ileus
Meconium Ileus (MI) is a neonatal intraluminal intestinal obstruction associated with
Cystic Fibrosis (10-20%). The distal ileum is packed with an abnormally thick, viscous,
inspissated meconium. The meconium has reduced water content the result of decreased
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pancreatic enzyme activity and a prolonged small bowel intestinal transit time. MI can be
classified as simple or complicated. Simple MI appears in the first 48 hrs of life with
abdominal distension and bilious vomiting. Complicated MI is more severe (< 24 hrs) with
progressive abdominal distension, respiratory distress, and peritonitis. X-Ray findings are:
dilated bowel loops, absent air-fluid levels, "soap-bubble" granular appearance of distal
ileum due to a mixture of air with the tenacious meconium. Therapy consists of
Gastrografin enema for simple cases: hyperosmolar solution draws fluid to the bowel
lumen causing an osmotic diarrhea. Operative therapy is reserved for failed gastrografin
attempts and complicated cases (associated to volvulus, atresias, gangrene, perforation
or peritonitis). Surgical procedures have included: ileostomy with irrigation, resection with
anastomosis, and resection with ileostomy (Mikulicz and Bishop- Kopp). Post-operative
management includes: 10% acetylcysteine p.o., oral feedings (Pregestimil), pancreatic
enzyme replacement, and prophylactic pulmonary therapy. Long-term prognosis depends
on the degree of severity and progression of cystic fibrosis pulmonary disease.
2. Meconium Peritonitis
Meconium peritonitis (MP) is a chemical peritonitis that occurs following bowel
perforation during fetal life. It is generally looked upon as benign, resulting in no long-
term sequelae. The peritonitis occurs when the meconium leaves the bowel, enters the
peritoneal cavity and spreads throughout causing a sterile inflammatory reaction. Most
common site of bowel perforation is the distal ileum, and 50% of babies with MP develop
intestinal obstruction. Prenatal ultrasound findings include ascites, intraabdominal
masses, bowel dilatation and the development of intraabdominal calcifications. Bowel
disorders which lead to MP in utero are those resulting in bowel obstruction and
perforation, such as small bowel atresias, volvulus and meconium ileus. MP can be divided
into simple or complex. Cases with spontaneously healed perforation (simple MP) need
observation as they rarely develop symptoms. Newborns with complex MP are born with
bowel obstruction a/or pseudocyst formation (localized collection of meconium contained
in a cyst made of fibrous granulation tissue). Complex MP needs surgical therapy.
3. Meconium plug syndrome/Left hypoplastic colon syndrome
Colonic obstruction in the newborn child could be the result of necrotizing
enterocolitis, atresia, meconium plug syndrome, duplication cyst, Hirschsprung disease
or the small left colon syndrome. In meconium plug syndrome the baby expels a grey-
meconium and the obstruction subsides.
Meconium plug syndrome can be associated with Hirschsprung’s disease so a rectal
biopsy is in order.
The left (small) hypoplastic colon syndrome (LHCS) is a very rare cause of colonic
obstruction identified in newborns with characteristic roentgenographic features
resembling those of Hirschsprung's disease. Manifesting in the first 24-48 hours of life,
LHCS is a functional disturbance related to immaturity of the intrinsic innervation of the
colon that is especially common in low birth weight neonates or of diabetic mothers.
Intestinal perforation, sepsis, hypoglycemia and death may occur. The diagnosis is
suggested in a barium enema when the caliber of the left colon is small with a transitional
zone at the splenic flexure. Management consists of hypoglycemia correction, antibiotics,
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nasogastric decompression and observation. In most babies the obstruction clears in 48-
72 hours. When the clinical diagnosis is not readily apparent a rectal biopsy and sweat
chloride test should be done to differentiate LHCS from Hirschsprung disease and cystic
fibrosis respectively. The narrowed left colon remains narrow in follow-up.
IV. HERNIAS and ABDOMINAL WALL DEFECTS
A. Diaphragmatic Hernia
1- Congenital Diaphragmatic Hernia (Bochdalek)
The most common congenital diaphragmatic hernia (CDH) is that which occurs
through the posterolateral defect of Bochdalek. It is caused by failure of the
pleuroperitoneal membrane to develop adequately and close before the intestines
returning to the abdomen at the tenth week of gestation. The intestines then enter the
pleural cavity and cause poor lung development leading to pulmonary hypoplasia (a
reduced number of alveoli per area of lung tissue). This defect is postero-lateral in the
diaphragm and may vary in size. Stomach, liver or spleen may be partly in chest as well.
Frequency is 1:2000 live births and the natural history in prenatally diagnosed CDH is that
60% will die. The clinical presentation is that the newborn becomes rapidly cyanotic,
acidotic, and has poor ventilation. Major findings relate to the degree of pulmonary
maldevelopment. Chest films will show intestines in the chest. Left sided hernias are more
common than right (90% on left). Placement of a radiopaque nasogastric tube may show
the tube coiled in the lower left chest. Higher risk factors are: early appearance of
symptoms in life, prematurity and associated anomalies. Treatment consists of rapid
intubation and ventilation with use of muscle relaxants, placement of a nasogastric tube
to prevent gaseous distension of the intestines and preoperative stabilization of arterial
blood gases and acid-base status. Surgery can be undertaken when one of the following
objectives are met: (1) blood gases normalize with no significant changes between
preductal and postductal samples, (2) echocardiogram demonstrate reduce pulmonary
pressure and pulmonary peripheral resistance.
Operative management consists of abdominal approach, closure of hernia by
primary repair or use of mesh, and correction of malrotation. Postoperative management
is very difficult. Due to hypoplastic lungs, there is frequently pulmonary hypertension
leading to right-to-left shunting and progressive hypoxemia, hypercarbia, and acidosis
that worsens the pulmonary hypertension. The use of chest tubes may cause
overstretching of the already hypoplastic alveoli causing: increase pulmonary
hypertension, reduce functional residual capacity and reduce lung compliance.
Postoperatively, the infant should be kept paralyzed and ventilated and only very slowly
weaned from the ventilator. The severity of pulmonary hypoplasia, both ipsilaterally and
contralaterally, is the main determinant of outcome. ECMO (extracorporeal membrane
oxygenator) has come to reduce somewhat the mortality of this condition.
The mortality of CDH is directly related to the degree of lung hypoplasia associated.
Death is caused by persistent pulmonary hypertension and right ventricular failure.
Prospective studies of prenatally diagnosed fetus prior to 25 wk. gestation have shown
that 60% will die despite optimal postnatal care. This unsolved problem has prompted
investigators to develop new treatment options such as preoperative stabilization,
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jetfrequency ventilation, and ECMO. Another area of development is intrauterine fetal
surgical repair. To achieve success fetal surgery should: (1) pose no risk to the mother
(innocent bystander) or her future reproductive capacity; (2) tocolytic therapy in the post-
op weeks should proved effective to avoid prenatal stillbirths; and (3) the procedure
should be superior to conventional therapy. Intrauterine repair has meet with limited
success due to herniation of the fetal liver into the chest through the defect. Disturbance
of the umbilical circulation during or after liver reduction causes fetal death. Positive-
pressure ventilation after birth reduces the liver before the baby comes for surgical repair.
Dr. Harrison (USFC Fetal Treatment Center) has devised separate fetal thoraco-abdominal
incisions to deal with this problem ("two-step dance"), reducing or amputating the left
lateral segment of the liver. Another less invasive approach is enlarging the hypoplastic
lungs by reducing the normal egress of fetal lung fluid with controlled tracheal obstruction
called PLUGS (Plug Lung Until it Grows).
Delayed presentation beyond the neonatal period is rare, estimated to occur in 4-
6% of cases. Infants and children will present with either respiratory or gastrointestinal
symptoms such as: chronic respiratory tract infection, vomiting, intermittent intestinal
obstruction, and feeding difficulty. Occasionally the child is asymptomatic. The small size
of the defect protected by either the spleen or the liver and the presence of a hernial sac
may delay the intestinal herniation into the chest. A rise intraabdominal pressure by
coughing or vomiting transmitted to any defect of the diaphragm makes visceral
herniation more likely. Diagnosis is confirmed by chest or gastrointestinal contrast
imaging. Management consists of immediate surgery after preop stabilization. Most
defects can be closed primarily through an abdominal approach. Chest-tube placement in
the non-hypoplastic lung is of help. Surgical results are generally excellent. A few deaths
have resulted from cardiovascular and respiratory compromise due to visceral herniation
causing mediastinal and pulmonary compression.
2. Morgagni Hernias
Morgagni Hernias (MH) are rare congenital diaphragmatic defects close to the
anterior midline between the costal and sternal origin of the diaphragm. They occur
retrosternally in the midline or more commonly on either side (parasternally) of the
junction of the embryologic septum transversum and thoracic wall (see the figure)
representing less than 2% of all diaphragmatic defects. Almost always asymptomatic,
typically present in older children or adults with minimal gastrointestinal symptoms or as
incidental finding during routine chest radiography (mass or air-fluid levels). Infants may
develop respiratory symptoms (tachypnea, dyspnea and cyanosis) with distress. Cardiac
tamponade due to protrusion into the pericardial cavity has been reported. The MH defect
contains a sac with liver, small/ large bowel as content. Associated conditions are: heart
defects, trisomy 21, omphalocele, and Cantrell? pentalogy. US and CT-Scan can
demonstrate the defect. Management is operative. Trans-abdominal subcostal approach
is preferred with reduction of the defect and suturing of the diaphragm to undersurface
of sternum and posterior rectus sheath. Large defects with phrenic nerve displacement
may need a thoracic approach. Results after surgery rely on associated conditions.
3. Hiatal Hernia
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Hiatal hernia is rarely a problem in infants unless associated with gastroesophageal
reflux or severe anatomic dysfunction of the stomach (upside-down intrathoracic
stomach).
Two types of esophageal hernia recognized are the hiatal and paraesophageal
hernia. Diagnosis is made radiologically always and in a number of patients
endoscopically. The hiatal hernia (HH) refers to herniation of the stomach to the chest
through the esophageal hiatus. The lower esophageal sphincter also moves. It can consist
of a small transitory epiphrenic loculation (minor) up to an upside-down intrathoracic
stomach (major). HH generally develops due to a congenital, traumatic or iatrogenic
factor. Most disappear by the age of two years, but all forms of HH can lead to peptic
esophagitis from Gastroesophageal reflux. Repair of HH is determined by the pathology
of its associated reflux (causing failure to thrive, esophagitis, stricture, respiratory
symptoms) or the presence of the stomach in the thoracic cavity. In the paraesophageal
hernia (PH) variety the stomach migrates to the chest and the lower esophageal sphincter
stays in its normal anatomic position. PH is a frequent problem after antireflux operations
in patients without posterior crural repair. Small PH can be observed. With an increase in
size or appearance of symptoms (reflux, gastric obstruction, bleeding, infarction or
perforation) the PH should be repaired. The incidence of PH has increased with the advent
of the laparoscopic fundoplication.
4. Paraesophageal Hernias
Paraesophageal hernia (PEH), a rare entity in children, occurs when the stomach
protrudes laterally through the esophageal hiatus toward the chest while the gastro-
esophageal junction stays in anatomic position. Though most cases remain asymptomatic,
PEH can cause upper bowel obstruction, gastroesophageal reflux, gastric volvulus,
bleeding and perforation. Most PEH in children are acquired resulting after fundoplication.
A small group of children are born with the PEH. Groups of patients with a higher incidence
of developing PEH after fundoplication includes infants under the age of one, neurologic
impaired children and surgical patients where a crural repair is not done after
fundoplication. PEH is linked to gagging before an antireflux procedure in children.
Diagnosis of PEH is confirmed during a barium swallow and upper gastrointestinal series.
A small PEH can be managed non-operatively if the child is asymptomatic. With the
presence of symptoms or enlargement of the hernia operative repair must be done. A
transabdominal approach is preferred for reducing the stomach and crural repair of the
diaphragm. The use of mesh hiatal reinforcement is recommended for patients
undergoing reoperation for PEH and recurrent gastroesophageal reflux or if the
diaphragmatic crura is thought to require reinforcement at the time of the original
surgery.
5. Traumatic Diaphragmatic Hernia
Motor vehicle trauma is the leading cause of an acquired diaphragmatic hernia in a
child and adult. The traumatic event can either be penetrating directly injuring the
diaphragm, or most commonly blunt abdominal causing a sharp increase in
intraabdominal pressure with rupture of the diaphragmatic muscle. The more medial and
lateral fibers of the posterior diaphragm arising from the lumbocostal arch and the
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vertebrocostal trigone are the weakest points of rupture. The posterolateral portion is
virtually always the area that ruptures with trauma.
Diaphragmatic injuries are difficult to diagnose preoperatively and can be missed
easily. Traumatic diaphragmatic hernia should be suspected on the basis of an abnormal
chest radiograph in the trauma victim with multiple injuries. If diaphragmatic injury is
suspected, ultrasound or CT Scan investigation must be performed. Most cases involve
the left diaphragm due to the buttressing effect of the liver. The incidence of bowel
strangulation is high in traumatic diaphragmatic hernias. In the acute setting,
transabdominal repair after palpation of both hemidiaphragms is the procedure of choice
because of the high incidence of associated trauma. Injury severity score and hemorrhagic
shock upon admission strongly influence the outcome. Delayed presentation can be
repaired through the chest .
To be contined,,,