LECTURE№1
THEME: Acquired intestinal ileus.
(Adhesive Intestinal Obstruction, intussusception, and dynamic intestinal obstruction).
Digestive tract bleeding in children. Portal hypertension.
(Peptic ulcer Disease, Portal Hypertension, Meckel’s diverticulum bleeding, Colonic polyposis, Anal Fissure, Hemorrhoids).
Plan:
1. Acquired intestinal ileus:
1.1. Adhesive Intestinal Obstruction.
1.2. Intussusception.
1.3. Dynamic intestinal obstruction.
2. Digestive tract bleeding in children.
2.1. Peptic ulcer Disease.
2.2. Meckel’s diverticulum bleeding.
2.3. Colonic polyposis.
2.4. Anal Fissure.
2.5. Hemorrhoids.
3. Portal hypertension
1. Acquired intestinal ileus.
1.1. Adhesive Intestinal Obstruction
Etiology Adhesions are fibrous bands of tissue that form between loops of bowel or between the bowel and the abdominal wall after intraabdominal inflammation.
Clinical Presentation Children with a mechanical obstruction present with cramping abdominal pain, distension, and vomiting. For prolonged McBurneys points the vomitus becomes bilious or even feculent. Inspection of the abdomen may reveal obvious dilated loops of bowel and distension. If observed early in the clinical course, the patients vital signs are within the normal range and the abdomen is not tender. In contrast, children with compromised bowel or a prolonged obstruction, present with abdominal pain, vomiting, fever, tachycardia, decreased blood pressure, abdominal tenderness, and leukocytosis.
Treatment
Nonoperative management includes resuscitation with isotonic saline solutions, nasogastric decompression, correction of electrolyte abnormalities, IV antibiotics, and serial examinations. Within 24 hours, children with ileus and simple mechanical obstruction will improve as indicated by a return of bowel function, a normalization of vital signs and a normal WBC. Indications for operation include obstipation for 24 hours, continued abdominal pain with fever and tachycardia, decreased blood pressure, increasing abdominal tenderness, and leukocytosis despite adequate resuscitation and medical treatment.
The abdomen is opened through a previous incision, if present, and midline, if not. The cecum is identified and the collapsed ileum is followed proximally until dilated bowel and the point of obstruction is identified. The offending adhesive bands are disrupted and the abdomen is closed. Laparoscopic lysis of adhesions is another option and may allow a shorter postoperative recovery and hospital stay.
Postoperatively, nasogastric decompression and intravenous fluids are continued until return of bowel function and the volume of gastric aspirate decreases.
1.2. Intussusception
Intussusception, the telescoping or invagination of a proximal portion of intestine (intussusceptum) into a more distal portion (intussuscipiens), is one of the most common causes of bowel obstruction in infants and toddlers.
Four varieties are described: ileocolic, colocolic, ileoilealcolic and ileoileal, this latter being the least frequent.
Ileocolic – the small intestine invaginates into the right colon; this is the most common intussusception
Ileoileal – the small intestine invaginates into itself
ileoilealcolic
Colocolic – the large intestine invaginates into itself
When an older child or adult develops intussusception, it is often the result of a Meckels diverticulum, intestinal duplication, tumor and polyps.
Predisposing factors
Recent upper respiratory illness
Recent diarrheal illness
Henoch-Schönlein purpura
Cystic fibrosis
Chronic indwelling GI tubes
Processes that result in a mechanical lead point
Meckel diverticulum
Intestinal polyp (eg, Peutz-Jeghers syndrome, familial polyposis coli, juvenile polyposis)
Intestinal lymphosarcoma
Blunt abdominal trauma with intestinal or mesenteric hematomas
Hemangioma
Foreign body
Henoch-Schönlein purpura (small bowel hematomas cause small bowel intussusception)
Age. Intussusception is the most common cause of intestinal obstruction in patients aged 5 months to 3 years.
Clinical manifestations
History. Symptoms include the following:
Pain is colicky, severe, and intermittent. Initially, vomiting is nonbilious and reflexive, but when the intestinal obstruction occurs, vomiting becomes bilious. Parents also report the passage of stools that look like currant jelly. Diarrhea also can be an early sign of intussusception.
Physical: On physical examination, the patient is usually chubby and in good health. Intussusception is uncommon in children who are malnourished. The child is found to have periods of lethargy alternating with crying spells, and this cycle repeats every 15-30 minutes. The infant can be pale, diaphoretic, and hypotensive if shock has occurred.
The hallmark physical findings in intussusception are a right hypochondrium sausage-shaped mass and emptiness in the right lower quadrant (Dance sign). This is hard to detect and is palpated best when the infant is quiet between spasms of colic.
Patients with intussusception often have no classic signs and symptoms, which can lead to an unfortunate delay in diagnosis and can have disastrous consequences.
Imaging Studies:
Plain abdominal x-ray On abdominal radiographs, the classical description of an intussusception is a mass lesion seen indenting the colon with or without signs of bowel obstruction. There is a paucity of right-sided colonic gas. Intussusceptions may present anywhere along the colon and even present in the rectum. The typical location is from the hepatic flexure to mid descending colon. A normal abdominal radiograph does not exclude intussusception.
Ultrasonography. Characteristic findings include a target sign visible on transverse section and a pseudo kidney sign viewed on longitudinal section.
Colour Doppler has been used to assess bowel viability and as a prognostic sign that reduction will be successful, no colour signal of the intussusception being regarded as having a poor prognosis. This finding is still under debate. One may sometimes see intestinal lymphadenopathy with intussusception.
Computed tomography (CT) scan also has been proposed to be useful making the diagnosis of intussusception; however, CT findings are unreliable, and use of CT carries the risks associated with intravenous contrast administration, radiation exposure, and sedation.
Diagnostic and therapeutic enema
Once the diagnosis of intussusception is entertained, surgical personnel should be notified and an intravenous (IV) line and nasogastric tube should be placed. The surgeon preferably is present in the radiology suite at the time of the contrast enema examination.
The presence of peritonitis and any evidence of perforation revealed on plain radiographs are the only 2 absolute contraindications to an attempt at nonoperative reduction with a therapeutic enema. Therapeutic enemas can be hydrostatic, with either barium or water-soluble contrast, or pneumatic, with air insufflation. Therapeutic enemas can be performed under fluoroscopic or ultrasonic guidance. The technique chosen is not important as long as the radiologist performing the enema is comfortable with the method. Preferably, the pediatric surgeon involved is present at the reduction.
When performing a therapeutic enema, the recommended pressure of air insufflation should not exceed 120 cm of water. When using barium or water-soluble contrast, the column of contrast should not exceed 100 cm above the level of the buttocks. An attempt is not considered successful until the reducing agent, whether air, barium, or water-soluble contrast, is observed refluxing back into the terminal ileum. Otherwise, the intussusception can remain at the ileocecal region and can resume its progression.
Treatment
Preoperative details. Preoperatively, IV crystalloid resuscitation is begun (10 mL/kg x 2, plus 1.5 x maintenance fluid). A Foley catheter is placed to guide fluid resuscitation. A nasogastric tube is placed. Broad-spectrum IV antibiotics are administered. Body temperature must be preserved in the operating room. A type and screen of the patient’s blood should be obtained. As with any patient with a bowel obstruction, careful induction (ie, rapid sequence) of anesthesia should take regurgitation and risk of aspiration into consideration.
Surgery. Mostly, a right transverse incision supra-umbilical at the umbilicus or lower is recommended, adapted to the position of the apex of intussusception.A midline longitudinal incision is an easier and quicker approach and may be used as well.
Manual reduction has to be performed very carefully and slowly. Taking the apex of intussusception between fingers and cup of the surgeon’s hand at the distal end, the intussusception is squeezed gently in a retrograde direction distally to proximally. In recurrent intussusception it is of definite benefit, since the ileocecal valve is widened. For closure the abdominal cavity is irrigated with warm saline. No drainage is used. The peritoneum and posterior rectus sheet is closed at the same time by running 3/0 sutures. Continuous suturing is also sufficient for anterior rectus sheet.A subcuticular 4/0 running suture provides a good skin adaptation and a cosmetically good scar. Skin closure by intracuticular suture line, by fibrin sealant or metal clips is optional. Indications for resection include irreducible intussusception, gangrenous bowel or perforation of the bowel. After resection of the bowel, end-to-end intestinal anastomosis is completed
Postoperative details. IV fluid resuscitation is continued and calculated, taking into consideration maintenance requirements and third-space losses. Upon resolution of ileus, diet is advanced at the discretion of the surgeon.
1.3. Dynamic intestinal obstruction
Acute Paralytic Ileus
Essentials of Diagnosis
■ Precipitating factors: surgery, peritonitis, electrolyte abnormalities, medications, severe medical illness.
■ Nausea, vomiting, obstipation, distention.
■ Minimal abdominal tenderness; decreased bowel sounds.
■ Plain abdominal radiography with gas and fluid distention in small and large bowel. General Considerations
Clinical Findings
SYMPTOMS AND SIGNS
Patients who are conscious report mild diffuse, continuous abdominal discomfort with nausea and vomiting. Generalized abdominal distention is present with minimal abdominal tenderness but no signs of peritoneal irritation (unless due to the primary disease). Bowel sounds are diminished to absent.
LABORATORY FINDINGS
The laboratory abnormalities are attributable to the underlying condition. Serum electrolytes, including potassium, magnesium, phosphorus, and calcium, should be obtained to exclude abnormalities as contributing factors.
IMAGING
Plain film radiography of the abdomen demonstrates distended gas-filled loops of small and large intestine. Air-fluid levels may be seen. Under some circumstances, it may be difficult to distinguish ileus from partial small bowel obstruction. A limited barium small bowel series or a CTscan maybe useful in such instances to exclude mechanical obstruction, especially in postoperative patients.
Differential Diagnosis
Ileus must be distinguished from mechanical obstruction of the small bowel or proximal colon. Pain from small bowel mechanical obstruction is usually intermittent, cramping, and associated initially with profuse vomiting. Acute gastroenteritis, acute appendicitis, and acute pancreatitis may all present with ileus.
Treatment
The primary medical or surgical illness that has precipitated adynamic ileus should be treated. Most cases of ileus respond to restriction of oral intake with gradual liberalization of diet as bowel function returns. Severe or prolonged ileus requires nasogastric suction and parenteral administration of fluids and electrolytes. Alvimopan is a new peripherally acting mu-opioid receptor antagonist with limited absorption or systemic activity that reverses opioid- induced inhibition of intestinal motility. This agent is not yet approved by the FDA. However, in five randomized controlled trials, it reduced the time to first flatus, bowel movement, solid meal, and hospital discharge compared with placebo in postoperative patients.
2. Digestive tract bleeding in children.
2.1. Peptic ulcer Disease,
Frequency. PUD is an uncommon disease of childhood, with an estimated frequency of 1 case in 2500 hospital admissions. The estimated prevalence of childhood PUD in large general pediatric practices is 1.7%. The true incidence of secondary ulcers is unknown and depends on the frequency of systemic illness, traumatic injury, other chronic diseases, and injurious drug use.
Age. Primary PUD is rare in infants and children younger than 10 years. Prevalence of primary PUD increases during adolescence. Secondary PUD can be found in patients of all ages but has a higher prevalence in patients younger than 6 years.
Sex. Primary PUD has a 2- to 3-fold higher incidence in boys than in girls; however, no sex difference in incidence rates in primary PUD has beeoted in infants or very young children.
Clinical manifestation.
In children in whom PUD is suspected, include the following in the history:
Review of past illnesses and chronic medical conditions
Family history of ulcer disease or GI tract conditions (eg, Crohn disease)
Character, location, frequency, duration, severity, and exacerbating (especially meals in children) and alleviating factors of abdominal pain
Vomiting and description of gastric material
Bowel habits and description of stool
Medications
Prior diagnostic testing and specific GI therapies
Appetite, diet, and weight changes
Family and social stressors
Alcohol ingestion and smoking habits
Abdominal pain is the most common symptom of childhood PUD. The pain is usually dull and vague in character and may be poorly localized or localized to the periumbilical or epigastric areas. In preschool-aged children, pain is typically periumbilical and is worse after eating. After age 6 years, the child’s description of pain may be quite similar to the description made by adults. The classic pain of PUD (ie, pain that awakens the child, worsens with food, and is relieved by fasting) is described infrequently, but it helps distinguish GI tract and psychogenic pathology when present. Pain is more likely to be dull and aching rather than sharp and burning, as is described by adults. Frequent exacerbations and remissions of pain extend over weeks to months. The pain is often worsened by food intake, which is the opposite of the adult pattern.
Vomiting in infants and toddlers may be associated with slow growth. Recurrent vomiting is also noted in preschool-aged and school-aged children.
GI tract bleeding (eg, melena, hematochezia, hematemesis) may be another presentation in children; however, in infants, particularly in the first month of life, serious underlying illness and stress ulceration present most commonly with acute perforation or hemorrhage.
Hemoglobin and hematocrit
Iron studies (serum iron, total iron-binding capacity [TIBC], ferritin, reticulocyte count, peripheral smear) – to determine presence of IDA.
H pylori serology – to detect H pylori infection in children who have not been previously diagnosed or treated.
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) – to identify coagulopathy in patients with sepsis, multiple injuries, or massive GI tract bleeding, or in those at risk for diffuse intravascular coagulation (DIC).
Type and cross-match blood – for transfusion in patients in whom the condition is unstable or the illness is critical.
Electrolyte and creatinine levels – for assessment in patients with volume depletion or who require fluid resuscitation.
Arterial blood gas – to assess degree of acidosis in the patient with systemic illness, respiratory failure, or severe hypovolemia or in patients with severe burns or trauma.
Urinalysis – to assess hydration status and to screen for infection or stone.
WBC count and differential – to detect peripheral eosinophilia in children with eosinophilic gastritis.
Serum gastrin and gastrin-releasing peptide levels – to exclude Zollinger-Ellison syndrome in patients with refractory ulcers.
Examine and perform guaiac testing on the stool to confirm GI tract bleeding. Melena is usually the result of an upper GI tract bleed, although blood from a duodenal ulcer that quickly transits the intestinal tract may be visible as red or maroon blood in the stool.
Imaging Studies.
Abdominal and/or chest radiograph findings assist in the diagnosis of perforation. Upper GI series can depict PUD in approximately 70% of children who are studied. A double-contrast study has a higher detection rate but requires an older cooperative child and results in higher radiation exposure. The false-positive rate may be 30%. Sensitivity is higher for detection of duodenal ulcers than for detection of gastric ulcers. Radiologic findings of duodenal ulcers include filling defects or duodenal bulb deformities. The presence of a fibrinous clot in the ulcer may lead to false-negative findings. False-positive findings on barium studies have beeoted as especially high in the pediatric patient population, up to 30-40%.
Gastric outlet obstruction, the result of pyloric lesions, can be detected using upper gastrointestinal imaging (UGI).
Procedures. Consider nasogastric (NG) lavage in a child who is ill and in whom an upper GI tract hemorrhage is suspected, as evidenced by hematemesis or melena. Esophagogastroduodenoscopy (EGD) is the procedure of choice for the detection of PUD in the pediatric population. EGD allows direct visualization of the mucosa, localization of the source of bleeding, and diagnosis of H pylori infection via analysis of biopsy specimens, culturing, or detection of urease activity.
Therapeutic endoscopy for acute bleeding (coagulation of a bleeding ulcer with a heater probe or injection with vasoconstricting agents) is another important indication for EGD.
Complications. Hemorrhage accompanies PUD in 15-20% of patients. An acute abdomen resulting from GI tract perforation occurs in 5-10% of children with PUD. Obstruction of the gastric outflow tract because of edema or scarring most often occurs in the setting of duodenal or pyloric channel ulcers.
Treatment. Assess airway, breathing, and circulation (ABC).
Administer oxygen and provide ventilatory support as appropriate. Establish IV access, place cardiorespiratory monitors, begin volume replacement, and prepare transfusions in children who are unstable and bleeding. Place an NG tube and perform lavage in the stomach of children in whom an upper GI tract bleed is suspected. Consider IV infusion of a histamine H2-receptor antagonist.
Surgical intervention A bleeding ulcer can be treated with a simple plication or oversewing of the bleeding source. A more definitive procedure may be required, such as vagotomy and pyloroplasty.Medications used in patients with PUD reduce gastric acidity and serve to eradicate H pylori infection.
Diet. Recommend abstinence from all caffeine and alcohol. In hospitalized children, milk feedings have been found to raise the gastric pH level and to prevent GI tract bleeding.
Activity. Allow common sense to dictate appropriate activity restrictions in children with chronic symptoms.
Further Outpatient Care.Carefully monitor medication doses, adverse effects of medications, and relief or persistence of symptoms.
Prescribe edications include blockers of gastric acid secretion, acid neutralizers, and antibiotics.
Avoid all irritative medications, including NSAIDs, aspirin, and corticosteroid preparations.
IDA may require iron replacement therapy.
Prognosis.Mortality rates are very low in older children with primary ulceration and H pylori infection.
Mortality rates remain highest ieonates, as well as infants and children with systemic illness or injury, who present with acute bleeding or perforation.
2.2. Meckel’s diverticulum bleeding
Meckel diverticulum is the most common form of congenital abnormality of the small intestine, resulting from an incomplete obliteration of the vitelline duct
Embryology, pathophysiology. Examples of of vitelline duct anomalies include (1) a persistent vitelline duct (appearing as a draining fistula at the umbilicus), (2) a fibrous band connecting the ileum to the inner surface of the umbilicus, (3) a patent vitelline sinus beneath the umbilicus, (4) an obliterated bowel portion, and (5) a vitelline duct cyst.
Meckel diverticulum occurs on the antimesenteric border of the ileum, usually 60 cm proximal to the ileocecal valve. On average, the diverticulum is 2.99 cm long and 1.92 cm wide. Meckel diverticulum is a true diverticulum because it contains all layers of the intestinal wall.
The heterotopic mucosa is likely to be gastric in origin in 80% of cases of Meckel diverticulum. This is important because peptic ulceration of this or adjacent mucosa can lead to pain, bleeding, and/or perforation.
Clinical manifestations.
History. Most patients are asymptomatic
. Complications of Meckel diverticulum included bowel obstruction (35%), hemorrhage (32%), diverticulitis (22%), umbilical fistula (10%), and other umbilical lesions (1%).
In children, bleeding is the most common presenting sign. Although intestinal obstruction is not considered a major presenting clinical sign, it occurs in 25-40% of pediatric patients. Obstruction can occur as a result of various mechanisms: Omphalomesenteric band (most frequent cause),Internal hernia through vitelline duct remnants, Volvulus occurring around vitelline duct remnants, T-shaped prolapse of both efferent and afferent loops of intestine through a persistent vitelline duct fistula at the umbilicus in a neonate
Intussusception is another serious and common complication of the Meckel diverticulum. The diverticulum may itself act as a lead point for an ileocolic or ileoileal intussusception. None of the clinical features are pathognomonic, and the diagnosis is rarely made preoperatively.
Diverticulitis usually is seen in older patients. The clinical presentation includes abdominal pain in the periumbilical area that radiates to the right lower quadrant. Abdominal pain is present more in the periumbilical region than the pain of appendicitis.
Diagnosis.
Lab Studies. Routine laboratory studies, such as CBC, electrolyte tests, glucose test, creatinine test, and coagulation screen, are not helpful in establishing the diagnosis but are helpful in the general workup. Hemoglobin and hematocrit are low in the setting of anemia or bleeding. Patients with significant bleeding can develop anemia.
Imaging Studies. History and physical examination are of paramount importance for establishing a clinical diagnosis. Imaging studies are performed to confirm a clinical suspicion of Meckel diverticulum.
Plain radiographs of the abdomen may depict signs of intestinal obstruction or perforation.
When a patient presents with bleeding and with suspicion of Meckel diverticulum, the diagnostic evaluation should include a technetium Tc 99m–pertechnetate scintiscan, or so-called Meckel scan. Scintiscan is especially helpful in infants who present with lower GI bleeding.
Treatment.
Medical Care. The emergency department evaluation and treatment of patients depends on the clinical presentation.
Because most symptomatic patients are acutely ill, establish an intravenous line immediately, start crystalloid fluids, and keep the patient oothing by mouth (NPO) status.
If significant bleeding occurs, perform a transfusion of packed red cells.
A patient presenting with intestinal obstruction may require nasogastric decompression.
Administer a regimen of antibiotics, , whenever acute Meckel diverticulitis, strangulation, perforation, or signs of sepsis are present
Surgical Care. The presence of peritoneal signs or hemodynamic instability demands urgent surgical intervention.
Definitive treatment of a complication, such as a bleeding Meckel diverticulum, is the excision of the diverticulum along with the adjacent ileal segment. Excision is carried out by performing a wedge resection of adjacent ileum and anastomosis, with the use of a stapling device. Adjacent ileum is included in the resection because ulcers frequently develop in the adjacent part of the ileum.
Successful resection of a Meckel diverticulum can also be accomplished through laparoscopy, using an endoscopically designed autostapling device.
In some cases of Meckel diverticulum, a primitive persistent right vitelline artery originating from the mesentery has been found during operation. When present, the artery is found to supply the Meckel diverticulum; therefore, it must be identified and ligated during the operation.
2.3. Colonic polyposis
Incidence Intestinal polyps are much less common in children than in adults, and their association with syndromatic clusters is very common. Malignant transformation except in the syndromatic cases is less than in adults, and the approach to management is more expectant. Approximately 1% of children have asymptomatic intestinal juvenile polyps which are benign. Other types of polyps are much rarer.
Etiology and Pathology The etiology of polyps in children is multifactorial and depends on the type of polyp. Etiologies and pathologic features will be discussed individually in the classification section.
Clinical Presentation Bleeding,Pain, Intussusception
Diagnosis The diagnosis of polypoid lesions depends primarily on two modalities: intestinal contrast studies and endoscopy.
Classification
Benign
Isolated Juvenile polyps
These are the most common polypoid lesion of infancy and childhood. The peak age of incidence is between the ages of 3 and 10 years. As with most polyps, crampy abdominal pain and bleeding with bowel movements are the presenting symptoms. Juvenile polyps are hamartomatous excrescencies of the intestinal mucosa. They appear to lengthen from traction caused by peristalsis and the flow of intestinal contents. There is no malignant potential, and juvenile polyps naturally auto-amputate if given enough time. Seventy-five percent of juvenile polyps occur in the rectum and sigmoid colon, but juvenile polyps may occur in the right colon as well.
Peutz-Jeghers Syndrome
This well-known syndrome causes polyps predominantly in the small bowel. Its hallmark distinguishing feature is the pigmented lesions observed on the buccal mucosa and lips of these patients. Malignant degeneration can occur, and lifelong surveillance is necessary.
Adenomatous Polyp
This lesion is rare but known to occur in childhood (Fig. 52.1). Malignant degeneration can occur as in the adult-type lesion. Familial adenomatous polyposis (FAP) is a syndrome that results in multiple colorectal polyps (see below). Traditionally, the presence of at least one hundred individual polyps is required to make this diagnosis.
Hemangiomatous Polyps
Hemangiomatous polyps cause profuse bleeding and occur predominantly in the distal small bowel. Profuse bleeding may require excision if it occurs repeatedly. They tend to regress with time as do most hemangiomas after the age of two years.
Malignant
Juvenile Polyposis and Familial Adenomatous Polyposis (FAP)
Juvenile polyposis is an autosomal dominant disorder which causes polyps predominantly in the large and small bowel. The lesions resemble adenomatous polyps individually but are actually mucous-retention polyps. These polyps can occur anywhere along the gastrointestinal tract. It is considered a premalignant condition and 6% of these children will eventually develop malignancy. Familial adenomatous polyposis is characterized by hundreds of adenomatous polyps in the rectum and colon causing diarrhea and bleeding. It also shares an autosomal dominant pattern of inheritance. Malignant degeneration in one or more polyp is virtually certain before the age of twenty years.
Adenocarcinoma
Although rare, isolated colonic or small bowel adenocarcinoma can occur in childhood. It can be mistaken for a juvenile polyp until it has advanced beyond the stage where it can be excised completely. Adenocarcinomas usually arise from villous adenomas.
Lymphoma
Small bowel lymphoma is usually a non-Hodgkin’s B cell lymphoma. The two most common gastrointestinal sites of non-Hodgkin’s lymphoma are the distal small bowel and the stomach. Proximal gastric lesions may be visualized and biopsied endoscopically although the lesion originates in the submucosa. In the small bowel, CT scanning can usually image the lesion if it has attained sufficient size to cause symptoms. Lymphoma of the bowel is rare in infancy, but the incidence increases with advancing age peaking in adolescence. Bleeding is the main symptom from gastric lesions. Small bowel lymphomas cause crampy abdominal pain, and may result in intussusception. Some may erode and perforate into the free abdominal cavity presenting as gastrointestinal perforation.
Treatment
The treatment of polyps of the GI tract in children can vary from simple observation of benign lesions to wide excision and chemotherapy for malignant ones. Juvenile polyps should be removed endoscopically once diagnosed. This is done to stop the symptoms as well as establish the diagnosis. Most are within easy reach of a flexible sigmoidoscope and can be snared around the stalk.
Treatment of children with familial adenomatous polyposis (FAP) A Soave type operation (endorectal pullthrough) is the one most commonly used.
2.4. Anal Fissure
Incidence
An anal fissure is a tear in the mucosa and die anoderm lining the anal canal. These lesions are common in infancy and are the most common cause of bright red blood per rectum in that age group.
Etiology
Anal fissures occur in the setting of constipation and passage of large, hard stools that cause a mechanical rear of the anal mucosa. Diarrhea can cause a chemical irritation from stool alkalinity. Pain associated with anal fissures may potentiate constipation and seems to be related to hyper tonicity of the anal sphincters.
Clinical Presentation
Anal fissures in children most commonly occur during infancy The usual presenting symptom in that age group is bright red blood per rectum. Crying with bowel movements and hard stool streaked with bright-red blood are the common findings observed by the parents.
Gently spreading the anus (also having the older child bear down), exposes the dentate line and the longitudinal tear comes into view. Fissures are most commonly located in the posterior midline and distal to the dentate line.
An unhealed fissure may become infected and evolve into a chronic ulcer. If this occurs a sentinel skin tag forms distal to the fissure, and the anal papilla may hypertrophy. Fissures are sometime multiple and may occur anteriorly Fissures located laterally suggest Crohn’s disease or immunodeficiency states. Chronic anal fissures in older children may indicate inflammatory bowel disease.
Diagnosis and Treatment
Anal fissures are diagnosed from history and physical. Acute fissures respond to gentle anal dilation, stool softeners, laxatives, and Sitz baths. If fissures are secondary to underlying conditions, treatment is directed to these conditions as well. Fissures associated with inflammatory bowel disease may be treated with metronidazole. Topical anesthetic ointments alter each bowel movement reduce sphincter spasm and pain. A hypertonic anal sphincter may be treated with botulinum toxin and topical nitroglycerine or a lateral subcutaneous internal sphincterotomy. Chronic anal ulcers are surgically excised eliminating granulation/scar tissue while preserving the sphincters. Leukemia and chronic immunosuppression are contraindications to surgical intervention since such fissures fail to heal until these problems are addressed.
Outcomes
Most acute fissures respond to conservative measures and heal within 10-14 days. Recalcitrant fissures respond to lateral internal sphincterotomy This procedure quickly relieves symptoms in 95% of cases and recurrence is less than 5%.
2.5. Hemorrhoids
Hemorrhoids in children are unusual. Four to five percent of children with portal hypertension may develop symptomatic bleeding rectal varices. The clinical presentation is variable with thrombosis occurring most frequently in teenagers. Hemorrhoid thrombosis is frequently associated with heavy physical activity Symptoms may be a report of a perianal mass that prolapses, rectal bleeding, or perianal itching. Children with hemorrhoids frequently have an anal ulcer with a prominent skin tag, rectal prolapse, or rectal polyp. Rectal duplications can rarely present as an external hemorrhoid. Physical exam and history are usually adequate to establish the diagnosis.
Treatment
When bleeding occurs in children with portal hypertension, sclerotherapy may be attempted, however, direct oversewing is the definitive therapy. In children with thrombosed hemorrhoids therapy depends on timing of presentation. If seen within the first 24 hours of symptoms, incision and clot removal provides immediate relief if pain is the presenting symptom. After the first day, spontaneous resolution is underway. Rest, analgesics, stool softeners, and Sitz baths are then the treatment of choice. Hemorrhoidectomy, the surgical procedure of choice, is reserved for chronic hemorrhoids that do not respond to medical therapy. It has a low recurrence rate (< 0.5%). Hemorrhoid surgery is contraindicated in most children who are immunocompromised. Sclerotherapy or rubber-band ligation are recommended over formal hemorrhoidectomy in children with hemorrhoids and concomitant inflammatory bowel disease.
3. Portal Hypertension
Portal hypertension may be defined as a portal pressure gradient of 12 mm Hg or greater and often is associated with varices and ascites.
Pathophysiology. Two important factors exist in the pathophysiology of portal hypertension: vascular resistance and blood flow.
Classification
I. PRESINUSOIDAL
extrahepatic:
portal vein obstruction (extrinsic compression, phlebitis, coagulopathy, tumor invasion, pancreatitis, neonatal omphalitis)
dynamic: traumatic/neoplastic arterioportal fistula
segmental portal HTN: splenic/SMV occlusion
intrahepatic (obstruction of portal venules):
congenital hepatic fibrosis
myelofibrosis
schistosomiasis
idiopathic noncirrhotic fibrosis
reticuloendotheliosis
chronic malaria
toxic fibrosis (arsenic, copper, PVC vapors)
SINUSOIDAL
cirrhosis
POSTSINUSOIDAL
Budd-Chiari syndrome (obstruction of major hepatic veins; etiology: thrombus (dehydration, sepsis, polycythemia vera, paroxysmal nocturnal hemoglobinuria), congenital (web in hepatic v. or IVC), tumor or other mass (eg, hydatid cyst), sickle cell anemia, trauma)
constrictive pericarditis
congestive heart failure.
Symptoms, Signs
The most important are esophageal varices, striking dilation and prominence of the collateral vessels on the anterior abdominal wall with centrifugal radiation outward from the umbilicus, a pattern known as caput medusae. The latter results in large dilated, inferior rectal veins, often mistaken as gross hemorrhoids. Rarely, collaterals can develop in atypical sites (eg, duodenum, colon, or vagina). Determining the presence of the complications of portal hypertension involves the following: Hematemesis or melena (gastroesophageal variceal bleeding or bleeding from portal gastropathy), Mental status changes such as lethargy, increased irritability, and altered sleep patterns (presence of portosystemic encephalopathy),Increasing abdominal girth (ascites formation),Abdominal pain and fever (spontaneous bacterial peritonitis [SBP], which also presents without symptoms),Hematochezia (bleeding from portal colopathy)
Mortality/Morbidity: Variceal hemorrhage is the most common complication associated with portal hypertension. Almost 90% of patients with cirrhosis develop varices, and approximately 30% of varices bleed. The first episode of variceal hemorrhage is estimated to carry a mortality rate of 30-50%.
Lab studies include the following:
Liver function tests,Prothrombin time,Albumin,Viral hepatitis serologies,Platelet count,Antinuclear antibody, antimitochondrial antibody, antismooth muscle antibody,Iron indices,Alpha1-antitrypsin deficiency,Ceruloplasmin, 24-hour urinary copper – To be considered only in individuals aged 3-40 years who have unexplained hepatic, neurologic, or psychiatric disease
Imaging studies.
Duplex-Doppler ultrasonography. CT scan, Magnetic resonance imagin (MRI)
Treatment
Gastroesophageal variceal hemorrhage is the most dramatic and lethal complication of portal hypertension. Bleeding from esophageal varices ceases spontaneously in as many as 40% of patients. Each episode of variceal bleeding is associated with a 30% mortality rate and occurs mostly in patients with severe liver disease and in those with early rebleeding. Rebleeding occurs in 40% of patients within 6 weeks. Emergent treatment-following resuscitation, treatment of acute variceal bleeding includes control of bleeding (24 h without bleeding within the first 48 h after starting therapy) and prevention of early recurrence.
All patients with cirrhosis and upper GI bleeding are at a high risk of developing severe bacterial infections, which are associated with early rebleeding. The use of prophylactic antibiotics has been demonstrated to decrease the rate of bacterial infections and increase survival rates.
Specific treatment of bleeding lesion.
Pharmacological therapy: Somatostatin,Octreotide,Vasopressin
Endoscopic therapy
Endoscopic injection sclerotherapy involves injecting a sclerosant solution into the bleeding varix. Endoscopic variceal ligation (EVL), Endoscopic administration of cyanoacrylate monomer (superglue) in gastric varices is another intervention.
Balloon-tube tamponade.
Balloon-tube tamponade should be used only in massive bleeding as a temporizing measure until definitive treatment can be instituted (Minnesota tube).
Surgical Care
Surgical care includes decompressive shunts, devascularization procedures, and liver transplantation.
