From Joseph Levy. A Guide to Children's Digestive and Nutritional Health. 2001. With permission.
Not all that is red or black is blood, but when a child vomits what appears to be blood or passes maroon, tarry, or bright red stools, fright is the parent's immediate reaction, and medical attention is usually quickly sought.
Confirming the presence of blood and assessing the severity of the bleeding are the priorities of the practitioner. Prompt referral to a hospital will be indicated in the majority of cases of documented upper GI bleed, while passage of blood per rectum will in many cases be of a less emergent nature.
DEFINITIONSHematemesis refers to the vomiting of blood, and it can be bright red or dark, depending on whether there has been sufficient time for the hemoglobin to be acid-denatured in the stomach. Coffee ground vomitus is a graphic term that describes this darker appearing hemoglobin. Hematemesis results from lesions in the esophagus, stomach, and sometimes from the duodenum. Bleeding from the nasopharynx and oral structures (gums, tongue, or teeth) can be inapparent and can present as hematemesis. Blood is a relatively potent emetic. Blood passed per rectum can be bright red - hematochezia - or tarry black and sticky with a very characteristic smell - melena. Hematochezia usually results from lesions in the colon or terminal ileum while melena is typical of sources above the ligament of Treitz and upper small intestine. Because blood is also a cathartic, profuse upper intestinal bleed can present as hematochezia; on the other hand, blood can become dark if it remains in the colon for a long enough time.
CONFIRMING THE PRESENCE OF BLOOD
One of the first considerations is to determine whether blood is indeed present in the vomiting or stool. Food coloring added to cereals, drinks, medications, gelatine desserts, ketchup, and other tomato dishes can be deceivingly similar to blood, especially to an anxious parent. Dark vegetables, bismuth compounds such as found in Pepto-Bismol, iron-fortified cereals, Oreo cookies, or medicinal iron supplements can turn the stools black. Confirmation of the presence of hemoglobin in body fluids can be accomplished with readily available test tablets or slides. This is particular important in the workup of suspected occult bleeding as a source of unexplained anemia.
Identification of blood containing products is based on the interaction of peroxidase activity found in hemoglobin and various reagents. Among the most commonly used are guaiac (as found in the Hemoccult II slides), orthotoluidin (Hematest tablets) or benzidine. Because of the benzidine reaction is very sensitive, a high rate of false positive results limits its usefulness. Guaiac-based tests are most reliable, but still have a false positive rate of 1%-2%. High doses of vitamin C will produce false negative guaiac tests, and diets containing radishes, turnips, and horseradish will cause false positives due to their high content of peroxidase. Hemoglobin in red meat will also result in a false positive test. Developing of the slides with the peroxide-containing reagent should be done within 3-6 days. None of the tests are 100% specific, and sensitivity varies depending on whether the reaction takes place in acid (gastric contents) or neutral pH. Products such as the Gastroccult have improved the sensitivity for detecting GI bleeding in vomitus or gastric contents. Several consecutive stools should be sampled when searching for occult bleeding, since polyps and other lesions can bleed only intermittently. In the adult, loss of more than 2.5 cc of blood per day is considered abnormal. Actual quantitation of the hemoglobin present per gram of stool has emerged as an accurate diagnostic test mainly used in adults for carcinoma screening purposes.
HEMODYNAMIC EFFECTS OF BLEEDING
Once we have determined that the child is losing blood, the severity of the bleeding and its hemodynamic effects need to be assessed as accurately as possible. These effects are more prominent when the patient has bled acutely. Slow GI bleeds can be tolerated remarkably well and might present only with tiredness, pallor, dizziness, or fainting. Remembering that the circulating blood volume of a child is about 80-85 ml/kg and that orthostatic changes appear when there has been more than 20% reduction of blood volume, one can roughly appraise the severity of the bleed and the need for intensive care. Orthostatic changes are present when the pulse accelerates by 20 beats/minute or the systolic blood pressure drops by 10 mm Hg when the patient's position is changed from recumbent to seating.
MOST COMMON ETIOLOGIES OF GI BLEEDING ACCORDING TO AGE GROUPS
In the immediate perinatal period, one of the most commons reasons for hematemesis or even melena is the ingestion of maternal blood during delivery. Because fetal hemoglobin is more resistant to alkali denaturation than adult hemoglobin, it's presence can be identified easily. Thus, the Apt test can be done at the bedside and requires a 1% solution (0.25 M) of sodium hydroxide. The stool or vomitus blood is diluted 1:10 in water (to effect hemolysis), and after filtration or centrifugation, the hydroxide is added to the clear supernatant. A brown color reflects denatured maternal hemoglobin while dissolved fetal hemoglobin, unaffected by the alkali, will appear pink.
Another less commonly recognized source of apparent bleeding is from inadvertent ingestion of blood during breast feeding. Often, the mother is unaware of a crack in her nipple, and it is surprising how much blood can be sucked and swallowed by a hungry nursing infant. In the nursery, more serious bleeding results from hemorrhagic disease, seen much less commonly since the widespread prophylactic administration of vitamin K. A bleeding diathesis can be precipitated by antibiotic use and feeding of formulas low in vitamin K. It is also more likely to occur in exclusively breast-fed infants. The vitamin K-dependent clotting factors include prothrombin (II), proconvertin (VII), plasma thromboplastin component (IX), and Stuart-Prower factor (X). Vitamin K deficiency can develop in conditions resulting in fat malabsorption and steatorrhea such as cystic fibrosis and cholestatic syndromes.
Additional hemorrhagic disorders to be ruled out in the bleeding infant include disseminated intravascular coagulation and von Willebrand's disease. The first is often a complication of gram negative septicemia and endotoxemia, while von Willebrand's disease is an inherited defect involving platelet adhesiveness and abnormal factor VII concentrations and function. Special coagulation studies, measuring fibrin degradation products, platelet function, and the response of factor VII to plasma infusions are necessary to accurately diagnose these conditions. Bleeding diathesis can result in hematemesis from diffuse gingival and gastric erosions. Subcutaneous hemorrhages and intraventricular bleeds can be major complications. Necrotizing enterocolitis presents with GI bleeding in all but the mildest forms. Bleeding can range from faintly heme positive gastric aspirates to massive hematochezia. Necrotizing enterocolitis (NEC) must be suspected in any infant (particularly if premature and stressed) who develops apnea/bradycardia, hypo- or hyperthermia, decreased gastric emptying, abdominal distension, or heme positive stools.
The entire bowel can be affected, but it occurs more often in the right colon and terminal ileum. Intestinal ischemia resulting from arteriolar thrombi, mucosal ulcerations, and hemorrhage into the submucosa can rapidly progress to partial or total pneumonatosis intestinalis, perforation, and bowel gangrene. Healing can be complete or result in strictures (often multiple) in over one-third of the patients.
The etiology of NEC has remained elusive but is most likely multifactorial. The role of hypertonic formulas high in carbohydrates that cannot be completely digested and absorbed and might promote bacterial overgrowth has been implicated in several outbreaks. Nurseries in which enteral feedings of isotonic formulas are advanced very slowly report a much lower incidence of NEC. Bacterial toxins and enteroinvasive organisms have also been involved in epidemics. Breast milk appears to be protective. Treatment consists of nasogastric decompression intravenous antibiotics, close radiologic and clinical monitoring to diagnose perforation, and surgery if this has occurred or if no improvement follows intensive supportive therapy.
Midgut volvulus, arteriovenous malformations, and duplication cysts of the intestine can all present with bleeding in the neonatal period, sometimes with catastrophic severity. The infant will have signs of intestinal obstruction and appear ill, and bleeding resulting from gangrenous bowel is ominous. Bleeding from esophageal varices is not common in the neonatal period but has been described in children with severe cytomegalovirus neonatal hepatitis. This diagnosis is suggested by the presence of a jaundiced neonate showing signs of hepatic decompensation (ascites, bleeding). Gastric and duodenal ulcers can occur in stressed and (much less commonly) nonstressed neonates. Hematochezia can result from brisk bleeding.
Rectal Bleeding in the Neonate
Perianal irritation and excoriations can result in small amounts of occult or streaky bleeding. Fissures can develop at any age and can also result in streaks of blood. The rectal mucosa at this young age is delicate, and if nodular lymphoid hyperplasia is present, friability can be sufficient to cause superficial bleeding with straining or passage of frequent stools. Anal and rectal fissures are often exquisitely painful and can be the underlying reason for irritability and distressed crying. Irritability due to painful defecation can be mistakenly confused with esophagitis and GE reflux since a straining and crying infant is more prone to vomit and the gastrocolic reflex will stimulate a bowel movement at the time of feedings.
Anal fissures are apparent by gently spreading the buttocks. The shiny mucosa will most often occur posteriorly or a small skin tag (a "sentinel pile") might be present between the anus and the perineum. Deeper rectal fissures can be felt by digital palpation with a well-lubricated glove. Use of the pinky is recommended for infants lest a fissure be produced by the examination itself. Examination with a test tube is to be discouraged. Accidental breaks can occur with serious consequences, and visibility is difficult in the best of circumstances. A pediatric proctoscope can readily detect fissuring, provide additional important information about the rectal mucosa, and show evidence of generalized involvement with inflammation or the appearance of blood above the reach of the instrument. If a pediatric proctoscope is not available, an otoscope with a medium-sized speculum can at least provide visualization of a limited segment of the anal canal in a small child and give bright illumination for inspection of the perianal area.
Loose stools mixed in with blood should raise the possibility of milk-induced or postantibiotic colitis. A stool smear will identify polymorphonuclear leukocytes and Charcot-Leyden crystals (remnants of eosinophils). A much more serious cause of colitis and bloody diarrhea in the neonate is the enteritis associated with Hirschsprung's disease. Prompt recognition is imperative since mortality is high. Colonic dilatation, toxemia, and shock can develop rapidly. The underlying aganglionosis is at times unsuspected at this stage. Aggressive treatment of fluid and electrolyte disturbances, rectal decompression and irrigations, antibiotics, and nasogastric intubation are necessary to avert progression to perforation and irreversible shock.
Bleeding in the First 5 Years of Life
Upper gastrointestinal bleeding in this age group is most frequently due to esophagitis, gastritis, or peptic ulcers. If the bleeding develops after forceful vomiting, a Mallory-Weiss tear has to be suspected. The longitudinal laceration occurs most frequently in the esophagogastric junction. Bleeding from a Mallory-Weiss tear can also present as melena. Diagnosis is made endoscopically, and management is conservative in most cases, unless bleeding goes on unabated.
Foreign bodies can damage the tongue, pharynx, esophagus, or stomach. Initial bleeding can subside shortly after the ingestion only to reappear when erosion into a vessel or perforation develop.
Enteric duplication cysts containing ectopic gastric mucosa can be present along the mesenteric side of any part of the intestinal tract. Their lumen can communicate with the lumen of the intestine, in which case erosion or ulceration of adjacent mucosa will result in bleeding. Cysts can also be leading points for intussusception or result in intestinal obstruction. Intestinal tumors are a much less common source of hematemesis.
Rectal bleeding will accompany bacterial infections, protein allergy, or localized rectal lesions. The clinical presentation will give useful information and will help determine the most likely diagnosis.
Painless bleeding, typically maroon colored alternating with bright red, will most likely result from a Meckel's diverticulum or a polyp. The diverticulum is a remnant of the omphalomesenteric duct which connected the yolk sac to the intestine. It is always on the antimesenteric border of the ileum, usually within a foot of the ileocecal valve. One-third of the diverticula contain gastric or pancreatic mucosa, and it is for this reason that bleeding occurs. The erosions are either at the base of the diverticulum or in the ileum adjacent to it. When a large vessel is involved, the bleeding can be severe. Bleeding from a Meckel's diverticulum can occur at any age, but is more common in the first 2 years of life. Other complications associated with this anomaly are intussusception, volvulus around a long omphalomesenteric band, bowel gangrene, and, rarely, diverticulitis with or without a foreign body. The diagnosis is most frequently made on clinical grounds since radiological demonstration of the lesion is rare. The parietal cells in gastric epithelium concentrate technetium 99m pertechnetate and can help identify the diverticulum if enough ectopic mucosa is present in it. A negative test is never considered a sufficient reason not to explore a patient in whom the diagnosis is strongly suspected clinically.
Colonic polyps (inflammatory, juvenile polyps) are benign lesions in their vast majority, and often present as painless rectal bleeding. Male children in the age group 2 to 6 years are most affected. In the majority of cases, the polyp is single. On occasion, it will autoamputate by trauma or by infarction of the feeding vessels at the pedicle. Luckily, 90% of the polyps arise in the rectosigmoid and are easily visualized and managed endosco[ically.
Other colonic polyps appear later and can be associated with familiar syndromes inherited in most of the cases as autosomal dominant and important because of the extremely high risk of malignancy. In familial colonic polyposis, the lesions are adenomatous polyps. In Gardner's syndrome, adenomas are found in association with soft tissue tumors, osteomas, and epidermal cysts. In both of these conditions, prophylactic colectomy is indicated. The ileoanal endorectal pullthrough offers an excellent chance for continence. Screening of all family members by means of colonoscopy or air contrast barium enemas must be done diligently.
In contrast, the intestinal polyps in the Peutz-Jeghers syndrome are located mainly in the small intestine. Pathologically, the polyps are hamartomas, and only in rare instances has malignant transformation been reported. The typical skin lesions are pigmented maculas present in the oral and labial mucosa. Clinical presentation includes anemia, recurrent abdominal pains, and intermittent intestinal obstruction with intussusception and melena. The pigmented lesions appear in late childhood and early adolescence.
Bleeding in the Older Child and Adolescent
Upper gastrointestinal bleeding in this age group is most frequently due to peptic ulcer disease (duodenal and gastric), gastritis, and esophageal varices. Peptic ulcer disease is more common in males. Melena can be the presenting symptom in half of the patients. Variceal bleeding is usually painless and profuse, and fortunately is well tolerated initially. Even in the presence of esophageal varices, another source of bleeding (gastric varices, duodenal ulcer) can be found in about 40% of patients, and the exact source of an upper GI bleed can now be accomplished in most cases endoscopically. Therapeutic intervention is also possible, whether laser or bipolar coagulation of bleeding vessels or with injection of sclerosing solutions or banding of esophageal varices.
Variceal bleeding can sometimes be the initial presentation of portal hypertension, usually when the underlying etiology is extrahepatic portal hypertension. Cavernous transformation of the portal vein, a complication of omphalitis or umbilical vein catheterization, and congenital hepatic fibrosis are the most common entities.
The association of intestinal bleeding and renal manifestations can be found in the hemolytic uremic syndrome and Henoch-Schonlein purpura. Vasculitis is responsible for edema of the bowel, rectal bleeding, intestinal obstruction, and perforation. In Henoch-Schonlein purpura, the intestinal manifestations can precede the rash which is initially urticarial and later turns ecchymotic and purpuric. Buttocks and lower extremities are preferentially involved. Hematuria and proteinuria can be prominent or microscopic, and the renal involvement ultimately determines the prognosis, since some patients can progress to renal failure. Intestinal bleeding can be severe and recurrent, and intussusception can develop, with edematous loops of bowel at the lead point. Close observation is necessary to ward off ischemic necrosis and perforation. Symptoms improve on steroid therapy. Prednisone 1-2 mg/kg/day can result in dramatic resolution of the abdominal pains, which can be severe.
The hemolytic uremic syndrome can be accompanied by an ischemic colitis presenting with diarrhea and rectal bleeding. There is oliguria and pallor, and the youngster or child can appear quite ill with abdominal guarding, vomiting, and lethargy. Intussusception needs to be ruled out, and prognosis is dependent on the renal lesion. Familial forms have been described and have a worse prognosis. Clustering of cases in certain geographical areas suggests an infectious agent might be involved as the initial trigger for what then develops into a microangiopathic lesion. There is laboratory evidence of hemolysis and later, azotemia. Abnormal liver function tests reflect involvement of the liver by the vasculitic process. Management in supportive and intensive, since recovery of renal function is possible even in the face of prolonged renal failure.
SUGGESTIONS FOR THE INVESTIGATION OF GI BLEEDING
After the initial evaluation of the hemodynamic stability of the patient and as the immediate measures for adequate venous access are instituted, as much information as possible is gathered on pertinent points in the history. A preliminary differential diagnosis is sketched based on the nature and amount of the bleed, age of the patient, and clinical features: fever, vomiting, pain, decreased urine output, diarrhea, mental changes, skin lesions, etc. Even if the suspected source are esophageal varices, no harm will be done if a well lubricated nasogastric tube is inserted. This should be one of the first steps in the diagnostic approach of the patient with GI bleeding, whether it presents as melena or hematemesis. A 10 to 14F sump tube should be used. Finding clots of blood, coffee ground material, or fresh blood suggests an esophageal or gastric source, but blood from the duodenum can sometimes flow retrogradely and appear in the aspirates as well.
If blood is found in the stomach, repeated lavage with saline will help assess the briskness of the bleed. Recent studies suggest that the old practice of using ice-cold lavage solution is not any more effective than using it at room temperature. Of greater concern are the reports of abnormal coagulation function induced by the iced solution and potentially detrimental changes in mucosal blood flow. Ice-cold lavage has joine other long lasting and firmly believed medical traditions abandoned for more rational and experimentally proven ones.
If the bleeding does not subside after repeated lavage, the next step will depend on the severity of the bleed. If the rate is profuse, interventive endoscopy will often provide effective treatment. The bleeding can be controlled with epinephrine injections around the responsible vessel and cautery can obliterate it.
If the bleeding is intermittent and severe and no sources are found after upper endoscopy (if indicated) or colonoscopy, an arteriography should be planned if labeled red cell scanning fails to document a bleeding site. A bleeding rate of at least 0.5 cc/min is needed to permit visualization by angiography.
The infusion of vasopressin or octeotride shunts blood away from the splanchnic circulation and tends to control bleeding from varices, gastritis, or other unidentified sources. Close monitoring of serum electrolytes (increased risk of hyponatremia when using vaspressin), cardiovascular status, and peripheral circulation is mandatory.
In summary, after stabilizing the patients vital signs, nasogastric aspiration becomes the first, simplest, and most revealing diagnostic step. Once the source is identified (endoscopy, air/barium contrast studies, nuclear medicine, arteriography), the therapeutic options will be adjusted to the address the case at hand.
The gastric and duodenal mucosa of children is not immune to damage by pepsin, acid and chemicals. Factors determining the formation of a superficial erosion or a deeper ulcer are not fully understood, but the importance of hydrochloric acid and pepsin is well established ("no acid, no ulcer"). Also important are mucosal protective factors mediated by prostaglandins and the quality and quantity of the mucinous secretions lining the epithelial cells. Normal perfusion and oxygenation are also protective, and disruption of cellular integrity often occurs during severe hypovolemia and hypoxia, especially in the newborn.
Gastric acid is produced by the parietal cells, found in higher density in the area of the antrum of the stomach. The parietal cell mass is believed to be high in newborns, and its control is under the influence of neurohormonal factors (vagal, gastrin, other).
Despite the hypergastrinemia found in newborns, acid production is lower at that time and does not reach adult levels until about 6 months of age. A decrease in the number of gastrin receptors or an insensitivity to gastrin has been postulated. Gastrin is released by vagal stimulation after gastric dilatation and by certain peptones and amino acids in the diet, as well as by caffeine, aminophylline, alcohol, and calcium salts. Histamine released from mast cells closely apposed to blood vessels under the mucosa and synthesized in oxyntic cells is also a powerful stimulator of acid production.
The maximal secretory capacity after stimulation with a histamine analog (Histalog) or pentagastrin is commonly used to assess gastric secretion. Unfortunately, there is a great deal of overlap between the basal and maximal acid outputs in patients with peptic ulcer disease of the stomach and controls. In general, maximal and peak acid output tends to be higher in patients with primary duodenal ulcers. Similarly, postprandial serum gastrin levels in patients with peptic disease is not different from controls. Serum gastrin is elevated in the Zollinger-Ellsion syndrome and in some hypercalcemic states. Pepsinogen I also originates in the oxyntic cells in the stomach and, according to recent studies, its concentration in the serum appears to be higher in some patients with duodenal ulcers.
Predisposition for duodenal ulcers is a familiar trait. Fathers of children with primary duodenal ulcers often also give a positive ulcer history. There is a threefold increased incidence in identical twins. The HLA-B5 and BW phenotypes were thought to found with increased frequency in patients with duodenal ulcers, but more extensive does not confirm those findings. There is an excess of blood group O in patients developing ulcers in their 30s.
Peptic ulcer disease is not a common reason for hospitalization (2-5 of 10,000 pediatric admissions), but the true prevalence for these disorders is unknown. Given the nonspecific nature of the symptoms in infants and young children, we are most probably underestimating its occurrence.
The role of Helicobacter pylori infection in the etiology of peptic disease in children is the subject of a separate document.
Clinical PresentationThe younger the child, the higher the likelihood of peptic ulcer disease presenting with a serious complication: perforation, bleeding, shock, abdominal distention, or high obstruction. In the newborn, ulcers are more common in the stomach, and perforations occur close to the greater curve. As previously mentioned, gastric ulcers in the newborn are more common following a stressful delivery, prematurity, sepsis, hypoglycemia, or hypoxia. They also occur in infants with none of these risk factors. There is no sex predilection.
Up to the preschool years, vomiting is the most common symptom. Decreased oral intake, anorexia, weight loss, and irritability should always be carefully assessed. These symptoms can persist for months since the diagnosis and specific treatment is often not even considered. A high index of suspicion is necessary when dealing with the child with poor feeding habits, excessive crying, or vomiting. Anemia or bleeding, rather than perforation, is the more common serious complication in this age group.
In children older than 6 years, pain is the most common presenting symptom. Only one-third of the patients will give a history of typical pain, i.e., hunger-related, improved by eating, nocturnal. The location of the pain tends to become more epigastric as the child gets older and is able to express and localize discomfort. Periumbilical pain, early morning, and postprandial symptoms are also common. Hematemesis or melena occur in half of the patients in this age group. Boys are almost four times more involved than girls.
Ulcers occurring in the context of severe disease or associated with stress are termed secondary. Interestingly, they are not always associated with hypergastrinemia or hyperacidity. Postulated mechanisms have included changes in membrane permeability, steroid-mediated effects on gastric mucus, and increased histamine release. Special names have been coined for the ulcers developing during head trauma, surgery, or CNS infection (Cushing's ulcers), or following burns (Curling's ulcers). Their etiology remains unclear, although increased acid secretion has been demonstrated in Cushing's ulcers.
Peptic ulcer is the major diagnostic consideration when a child presents with GI bleeding, either hematemesis or melena. When the bleeding is massive, as it can be, aggressive management will be needed to stabilize the patient. Reassessment of the hemodynamic changes occurring as a result of blood loss takes precedence in the evaluation. Surgical consultation is often indicated early on to prepare for eventual failure of medical therapy. A high index of suspicion helps diagnose peptic ulcer disease presenting with abdominal pain and vomiting.
Major considerations in the differential diagnosis of peptic ulcer disease include gastroesophageal reflux with or without esophagitis, H. pylori gastritis, pancreatitis, inflammatory bowel disease, food intolerance, and gallbladder pathology (with or without stones).
Once the diagnosis is entertained, a number of investigations are available for its evaluation. Because of the atypical nature of the pain, the inconsistent association with meals, and the spontaneous improvement in the symptoms with unpredictable recurrences, the diagnosis can be very difficult at times. The presence of anemia, guaiac positive stools, and obviously blood-streaked vomitus will naturally prompt a more extensive workup.
Upper endoscopy can be done in children of all ages. New endoscopes are as small (or big) as a 14F tube and can be introduced without compromise to the airway. Endoscopy offers the highest yield for diagnosing gastritis and bleeding secondary ulcers. It is also indicated in the investigation of persistent symptoms despite adequate therapy or when mucosal irregularities detected radiologically remain unchanged after treatment.
The mainstay of therapy of peptic ulcer disease in the absence of serious complications is the suppression of acid production or the neutralization of gastric acidity with antacids. Maintaining gastric pH above 4.0 inactivates pepsin and promotes healing. If a diagnosis of H.pylori gastritis is made, treatment protocols include triple therapy with clarithromycin, a proton pump inhibitor and metronidazole or with amoxacillin, a histamine-2 receptor antagonist and bismuth subsalicylate are effective in 70-90%. Recurrence is in the range of 10-20%.
Antacids. - Aluminum hydroxide is constipating while magnesium hydroxide is a cathartic. Products containing mixtures of both ingredients or alternating preparations are best tolerated. Dosage is empiric, and is mostly used for management of breakthrough dyspepsia while on acid suppression therapy.
H-2 Receptor Antagonists. - Both cimetidine (Tagamet) and ranitidine (Zantac) are powerful inhibitors of acid secretion, and for a long time had been the therapy of choice to treat peptic ulcers. More recently, proton pump inhibitors are taking their place as more potent acid suppressants. Lack of availability of IV preparations, still make the use of H-2 receptor antagonists widespread.
Sucralfate. - This is a complex of aluminum hydroxide and sulfated sucrose. It dose not get absorbed to any significant degree and seems to exert its effect locally by binding to the exudate of the ulcer and perhaps by preventing back diffusion of hydrogen ions. Sucralfate also absorbs bile acids and inactivates pepsin. Experience in adults has been favorable when used an hour before meals and at bedtime. The 1-gm tablets are large for use in young children, and a liquid form is available. Its role in the long-term management of peptic ulcer disease or peptic esophagitis in adults and children has not been established. Because of the potential for toxic accumulation, use of sucralfate should be avoided in conditions of impaired renal clearance.
Diet. - It will come as a surprise to most patients and their parents to hear that there is no need for drastic dietary changes. There is no evidence that a bland diet influences ulcer healing. Drinking citrus juices will sometimes exacerbate dyspepsia, and any other associations between food and symptoms should be assessed on an individual basis. Since food itself stimulates acid production, frequent small meals should be avoided. Three meals a day are preferable.
Following an upper GI bleed, diet should be initially light to test gastric emptying and give a chance for normal function to return. Alcohol ingestion should be discouraged in the adolescent. Smoking delays ulcer healing and should also be avoided. Of course, aspirin and other nonsteroidal anti-inflammatory medications should not be used. Acetaminophen does not adversely influence ulcer healing and can be safely used in these patients.