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Cardiac Pharmacology: CHF & (+) Inotropic Drugs
What Is Asperger Syndrome?
Endocarditis Prophylaxis
The Digestive Process
Basic Pharmacology - Pharmacodynamics
Tetanus prophylaxis


A. Upper GI bleeding (Neonate)

Initially do an Apt test to determine if blood comes from fetal origin or maternal origin (blood swallowed by the fetus). If its of fetal origin then consider a coagulation profile (PT, PTT). If this coagulation profile is normal the possibilities are either stress gastritis or ulcer disease. If the coagulation profile is abnormal then consider hematologic disease of the newborn and manage with vitamin K. The apt test is performed by mixing 1 part of vomitus with 5 part H2O, centrifuge the mixture and remove 5 ml (pink). Then add 1 ml 1% NaOH, wait 2 minutes and if it remains pinks is fetal blood, if it turns brown-yellow its maternal blood.

B. Lower GI bleeding (Neonate)

Again start with an Apt test, if itís positive its maternal swallow blood, if its negative do a PT, PTT. If the coagulation profile is abnormal give Vit K for hematologic disorder of newborn. If it's normal do a rectal exam. A fissure could be the cause, if negative then consider either malrotation or Necrotizing enterocolitis.

1- Necrotizing Enterocolitis (NEC)

Although the exact pathogenesis of NEC is not known, the most widely held theory is that of perinatal stress leading to selective circulatory ischemia. The stress includes prematurity, sepsis, hypoxia, hypothermia, and jaundice. These babies frequently have umbilical artery, vein catheters, have received exchange transfusions or early feeds with hyperosmolar formulas. The intestinal mucosal cells are highly sensitive to ischemia and mucosal damage leads to bacterial invasion of the intestinal wall. Gas-forming organisms produce pneumatosis intestinalis (air in the bowel wall readily seen on abdominal films). Full-thickness necrosis leads to perforation, free air and abscess formation. These usually premature infants develop increased gastric residuals, abdominal distension, bloody stools, acidosis and dropping platelet count. The abdominal wall becomes reddened and edematous. There may be persistent masses and signs of peritonitis. Perforation leads to further hypoxia, acidosis and temperature instability. The acid-base status is monitored for worsening acidosis and hypoxia. Serial platelet counts are obtained and, with increasing sepsis, the platelet count drops <50,000, indicating intravascular coagulation and decreased bone marrow production. The white blood cell count may be high, low or normal and is not generally of help. Serial abdominal films are obtained to look for evidence of free abdominal air, a worsening picture of pneumatosis intestinalis, or free portal air. Therapy consists initially of stopping feeds, instituting nasogastric suctioning and beginning broad-spectrum antibiotics (ampicillin and gentamycin). Persistent or worsening clinical condition and sepsis or free air on abdominal films requires urgent surgical intervention. Attempts to preserve as much viable bowel as possible are mandatory to prevent resultant short gut syndrome.

Complicated NEC is the most common neonatal surgical emergency of modern times, has diverse etiologies, significant mortality and affects mostly premature babies. The use of primary peritoneal drain (PPD) in the management of NEC dates from 1977. The technique is used in the very low birth weight premature infant (<1500 gm) with pneumoperitoneum, metabolic and hemodynamic instability. Consist of a right lower quadrant incision and placement of drainage (penrose or catheter) under local anesthesia with subsequent irrigation performed bedside at the NICU. Initially used as a temporizing measure before formal laparotomy, some patient went to improvement without the need for further surgery (almost one-third). They either had an immature (fetal type) healing process or a focal perforation (not associated to NEC?) which healed spontaneously. Those babies not improved by PPD either die (20%), go on to laparotomy and half die (20%) or develop complications (24%). Some suggestion made are: PPD should be an adjunct to preop stabilization, before placing drain be sure pt has NEC by X-rays, persistent metabolic acidosis means uncontrolled peritoneal sepsis, do not place drain in pts with inflammatory mass or rapid development of intraperitoneal fluid, the longer the drainage the higher the need for laparotomy.

C. Upper GI Bleeding (Older Children)

In the initial evaluation a history should be obtained for bleeding disorders, skin lesions, and aspirin or steroid ingestion. The physical exam for presence of enlarged liver, spleen, masses, ascites, or evidence of trauma or portal hypertension. Labs such as bleeding studies and endoscopy, contrast studies if bleeding stops. Common causes of Upper GI bleeding are:

1. Esophagus

(a) Varices- usually presents as severe upper gastrointestinal bleeding in a 2-3 year old who has previously been healthy except for problems in the neonatal period. This is a result of extrahepatic portal obstruction (portal vein thrombosis most commonly), with resulting varices. The bleeding may occur after a period of upper respiratory symptoms and coughing. Management is initially conservative with sedation and bedrest; surgery ir rarely needed.

(b) Esophagitis- this is a result of persistent gastroesophageal reflux leading to inflammation and generally slow, chronic loss of blood from the weeping mucosa. Treatment consists of antacids, frequent small feeds, occasionally medications and if not rapidly improved then surgical intervention with a fundoplication of the stomach.

Mallory-Weiss- this is a tear of the distal esophagus and/or gastroesophageal junction secondary to severe regurgitation. This was thought to be uncommon in children because it was not looked for by endoscopy. It probably occurs more often than previously thought. Treatment initially is conservative and, if persistent, oversewing of the tear through an incision in the stomach will be successful.

(d) Duplication cysts- Rare cause, they are seen on the mesenteric side of the intestine anywhere from the esophagus to the anus. They bleed when there is ectopic gastric mucosa present. Total excision is curative.

2. Stomach

(a) Gastric Erosions- managed medically in most cases.

(b) Ulcer- treated medically unless there is persistent hemorrhage, obstruction or perforation.

(c) Hematoma- usually secondary to trauma or bleeding disorders.

3. Duodenum

(a) Duodenitis- associated to acid peptic disease.

(b) Hematobilia- secondary to blunt or penetrating abdominal injury. Occasionally requires surgical intervention with local repair or ligation of hepatic vessels.

D. Lower GI bleeding (Older Children)

1- Anal Fissure

Anal fissure is the most common cause of rectal bleeding in the first two years of life. Outstretching of the anal mucocutaneous junction caused by passage of large hard stools during defecation produces a superficial tear of the mucosa in the posterior midline. Pain with the next bowel movement leads to constipation, hardened stools that continue to produce cyclic problems. Large fissures with surrounding bruising should warn against child abuse. Crohn's disease and leukemic infiltration are other conditions to rule‑out. The diagnosis is made after inspection of the anal canal. Chronic fissures are associated with hypertrophy of the anal papilla or a distal skin tag. Management is directed toward the associated constipation with stool softeners and anal dilatations, warm perineal baths to relax the internal muscle spasm, and topical analgesics for pain control. If medical therapy fails excision of the fissure with lateral sphincterotomy is performed. 

2- Meckelís Diverticulum

Meckel's diverticulum denotes those anatomic structures resulting from the umbilical and intra-abdominal persistence of the embryonic vitelline duct (yolk stalk). Meckel's diverticulum is clinically significant, either when discovered incidentally at celiotomy or recognize as the cause of symptoms, which are intestinal bleeding, abdominal pain, or intestinal obstruction. Children with symptomatic Meckel are present with hemorrhage (40%), intestinal obstruction (30%), diverticulitis (20%), and umbilical discharge or disease (6%). Diagnosis is related to presentation. Intermittent rectal bleeding may be diagnosed on occasion by 99mTc sodium pertechnetate. Barium studies are unreliable. Persistent bleeding requires laparotomy even if the Meckel's scan is negative. Diverticulitis or perforation presents with finding similar to appendicitis. Obstruction secondary to intussusception is diagnosed by clinical findings and barium enema. Incidental Meckel's diverticulum is generally handled by simple wedge excision in children. Bleeding Meckel's is managed by resection of the bowel and end-to-end anastomosis. Diverticulitis is handled by either method. Asymptomatic Meckelís diverticula identified incidentally should be removed if upon palpation there is questionable ectopic (gastric or pancreatic) mucosa.

3- Polyps

Juvenile Polyps comprise 80% of childhood polyps. This is a mucous retention polyp and histologically features a cluster of mucoid lobes surrounded by flattened mucus-secreting glandular cells. There is no malignant potential. These polyps are most commonly seen in children age 3-10 with a peak at age 5-6. 85% of children have a solitary polyp. The most common complaint is rectal bleeding and occasionally the polyps may prolapse out the rectum. Diagnosis is by barium enema, rectal exam and/or endoscopy. Removal by endoscopy is the treatment of choice. rarely, exploratory lap with colotomy and excision is required. Lymphoid polyps are not polyps at all, but rather localized elevations of colonic mucosa that on barium enema produce filling defects resembling polyps. They are produced by hyperplasia of submucosal lymphoid tissue. These make up about 15% of childhood polyps. They begin to appear during the first year of life, peak at about the third year of life, and diminish in number by 5 years of age. These are multiple and may present with mild chronic blood loss. Diagnosis is made by barium enema, endoscopy and biopsy. No treatment is necessary since they will regress spontaneously.

Peutz-Jeghers syndromes are polyps associated with melanin hyperpigmentation of the lips and oral mucosa. The polyps are usually multiple and hamartomas. They will appear anywhere, but the majorities are limited to the jejunum and ileum. Chronic blood loss anemia in a child with repeated bouts of colicky abdominal pain secondary to actual or incipient intussusception are typical. Diagnosis is by contrast studies. GI malignancy has been reported in 2-3% of patients. Females with Peutz-Jeghers syndrome seem predisposed to develop ovarian tumors, usually in adolescence. Treatments depend on the severity of symptoms and extend of involvement.

Familial Polyposis Coli has an autosomal dominant inheritance. Hundreds of adenomatous colonic polyps with virtually all developing adenocarcinoma of colon by the third decade of life. The most common and best-recognized variant is patients with Gardner's syndrome, which combines the premalignant adenomatous colonic polyps with soft and hard tissue tumors. Diagnosis is by family history, and contrast studies followed by biopsy. Treatment is total colectomy with ileostomy or endorectal pull-through with ileo-anal anastomosis.

E. Peptic Ulcer Disease

With the advent of more powerful acid inhibiting drugs (H2 antagonists) and proton pump inhibitors, surgery for refractory peptic ulcer disease (PUD) is becoming something of the past. We now manage rare complications of PUD such as bleeding, perforation and obstruction. PUD is either primary or secondary in origin. Secondary PUD are more common and primarily seen in infants the result of an associated condition such as prematurity, steroids, burns, trauma, immune deficiency and brain tumors. Primary PUD occurs more commonly in older children and adolescents the result of an imbalance between acid secretion and gastric mucosal protection. Helicobacter pylori infestation plays a crucial role in the genesis of gastritis and primary duodenal ulcer formation. Successful management of PUD disease encompasses eradication of Helicobacter infection. Initial management of PUD includes medication to reduce acid production (omeprazole, ranitidine, cimetidine) combined with agents that improve mucosal defense (sucralfate). Bleeding PUD manifests itself with either melena or hematochezia. The bleeding site must be visualized during upper endoscopy. Most cases will stop with prompt medical management or endoscopic diathermy. Beyond 50% blood volume loss in a short period of time (8-24 hours) is an indication for surgery.  Infants benefit from duodenotomy and bleeding ulcer ligation, while older children will need more definite ulcer surgery (vagotomy and pyloroplasty). Perforated PUD is the manifestation of a coexisting illness. Simple surgical closure with an omental patch is sufficient. Obstruction produces chronic vomiting due to pyloric scarring.

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