Sarah A. Martin
Appendicitis is the most common reason for abdominal surgery in children in the United States.
Although it can occur at any age, it is most commonly diagnosed between 10 and 12 years of age and occurs more often in males than females.
Perforation rates may be as high as 60% in children <5 years of age and 100% in infants.
A progressive inflammatory process of the appendix, which is a finger-like structure projecting from the cecum, which is usually located in the right lower quadrant. The function of the appendix is not known.
Appendicitis is thought to occur from the occlusion of the appendiceal lumen with an appendicolith or fecalith (feces which has formed a stone), lymph node proliferation, ingested foreign body, tumor, or parasitic infection.
The trajectory of appendicitis has been described as acute progressing to suppurative with further progression to gangrenous, and eventual perforation, and finally abscess formation.
Two major types: nonperforated or acute, and perforated.
Perforated appendix results in increased morbidity, with the diagnosis often made upon presence of an intra-abdominal abscess on diagnostic imaging.
Initially, there is occlusion of the appendiceal lumen, which blocks mucus and bacterial drainage, causing distension, and raising the appendiceal intraluminal pressure.
Appendiceal distension causes stimulation of the 8th to 10th visceral afferent thoracic nerve, leading to periumbilical pain.
Increased intraluminal pressure impairs appendiceal perfusion with eventual gangrene, leading to perforation.
The classic clinical presentation consists of the report of periumbilical pain with progression to right lower quadrant pain (McBurney point) accompanied by anorexia and eventually vomiting and diarrhea.
Nearly 50% of children will have atypical presentations.
A recent systematic review of clinical prediction rules for children with acute abdominal pain concluded that the Pediatric Appendix Score and the Modified Alvarado score were the most validated (Kulik, Uleryk, & Maguire, 2013).
Common signs and symptoms include: fever (more common with perforation), decreased activity level, point tenderness at McBurney point (anatomic marker for the usual location of the appendix, which is one third the distance along a line from the umbilicus to the right anterior iliac spine), and rebound tenderness related to peritonitis associated with perforation.
Rebound tenderness: an increase in pain with the release of pressure rather than the application of pressure.
Specific signs of appendicitis.
Psoas sign—Concomitant irritation of the psoas muscle and associated pain will be present with passive extension or flexion of the right lower extremity.
Obturator sign—If appendix lies on the obturator internus muscle, pain may be present with internal rotation of the right thigh.
Rovsing sign—Pain reported in the right lower quadrant with palpation of the left lower quadrant.
Complete blood count (CBC).
Leukocytosis with a white blood cell (WBC) count >10,000 to 15,000 cells/mm3, and bandemia.
Complete metabolic panel may be done to evaluate for other abnormalities (e.g., dehydration, liver abnormalities).
Urinalysis for presence of a urinary tract infection.
Pregnancy test in appropriate-age female adolescents.
Pros: no radiation exposure, portable, fast, diagnostic for gynecologic disease.
Cons: study limited by appendix position, bowel gas pattern, obesity (not recommended if BMI > 25 in adults), operator experience.
Diagnostic indicators: noncompressible, fluid filled, >6 mm in diameter, and wall that is irregular or >2 mm thick; following perforation, appendix may not be visible or may see focal periappendiceal or pelvic fluid collections.
Computed tomography (CT).
Pros: most sensitive test.
Cons: exposure to ionizing radiation with potential for radiation-induced malignancies, use of contrast, possible sedation.
Diagnostic indicators: Distended appendiceal diameter >7 mm in maximal diameter, appendiceal wall thickening, surrounding fat stranding and a calcified appendicolith (target sign) or regional lymph node enlargement may be appreciated (Figure 15.1).
Equivocal examination findings.
Serial abdominal examination.
NPO, intravenous (IV) fluid administration, antipyretics, and analgesia as indicated.
Diet challenge as supported by response to hydration.
Children with viral illness usually improve with IV hydration; however, children with appendicitis do not.
FIGURE 15.1 • CT Acute Appendicitis. CT of a 12-year-old boy with right lower quadrant pain shows a thick, dilated appendix (arrow) with enhancing walls. There is surrounding inflammation.
Antibiotic coverage targeted toward bacterial flora in the appendix (Escherichia coli, Streptococcus group milleri, anaerobes, and Pseudomonas aeruginosa).
Laparoscopic or open appendectomy.
Generally performed within 6 to 24 hours while patients receiving IV antibiotics and fluids.
Acute: appendicitis; no postoperative antibiotics.
Gangrenous: IV antibiotics.
Diet advancement as tolerated.
IV analgesia transitioned to oral as tolerated.
Antibiotic therapy is generally prescribed for 5 to 7 days depending on patient response. Ceftriaxone and Flagyl for perforated appendix have proven to be adequate.
Interventional radiology abscess drainage, if feasible.
Consider placement of a percutaneously inserted central venous catheter at the time of abscess drainage.
Prolonged ileus may require parenteral nutrition (PN).
Interval appendectomy approximately 6 to 8 weeks later.
If child does not improve with nonoperative management (remains febrile, persistent pain), operative management indicated.
Sarah A. Martin
Although the majority of abdominal masses in children are benign conditions (e.g., organomegaly, constipation, umbilical hernia), approximately one third of the cancers in children <16 years of age are intra-abdominal in origin.
Benign cystic masses and the most common malignant abdominal masses including neuroblastoma, Wilms tumor, and hepatoblastoma will be described.
Additional information on common malignant tumors can be accessed after registering at the St. Jude Children’s Research Hospital “Cure4Kids” site at www.cure4kids.org/ums/home/ and in Section 10 (Hematology and Oncology).
Types of Masses
Benign cystic lesion.
Uncommon in children.
Types of cystic abdominal masses; choledochal cyst, polycystic kidney disease, duplication cyst, cystic teratoma.
Neuroblastoma is the most common extracranial tumor in children, age at presentation is 18 months, with the prevalence greatest in children <4 years (85%).
Wilms tumor is the most common renal tumor and the fifth most common pediatric malignancy, with a common presentation age of 1 to 5 years.
Hepatoblastoma is the most common malignant liver tumor with a mean age at diagnosis 1 year, occurring in the right lobe of the liver and associated with extreme prematurity, very low birth weight, Beckwith-Wiedemann syndrome, Gardner syndrome, and familial adenomatous polyposis disease.
Presentations are variable, and commonly, a mass is noted incidentally by a parent, caregiver, or health professional with an asymptomatic child.
General symptoms include: abdominal pain, abdominal distension, constipation, and anorexia.
Tumor-specific symptoms: Refer to Chapter 10 for details of malignant abdominal masses.
Radiologic—After the diagnosis of a mass is made (clinical examination, abdominal flat plate, ultrasound, CT), consider obtaining any additional imaging at a referral center with pediatric oncology, surgery, and radiology to minimize radiation exposure and optimize the required evaluation for the suspected lesion.
Neuroblastoma—CT preferred diagnostic test, coarse calcifications present in 90% of the cases; may detect liver metastases.
Wilms tumor—Ultrasound may confirm the site of origin, and a CT is used to better characterize the mass, evaluate the other kidney, and detect vascular invasion.
Hepatoblastoma—CT is done to evaluate for tumor extent and vascular involvement. An ultrasound, if done, will evaluate for the inferior vena cava and hepatic veins.
CBC, comprehensive metabolic panel, α-fetoprotein, serum ferritin, and tumor markers as indicated by suspected lesion. See tumor-specific oncological studies in section 10.
A tissue sample of lesion is needed for diagnosis and confirmation by pathology.
Benign cystic lesions.
Surgical excision as appropriate.
Based on staging/grading, tumor size, and vessel involvement.
Will include biopsy, tumor resection, chemotherapy.
Sarah A. Martin
The incidence of biliary atresia (BA) is 1:10,000 live births with approximately 300 new cases diagnosed each year in the United States.
BA is absence or obstruction (due to fibrosis) of the biliary tree, (extrahepatic) leading to intrahepatic bile duct obstruction and proliferation.
Specific etiology remains unknown and thought to be more than one type of this diagnosis.
Davenport (2012) contends there are four types: (1) syndromic BA and associated malformations (i.e., BA splenic malformation syndrome, cat-eye) and random malformations (e.g., esophageal atresia (EA), jejunal atresia, malrotation), (2) cystic BA—cystic change in an obliterated biliary tract, (3) cytomegalovirus-associated BA, in which the infants have positive serology, (4) isolated BA (largest group of infants).
Proposed nongenetic etiologies: infection, intrauterine infection, toxin exposure.
There is obstruction of bile flow from the liver due to an inflammatory process.
Fibrosis or scarring obliterates the ducts and prevents bile from being transported from the liver to the gastrointestinal (GI) tract.
Resultant cirrhosis and the eventual development of liver failure.
Physical examination findings: jaundice, acholic stool, and dark urine.
Laboratory findings: Fractionated bilirubin will reveal a conjugated hyperbilirubinemia, elevated liver transaminases from hepatocellular injury, and additional studies may be done to evaluate for other infectious causes (e.g., TORCH infections, viral hepatitis) and metabolic causes of cholestatic jaundice.
Abdominal ultrasound: gallbladder noted to be absent or small.
Hepatobiliary scintigraphy, in which there is no excretion of the isotope detected in the intestine.
Confirmatory cholangiogram is done at the time of laparotomy/laparoscopy for surgical intervention.
Kasai procedure or portoenterostomy.
Best results in children <2 months of age in experienced hands.
Excision of the extrahepatic biliary tract and anastomosis of a Roux-en-Y limb to the jejunal limb at the porta hepatis.
The goal of the procedure is to reestablish bile flow as evident by pigmented stool in the immediate postoperative period.
Deemed a successful operation if conjugated bilirubin level is <2 mg/dL at 3 months postop; long-term outcome is variable with a small percentage of children achieving lasting drainage that is effective.
Complications: bacterial cholangitis.
Medical therapy for children with chronic disease.
Require 130% to 150% of the recommended daily allowance, and many require 150 kcal/kg/day to achieve appropriate growth.
May require formulas with increased medium chain triglycerides as they do not require bile acids for digestion (e.g., breastmilk, Pregestimil, or Portagen).
Supplement with fat-soluble vitamins (A, D, E, and K).
Supplemental nocturnal feeds with a nasogastric (NG) tube may be necessary for growth failure.
Treatment of cholestasis.
Clinical symptoms include worsening jaundice and pruritis.
Pharmacologic therapy: actigal (decreases bile viscosity), questran (removes bile salts), phenobarbital (stimulates bile flow).
Bathing and skin comfort measures.
Treatment of portal hypertension.
Hepatosplenomegaly—Patients may sequester platelets with resultant thrombocytopenia.
Varices—Collateral vessels from the increased portal venous pressure in the esophagus and rectum. Treatment is controversial and requires treatment of hypovolemia with an acute bleed, administration of H2 blocker or proton pump inhibitor, and endoscopy for variceal banding or ligation.
Ascites—accumulation of fluid in the abdomen from increased capillary pressures and low oncotic pressure from decreased serum protein levels (low albumin and total protein). Possible fluid restriction, albumin infusion, use of diuretics (aldosterone antagonist).
BA is the most common indication for liver transplantation.
Sarah A. Martin
There is an increase in gallbladder disease in children mainly attributed to improved diagnostic modalities (ultrasound) and the obesity epidemic.
Known spectrum of gallbladder disease ranging from biliary colic/dyskinesia, cholelithiasis, acute acalculous cholecystitis, choledocholithiasis, and cholangitis.
Acute cholecystitis is often attributed to the presence of gallstones; however, there are a myriad of etiologies that contribute to gallstone disease for which the patient may or may not develop cholecystitis or experience an acute illness but undergo cholecystectomy as an elective procedure.
Cholecystitis is inflammation of the gallbladder, which is most commonly caused by gallstones. However, there are two types of disease: acalculous or calculous, depending on the presence of cholelithiasis.
Cholelithiasis (presence of gallstone[s]).
Four types of gallstones.
Cholesterol—70% to 100% cholesterol; associated with obesity and insulin resistance; most commonly seen in adolescents and adults.
Black pigment—calcium bilirubinate (calcium salts of unconjugated bilirubin); associated with hemolytic disease and PN administration.
Brown pigment—calcium bilirubinate and fatty acids and are associated with biliary tract infections.
Calcium carbonate—related to transient cystic duct obstruction.
Acalculous is most commonly caused by sepsis or a severe infection.
Calculous from nonhemolytic cholelithiasis; formation of gallstones in the absence of a hemolytic disease.
History of an ileal resection (e.g., in infants with necrotizing enterocolitis, atresia, volvulus).
Medications (e.g., ceftriaxone and furosemide).
Calculous, from hemolytic cholelithiasis; bile in these patients has an increased amount of unconjugated bilirubin, leading to the formation of gallbladder sludge, resulting in an increased risk of cholelithiasis.
Sickle cell disease, thalassemia, spherocytosis, Gilbert syndrome.
Stasis within the gallbladder.
Sludge formation and inflammation that may lead to obstruction and further inflammation in the presence of gallstones.
Bile stasis and bacterial overgrowth lead to the release of lysolecithin (phospholipid) and other proinflammatory agents, exacerbating the inflammatory response.
Pain is attributed to the increased pressure within the gallbladder.
Acalculous—fever, vomiting, right upper quadrant pain, and positive Murphy sign (pain on deep inspiration when the inflamed gallbladder is palpated).
Calculous—with cholelithiasis—“silent stones” that are recognized incidentally on imaging but without symptoms.
Range of presentation with fever, right upper quadrant/abdominal pain, positive Murphy sign, vomiting.
Liver transaminases, bilirubin, and WBC count may be elevated; obtain amylase and lipase.
Ultrasound; thickened gallbladder that contains debris; gallstones may or may not be present (Figure 15.2).
Endoscopic retrograde cholangiopancreatography (ERCP) can be done to evaluate the pancreas and common bile duct with possible stone removal, if present.
Magnetic resonance cholangiopancreatography can be done with no radiation exposure to define and evaluate the biliary structures; however, this is strictly diagnostic, and there can be no intervention.
Supportive care and antimicrobials for self-limiting cases.
Cholecystectomy for progressive gallbladder distension or clinical deterioration.
ERCP may be indicated if a stone is present with common bile duct dilation prior to a cholecystectomy.
Surgery may be delayed to allow for resolution of the inflammation.
Cholecystectomy; either by an open or laparoscopic technique.
Hospital stay of 1 to 2 days following a laparoscopic procedure, and 2 to 4 days if an open procedure is performed.
FIGURE 15.2 • Ultrasound Cholelithiasis. Right upper quadrant abdominal ultrasound revealing cholelithiasis.
Discharge criteria include tolerating diet, pain well controlled with oral analgesia, without fever.
Deiadra J. Garrett
Esophageal atresia (EA) is a congenital defect in which there is interruption of the continuity of the esophagus; the esophagus ends in a blind pouch; usually associated with tracheoesophageal fistula.
EA occurs in about 1 in 3,000 to 4,500 live births; duodenal atresia occurs in 1 in 5,000 to 10,000 live births.
In 50% to 75% of children with EA, at least one other anomaly is present.
Etiology/Types: Five Types of EA
Type A—EA without fistula.
Type B—EA with proximal fistula.
Type C—EA with distal fistula; most common type.
Type D—EA with proximal and distal fistulas.
Type E—Tracheoesophageal fistula without atresia.
Newborn with excessive oral secretions, drooling, accompanied by coughing, choking, or sneezing.
Feeding can cause cyanosis, choking, and emesis.
Failure to pass NG or orogastric tube into the stomach.
Chest radiograph—anteroposterior and lateral, which demonstrates NG tube coiled in upper esophagus.
Assess for VACTERAL (Vertebral, Anorectal, Cardiac, Tracheoesophageal, Renal, and Limb anomalies) association.
Separate tracheoesophageal fistula, if present.
Establish esophageal continuity.
Deiadra J. Garrett
Obstruction of proximal duodenum secondary to failure of recanalization.
Associated with Trisomy 21; approximately 30% of patients with duodenal atresia will have Trisomy 21.
Bilious emesis in the first hours of life.
Abdominal radiograph—double bubble sign representing the stomach and proximal duodenum (Figure 15.3).
Duodenoduodenostomy (bypass obstruction).
Malrotation is treated with a Ladd procedure.
Gastrointestinal Foreign Body Ingestion
Erin M. Garth
Entrance of a foreign body into the GI tract via the mouth.
Esophageal: dysphagia, emesis, food refusal, salivation, coughing, choking, gagging, or asymptomatic.
Gastric/intestinal: typically present after a witnessed or reported event.
May present with peritoneal signs if ingestion has led to intestinal perforation.
Anteroposterior radiograph of chest and/or abdomen.
Esophageal: endoscopy for removal of foreign body.
Batteries/sharp objects—Prompt endoscopy for removal with special consideration to button batteries; can cause mucosal injury within 1 hour. Observe for esophageal perforation.
Gastric/intestinal: conservative management. Majority of foreign bodies that have entered into the stomach will pass through the intestine.
Magnets—Ingestion of ≥2 magnets increases the risk of perforation and obstruction. Prompt surgical intervention warranted.
Sharp objects—Open safety pins warrant removal. All other sharp objects (e.g., glass, straight pins) can be managed conservatively with weekly assessments.
Erin M. Garth
Occurs when reflux is associated with symptoms or complications.
Risk factors: neurologic impairment, obesity, repaired EA or other congenital esophageal disease, cystic fibrosis, hiatal hernia, repaired achalasia, family history of gastroesophageal reflux disease (GERD).
Gastroesophageal reflux: the movement of gastric contents into the esophagus.
GERD: the symptoms or complications of gastroesophageal reflux.
Primary cause is transient relaxation of the lower esophageal sphincter, which allows gastric contents to move into the esophagus.
Upper GI: evaluates for anatomical malformations; not sensitive or specific for GERD.
pH probe: measures lower esophageal acidity over 24 hours; helpful in measuring esophageal acidity exposure, but does not establish relationship with symptoms or disease in most cases; does not measure nonacid reflux.
Combined multiple intraluminal impedance study and pH monitoring: measures both acid and nonacid exposure and is superior to pH monitoring alone in establishing a temporal relationship with symptoms and disease.
Endoscopy and biopsy: not sensitive for diagnosis of GERD, but can exclude other esophageal complications or disorders such as eosinophilic esophagitis.
Radionuclide scintigraphy (milk scan): not specific for diagnosis of GERD; useful in measuring gastric emptying.
Empiric trial of acid suppression: Expert opinion suggests an empiric trial of a proton pump inhibitor in the older child or adolescent with typical symptoms for up to 4 weeks is justified, though not specific for diagnosis of GERD.
Elevate head of crib 30°; can use reflux wedge, avoidance of overfeeding, upright position for 30 minutes after feeding.
Consider a 1-to-2 week trial of hypoallergenic formula.
Increase caloric density of formula, or consider tube feeding if poor weight gain.
Child or adolescent.
Elevated head of bed, left-sided positioning, avoidance of caffeine, chocolate, fatty or spicy foods, carbonated beverages.
Small frequent meals, avoid eating 2 to 3 hours before bedtime.
Lose weight if overweight.
H2 blockers are generally first-line choice, especially for infants.
Proton pump inhibitors; not indicated for infants <1 year of age.
Prokinetic agents can be used to promote stomach emptying.
Nissen fundoplication—the fundus of the stomach is wrapped around the lower esophagus to improve function of the lower esophageal sphincter.
Complication rates are higher in neurologically impaired children.
Due to the risk of complications, usually reserved for those children with multiple pneumonia episodes felt to be related to aspiration and those with intractable reflux unresponsive to medical therapy.
Acute gastroenteritis is defined as “nonspecific inflammation of the gut”.
Most commonly describes a transient viral infection of the GI tract.
Can also be bacterial or parasitic.
Rotavirus, adenovirus, astrovirus, calcivirus, coronavirus, sapovirus, parvovirus.
Salmonella, Shigella, Yersinia, Campylobacter, E. coli O157:H7, Yersinia, Aeromonas, Bacillus cereus, Clostridium difficile.
Cryptosporidium, Giardia, Enteromonas hominis.
Transmitted via fecal-oral route. Person to person, contaminated food/water, and/or fomites.
Lysis of mucosal enterocytes leads to a dysfunctional brush border and causes malabsorption.
Some viral infections (e.g., rotavirus) interfere with calcium channels and lead to loss of sodium and water.
Stimulation of the enteric nervous system leads to increased electrolyte secretion and intestinal water loss.
Toxin production by organism. Toxins bind to enterocyte receptors, which leads to increased fluid secretion, loss of water, stool, and electrolytes.
Organisms invade GI mucosal epithelial cells → villous atrophy → malabsorption.
History often includes travel, sick contacts, recent antibiotic use.
Vomiting, diarrhea, and fever are the hallmark symptoms, but all three may not be present.
Normal bowel movement but with increased frequency and larger water content.
Stool output of >3 bowel movements/day.
Acute diarrhea ≤14 days.
Persistent diarrhea >14 days.
Chronic diarrhea >30 days.
Symptoms may also include myalgias, headaches, and/or fatigue.
Refer to Section 8 (Fluid and Electrolytes) for classification, evaluation and assessment of dehydration.
Minimal to no clinical dehydration.
Manage at home with supportive care.
Oral rehydration solution (ORS) for maintenance hydration.
Continue age-appropriate diet.
Mild to moderate dehydration in acute care setting.
Oral rehydration therapy.
Rehydration (ORS) over 3 to 4 hours + replacement fluids for ongoing losses.
Resume age-appropriate diet as soon as losses have been replaced and vomiting subsides.
Observation until signs of dehydration are resolved and caregivers demonstrate efficient delivery of oral rehydration therapy for home management.
Severe dehydration in acute or intensive-care setting.
IV fluid replacement.
Stool replacement in addition to maintenance IV fluids.
Replacement of electrolytes and buffer if acidotic.
ORS via mouth or NG tube once patient is stable.
Antibiotics may be indicated in certain bacterial infections; contraindicated in E. coli 0157:H7.
Antipyretics and antiemetics can be useful as supportive care.
Do not recommend home use of antiemetics as persistent vomiting would require further investigation.
Hand hygiene is of paramount importance in preventing spread of disease.
Antidiarrheal medications often contain aspirin, which contributes to Reye syndrome and should be avoided.
Can be divided into upper GI tract and lower GI tract bleeding.
Division is anatomically made by the ligament of Treitz (division between the duodenum and the jejunum).
Upper GI tract.
Lesions of the GI mucosa.
Ulcers (gastric or duodenal); Helicobacter pylori is one possible cause.
Lower GI tract.
Infectious colitis: the most common cause of lower GI bleeding is infection.
Allergic colitis/milk-protein enteropathy.
Inflammatory bowel disease (IBD).
Crohn disease, ulcerative colitis.
Any lesion that obstructs intestinal blood flow (e.g., tumor).
Upper GI tract.
Nonsteroidal anti-inflammatory drugs use, Helicobacter pylori infection, prolonged NPO status.
Liver disease with portal hypertension.
Lower GI tract.
Colitis: infectious, inflammatory, ischemic, allergic.
Polyps: rarely cancerous in children; most common are juvenile polyps and familial polyposis syndromes.
Meckel diverticulum (ectopic gastric mucosa): most common in school-aged child.
Anal fissure: associated with constipation.
Upper GI tract.
Hematemesis/bright red blood from gastric tube.
Coffee-ground emesis/output from gastric tube.
Lower GI tract.
Melena: hemoccult positive stool with black, tarry appearance.
Hematochezia—important to differentiate painful versus painless.
Painful: streaks of blood on top of stool or bright red blood mixed into stool.
Painless: bright red blood per rectum.
Upper GI bleed.
Labwork: CBC, PT/PTT, blood type and cross-match, basic metabolic panel, panel for disseminated intravascular coagulation.
Consider urgent upper endoscopy with biopsies to locate source of bleed.
Consider gastric lavage.
Labwork: CBC, basic metabolic panel.
Upper endoscopy with biopsies.
Lower GI bleed.
Lab work: CBC, PT/PTT, blood type and cross-match, basic metabolic panel, panel for disseminated intravascular coagulation.
Upper endoscopy and colonoscopy with biopsies.
Consider tagged red blood cell (RBC) scan.
Must be bleeding briskly for scan to detect source of bleed.
Infectious stool studies.
Laboratory evaluation: CBC, basic metabolic panel.
Infectious stool studies.
Upper endoscopy and colonoscopy with biopsies.
Hemodynamically unstable (upper & lower GI bleeds).
Obtain IV access and administer fluid volume.
Initial fluids: normal saline, lactated Ringer solution, and/or packed RBCs (PRBCs).
Proton pump inhibitor; intravenously.
Consider octreotide for bleeding esophageal varices; may also require banding via upper endoscopy.
Consider vitamin K administration if coagulopathy noted.
Hemodynamically stable upper GI bleed.
Proton pump inhibitor.
Treat infectious etiology if identified (i.e., Helicobacter pylori).
Hemodynamically stable lower GI bleed: management is dependent on etiology.
Meckel diverticulum: surgical consult/evaluation.
Colonic polyps: colonoscopic removal with snare.
IBD: gastroenterology consult.
Treat infectious etiology if identified.
Erin M. Garth
Liver provides many functions in the body, including (1) metabolism of glucose, lipid, nitrogen, drugs, and toxins; (2) Synthesis of albumin and coagulation factors; (3) formation of bile and bile acids.
Inflammation or death of hepatocytes. Process can be self-limiting or can cause fibrosis and cirrhosis, leading to chronic liver disease or hepatic failure.
A—fecal-oral; common in child care centers; contaminated food/water.
B—blood, saliva, semen, transplacental; infants especially susceptible.
C—mother to infant, blood, saliva, semen (0.1%-2% of children in the United States).
Cytomegalovirus (CMV), HIV, Epstein-Barr virus (EBV).
Sepsis, urinary tract infection.
Toxins—alcohol, drugs: acetaminophen, nonsteroidal anti-inflammatory drugs, ACE inhibitors, nicotinic acid, isoniazid, sulfonamides, erythromycin; griseofulvin and fluconazole.
Metabolic/Genetic—α1-antitrypsin deficiency, Tyrosinemia, Galactosemia, Hypothyroidism, Progressive familial intrahepatic cholestasis.
Steatohepatitis and Nonalcoholic steatohepatitis.
Secondary to comorbidity—(e.g., cardiac, thyroid).
Hepatocellular injury can be due to functional or obstructive pathways.
Viral—Errors in RNA transcription lead to different genotypes.
Congenital disorders lead to abnormal development or malfunctioning of hepatocytes, biliary tree.
Asymptomatic with abnormalities in laboratory values.
Acute or chronic symptoms: chronic condition can present with acute changes.
General symptoms: fever, malaise, anorexia, nausea, vomiting, abdominal pain, diarrhea. jaundice, joint pains, low-grade fever.
Physical examination findings: jaundice, hepatomegaly, abdominal tenderness.
Liver function tests are not true tests of liver function. These tests are indirect markers of hepatobiliary disease.
AST, ALT, total/conjugated bilirubin, fractionated alkaline phosphatase, GGT, PT/PTT, INR, complete metabolic profile, ammonia, α1-antitrypsin.
Fractionated alkaline phosphatase and GGT can help distinguish if source is liver or other muscle/tissue etiology.
Rapid decrease in AST/ALT with increased coagulation and bilirubin suggests worsening hepatic failure.
Clotting factors, especially factor V, can help distinguish between liver disease and malnutrition (e.g., vitamin K deficiency).
Disease types based on lab values.
Viral—ALT > AST; peak 7 to 14 days; resolve 6 weeks.
A—Hep A IgM.
B—Hep B IgM core antibody.
C—Hep C antibody or RNA.
Autoimmune—immunoglobulin >3 g/dL; high protein-to-albumin ratio.
Drug—ALT and AST >10, 1000 IU/L.
Steatohepatitis—ALT/AST less than 4 × upper limit of normal; need to evaluate for other conditions (e.g., infection, coagulopathies).
Abdominal ultrasound with Doppler.
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