- Definitions: Gastroesophageal reflux (GER) is normal passage of gastric contents into the esophagus; GERD consists of symptoms and complications of GER; rumination is voluntary habitual regurgitation of gastric contents into the mouth for self-stimulation.
- Complications of GERD can be divided into three systems: Respiratory (asthma and /chronic cough, apnea and ALTE, recurrent aspiration pneumonia), ENT (hoarseness, laryngitis, sinusitis, dental erosions, recurrent OM), and GI (esophagitis, esophageal ulcers, esophageal strictures, Barrett’s esophagus).
- Prevalence of GER: 50% in infants age 0–3 mo; 67% in children age 4 mo; 5% of children age 10–12 mo; 1.4–8.2% in children age 3–17 yr (Arch Pediatr Adolesc Med. 1997;151:569). The prevalence of GERD is unknown.
- Diagnosis
- History and physical exam: A thorough H&P is sufficient for diagnosis. The clinical presentation is based on the age of the child:
- Infants and young children present with recurrent vomiting, arching of the back during feeds (Sandifer syndrome), irritability, and poor weight gain (2° to vomiting or dysphagia). Some present with wheezing or chronic cough, recurrent pneumonia, upper airway symptoms (eg, recurrent stridor), apnea, or ALTE.
- Older children and adolescents present with heartburn or retrosternal chest pain and regurgitation. Some present with dysphagia, hoarseness of the voice, weight loss, anemia, wheezing or chronic cough, recurrent pneumonia, food impaction, and Barrett’s esophagus (rare).
- History: Ask for details of meals (type, volume and frequency), recent change in appetite, reflux symptoms after feeding (regurgitation, pain, irritable, dyspepsia), presence of blood or bile, force of reflux, blood in the stool, trends in weight gain. Social history: Tobacco or alcohol use, psychological factors (eg, stressors, anxiety, depression). PMH: of eczema, neurologic issues (↑ or ↓ tone, hydrocephalus, presence of shunt), prematurity, surgery, ENT disease. Family history: Helicobacter pylori infection, reflux, atopic disease.
- Signs suggesting non-GER cause of vomiting: Bilious or forceful vomiting, GI bleeding, diarrhea, constipation, abdominal pain or distension, fever, lethargy, HSM, seizures, micro- or macrocephaly, FTT, genetic d/o (trisomy 21), other chronic diseases (eg, HIV).
- Infants and young children present with recurrent vomiting, arching of the back during feeds (Sandifer syndrome), irritability, and poor weight gain (2° to vomiting or dysphagia). Some present with wheezing or chronic cough, recurrent pneumonia, upper airway symptoms (eg, recurrent stridor), apnea, or ALTE.
- Laboratory studies/evaluation: None are required for the diagnosis of GERD. Consider H. pylori stool antigen testing for children and adolescents if the patient c/o abdominal pain ± dyspepsia or vomiting. In unclear cases, consider UGI to r/o anatomical abnormalities, esophageal pH monitoring or multichannel intraluminal impedance may be used to correlate reflux with symptoms; esophagoscopy may be used for complications (strictures, esophagitis) and to rule out anatomic abnormalities.
- History and physical exam: A thorough H&P is sufficient for diagnosis. The clinical presentation is based on the age of the child:
- Treatment
- Physiological GER: Reassurance
- GERD in infants:
- Step 1: Thicken formula or breast milk with rice cereal (add 1 Tbsp/oz of formula), reflux precautions (ie, sleeping supine at a 30- to 45-degree angle, small frequent feeds, frequent burping, maintain upright position for 30 min after feeding).
- Step 2: If step 1 interventions fail, add pharmacologic therapy:
- H2R antagonist (eg, ranitidine) or PPI (eg, lansoprazole; not currently FDA approved). PPIs are more effective at acid suppression and are most effective if given 30 min before morning feeds.
- Surface agents (eg, sucralfate, sodium alginate) help protect ulcerated gastric mucosa. Consider use in infants with esophagitis or ulcers.
- Consider changing to casein hydrolysate formula (ie, Nutramigen, Alimentum, Pregestemil) if milk-protein allergy is strongly suspected as the cause of GER.
- H2R antagonist (eg, ranitidine) or PPI (eg, lansoprazole; not currently FDA approved). PPIs are more effective at acid suppression and are most effective if given 30 min before morning feeds.
- Prokinetic agents are (eg, metoclopramide, bethanechol, erythromycin) generally not helpful. However, in severe cases a trial of bethanechol may be useful.
- Step 1: Thicken formula or breast milk with rice cereal (add 1 Tbsp/oz of formula), reflux precautions (ie, sleeping supine at a 30- to 45-degree angle, small frequent feeds, frequent burping, maintain upright position for 30 min after feeding).
- Surgical intervention: Nissen fundoplication is indicated in patients who failed or cannot be weaned off medical therapy and those with frequent aspiration related issues.
- Physiological GER: Reassurance
- Children and adolescents with GERD:
- Lifestyle changes: Sleep on the left side with the head of the bed elevated; avoid caffeine, chocolate, spicy food, tobacco exposure, alcohol; recommend weight loss for obese children; ± psychological evaluation and support; ± intermittent antacids (eg, magnesium hydroxide, aluminum hydroxide, calcium carbonate).
- If above interventions fail, provide a trial of H2RA or PPI.
- Surface agents (eg, sucralfate, sodium alginate) help protect ulcerated gastric mucosa. Consider use in children with esophagitis or ulcers.
- Lifestyle changes: Sleep on the left side with the head of the bed elevated; avoid caffeine, chocolate, spicy food, tobacco exposure, alcohol; recommend weight loss for obese children; ± psychological evaluation and support; ± intermittent antacids (eg, magnesium hydroxide, aluminum hydroxide, calcium carbonate).
Test | Description |
|---|---|
Upper GI series |
|
Esophageal pH monitoring |
|
Endoscopy |
|
Multichannel intraluminal impedance |
|
Nuclear GER study |
|
Gastric emptying study |
|
- Definition:
- Dysphagia: Difficulty swallowing
- Odynophagia: Painful swallowing, usually infectious in etiology (eg, herpes esophagitis).
- Dysphagia: Difficulty swallowing
- Etiology
- Food impaction – most common cause of acute dysphagia
- Structural anomalies of oral cavity, pharynx or esophagus (eg, esophageal webs, rings, and diverticula)
- Motor disorders of the esophagus
- External esophageal compression (eg, chest mass or vascular rings)
- Eosinophilic esophagitis
- Infectious esophagitis (especially immunocompromised or pts using inhaled corticosteroids)
- Peptic stricture secondary to chronic reflux
- Central and peripheral nervous system dysfunction
- Achalasia: loss of peristalsis in the distal esophagus and failure of LES relaxation
- Diffuse esophageal spasms (eg, the nutcracker esophagus)
- Muscular disorders
- Connective tissue d/o: Scleroderma, Sjogren’s syndrome
- History of caustic ingestion or radiation therapy to the neck and chest
- Food impaction – most common cause of acute dysphagia
- Diagnosis
- History:
- Prenatal and birth history
- Eating and swallowing history
- Do you have problems initiating a swallow (oropharyngeal dysphagia), or do you feel food getting stuck a few seconds after swallowing (esophageal dysphagia)?
- Timing of symptoms
- If symptom is before swallowing: Oral phase impaired
- If symptom is during swallowing: Pharyngeal phase dysfunction
- If symptom is after swallowing: Abnormal pharyngeal clearance
- If symptom is before swallowing: Oral phase impaired
- Do you cough or choke (suggests aspiration and oropharyngeal dysphagia) or does food come back through your nose after swallowing?
- Do you have problems swallowing solids (consider stricture), liquids, or both?
- Do you “wash down” solid foods? (consider achalasia)
- How long have you had problems swallowing? Have your symptoms progressed, remained stable, or are they intermittent?
- Could you point to where you feel food is getting stuck? (Usually unreliable; useful with oropharyngeal dysphagia.)
- Do you have problems initiating a swallow (oropharyngeal dysphagia), or do you feel food getting stuck a few seconds after swallowing (esophageal dysphagia)?
- Do you have other symptoms such as loss of appetite, weight loss, nausea, vomiting, regurgitation of food particles, heartburn, vomiting fresh or old blood, pain during swallowing, or chest pain?
- Foreign body or chemical irritant ingestion: What medications are you using now? (Ask specifically about potassium chloride, ferrous sulfate, quinidine, ascorbic acid, tetracycline, aspirin, and NSAIDs. Pill esophagitis may cause dysphagia.)
- Do you have medical problems such as diabetes mellitus, scleroderma, Sjogren syndrome, AIDS, neuromuscular disorders (stroke, myasthenia gravis, muscular dystrophy, multiple sclerosis), cancer, Chagas disease, or others?
- Have you had surgery on your larynx, esophagus, stomach, or spine?
- Have you received radiation therapy in the past?
- Do you have a family history of neurologic disorders or cleft lip or palate?
- Prenatal and birth history
- Physical exam:
- Thorough head and neck exam (nasal patency, oral cavity, lymph nodes, drooling)
- Detailed neurologic exam (special attention to gag reflex, CN 7 & 9-12 important)
- Observe patient feed and evaluate timing of symptoms and signs.
- Neurologic deficit: May not arouse normally for feeding
- Upper airway obstruction: Often arouses normally but has respiratory difficulty even before feeding begins
- Connections between digestive and respiratory tracts: Arouses and initially feeds well but begins choking in seconds
- Esophageal obstruction: Feeds well initially but may aspirate (ie, choke, cough) when the esophagus overfills
- Neurologic deficit: May not arouse normally for feeding
- Thorough head and neck exam (nasal patency, oral cavity, lymph nodes, drooling)
- Laboratory studies/evaluation:
- CBC (use to screen for infection and inflammatory conditions), serum protein and albumin (to assess nutritional status), TSH, free T4 (screen for hypo- and hyperthyroidism).
- May need ENT consult for bedside nasolaryngoscopy ± GI consult for further evaluation/treatment for dysphagia.
- CBC (use to screen for infection and inflammatory conditions), serum protein and albumin (to assess nutritional status), TSH, free T4 (screen for hypo- and hyperthyroidism).
- Treatment
- History:
Study | Reason |
|---|---|
CXR | If concern for foreign body or aspiration pneumonia (usually patient has fever) |
Lateral neck x-ray | If concern for foreign body |
Fluoroscopic swallow function study (modified barium swallow study) | To evaluate swallow function or presence of foreign body |
UGI | If concern for stricture, foreign body, external compression, structural anomalies |
EGD | If esophagitis suspected (dx of eosinophilic esophagitis requires endoscopy) |
Neck and chest CT | If concern for mass causing dysphagia |
Brain MRI | If concern for CNS reason for dysphagia |
Pharyngeal manometry | If suspicion of dysphagia is due to pharyngeal etiology (evaluates up to upper esophageal sphincter) |
Esophageal manometry | If suspicion of dysphagia is due to esophageal etiology |
US of neck | To evaluate submucosal and extramural lesions of the tongue |
Nuclear scintigraphy | To measure transit time & intraluminal volumes |
Etiology | Treatment |
|---|---|
Extrinsic esophageal compression | Surgical correction |
Intrinsic esophageal compression | Endoscopy or surgery |
Muscular disorder | Neuromuscular electrical stimulation Cricopharyngeal myotomy Botulinum toxin injection |
Eosinophilic esophagitis | Elemental formula, corticosteroids, food elimination diet |
Infectious esophagitis | Antimicrobial treatment |
Other causes | Speech or occupational therapy† |
- Definitions
- Hematemesis: Vomiting of blood → bright red or “coffee-ground” consistency
- Hematochezia: Bright red blood per rectum
- Melena: Black, tarry, shiny, sticky stool
- Occult blood: Determined with hemoccult (guaiac)
- Hematemesis: Vomiting of blood → bright red or “coffee-ground” consistency
- Diagnosis
- History and physical exam: First assess vital signs (tachycardia, orthostatic changes) and physical appearance (pallor, diaphoresis, restlessness, lethargy, abdominal pain). Once stable, quantify blood loss, frequency, duration of bleeding, assess for upper or lower GI bleed (see table below). Obtain history based on common causes for the patient’s age (see table below), food and medication history. The physical exam should particularly emphasize ENT, respiratory, abdominal, and digital rectal exam (with hemoccult, see table below).
Type of Bleed | Classic Presentation |
|---|---|
Upper GI bleed (above ligament of Treitz) | Hematemesis ± melena ± stool occult blood |
Lower GI bleed (below ligament of Treitz) | Bloody diarrhea or red blood coating normal stool |
Slow GI bleed | Coffee ground emesis + melena |
Fast GI bleed | Bright red blood per rectum |
Painless rectal bleed | Meckel diverticulum or polyp |
Infant (0–1 yr) | Child (1–12 yr) | Adolescent (12–18 yr) | |
|---|---|---|---|
Hematemesis ± pain | Swallowed maternal blood Esophagitis Gastric or duodenal ulcer Gastric erosion | Epistaxis Peptic esophagitis Caustic ingestion Esophageal varices Duodenitis or esophagitis Gastric or duodenal ulcer Hereditary hemorrhagic telangiectasia Henoch-Schönlein purpura | Esophageal ulcer Peptic esophagitis Gastric or duodenal ulcer Gastritis Hereditary hemorrhagic telangiectasia Henoch-Schönlein purpura |
Melena without pain | Duodenal ulcer Duodenal duplication Meckel diverticulum Gastric heterotopia | Duodenal ulcer Duodenal duplication Meckel diverticulum Gastric heterotopia | Duodenal ulcer Leiomyoma |
Melena with pain, obstruction ± peritonitis ± perforation | Necrotizing enterocolitis Intussusception Volvulus | Duodenal ulcer Intussusception Volvulus | Duodenal ulcer Crohn disease (ileal ulcer) |
Hematochezia with diarrhea ± crampy abdominal pain | Infectious colitis Sigmoid or rectal prolapse Pseudomembranous colitis Eosinophilic colitis Hirschsprung’s enterocolitis | Infectious colitis Henoch-Schönlein purpura Sigmoid or rectal prolapse Pseudomembranous colitis Crohn colitis Hemolytic uremic syndrome Lymphonodular hyperplasia | Infectious colitis Ulcerative colitis Crohn colitis Pseudomembranous colitis Hemolytic uremic syndrome Henoch-Schönlein purpura |
Hematochezia without diarrhea or abdominal pain | Constipation Milk protein allergy Anal fissure Eosinophilic colitis Rectal gastric mucosa heterotopia Colonic hemangiomas | Constipation Anal fissure Rectal ulcer Polyp Lymphonodular hyperplasia Colonic hemangiomas | Constipation Anal fissure Hemorrhoid Rectal ulceration Colonic arteriovenous malformation Colonic hemangiomas |
Negative Stool Occult Blood Result | Positive Stool Occult Blood Result |
|---|---|
False–negative result: Ascorbic acid, dry stool sample, outdated reagent, prior conversion of hemoglobin to porphyrin by bacteria Mimics melena: Iron, bismuth (Pepto-Bismol), chocolate, grape juice, spinach, blueberries | False-positive result: Red meat, peroxidase- containing food (eg, broccoli, radishes, cantaloupe turnips) Mimics hematochezia: Food coloring, beets, Jell-O, red medication |
Bleeding type | Laboratory and Other Studies as indicated |
|---|---|
Hematemesis |
|
Hematochezia |
|
Hematochezia |
|
Rectal bleeding with signs of colitis |
|
Rectal blood mixed with normal stool |
|
Occult GI blood loss |
|
- Treatment
- Supportive treatment: Stabilize hemodynamic status (NS or LR → blood transfusion); correct coagulation and platelet abnormalities ± iron supplementation.
- Treatment of hemodynamically unstable GI bleed: ABC → supportive treatment → admit to ICU with GI and surgery consults.
- Treatment of upper GI bleed: IV PPI preferred → octreotide preferred over vasopressin (better side effect profile) → endoscopic hemostasis (local epinephrine injection, thermal coagulation, clip placement). Band ligation preferred over injection sclerotherapy for esophageal varices.
- Treatment of lower GI bleed is based on etiology:
- Milk or soy protein allergy: Step 1: trial of milk and soy exclusion (from maternal diet of breast feeding neonates) → hydrolyzed formula (Nutramigen, Alimentum, or Pregestimil) → amino acid formula (Neocate or Elecare).
- C. difficile colitis: PO (or IV) metronidazole x 10 days. For treatment failure or serious illness → PO vancomycin. 25% of patients need a second course of antibiotics. Consider anion resin binders (eg, Questran) and Lactobacillus for recurrent disease. Surgical diversion or resection for severe disease (rare).
- Other infectious colitis: Antibiotics rarely required (see AAP Redbook for recommendation of treatment for specific pathogen).
- Intussusception: Air-contrast enema may be diagnostic and therapeutic
- Meckel diverticulum: Surgical resection.
- Polyps, bleeding ulcer, telagiectasia, small hemangioma, mucosal lesion: Endoscopy
- Bleeding blood vessels (eg, AVM): Coil embolization by angiography.
- Visible blood resolves within 2 weeks.
- Reintroduce soy or milk after 6 months → acceptable to trial milk at age 1 yr (if significant allergy, perform monitored milk challenge).
- Milk or soy protein allergy: Step 1: trial of milk and soy exclusion (from maternal diet of breast feeding neonates) → hydrolyzed formula (Nutramigen, Alimentum, or Pregestimil) → amino acid formula (Neocate or Elecare).
- Supportive treatment: Stabilize hemodynamic status (NS or LR → blood transfusion); correct coagulation and platelet abnormalities ± iron supplementation.
- Prevention: Consider H2RA, PPI, or sucralfate if applicable
Required Criteria | Supportive Criteria |
|---|---|
|
|
- Clinical presentation: Onset usually before age 5 yr (patients ≤2 yo may have CVS, but other diagnoses are more common). Vomiting episodes often start during sleep or in the early morning (3–4 am). The patient may have a 30 min prodrome of nausea and pallor without visual aura (68%). Vomit ≤12 (average 6) times per hr, which may last days (average, 41 hrs; rarely >72 h). Emesis may be bilious (76%), mucoid (72%), projectile (50%), or bloody (32%). Other symptoms include retching (76%) and anorexia (74%).
- 47% have true cycle, often every 2–4 wk; average, 12 episodes/yr.
- 47% have migraines. 47% have first-degree relatives and 72% have second-degree relatives with migraine.
- 62% have personal or family history of irritable bowel syndrome.
- 47% have true cycle, often every 2–4 wk; average, 12 episodes/yr.
- Triggers: Infection (41%; eg, chronic sinusitis),both positive and negative stress (34%; eg, birthdays, exams), food (26%; eg, cheese, chocolate, monosodium glutamate), hypoglycemia (eg, fasting), exhaustion or sleep deprivation (18%), menstruation (13%), atopic events (13%), motion sickness (9%), anxiety, excessive exercise, trauma.
Differential Diagnosis | Blood Tests | Urine and Stool Tests | Imaging and Other Evaluation |
|---|---|---|---|
Gastrointestinal Peptic injury Obstruction Malformations IBD Chronic appendicitis Hepatobiliary disorder
Pancreatitis Dysautonomia, pseudo-obstruction |
CBC, ESR ESR, CRP ALT, GGT
Amylase, lipase |
Stool guaiac |
EGD with biopsy Abdominal plain film UGI ± SBFT UGI ± SBFT Abdominal CT Gallbladder US, CCK-stimulated HIDA scan Abdominal US UGI ± SBFT gastric-emptying scan |
Neurologic Abdominal migraine Chronic sinusitis Increased subtentorial pressure Abdominal epilepsy | Consider sinus CT, ENT consult Head CT or MRI EEG | ||
Renal Acute hydronephrosis Nephrolithiasis |
UA, urine calcium:creatinine ratio |
Renal US | |
Metabolic and Endocrine | |||
Addison’s disease | Electrolytes, cortisol | ||
Diabetes mellitus | Glucose | Ketones | |
Pheochromocytoma | Fractionated metanephrines | Fractionated metanephrines | |
Organic acidemias | pH, bicarbonate, SAA’s | Organic acids | |
Disorders of fatty acid oxidation | Carnitine, acylcarnitine profile | UOAs | |
Mitochondrial disorders | Lactate, pyruvate | ||
Urea cycle defects | SAA’s | ||
Aminoacidurias | |||
Acute intermittent porphyria | Delta-aminolevulinic acid, porphobilinogen | ||
Hypothalamic surge | ACTH, ADH | ||
Disorders of ketolysis | glucose, pH, ketones | Ketones | |
Others Munchausen by proxy Anxiety, depression, secondary gain Pregnancy |
β-HCG |
Toxicology screen |
Psychology consult |
Acute management | |
|---|---|
Emergency Department |
|
Outpatient management | |
Lifestyle changes (for milder presentation, eg 1-2 episodes per month) |
|
Prophylaxis |
|
| |
- May represent intrinsic liver disease or result from systemic disease.
- The normal liver span by percussion at 1 week of age is 4.5–5 cm and at 12 years is 7–8 cm for boys and 6–6.5 cm for girls.
- A normal variant of the right lobe of the liver, called Reidel lobe, may extend far below the right costal margin and be confused as pathologic hepatomegaly.
Biliary | Infiltration |
|---|---|
Alagille syndrome Biliary atresia Choledochal cyst Cholelithiasis Biliary tumor | Primary neoplastic tumor Primary non-neoplastic tumor Cyst Hemophagocytic syndrome Extramedullary hematopoiesis |
Inflammation | Infection |
Sclerosing cholangitis Generalized systemic inflammation Neonatal hepatitis Autoimmune disease | Viruses: Hepatitis A–E, EBV, CMV, coxsackievirus, rubella, HSV Bacteria: Bartonella, gonococcus, TB Protozoa: Toxoplasma, amebiasis, schistosomiasis, malaria Other: Sepsis, abscess |
Toxins and Drugs | Trauma |
Acetaminophen (most common), corticosteroids, iron, INH, alcohol | Hemorrhage Subcapsular hematoma |
Inappropriate Storage | Tumor |
Carbohydrate: Glycogen storage disease, DM, parenteral nutrition Lipids: Wolman disease, Neimann-Pick disease, Gaucher disease, Fatty acid oxidation defects, obesity, DM, parenteral nutrition, mucopolysaccharidosis types I–IV Metals: Copper (Wilson disease), iron (hemochromatosis) Abnormal protein: α1-antitrypsin deficiency, glycoprotein deficiency, amyloidosis | Hemangioma Hemangioendothelioma Mesenchymal hamartoma Focal nodular hyperplasia Adenoma Congenital cyst Hepatoblastoma Hepatocellular carcinoma Metastatic tumor |
Genetic | Vascular Congestion |
Crigler-Najjar syndrome Galactosemia Homocystinuria Urea cycle disorders | Suprahepatic: CHF, restrictive pericardial disease, suprahepatic web, hepatic vein thrombosis (Budd-Chiari syndrome) |
Other | |
Reye Syndrome |
History Elements | Physical Exam |
|---|---|
HPI: Thorough history including fever, weight loss or gain, jaundice, pruritus, medications, diet or parenteral nutrition, trauma, abdominal pain, vomiting, diarrhea, bleeding or bruising, travel and sexual history. PMH: Pre- and post-natal exposure to infections, chronic illnesses (eg, IBD, immunodeficiency) FH: Early infant death, hepatic, neurodegenerative or psychiatric d/o (all suggest metabolic d/o) | General: Mental status, development HEENT: Microcephaly (eg, intrauterine growth retardation → suggest TORCH infection); cataract and chorioretinitis (eg, TORCH), posterior embryotoxin (Alagille syndrome), Kayser-Fleischer rings (Wilson disease) Abdomen/rectal: Percuss for liver span,* palpate liver for contour, consistency, tenderness, auscultate for liver bruit or friction rub, ascites, palpate for spleen size,† hemorrhoids, occult bleeding Skin: Cutaneous hemangioma, papular acrodermatitis (Gianotti Crosti syndrome) with viral hepatitis, purpura (eg, TORCH), bruising Neurologic: Full exam to look for signs of metabolic or storage diseases Extremities: Digital clubbing |
Laboratory and Other Studies | |
Routine Studies | Studies Based on Clinical Suspicion |
CBC, reticulocyte count, chem 10, LFT,‡ PT/PTT, ± abdominal US ± doppler flow | Suspect infection → hepatitis panel, monospot, EBV, and CMV IgM/IgG; ± Bartonella, Toxoplasma, HIV, HSV, rubella titers if suspect TORCH infection Other labs: ESR, ammonia, lactate, pyruvic acid, triglycerides, PAA, UOA, carnitine and acylcarnitine profile, fibrinogen, d-dimers, blood cx, iron profile, ANA, α-1 antitrypsin (Pi typing), anti–smooth muscle antibodies, anti-liver kidney microsomal antibodies, serum ceruloplasmin, 24-h urine copper Suspect drug or toxins→ serum acetaminophen level, serum alcohol level, UDS ± extended serum drug screen Radiology: Radiography of spine, abdominal CT/MRI, radionuclide biliary scan (HIDA scan), cholangiogram, ECHO Pathology: Liver or bone marrow biopsy, gastrointestinal biopsy (IBD) |
Test | Origin | Increased | Decreased | Comments |
|---|---|---|---|---|
AST | Liver Heart Skeletal muscle Kidney Brain RBCs | Liver injury 1. >1000 in acute viral hepatitis, ischemic hepatitis, toxin injury 2. ALT > AST in viral hepatitis, nonalcoholic steatohepatitis 3. AST/ALT >2 in alcoholic hepatitis, rhabdomyolysis, muscular dystrophy, hemolysis 4. AST > ALT in liver cancer | Vitamin B6 deficiency Uremia | May require several weeks to normalize after an acute injury May be elevated in thyroid or celiac disease May be normal in advanced liver disease |
ALT | Liver Kidney Skeletal muscle | |||
Alkaline phosphatase | Liver Biliary tract Bone Intestines Placenta Kidney Reticuloendothelial tissue | Liver injury Cholestasis Liver cancer Bone turnover Pregnancy Familial | Wilson’s disease Zinc deficiency Hypothyroidism Pernicious anemia Congenital hypophosphatasia Estrogen therapy Hyperbilirubinemia (falsesly low) | Check liver specificity of elevated alkaline phosphatase:
|
GGT | Biliary tract Kidney Intestines Pancreas Spleen Prostate | Cholestasis Newborns Enzyme-inducing drugs | Elevated by enzyme-inducing drugs (eg, alcohol, antiepileptics, and barbiturates) | |
5′-Nucleotidase (5′-NT) | Liver Intestines Brain Heart Blood vessels Pancreas | Cholestasis | Use in evaluation of nonpregnant patients Not elevated by enzyme-inducing drugs like GGT | |
Unconjugated bilirubin | Liver Spleen | Physiologic jaundice of newborn Breast milk jaundice Increased enterohepatic circulation Hemolysis Ineffective erythropoiesis Drugs or toxins Crigler-Najjar syndrome Gilbert syndrome Sepsis | Clinical jaundice when unconjugated bilirubin >2.5 mg/dL | |
Conjugated bilirubin | Liver | Cholestasis TORCH infections Dubin-Johnson syndrome Rotor syndrome Sepsis or infection | Increased urine bilirubin with conjugated hyperbilirubinemia | |
Albumin | Liver | Dehydration | Chronic liver failure Nephrotic syndrome Severe malnutrition Protein-losing enteropathy | half-life ∼20 days Negative acute phase reactant |
PT/INR | Deficient factor I, II, V, VII, or X Vitamin K deficiency Consumptive coagulopathy (eg, DIC) | Factors I, II, V, VII, X synthesized by liver → PT/INR elevated with liver failure |
- May represent an intrinsic spleen problem or result from systemic disease.
- 5%–10% of normal infants, children, and adolescents may have palpable spleen.
- Dullness to percussion beyond the 11th intercostal space suggests splenomegaly.
- Spleen edge > 2 cm below the costal margin is always abnormal.
- The spleen must be enlarged two to three times its normal size to be palpable on exam.
Nonsplenic Causes | Infiltration |
|---|---|
Large kidney Retroperitoneal tumor Adrenal neoplasm Ovarian cyst Pancreatic cyst Mesenteric cyst | Gangliosidoses Mucopolysaccharidoses Metachromatic leukodystrophy Wolman disease Gaucher disease Neimann-Pick disease Amyloidosis |
Neoplasia or Tumor | Infection |
Leukemia Lymphoma Hemangioma Lymphangioma Neuroblastoma Splenic hamartoma | Viruses: Hepatitis A and B, EBV, CMV Bacteria: Salmonella, Staphylococcus aureus, Rocky Mountain spotted fever, Bartonella, TB Protozoa: Toxoplasma, schistosomiasis, malaria Other: Bacteremia, sepsis, pneumonia |
Hematologic | Vascular Congestion |
Congenital and acquired: Hereditary spherocytosis, pyruvate kinase deficiency, G6PD deficiency, isoimmunization disorder, hemolytic anemia* Hemoglobinopathy: SCD, thalassemia, iron-deficiency anemia | Cirrhosis, portal vein thrombosis, splenic vein thrombosis, cavernous malformation of portal vein, right heart failure |
Other | |
Serum sickness Systemic inflammatory diseases (RA, SLE) Infant of a diabetic mother Cysts: Congenital or posttraumatic |
History | Physical Exam |
|---|---|
HPI: Fever, evaluate for infections, food and drug intake, abdominal pain, bleeding, bruising, pallor, jaundice, weight loss or gain, systemic symptoms (eg, joint pain, malaise), trauma PMH: Chronic illnesses, liver disease FH: Hemoglobinopathy, hemolytic anemia, liver disease | General: Mental status, development HEENT: Jaundice, signs of infection, lymphadenopathy Abdomen and rectal: Percuss for liver and spleen span*, palpate liver for contour, consistency, and tenderness, auscultate for liver or splenic bruit or friction rub, ascites, hemorrhoids, occult bleeding, caput medusa Skin: Cutaneous hemangioma, bruising, telangiectasia Neurological: Evaluate for neurologic manifestations of metabolic or storage diseases |
Laboratory and Other Studies | |
Routine Studies | Studies Based on Clinical Suspicion |
CBC, reticulocyte count, chem 10, liver panel, PT/ PTT, peripheral smear, direct/indirect Coombs, ± thick smear for malaria, ± abdominal ultrasound ± Doppler flow | Labs: Blood cx, if suspect infection → Monospot, EBV and CMV IgM/IgG, ± Toxoplasma, ± HIV, ± Bartonella Radiology: Abdominal CT or MRI, angiography to differentiate splenic cysts or tumor Pathology: Bone marrow biopsy |
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