Rosen & Barkin's 5-Minute Emergency Medicine Consult (523 page)

1 wk quadruple therapy:

• Bismuth subsalicylate 120 mg PO QID, tetracycline PO 500 mg QID, metronidazole 400 mg PO QID, esomeprazole 20 mg PO BID
  
• 80% eradication rate
  

FOLLOW-UP

• Gastric obstruction
  
• Perforation
  
• Active upper GI bleed
  
• Melena
  
• Uncontrolled pain
  
• Anemia requiring transfusion
  

• Unremarkable physical exam with normal CBC and heme-negative stools
  
• If heme-positive stools, discharge if stable vital signs, normal hematocrit, and negative NGT aspiration for upper GI hemorrhage
  

Outpatient GI evaluation and endoscopy

• High-risk patients include those with the following characteristics:
  
  • Bleeding with hemodynamic instability
    
  • Repeated hematemesis or any hematochezia
    
  • Failure to clear with gastric lavage
    
  • Coagulopathy
    
  • Comorbid disease
    
  • Advanced age
    
  • Patients with ulcer perforation or penetration require operative repair.
    
• All patients require primary care follow-up in 2–6 wk to evaluate efficacy of treatment.
  
• Patients >55 yr and patients with severe symptoms should receive GI referral for endoscopy and testing for
  H. pylori
  .
  

• H. pylori
  is the most common cause of PUD.
  
• NSAID-induced PUD is frequently silent.
  
• Dyspeptic symptoms are nonspecific.
  
• Endoscopy is diagnostic and should include
  H. pylor
  i screening.
  
• Treatment should include
  H. pylori
  eradication and H
  ₂
  blockers or PPIs.
  
• Complications include perforations, hemorrhage, anemia.
  
• Failure to follow up may result in failure to diagnose gastric cancer.
  

• Chey WD, Wong BC, Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection.
  Am J Gastroenterol.
  2007;102(8):1808–1825.
  
• Lanza FL, Chan FK, Quigley EM, et al. Guidelines for prevention of NSAID-related ulcer complications.
  Am J Gastroenterol.
  2009;104(3):728–738.
  
• Louw JA, Marks IN. Peptic ulcer disease.
  Curr Opin Gastroenterol
  . 2004;20(6):533–537.
  
• Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease.
  Lancet
  . 2009;374:1449–1461.
  
• Smoot DT, Go MF, Cryer B. Peptic ulcer disease.
  Prim Care
  . 2001;28(3):487–503.
  
• Yuan Y, Padol IT, Hunt RH. Peptic ulcer disease today.
  Nat Clin Pract Gastroenterol Hepatol
  . 2006;3(2):80–89.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Gastroesophageal Reflux Disease
  
• Gastritis
  
• Gastrointestinal Bleeding
  

CODES

• 531.30 Acute gastric ulcer without mention of hemorrhage or perforation, without mention of obstruction
  
• 532.30 Acute duodenal ulcer without mention of hemorrhage or perforation, without mention of obstruction
  
• 533.90 Peptic ulcer of unspecified site, unspecified as acute or chronic, without mention of hemorrhage or perforation, without mention of obstruction
  

BASICS

• Perforation/break in the containing walls of an organ with contents spilling into peritoneal cavity
  
• Inflammation/infection
  
• Ulceration
  
• Shearing/crushing or bursting forces in trauma
  
• Obstruction
  
• Chemical and/or bacterial peritonitis occurs as result of disruption of gastric or intestinal lining into peritoneal cavity.
  

• Peptic ulcer disease:
  
  • Majority of cases caused by NSAIDS and
    Helicobacter pylori
    
• Esophageal
  
• Small bowel:
  
  • Ischemia, foreign body, neoplasms, inflammatory bowel disease
    
• Large bowel:
  
  • Diverticular disease, foreign body, neoplasms, inflammatory bowel disease
    
• Appendicitis
  
• Penetrating or blunt trauma
  
• Iatrogenic:
  
  • Endoscopy, colonoscopy
    
• Radiation enteritis and proctitis
  

• Trauma is the more common cause of rupture:
  
  • Neonates with difficult birth/child abuse/motor vehicle accidents and falls
    
• Jejunum is the most common site of rupture.
  

DIAGNOSIS

• Sudden severe abdominal pain:
  
  • Initially local
    
  • Often rapidly becoming diffuse due to peritonitis
    
  • Consider persistent local pain due to abscess/phlegmon formation
    
• Rigidity
  
• Guarding
  
• Rebound tenderness
  
• Absent bowel sounds
  
• SIRS
  
• Hypovolemic or septic shock:
  
  • Hypotension
    
  • Tachycardia
    
  • Tachypnea
    

• 1/3 without complaints of PUD
  
• May not have dramatic pain/peritoneal findings on exam:
  
  • Less rebound and guarding due to less abdominal wall musculature
    
  • Chronic use of pain meds
    
• May present with altered mental status
  
• Hypothermic, suppressed tachycardia
  

Upright chest radiograph:

• Best demonstrates pneumoperitoneum
  
• When in upright position for 5–10 min, may detect as little as 1–2 mL of free air under diaphragm
  

• CBC
  
• Electrolytes, BUN/creatinine, glucose
  
• Lipase
  
• Urinalysis
  
• Liver function test, coagulation panel
  
• ABG
  
• Lactate
  
• Consider type and cross match for blood
  

• Upright CXR:
  
  • To detect air under diaphragm
    
  • Sensitivity ranges from 50% to 85%
    
• Abdominal radiographs:
  
  • Left lateral decubitus film more helpful than supine abdomen.
    
  • Double wall sign of perforated viscous:
    
    • Air in intestinal lumen and peritoneal cavity allows for visualization of both serosal (not normally seen) and mucosal surfaces of intestine.
      
• Abdominal CT:
  
  • Detects small amounts of free air from perforated viscous
    
• ECG
  

• Pneumomediastinum with peritoneal extension
  
• Appendicitis/cholecystitis/pancreatitis
  
• Pneumonia
  
• DKA
  
• Intra-abdominal abscess
  
• Peptic ulcer disease
  
• Inferior wall myocardial infarction
  
• Obstruction
  

Atypical symptoms of pain, lack of fever, absence of leukocytosis more likely due to population’s suppressed immunity, common comorbidities

• AAA
  
• Acute mesenteric ischemia
  
• Atypical presentations of conditions listed in DDx
  

Rule out ectopic pregnancy

TREATMENT