What is the cause of enlarging abdominal pain in a patient with a history of gout, potential kidney disease, and cardiovascular conditions?

Acute Mesenteric Ischemia Must Be Ruled Out Immediately

In a patient with gout, kidney disease, and cardiovascular conditions presenting with enlarging abdominal pain, acute mesenteric ischemia is the most critical diagnosis to exclude emergently, as it is nearly always fatal without treatment. 1

Immediate Diagnostic Approach

High-Risk Clinical Profile

This patient's combination of cardiovascular disease, potential chronic kidney disease, and gout creates a high-risk profile for acute intestinal ischemia:

• Cardiovascular disease history is present in most patients (approximately two-thirds) who develop acute mesenteric ischemia, with a median age of 70 years 1
• Chronic kidney disease is present in 53% of gout patients and 86% of those with severe hyperuricemia (≥10 mg/dL), creating additional vascular risk 1
• The combination of these comorbidities substantially elevates risk for arterial thrombosis or embolism 1

Classic Presentation to Recognize

• "Pain out of proportion to physical findings" is the hallmark—severe periumbilical abdominal pain with minimal peritoneal signs initially 1
• Pain is typically anterior, periumbilical, and severe enough to prompt immediate medical attention 1
• Laboratory findings show leukocytosis and lactic acidosis in most cases; amylase is elevated in approximately 50% 1

Imaging Strategy

• CT angiography is the diagnostic test of choice—it can identify arterial thrombosis, atherosclerotic disease, intestinal wall thickening, and late findings like pneumatosis intestinalis 1
• Duplex ultrasound is contraindicated in acute presentations due to abdominal distention and the time-sensitive nature of the condition 1

Alternative Gout-Related Causes

Intra-Abdominal Gout (Extremely Rare)

While extraordinarily uncommon, monosodium urate crystal deposition can occur intra-abdominally:

• Only one prior case of intra-abdominal gout mimicking a pelvic abscess has been reported in literature 2
• This manifests as an abdominal abscess with necrotic tissue containing polarizable needle-shaped crystals 2
• This diagnosis should only be considered after life-threatening causes are excluded 2

Acute Gout Flare with Referred Pain

• Gout can affect multiple joint sites including atypical locations (wrist, finger, elbow, knee) 3, 4
• Severe polyarticular flares can cause systemic symptoms and distress 1
• However, true abdominal pain is not a feature of typical gout flares 3, 4

Medication-Related Considerations

Colchicine Toxicity

If the patient is taking colchicine for gout:

• Severe gastrointestinal toxicity can occur, especially with renal impairment or drug interactions 1
• Colchicine must be avoided in severe renal impairment and with strong P-glycoprotein/CYP3A4 inhibitors (cyclosporin, clarithromycin) 1
• Symptoms include severe abdominal pain, nausea, vomiting, and diarrhea 1

NSAID-Related Complications

If NSAIDs are being used for gout management:

• Gastric perforation risk is elevated, particularly without proton pump inhibitor prophylaxis 1
• NSAIDs should be avoided in severe renal impairment, which may be present in this patient 1

Critical Action Algorithm

1. Obtain immediate CT angiography if clinical suspicion for mesenteric ischemia exists (cardiovascular disease + acute severe abdominal pain) 1

2. Check lactate, complete blood count, and amylase while imaging is being arranged 1

3. Involve surgical consultation emergently if mesenteric ischemia is confirmed, as most patients require laparotomy for assessment of bowel viability 1

4. Review medication list for colchicine, NSAIDs, or other agents that could cause gastrointestinal complications in the setting of renal impairment 1

5. Consider alternative diagnoses (peptic ulcer perforation, pancreatitis, nephrolithiasis) only after vascular catastrophe is excluded 1

Key Pitfall to Avoid

Do not delay imaging or surgical consultation while pursuing less urgent workup—acute mesenteric ischemia progresses rapidly to infarction, perforation, and death without intervention 1. The natural history without treatment is nearly always fatal, and re-establishment of flow after infarction can cause sudden systemic endotoxin release with disseminated intravascular coagulation and multiorgan failure 1.