Medical Causes of Acute Abdominal Pain: A Comprehensive Review

 

Medical Causes of Acute Abdominal Pain: A Comprehensive Review 

Dr Neeraj Manikath , claude.ai

Abstract

Acute abdominal pain represents a diagnostic challenge where medical causes are frequently overshadowed by surgical emergencies. This review examines the spectrum of non-surgical medical conditions that manifest with acute abdominal pain, emphasizing diagnostic pearls, clinical hacks, and contemporary management approaches essential for internists and postgraduate trainees.

Introduction

While acute abdominal pain prompts immediate consideration of surgical emergencies, medical conditions account for approximately 30-40% of cases presenting to emergency departments. Misdiagnosis or delayed recognition of medical causes can lead to unnecessary surgical interventions, prolonged morbidity, and increased healthcare costs. The internist's role in distinguishing medical from surgical pathology remains paramount, requiring systematic clinical acumen and judicious investigation.

Classification Framework

Medical causes of acute abdominal pain can be systematically categorized into metabolic, hematologic, infectious, inflammatory, vascular, and referred pain syndromes. This classification provides a structured approach to differential diagnosis when surgical pathology has been reasonably excluded.

Metabolic Disorders

Diabetic Ketoacidosis (DKA)

Abdominal pain occurs in 40-75% of DKA presentations, often preceding hyperglycemia recognition. The mechanism involves gastroparesis, hepatic capsular distension, and metabolic acidosis-induced ileus. Pain severity correlates with acidosis degree rather than glucose levels.

Clinical Pearl: The presence of acute abdominal pain with ketonuria in a diabetic patient should prompt immediate blood gas analysis before imaging studies. Surgical consultation for "acute abdomen" in unrecognized DKA leads to unnecessary laparotomy in 5-8% of cases.

Diagnostic Hack: A venous pH <7.2 with moderate-to-large ketonuria virtually excludes surgical pathology as the primary cause. The pain characteristically resolves within 12-24 hours of metabolic correction without specific analgesic intervention.

Acute Intermittent Porphyria (AIP)

This autosomal dominant disorder presents with severe, colicky abdominal pain in 85-95% of acute attacks. The pathophysiology involves autonomic neuropathy affecting the enteric nervous system. Associated features include neuropsychiatric symptoms, hyponatremia, and port-wine colored urine upon standing.

Oyster of Wisdom: Consider AIP in young females with recurrent acute abdominal pain, especially if triggered by medications (barbiturates, sulfonamides, alcohol), fasting, or the luteal phase of menstruation. The Watson-Schwartz test provides rapid screening, though urinary porphobilinogen quantification confirms diagnosis.

Management Hack: Intravenous hemin (3-4 mg/kg daily for 4 days) remains the definitive treatment, reducing attack duration from weeks to days. Avoid morphine derivatives; use gabapentin for pain management.

Hypercalcemic Crisis

Serum calcium >14 mg/dL causes acute abdominal pain through smooth muscle dysfunction, constipation, and acute pancreatitis. Primary hyperparathyroidism and malignancy account for 90% of hypercalcemic emergencies.

Clinical Pearl: The mnemonic "stones, bones, groans, and psychiatric overtones" understates the acute presentation. Hypercalcemia can mimic acute pancreatitis, peptic ulcer perforation, or bowel obstruction.

Hematologic Emergencies

Sickle Cell Crisis

Vaso-occlusive crises produce severe abdominal pain in 50% of sickle cell patients, primarily affecting the mesenteric vessels, spleen, and liver. The pain results from microvascular occlusion and tissue ischemia.

Diagnostic Challenge: Differentiating vaso-occlusive crisis from acute cholecystitis, hepatic sequestration, or splenic infarction requires high clinical suspicion. Elevated lactate dehydrogenase (LDH) >600 U/L and reticulocytosis suggest hemolysis, but imaging may be necessary to exclude surgical complications.

Management Pearl: Aggressive hydration (1.5 times maintenance), opioid analgesia, and early exchange transfusion for severe crises (Hb <5 g/dL or >30% reduction from baseline) reduce complications. Screen for acute chest syndrome, which complicates 15-20% of abdominal crises.

Acute Hemolytic Anemia

Intravascular hemolysis from various causes (autoimmune, microangiopathic, drug-induced) produces abdominal pain through hepatosplenomegaly, biliary colic from pigment stones, and mesenteric ischemia from profound anemia.

Hack for Recognition: The triad of acute abdominal pain, jaundice, and dark urine with a negative hepatitis panel should prompt hemolysis workup. Peripheral smear examination provides immediate diagnostic information.

Infectious and Inflammatory Conditions

Acute Hepatitis

While typically gradual, acute viral hepatitis (particularly hepatitis A and E) can present with sudden right upper quadrant pain mimicking cholecystitis. Fulminant hepatic failure develops in 1-2% of hepatitis A cases, more commonly in hepatitis E.

Diagnostic Pearl: Aminotransferase elevation >1000 U/L with alkaline phosphatase <3 times upper limit normal distinguishes hepatocellular from cholestatic patterns. Hepatitis serology should precede abdominal imaging in appropriate clinical contexts.

Familial Mediterranean Fever (FMF)

This autoinflammatory condition affects Mediterranean populations, presenting with recurrent acute peritonitis-like episodes lasting 12-72 hours. Peritoneal inflammation results from interleukin-1β overproduction.

Oyster Insight: Consider FMF in patients with recurrent acute abdominal pain requiring multiple emergency visits, particularly those of Armenian, Turkish, Arab, or Sephardic Jewish ancestry. Between attacks, patients are completely asymptomatic—a distinctive feature.

Diagnostic Approach: Elevated acute-phase reactants during attacks with complete normalization between episodes suggests FMF. MEFV gene mutation analysis confirms diagnosis. Colchicine (0.6-1.2 mg daily) prevents 60% of attacks and essentially eliminates secondary amyloidosis risk.

Acute Gastroenteritis with Severe Dehydration

While common, severe gastroenteritis deserves mention as it frequently causes acute abdominal pain through bowel distension, electrolyte disturbances, and prerenal azotemia. Complications include acute mesenteric ischemia in elderly patients with atherosclerotic disease.

Clinical Hack: A blood urea nitrogen/creatinine ratio >20:1 with hemoconcentration indicates significant volume depletion. Rapid fluid resuscitation often resolves pain within 2-4 hours without further intervention.

Vascular Causes

Mesenteric Ischemia

Non-occlusive mesenteric ischemia (NOMI) accounts for 20-30% of acute mesenteric ischemia cases, occurring without arterial or venous thrombosis. Vasospasm from low cardiac output states precipitates this condition.

High-Stakes Pearl: "Pain out of proportion to examination findings" remains the hallmark, but this develops late. Earlier recognition requires high suspicion in patients with recent myocardial infarction, heart failure, or septic shock presenting with abdominal discomfort.

Diagnostic Strategy: Serum lactate >2 mmol/L with metabolic acidosis raises suspicion. CT angiography showing diffuse bowel wall thickening without arterial occlusion suggests NOMI. Early papaverine infusion into the superior mesenteric artery can reverse vasospasm.

Abdominal Aortic Aneurysm—Contained Rupture

While classically surgical, small contained ruptures may present subtly with abdominal or back pain, allowing medical stabilization before repair. The mortality difference between ruptured and electively repaired AAA exceeds 80%.

Critical Recognition Hack: Any patient >60 years with acute abdominal or back pain and hypotension requires immediate AAA consideration. Bedside ultrasound demonstrating aortic diameter >5.5 cm with retroperitoneal fluid mandates immediate vascular surgery consultation without CT delay.

Referred and Neurogenic Pain

Herpes Zoster (Pre-eruptive Phase)

Varicella-zoster reactivation causes dermatomal pain 2-7 days before vesicular eruption. Thoracic dermatomes (T6-T10) commonly affected produce acute abdominal pain indistinguishable from intra-abdominal pathology.

Diagnostic Pearl: Unilateral distribution of pain respecting the midline, associated with burning or tingling quality, suggests radicular pathology. The appearance of vesicles confirms diagnosis retrospectively, but early antiviral therapy (within 72 hours) significantly reduces postherpetic neuralgia.

Spinal Cord Pathology

Thoracic cord lesions (transverse myelitis, epidural abscess, infarction) occasionally present with acute abdominal pain before motor or sensory deficits emerge. The mechanism involves spinothalamic tract involvement.

Oyster of Caution: Acute abdominal pain with bladder dysfunction, bilateral leg weakness, or sensory level mandates urgent spinal imaging before attributing symptoms to intra-abdominal pathology. The window for intervention in compressive myelopathy is narrow—ideally within 24 hours.

Toxicologic and Drug-Induced Causes

Lead Poisoning

Though rare in developed nations, chronic lead exposure produces acute abdominal crises. Occupational exposure (battery manufacturing, renovation of old buildings) and contaminated herbal remedies represent modern sources.

Recognition Pattern: The combination of colicky abdominal pain, constipation, peripheral neuropathy (wrist drop), and basophilic stippling on blood smear suggests plumbism. Blood lead levels >70 μg/dL require chelation therapy.

Opioid-Induced Constipation

Chronic opioid therapy paradoxically causes acute abdominal pain through severe constipation, pseudo-obstruction, or opioid-induced bowel dysfunction syndrome. This affects 40-80% of chronic opioid users.

Management Hack: Peripheral μ-opioid receptor antagonists (methylnaltrexone, naloxegol) reverse opioid-induced gut dysmotility without precipitating systemic withdrawal or affecting analgesia. These agents work within 4-24 hours, avoiding surgical intervention.

Diagnostic Approach: A Systematic Framework

The evaluation of suspected medical causes requires systematic exclusion of life-threatening surgical conditions while pursuing specific medical diagnoses:

Step 1: Assess hemodynamic stability and exclude peritonitis. True peritoneal signs (rebound, guarding, rigidity) mandate surgical evaluation regardless of suspected medical etiology.

Step 2: Obtain targeted laboratory evaluation: complete blood count, comprehensive metabolic panel, lipase, liver function tests, lactate, and urinalysis. Abnormal patterns guide specific testing.

Step 3: Consider point-of-care ultrasound for rapid assessment of free fluid, aortic diameter, and gallbladder pathology before formal imaging.

Step 4: CT abdomen/pelvis with IV contrast remains the gold standard when imaging is necessary, but clinical probability should guide whether imaging precedes or follows specific metabolic testing.

Step 5: Therapeutic trials may provide diagnostic information. Resolution of pain with metabolic correction (DKA, hypercalcemia) or specific therapy (colchicine for FMF) confirms medical causation.

Contemporary Management Principles

Pain management in medical causes of acute abdomen differs fundamentally from surgical approaches. Analgesics do not mask evolving peritonitis in medical conditions and should be administered promptly. Opioid-sparing strategies using ketorolac (if renal function permits), acetaminophen, and lidocaine infusions reduce opioid-related complications.

Specific therapies targeting underlying pathology provide definitive treatment:

  • Insulin and fluid resuscitation for DKA
  • Hemin for acute porphyria
  • Aggressive hydration and transfusion for sickle cell crisis
  • Colchicine for familial Mediterranean fever
  • Chelation for heavy metal poisoning

Conclusion

Medical causes of acute abdominal pain represent a heterogeneous group of conditions requiring high clinical suspicion, systematic evaluation, and targeted management. Recognition of characteristic patterns—pain resolution with metabolic correction, recurrent self-limited episodes, systemic features suggesting specific diagnoses—enables accurate diagnosis and prevents unnecessary surgical intervention. For postgraduate trainees, developing expertise in distinguishing medical from surgical acute abdomen remains a fundamental clinical skill, requiring integration of history, examination, laboratory findings, and judicious imaging interpretation. The internist's systematic approach, complementing the surgeon's readiness to intervene, ultimately serves patients best.

Key Teaching Points

  1. Always consider metabolic causes (DKA, hypercalcemia, porphyria) before proceeding to imaging
  2. Hematologic emergencies (sickle cell crisis, hemolysis) frequently cause acute abdominal pain
  3. Pain severity correlating with specific metabolic parameters (pH in DKA, calcium levels) suggests medical rather than surgical pathology
  4. Recurrent episodes with complete resolution between attacks characterize autoinflammatory conditions
  5. Early specific therapy (hemin, colchicine, chelation) dramatically alters disease course in specific medical causes

 This review synthesizes current evidence from major gastroenterology, internal medicine, and emergency medicine literature through 2025.

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