Persistent Vomiting in Adults: A Comprehensive Approach for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Persistent vomiting represents a diagnostic and therapeutic challenge in internal medicine, with etiologies ranging from benign self-limited conditions to life-threatening emergencies. This review provides a structured approach to evaluation and management, emphasizing pattern recognition, strategic investigation, and evidence-based interventions. We highlight diagnostic pearls and common pitfalls to enhance clinical decision-making in this frequently encountered symptom.

Introduction

Vomiting, defined as the forceful expulsion of gastric contents through the mouth, becomes clinically significant when persistent—generally defined as lasting beyond 48 hours or requiring medical intervention. Unlike the acute presentations commonly seen in emergency departments, persistent vomiting in the ambulatory or inpatient internal medicine setting demands systematic evaluation to identify potentially serious underlying pathology while avoiding diagnostic anchoring on common causes.

The prevalence of persistent vomiting varies across clinical contexts, affecting approximately 3-8% of hospitalized patients and representing a significant source of morbidity through dehydration, electrolyte disturbances, and nutritional compromise. Understanding the pathophysiology and systematic approach to this symptom is essential for internists.

Pathophysiology: Understanding the Vomiting Center

Vomiting is coordinated by the vomiting center in the medullary reticular formation, which integrates inputs from multiple sources: the chemoreceptor trigger zone (CTZ) in the area postrema, vestibular apparatus, cerebral cortex, and peripheral afferents from the gastrointestinal tract and other viscera. This explains the diverse etiologies and therapeutic targets.

Pearl #1: The CTZ lies outside the blood-brain barrier, making it uniquely susceptible to circulating toxins, metabolic derangements, and medications—a key consideration when evaluating drug-induced vomiting.

Clinical Assessment: Beyond the Obvious

History: The Devil in the Details

The temporal pattern provides critical diagnostic clues:

Morning vomiting suggests increased intracranial pressure, pregnancy, uremia, or chronic alcohol use
Postprandial vomiting (immediate) points to psychogenic causes or esophageal pathology; delayed (>1 hour) suggests gastroparesis or gastric outlet obstruction
Projectile vomiting classically indicates pyloric stenosis or increased intracranial pressure
Cyclical vomiting suggests cannabinoid hyperemesis syndrome or cyclical vomiting syndrome

Pearl #2: The presence of bile indicates patency beyond the pylorus, essentially excluding gastric outlet obstruction. Conversely, persistent non-bilious vomiting with abdominal distension should raise concern for pyloric or proximal small bowel obstruction.

Character of vomitus matters: feculent vomiting indicates distal small bowel obstruction or gastrocolic fistula; coffee-ground appearance suggests upper gastrointestinal bleeding with gastric stasis.

Oyster #1: Don't be fooled by "gastroenteritis" in a patient over 50 with new-onset vomiting. Acute gastroenteritis is primarily a disease of the young and immunocompromised. In older adults, consider ischemic bowel, acute coronary syndrome, or other serious pathology.

Physical Examination: Looking Beyond the Abdomen

While abdominal examination remains central, persistent vomiting demands a comprehensive assessment:

Vital signs: Orthostatic hypotension indicates significant volume depletion
Skin: Poor turgor, dry mucous membranes; look for hyperpigmentation (Addison's disease)
Neurological: Papilledema, focal deficits, nystagmus
Cardiovascular: Irregular rhythm suggesting digoxin toxicity
Abdominal: Succession splash (gastroparesis, obstruction), surgical scars, masses

Hack #1: The "eyeball test" for volume status: if the patient looks well-perfused with normal mentation despite claiming severe vomiting, reconsider functional or factitious disorders.

Differential Diagnosis: A Framework Approach

Gastrointestinal Causes

Mechanical Obstruction: Small bowel obstruction from adhesions, hernias, or malignancy remains common, particularly post-surgical patients. Large bowel obstruction typically presents with constipation before vomiting.

Gastroparesis: Increasingly recognized, particularly in diabetics. The classic triad: early satiety, postprandial fullness, and nausea/vomiting. Diabetes, post-viral syndromes, and medications (opioids, anticholinergics) are common culprits.

Pearl #3: Gastric outlet obstruction from peptic ulcer disease has become rare in the proton pump inhibitor era. When encountered, consider malignancy (gastric/pancreatic) or Bouveret's syndrome (gallstone ileus at the pylorus).

Functional Disorders: Chronic nausea and vomiting syndrome, cyclical vomiting syndrome, and rumination syndrome are diagnoses of exclusion but increasingly recognized entities with specific treatments.

Infectious and Inflammatory

Beyond acute gastroenteritis, consider:

Chronic infections: H. pylori, parasitic infections (Giardia, Strongyloides)
Inflammatory bowel disease with stricturing
Acute hepatitis or cholecystitis
Chronic mesenteric ischemia ("intestinal angina")

Metabolic and Endocrine

Oyster #2: Hypercalcemia is easily missed if ionized calcium isn't checked or corrected for albumin. Remember the mnemonic "groans, stones, moans, and bones"—persistent vomiting may be the "groan."

Other metabolic causes include:

Uremia (often with BUN >100 mg/dL)
Diabetic ketoacidosis
Adrenal insufficiency (Addison's disease)
Hyperthyroidism
Hyponatremia (particularly when Na+ <120 mEq/L)

Hack #2: Check a morning cortisol in anyone with persistent vomiting and hypotension despite adequate fluid resuscitation. Adrenal insufficiency can masquerade as gastroenteritis but responds dramatically to corticosteroids.

Medications and Toxins

Pearl #4: Obtain a meticulous medication history including over-the-counter drugs, supplements, and recently discontinued medications. Common culprits include:

Opioids
Chemotherapy agents
Digoxin
Antibiotics (particularly erythromycin, though paradoxically used as prokinetic)
NSAIDs
Levodopa

Cannabinoid Hyperemesis Syndrome (CHS): An increasingly recognized cause in chronic cannabis users. The pathognomonic feature is compulsive hot bathing for symptom relief.

Hack #3: For suspected CHS, ask: "Do hot showers help your symptoms?" A positive response has high specificity. Capsaicin cream to the abdomen may provide therapeutic benefit.

Neurological Causes

Increased Intracranial Pressure: From tumors, hydrocephalus, or idiopathic intracranial hypertension. Morning vomiting with headache is the classic presentation.

Vestibular Disorders: Labyrinthitis, Ménière's disease, posterior circulation stroke.

Migraine: Cyclical vomiting with headache; consider abdominal migraine in younger patients.

Cardiac Causes

Oyster #3: Acute myocardial infarction, particularly inferior wall MI, can present primarily with nausea and vomiting. Maintain low threshold for ECG in patients over 40 with risk factors.

Diagnostic Approach

Initial Laboratory Evaluation

Essential first-tier tests:

Complete metabolic panel (electrolytes, renal function, glucose, calcium)
Complete blood count
Liver function tests
Urinalysis and pregnancy test (when applicable)
Thyroid-stimulating hormone
Morning cortisol if clinically indicated

Pearl #5: The pattern of electrolyte abnormalities provides clues:

Hypokalemic, hypochloremic metabolic alkalosis: classic for protracted vomiting
Hypokalemia with acidosis: suggests concurrent diarrhea or renal tubular acidosis
Hyperkalemia: consider adrenal insufficiency

Imaging Studies

Plain Radiography: Upright abdominal films may reveal air-fluid levels (obstruction), free air (perforation), or gallstones.

CT Abdomen/Pelvis: Gold standard for evaluating obstruction, inflammation, and malignancy. Consider oral and IV contrast when possible.

Upper Gastrointestinal Series: Useful for suspected malrotation or intermittent obstruction.

MRI Brain: When neurological symptoms present or increased intracranial pressure suspected.

Functional Testing

Gastric Emptying Study: Definitive test for gastroparesis. Normal emptying at 4 hours is >90% (scintigraphy remains gold standard).

Upper Endoscopy: Essential for suspected mucosal disease, outlet obstruction, or when empiric therapy fails.

Wireless Motility Capsule: Emerging technology assessing transit throughout GI tract.

Hack #4: Before ordering expensive gastric emptying studies, try a therapeutic trial. Response to metoclopramide or erythromycin supports gastroparesis diagnosis and provides immediate benefit.

Management Strategies

Immediate Stabilization

Volume Resuscitation: Most patients require 2-3 liters IV crystalloid initially. Monitor urine output and orthostatic vital signs.

Electrolyte Correction:

Potassium replacement (typically 40-80 mEq deficit per 1 mEq/L drop)
Magnesium (hypomagnesemia impairs potassium repletion)
Cautious correction of hyponatremia (<10-12 mEq/L/24h to avoid osmotic demyelination)

Pharmacological Management

First-Line Antiemetics:

Dopamine Antagonists:

Metoclopramide 10 mg IV/PO q6-8h (prokinetic benefit; beware extrapyramidal effects)
Prochlorperazine 5-10 mg IV/PO q6h

Serotonin Antagonists:

Ondansetron 4-8 mg IV/PO q8h (excellent for chemotherapy-induced, less effective for gastroparesis)

Pearl #6: Ondansetron can worsen constipation and may paradoxically slow gastric emptying in gastroparesis. Consider alternative agents for diabetic gastroparesis.

NK1 Receptor Antagonists:

Aprepitant 125 mg PO day 1, then 80 mg days 2-3 (expensive but highly effective for refractory cases)

Second-Line Agents:

Promethazine 12.5-25 mg q4-6h (sedating; useful for vestibular causes)
Trimethobenzamide 300 mg PO q6-8h
Dronabinol 2.5-5 mg BID (paradoxically useful despite CHS)

Prokinetic Agents:

Metoclopramide (as above)
Erythromycin 250 mg IV q6h (acute tachyphylaxis limits use beyond 2-4 weeks)
Domperidone 10-20 mg QID (limited US availability)

Hack #5: For refractory gastroparesis unresponsive to standard prokinetics, consider off-label prucalopride (5-HT4 agonist) 2 mg daily. Limited evidence but anecdotal success in clinical practice.

Non-Pharmacological Interventions

Dietary Modifications: Small, frequent meals; low-fat, low-fiber diet for gastroparesis; liquid supplements may be better tolerated.

Gastric Electrical Stimulation: For refractory diabetic gastroparesis unresponsive to medical management.

Nasogastric Decompression: Temporary relief for obstruction or severe gastroparesis; not a long-term solution.

Psychological Support: Essential for functional disorders; consider tricyclic antidepressants (amitriptyline 10-25 mg qHS) or mirtazapine 15-30 mg qHS.

Special Considerations

Cannabinoid Hyperemesis Syndrome

Pearl #7: Cessation of cannabis is curative but challenging. Capsaicin 0.1% cream applied to abdomen provides rapid relief. Haloperidol 5 mg IV may be more effective than ondansetron in acute presentations.

Pregnancy-Related Vomiting

Hyperemesis gravidarum requires aggressive management with IV fluids, thiamine (prevent Wernicke's), and combination antiemetics. Consider hydrocortisone in refractory cases.

Palliative Care Settings

Oyster #4: Octreotide 300-600 mcg/day subcutaneously may reduce secretions and vomiting in malignant bowel obstruction when surgery isn't an option—an underutilized intervention.

Red Flags Requiring Urgent Intervention

Feculent vomiting (complete obstruction or fistula)
Severe abdominal pain with peritoneal signs
Hematemesis with hemodynamic instability
Progressive neurological symptoms
Profound electrolyte abnormalities (K+ <2.5 or >6.5 mEq/L)
Signs of acute myocardial infarction

Conclusion

Persistent vomiting demands systematic evaluation beyond simple antiemetic prescription. Pattern recognition through detailed history, comprehensive physical examination, and judicious investigation identifies serious underlying pathology while avoiding unnecessary testing. Understanding the diverse etiologies—from metabolic derangements to mechanical obstruction—enables targeted therapy and improved outcomes. As internists, maintaining diagnostic humility and broad differential thinking prevents premature closure and diagnostic error in this complex presenting symptom.

Key Takeaways

Temporal patterns and vomitus characteristics narrow differential diagnosis significantly
Don't diagnose "gastroenteritis" in older adults without excluding serious pathology
Check metabolic parameters early; electrolyte patterns provide diagnostic clues
Consider cannabinoid hyperemesis in chronic cannabis users with compulsive bathing
Response to empiric prokinetic therapy supports gastroparesis diagnosis
Adrenal insufficiency masquerades as gastroenteritis but responds dramatically to corticosteroids
Maintain low threshold for cardiac evaluation in older adults with risk factors

References

Hasler WL, Chey WD. Nausea and vomiting. Gastroenterology. 2003;125(6):1860-1867.
Camilleri M, Parkman HP, Shafi MA, et al. Clinical guideline: management of gastroparesis. Am J Gastroenterol. 2013;108(1):18-37.
Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology. 2004;127(5):1592-1622.
Simonetto DA, Oxentenko AS, Herman ML, Szostek JH. Cannabinoid hyperemesis: a case series of 98 patients. Mayo Clin Proc. 2012;87(2):114-119.
Scorza K, Williams A, Phillips JD, Shaw J. Evaluation of nausea and vomiting. Am Fam Physician. 2007;76(1):76-84.
Quigley EM, Hasler WL, Parkman HP. AGA technical review on nausea and vomiting. Gastroenterology. 2001;120(1):263-286.
Guttman J, Kowal JB. Cannabinoid hyperemesis syndrome: novel treatment using capsaicin cream. Am J Emerg Med. 2017;35(12):1977.e3-1977.e4.

Word count: 2,000 words

Disclosure: The author has no conflicts of interest to declare.

Search This Blog

Internal medicine