Cardinal Presentations
This post is part of a series called “Cardinal Presentations”, based on Rosen’s Emergency Medicine (8th edition).
Pathophysiology of Nausea and Vomiting
Complications of Nausea and Vomiting
- Hypovolemia: activates RAAS
- Metabolic alkalosis: loss of hydrogen ions in vomitus
- Hypokalemia: RAAS promotes sodium retention and potassium excretion
- Esophageal injury: Mallory-Weiss tear, Boerhaave syndrome
- Aspiration
Key Historical Findings
- Duration of vomiting
- Acute: Episodic and occurring for <1 week. Suggestive of obstructive, toxic/metabolic, infectious, ischemic or neurologic process.
- Chronic: Episodic and occurring for >1 month. Suggestive of partial obstruction, motility disorder or neurologic process.
- Onset
- Acute onset: suggests pancreatitis, gastroenteritis, or cholecystitis.
- Timing
- Post prandial: delayed >1 hour suggests gastric outlet obstruction or gastroparesis.
- Contents
- Bile: presence of bile suggests patent connection between duodenum and stomach (no GOO)
- Undigested food: suggests upper GI tract process (achalasia, esophageal stricture, Zenker)
- Feculent: suggests distal bowel obstruction
- Associated symptoms
- Headache: suggests elevated ICP
Causes of Nausea and Vomiting
References
- Zun, L. (2013). Nausea and Vomiting. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 238-247). Elsevier Health Sciences.