ArticleCureus2026
Spiked Helmet Sign Associated With Acute Gastric Distension and Hemodynamic Instability: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 author.
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Abstract
The spiked helmet sign is an uncommon pseudo-ST-segment elevation pattern reported in critical illness and recognized by an upward baseline shift beginning before the QRS complex and a dome-and-spike contour. Its distinction from acute coronary occlusion is clinically important but can be difficult when myocardial injury, left ventricular hypertrophy, electrolyte abnormalities, or post-resuscitation changes coexist. We report a 34-year-old male with end-stage kidney disease on hemodialysis, hypertension, hypertrophic cardiomyopathy, and thrombotic microangiopathy who developed aspiration-related respiratory failure, peri-intubation asystolic cardiac arrest, septic shock, and marked gastric distension. During peak instability, an electrocardiogram showed sinus tachycardia at 135 beats/min, left ventricular hypertrophy with secondary repolarization abnormalities, and a spike-helmet morphology that was most prominent in lead II and less distinct in V3. Urgent nasogastric decompression evacuated gas and gastric contents. A repeat tracing obtained 20 minutes later showed a lower heart rate and partial attenuation of the dynamic morphology. A late tracing, obtained after resolution of gastric distension and hemodynamic stabilization, showed sinus rhythm at 83 beats/min and disappearance of the pre-QRS dome-and-spike configuration in lead II and V3, while baseline hypertrophy-related repolarization abnormalities persisted. The serial relationship supports a reversible extracardiac contribution, but incomplete serial biomarkers, echocardiographic assessment, intra-abdominal pressure measurements, and electrode-position documentation prevent definitive exclusion of concurrent myocardial injury or artifact. This case emphasizes integrating electrocardiographic morphology with bedside physiology, abdominal examination, imaging, and response to reversible interventions while continuing to evaluate for true myocardial ischemia.
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