# Profound Hypokalaemia and Functional Weakness Secondary to Gastric Outlet Obstruction: A Rare Case

## TL;DR

A man with a history of gastric outlet obstruction developed severe low potassium and muscle weakness, mimicking heart and nerve issues, requiring multidisciplinary care.

## Contribution

This case highlights the rare but critical link between gastric outlet obstruction and severe electrolyte imbalance causing neuromuscular and cardiac symptoms.

## Key findings

- Profound hypokalaemia and electrolyte imbalance led to quadriparesis and elevated troponin, mimicking acute coronary syndrome.
- Neurological symptoms resolved with electrolyte correction, emphasizing the metabolic origin of the weakness.
- Persistent pyloric stricture necessitated surgical referral after multiple unsuccessful dilatations.

## Abstract

We present the case of a 44-year-old male patient with a known history of pyloric stricture secondary to peptic ulcer disease who was admitted with quadriparesis, vomiting, and chest pain. He had a background of multiple endoscopic dilatations for gastric outlet obstruction and was severely malnourished at presentation. Clinical findings included markedly low serum potassium, phosphate, and magnesium, elevated creatine kinase, and ECG changes suggestive of myocardial strain. High-sensitivity troponin was also elevated, prompting evaluation for acute coronary syndrome and aortic dissection. Imaging ruled out structural cardiovascular pathology, and a diagnosis of type 2 myocardial infarction was made, likely secondary to electrolyte imbalance and volume depletion.

Despite correction of electrolyte abnormalities, the patient’s neuromuscular weakness persisted, prompting neurologic evaluation and spinal imaging to exclude Guillain-Barré Syndrome and compressive pathology. MRI spine was unremarkable. Over the course of his intensive care admission, the patient received central electrolyte replacement, cautious nutritional rehabilitation, and multidisciplinary input from neurology, cardiology, gastroenterology, and dietetics. As electrolyte levels improved, so did his neurological function, and he regained significant muscle strength.

He was subsequently transferred to the gastroenterology ward, where further endoscopic assessment confirmed ongoing pyloric narrowing. Given his history of multiple unsuccessful dilatations and persistent symptoms, he was referred to surgical services for consideration of a definitive gastrojejunostomy.

This case highlights the importance of considering gastrointestinal causes of profound electrolyte disturbances and the potential for these metabolic abnormalities to mimic primary neuromuscular or cardiac pathologies. It also underscores the critical role of multidisciplinary collaboration in managing complex cases involving metabolic, nutritional, and functional decline. Early recognition and a systematic approach to diagnosis and treatment can prevent complications, improve outcomes, and avoid unnecessary interventions.