Asian Research Journal of Current Science

Background: Acute hypokalaemic paralysis is a neurological emergency presenting as rapidly progressive flaccid weakness due to acute hypokalaemia. Deep tendon reflexes may be lost (hyporeflexia/areflexia) during attacks, but they may also be preserved, creating an under-recognised diagnostic challenge that can be confused with GBS, myelopathy, or functional paralysis.

Case Presentation: A previously asymptomatic, well 55-year-old man was admitted with a 24 h history of rapidly progressive, symmetrical limb weakness resulting in severe flaccid quadriparesis (power 2/5–3/5 below the knees and 3/5–4/5 above), with bilateral flexor plantar responses. Cranial nerve examination was normal, as was sensation. Despite the marked flaccid quadriparesis, deep tendon reflexes were well preserved (2+ bilaterally throughout), an unusual but recognised feature of hypokalaemic paralysis. There was no goitre. Laboratory investigations showed no abnormality apart from severe hypokalaemia (lowest serum potassium concentration, 1.7 mmol/L by central laboratory measurement), mild elevation of serum creatine kinase (348 U/L), and normal thyroid function tests. Hepatitis B surface antigen was positive. Arterial blood gases showed a pH of 7.40, pCO2 of 32 mmHg, bicarbonate of 19.8 mmol/L, and base excess of -5.0 mmol/L. These results indicate mild systemic metabolic acidosis superimposed on respiratory alkalosis rather than isolated compensated systemic metabolic acidosis, because the pCO2 (32 mmHg) is lower than the value predicted for respiratory compensation using Winter's formula. There was a large discrepancy between the potassium concentration measured by a whole-blood gas analyser (3.2 mmol/L; direct ion-selective electrode [ISE]) and the central laboratory serum potassium concentration (1.7 mmol/L; indirect ISE). Because such a large difference cannot be reliably explained solely by differences between direct and indirect ISE methods or by the effects of heparin, the specimens should be repeated using simultaneously collected and appropriately transported samples so that pre-analytical or analytical causes (such as dilution or specimen contamination) can be excluded before a diagnosis of primary hypokalaemic periodic paralysis is considered. The 12-lead ECG showed classical features of severe hypokalaemia, including prolongation of the PR interval (182 ms), widening of the QRS complex (124 ms), ST depression, T-wave flattening, and U-wave prominence with T-U fusion, producing an apparent prolongation of the QT/QTc interval (490 ms as calculated by QTc = QT/√RR; machine-reported QTc, 487 ms). The patient's condition improved rapidly with potassium replacement (potassium chloride 40 mEq in isotonic saline infused at 10 mEq/h together with oral potassium therapy and appropriate clinical and ECG monitoring). His neurological deficits resolved within 24 h of treatment, with complete restoration of power and no clinically significant rebound hyperkalaemia. The associated ECG abnormalities also resolved within 24 h. In acute hypokalaemic paralysis, the clinical presentation, neurological features, and rapid response to potassium therapy are characteristic; however, the first presentation at 55 years of age and the associated systemic acidosis suggest that other causes of hypokalaemia (such as renal and gastrointestinal potassium losses and renal tubular disorders) should be carefully sought and excluded before a diagnosis of hypokalaemic periodic paralysis is established.

Conclusion: This case highlights that preserved deep tendon reflexes do not rule out severe hypokalaemic paralysis. Emergency and intensive-care clinicians should remain alert to possible hypokalaemic paralysis, examine the 12-lead ECG in patients with acute flaccid quadriparesis, and promptly measure venous serum electrolytes. This approach may reduce misdiagnosis and unnecessary invasive procedures while helping to prevent potentially fatal ventricular tachyarrhythmias.