Chloride: 112 mEq\/L<\/p>\n
Creatinine: 1.6 mg\/dL<\/strong><\/p>\n ECG: sinus Bradycardia With PR: 55, U waves in V2-V6<\/p>\n A \u2013 Allergies<\/p>\n No known drug allergies<\/p>\n No known food allergies<\/p>\n M \u2013 Medications<\/p>\n Not on any regular medications<\/p>\n No history of recent medication intake<\/p>\n P \u2013 Past Medical History<\/p>\n History of cerebrovascular accident (CVA) 2 years ago<\/p>\n Previous medical records not available<\/p>\n Not on antiplatelets or any long-term treatment<\/p>\n No other known comorbidities<\/p>\n L \u2013 Last Meal<\/p>\n Last meal consumed approximately 2 hours prior to presentation<\/p>\n E \u2013 Events Leading to Presentation<\/p>\n Sudden onset left upper limb weakness associated with reduced grip strength since 8:00 AM on the day of presentation<\/p>\n The patient was admitted to the Intensive Care Unit for close monitoring and aggressive electrolyte correction. Given the severity of hypokalemia (serum potassium 1.4 mmol\/L) and associated electrocardiographic changes, continuous cardiac monitoring was instituted. A cumulative dose of 200 mEq of intravenous potassium chloride was administered over the first 24 hours, along with magnesium supplementation and serial electrolyte monitoring. The patient demonstrated progressive improvement in muscle strength with correction of serum potassium levels. Further evaluation revealed hyperchloremic normal anion gap metabolic acidosis consistent with distal renal tubular acidosis (Type 1 RTA). Autoimmune workup showed positive antinuclear antibody (ANA) positivity, and subsequent evaluation led to a diagnosis of Sj\u00f6gren\u2019s syndrome, which was considered the underlying cause of distal RTA. The patient\u2019s neurological deficits resolved completely, and he became symptomatically better by the second day of hospitalization. He was subsequently shifted to the ward and discharged in a stable condition with oral potassium supplementation and sodium bicarbonate (Tab Nodosis), with advice for nephrology and rheumatology follow-up.<\/p>\n Acute unilateral limb weakness is a time-sensitive presentation in the Emergency Department, with acute ischemic stroke often being the foremost consideration. However, a small but clinically significant proportion of patients presenting with focal neurological deficits are ultimately diagnosed with stroke mimics. Among these, hypokalemic periodic paralysis (HPP) remains an uncommon but completely reversible condition when recognized early. The present case highlights the diagnostic challenge posed by severe hypokalemia presenting as isolated left upper limb weakness, closely resembling an acute cerebrovascular event.<\/p>\n Hypokalemic periodic paralysis is characterized by episodic muscle weakness resulting from severe potassium depletion or intracellular potassium shifts. Classically, patients present with symmetrical proximal muscle weakness involving the lower limbs, with progression to quadriparesis in severe cases. Isolated unilateral limb weakness is rare and can create significant diagnostic uncertainty, particularly in patients with a previous history of stroke. In our patient, the sudden onset of left upper limb weakness and reduced hand grip strength initially raised concern for an acute neurological event. However, the absence of cortical signs, preserved higher mental functions, normal cranial nerve examination, intact reflexes, and lack of upper motor neuron findings prompted consideration of alternative diagnoses.<\/p>\n This case underscores the pivotal role of Emergency Medicine in rapidly differentiating true cerebrovascular events from reversible metabolic causes. While stroke pathways appropriately prioritize rapid neuroimaging and reperfusion decisions, simultaneous bedside evaluation remains crucial. In the present case, early ECG interpretation and point-of-care blood gas analysis proved invaluable. The presence of sinus bradycardia, right bundle branch block, and prominent U waves in leads V2\u2013V6, together with a serum potassium level of 1.4 mmol\/L, immediately redirected attention towards severe hypokalemia as the likely etiology of the neurological deficit.<\/p>\n A serum potassium concentration of 1.4 mmol\/L represents profound potassium depletion and constitutes a medical emergency. Such severe hypokalemia is associated with potentially fatal cardiac arrhythmias, respiratory muscle weakness, rhabdomyolysis, and cardiac arrest. Importantly, the severity of clinical manifestations often reflects the total body potassium deficit rather than the serum potassium value alone. Consequently, serum potassium concentrations may underestimate the magnitude of potassium depletion, particularly in patients with ongoing renal losses.<\/p>\n Recognition of this life-threatening electrolyte abnormality in the Emergency Department facilitated immediate initiation of potassium replacement therapy. The patient initially received intravenous potassium chloride and magnesium supplementation in the ED, followed by admission to the Intensive Care Unit for continuous cardiac monitoring and serial electrolyte assessment. A cumulative dose of 200 mEq of potassium chloride was required during the first 24 hours, highlighting the extent of total body potassium deficit. Current recommendations suggest that intravenous potassium replacement may be administered at rates of up to 20 mEq\/hour under continuous cardiac monitoring, preferably through central venous access, with appropriate dilution protocols. Adherence to these principles allowed safe and effective correction of hypokalemia in our patient, resulting in rapid neurological recovery and avoidance of potentially catastrophic cardiac complications.<\/p>\n An equally important aspect of this case was the identification of the underlying cause of potassium depletion. The presence of hyperchloremic normal anion gap metabolic acidosis suggested an underlying renal tubular disorder rather than isolated intracellular potassium shifting. Subsequent nephrological evaluation confirmed distal renal tubular acidosis (Type 1 RTA), a condition characterized by impaired hydrogen ion secretion in the distal nephron, resulting in chronic metabolic acidosis and renal potassium wasting. Distal RTA is a recognized but often underdiagnosed cause of recurrent hypokalemic paralysis and should be actively considered in patients presenting with severe hypokalemia and metabolic acidosis.<\/p>\n Further autoimmune workup revealed ANA positivity, and the patient was subsequently diagnosed with Sj\u00f6gren\u2019s syndrome. Renal involvement is a well-recognized extraglandular manifestation of Sj\u00f6gren\u2019s syndrome, with distal renal tubular acidosis representing one of its most common renal complications. Interestingly, hypokalemic paralysis may precede the development of classical sicca symptoms and may be the first clinical manifestation leading to diagnosis. In the present case, the episode of paralysis served as the initial clue to an underlying autoimmune disorder that might otherwise have remained undiagnosed for a prolonged period.<\/p>\n From an Emergency Medicine perspective, this case illustrates the importance of maintaining a broad differential diagnosis when evaluating acute neurological presentations. While rapid identification of stroke remains a priority, clinicians must remain vigilant for reversible stroke mimics, particularly electrolyte disturbances that can be rapidly identified and treated. The diagnosis in this patient was not established by a single investigation but rather through a systematic emergency approach integrating focused neurological examination, ECG interpretation, point-of-care testing, and multidisciplinary collaboration with neurology and nephrology teams.<\/p>\n Ultimately, this case represents more than a rare presentation of hypokalemic paralysis. It demonstrates how a seemingly straightforward stroke presentation can uncover severe electrolyte derangement, distal renal tubular acidosis, and previously undiagnosed Sj\u00f6gren\u2019s syndrome. Early recognition in the Emergency Department, prompt initiation of potassium replacement, adherence to safe correction protocols, and investigation of the underlying etiology resulted in complete neurological recovery and prevention of future recurrences. Awareness of such atypical presentations is essential for emergency physicians, as timely diagnosis can transform a potentially fatal condition into a completely reversible one.<\/p>\n Hypokalemic periodic paralysis is a rare but important reversible stroke mimic that may present with acute unilateral limb weakness. Early recognition of severe hypokalemia through careful clinical assessment, ECG interpretation, and point-of-care testing is crucial for timely diagnosis and management. In our patient, prompt potassium replacement resulted in complete neurological recovery, while further evaluation revealed distal renal tubular acidosis secondary to Sj\u00f6gren\u2019s syndrome as the underlying cause. This case highlights the importance of considering metabolic causes in patients presenting with focal neurological deficits and demonstrates the pivotal role of the Emergency Department in identifying and managing potentially life-threatening yet reversible conditions.<\/p>\n Koul PA, et al. Hypokalemic paralysis as a stroke mimic. Ann Indian Acad Neurol. 2013.<\/p>\n Dr. Avinash SSecondary Survey<\/h2>\n
Initial management in ED<\/h2>\n
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Discussion<\/h2>\n
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\nDepartment of Emergency Medicine,
\nKauvery Hospital, Chennai.<\/a><\/b><\/p>\n<\/div>\n<\/div>\n
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