Hyperkalemic quadriplegia – Secondary to diabetic ketoacidosis

INTRODUCTION

Patients with DKA present with a wide spectrum of symptoms, but flaccid quadriplegia (FQ) is not commonly seen.^[1] This is due to hyperkalemia caused by acidosis and is therefore termed secondary hyperkalemic paralysis (SHP).

CASE REPORT

A 51-year-old male with uncontrolled type 2 diabetes and chronic kidney disease on regular hemodialysis as co-morbidities presented to the emergency department with complaints of the sudden onset of symmetrical weakness in bilateral upper and lower limbs for 1 day. There is no history relevant to cervical spine injury, unknown (snake) bite, myasthenia gravis, or recent fever (to rule-out [r/o] Guillain–Barré syndrome [GBS]). Initially, he presented to an outside hospital, where stroke was suspected and brain imaging was done, which turned out to be normal. Hence, he was referred to our institute for further evaluation. On arrival, the patient was conscious and oriented. Vitals on presentation were pulse rate 66/min, blood pressure 120/80 mmHg, SpO₂ 96% on room air, and Glasgow Coma Scale 15/15. Examination revealed hypotonia in all four limbs with power of 0/5 and absent tendon reflexes. All cranial nerve functions were inta ct. The initial electrocardiogram (ECG) revealed severe hyperkalemic changes, including flattening of the P wave, widening of the QRS complex, and tall, peaked T waves [Figure 1]. Initial blood gas results suggested severe, uncompensated metabolic acidosis (pH 6.84) with high blood sugar levels (>500) and a potassium level of 8.3 mmol/L [Table 1]. Urine ketones turned out to be positive (3+). Diagnosis of diabetic ketoacidosis with secondary hyperkalemic paralysis (SHP) was made. Treatment was initiated with intravenous normal saline, calcium gluconate, insulin infusion, salbutamol nebulization, and sodium bicarbonate.^[2]

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Figure 1:

Initial electrocardiogram with severe hyperkalemic changes – flattening of P wave, widening of QRS complex, tall peaked T waves.

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Consequent blood gas analysis revealed a decline in K+ levels to 4.4 mmol/L [Table 1], with corresponding resolution of the ECG changes [Figure 2]. Muscle power also gradually improved with complete resolution within a few hours of initiating treatment.

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Figure 2:

Post-treatment electrocardiogram showing resolution of hyperkalemic changes.

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DISCUSSION

Common presentations of diabetic ketoacidosis^[3] include dehydration, polyuria, vomiting, abdominal pain, Kussmaul breathing, bradycardia/tachycardia, and altered sensorium . Primary hyperkalemic paralysis is a congenital, autosomal dominant disorder caused by a mutation in the SCN4a gene^[4], leading to an increased influx of Na⁺ (sodium ion) into cells^[5], initially described in horses. Reported causes^[6] of SHP include renal failure,^[7] Addison’s disease,^[8] and drugs (angiotensin-converting enzyme^[9]/angiotensin receptor blockers inhibitors, spironolactone, and digitalis).^[10] The pathophysiology of SHP is still unclear.

Emergency management of both primary and SHP remains the same. Insulin infusion, sodium bicarbonate, and beta-2 agonists enhance the intracellular shift of potassium. Calcium acts as a cardiac membrane stabilizer, thus preventing arrhythmias. This case report emphasizes the importance of bedside ECG as an initial investigation for patients with risk factors of hyperkalemia presenting with paralysis. GBS,^[11] spinal lesions, hypokalemia, and toxins are common differentials of acute flaccid quadriplegia (AFQ), and these require time-consuming investigations.

Hyperkalemic paralysis can rapidly progress to involve the respiratory muscles^[12] and lead to respiratory arrest. Hence, knowledge about SHP plays a vital role in early intervention and in avoiding treatment delays for obtaining neuro-imaging, to rule out other causes of AFQ.

CONCLUSION

Acute flaccid paralysis is a very dangerous presentation of hyperkalemia, and when respiratory muscles are involved, it can lead to respiratory acidosis (potentially aggravating the effect of metabolic acidosis if present) and also respiratory arrest if untreated. Consider SHP in high-risk patients like chronic kidney disease, certain drugs (mentioned previously), and DKA.