Electrolyte Abnormalities Causing Flaccid Quadriparesis
The primary electrolyte abnormalities that cause flaccid quadriparesis are hyperkalemia and hypokalemia, with hyperkalemia being particularly dangerous as it can rapidly progress to cardiac arrest. 1
Hyperkalemia
Severe hyperkalemia (>6.5 mmol/L) is a life-threatening cause of flaccid quadriparesis that requires immediate recognition and treatment. 1
Clinical Presentation
- Flaccid paralysis is a cardinal manifestation of severe hyperkalemia, often accompanied by paresthesias of the extremities, depressed deep tendon reflexes, and respiratory difficulties. 1
- The first clinical indicator may be ECG changes showing peaked T waves, which can progress to flattened P waves, prolonged PR interval, widened QRS complex, and ultimately sine-wave pattern leading to cardiac arrest. 1
- Hyperkalemia most commonly occurs from renal failure or release of potassium from cells. 1
Management Priority
For cardiac arrest or severe cardiotoxicity from hyperkalemia, IV calcium must be administered immediately in addition to standard ACLS care. 1
The treatment sequence is:
- Stabilize myocardial membrane: Calcium chloride 10% (5-10 mL IV over 2-5 minutes) or calcium gluconate 10% (15-30 mL IV over 2-5 minutes) 1
- Shift potassium into cells: Sodium bicarbonate 50 mEq IV over 5 minutes, glucose (25g) plus insulin (10 U regular) IV over 15-30 minutes, or nebulized albuterol 10-20 mg over 15 minutes 1
- Promote excretion: Furosemide 40-80 mg IV, Kayexalate 15-50g, or dialysis 1
Critical Pitfall
IV bolus administration of potassium for cardiac arrest in suspected hypokalemia is NOT recommended as it can be harmful. 1
Hypokalemia
Severe hypokalemia causes flaccid quadriparesis through altered cardiac and skeletal muscle excitability. 2, 3, 4, 5
Clinical Features
- Potassium depletion manifests as weakness, fatigue, cardiac rhythm disturbances, prominent U-waves on ECG, and in advanced cases, flaccid paralysis and impaired ability to concentrate urine. 2
- Hypokalemia typically occurs with diuretic therapy, hyperaldosteronism, diabetic ketoacidosis, severe diarrhea with vomiting, or inadequate replacement during parenteral nutrition. 2
- The intoxication signs from potassium phosphate include paresthesias of extremities, flaccid paralysis, listlessness, mental confusion, weakness and heaviness of legs, and cardiac arrhythmias. 3
Associated Conditions
- Thyrotoxic periodic paralysis can present with rapid onset flaccid quadriparesis associated with severe hypokalemia (as low as 1.5 mmol/L) and hypophosphatemia. 4
- Distal renal tubular acidosis (dRTA), particularly associated with primary Sjögren's syndrome, causes recurrent hypokalemia leading to flaccid quadriparesis in fewer than 2% of Sjögren's cases. 5, 6
Management Approach
- Correct the underlying cause (e.g., discontinue diuretics, treat diarrhea). 2
- Replace potassium with high-potassium foods or potassium chloride supplements when metabolic alkalosis is present. 2
- In metabolic acidosis with hyperchloremia (e.g., renal tubular acidosis), use potassium salts other than chloride such as potassium bicarbonate, citrate, acetate, or gluconate. 2
Hypophosphatemia
Severe hypophosphatemia (<0.32 mmol/L) contributes to respiratory failure and prolonged mechanical ventilation but is less commonly a direct cause of quadriparesis compared to potassium abnormalities. 1
- Hypophosphatemia occurs in 60-80% of ICU patients, particularly with intensive kidney replacement therapy and refeeding syndrome. 1
- Associated with worsening respiratory failure, cardiac arrhythmias, and prolonged hospitalization. 1
Hypomagnesemia
Hypomagnesemia (<0.70 mmol/L) prolongs the QT interval and can lead to ventricular arrhythmias but typically does not cause isolated flaccid quadriparesis. 1
- Occurs in up to 60-65% of critically ill patients, particularly with kidney replacement therapy using citrate anticoagulation. 1
- For cardiac arrest from severe hypomagnesemia, IV magnesium is recommended in addition to standard ACLS care. 1
Key Monitoring Recommendations
Electrolytes must be closely monitored in hospitalized patients with kidney disease receiving kidney replacement therapy, as electrolyte abnormalities occur in up to 65% of critically ill patients. 1