Angiotensin converting enzyme inhibitor induced hyperkalaemic paralysis

Dutta, Dibyendu; Fischler, Manuel; McClung, A

doi:10.1136/pmj.77.904.114

Cited by 19 publications

(7 citation statements)

References 11 publications

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“…5 One case report described hyperkalemiainduced paralysis in a 78-year-old man that was presumably due to enalapril. 6 Consistent with these reports, our patient was experiencing renal insufficiency and receiving an angiotensinconverting enzyme inhibitor (lisinopril) and a nonsteroidal antiinflammatory drug (naproxen). In the case reports, potassium levels ranged from 8.1-9.2 mEq/L.…”

Section: Discussionsupporting

confidence: 82%

Hyperkalemia‐Induced Paralysis

et al. 2009

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Hyperkalemia is an electrolyte abnormality that can lead to severe consequences. Paralysis induced by hyperkalemia has been described in only a few reports. We describe a 60-year-old man who experienced paralysis presumably due to hyperkalemia. He presented to the emergency department with severe weakness in all extremities. The patient's serum potassium concentration was greater than 8 mEq/L and his serum creatinine concentration was 7 mg/dl. Findings on electrocardiography were abnormal. Of note, his drug therapy included lisinopril and naproxen. After treatment for hyperkalemia, the patient's symptoms resolved; however, he was admitted for further workup for renal failure. The patient was discharged after approximately 1 week with a diagnosis of end-stage renal disease. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 5) between the patient's paralysis and hyperkalemia. Although hyperkalemia as a cause of paralysis is extremely rare, clinicians should be aware of this potentially life-threatening, noncardiac toxicity.

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Section: Discussionsupporting

confidence: 82%

Hyperkalemia‐Induced Paralysis

et al. 2009

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“…The weakness has been attributed to abnormalities at numerous locations in the motor axis, including the muscle, nerve, and neuromuscular junction. 3,14 However, the mechanism of secondary hyperkalemic paralysis could be similar to that of primary hyperkalemic periodic paralysis, which results from a primary sodium channelopathy in muscle. 4 One possible hypothesis is that the increase in plasma potassium concentration reduces the ratio of intracellular potassium concentration to that of the extracellular fluid, resulting in a persistent relative depolarization in the nerve membrane.…”

Section: Hyperkalemia Is a Cause Of Acute Flaccid Paralysis In Patienmentioning

confidence: 99%

Acute Quadriplegia From Hyperkalemia

et al. 2010

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“…While primary hyperkalemic paralysis is secondary to a defective sodium channel, a number of aetiologies have been reported as leading to secondary hyperkalemic paralysis. The primary aetiology could be one of renal failure [ 1 ], Addison's disease [ 2 , 3 ], potassium sparing diuretics [ 4 ], potassium supplements, and dietary excess [ 5 ]. Coconut water, when consumed in excess, has been reported to cause severe hyperkalemia [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Acute Ascending Flaccid Paralysis Secondary to Multiple Trigger Factor Induced Hyperkalemia

Hemachandra

Dayasiri

Kannangara

2018

Case Reports in Neurological Medicine

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Background Acute flaccid paralysis is an uncommon, but potentially life threatening, sequel of severe hyperkalemia. Reported primary aetiologies include renal failure, Addison's disease, potassium sparing diuretics, potassium supplements, and dietary excess. Coconut water, when consumed in excess, has been reported to cause severe hyperkalemia. We report the case of acute ascending flaccid paralysis secondary to hyperkalemia induced by multiple trigger factors—king coconut water, renal failure, diabetes, metabolic acidosis, and potassium sparing diuretics. Case Presentation A 78-year-old man presented with acute ascending type flaccid paralysis over five-hour duration and subsequently developed preterminal cardiac arrhythmias secondary to severe hyperkalemia (serum potassium: 7.02 mEq/L). He was on Losartan and Spironolactone for ischemic heart disease. Dietary history revealed excessive intake of king coconut water (Cocos nucifera) over past one week. Electrocardiogram returned to normal rhythm and serum potassium was 6.1 mEq/L within 2 hours of institution of emergency management for life threatening hyperkalemia. Neurological symptoms completely recovered within twenty-four hours without the need for dialysis. Electromyogram three days after the initial presentation revealed normal findings. Conclusions The report describes a rare case of secondary hyperkalemic flaccid paralysis induced by multiple trigger factors. It is important that patients with risk factors for hyperkalemia are educated regarding avoiding excess dietary potassium. Regular follow-up of these patients is mandatory with review of medication related side effects and serum electrolytes.

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Angiotensin converting enzyme inhibitor induced hyperkalaemic paralysis

Cited by 19 publications

References 11 publications

Hyperkalemia‐Induced Paralysis

Hyperkalemia‐Induced Paralysis

Acute Quadriplegia From Hyperkalemia

Acute Ascending Flaccid Paralysis Secondary to Multiple Trigger Factor Induced Hyperkalemia

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