Hypokalemic periodic paralysis: Difference between revisions

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==Background==
==Background==
*Autosomal dominant channelopathy<ref>June-Bum Kim, MD, PhD. Channelopathies. Korean J Pediatr. 2014 Jan;57(1):1-18 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935107/ Full Text]</ref>
*Autosomal dominant channelopathy<ref>June-Bum Kim, MD, PhD. Channelopathies. Korean J Pediatr. 2014 Jan;57(1):1-18 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935107/ Full Text]</ref>
*Acquired hypokalemia from barium poisoning, hyperthyroidism, renal disorders, and GI losses<ref>Ahlawat SK and Sachdev A. Hypokalemic paralysis. Postgrad Med J. 1999; 75(882):193-197.</ref>
*Acquired [[hypokalemia]] from barium poisoning, hyperthyroidism, renal disorders, and GI losses<ref>Ahlawat SK and Sachdev A. Hypokalemic paralysis. Postgrad Med J. 1999; 75(882):193-197.</ref>
*Most first attacks happen by age 16
*Most first attacks happen by age 16
*Young males, Asian
*Young males, Asian
*There is no decrease in total body potassium. Blood potassium level is normal between attacks.<ref>Mount DB, Zandi-Nejad K. Disorders of potassium balance. In Taal MW, Chertow GM, Marsden PA, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia, Pa: Elsevier Saunders; 2011:chap 17.</ref>
*There is no decrease in total body potassium. Blood potassium level is normal between attacks.<ref>Mount DB, Zandi-Nejad K. Disorders of potassium balance. In Taal MW, Chertow GM, Marsden PA, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia, Pa: Elsevier Saunders; 2011:chap 17.</ref>
*Associations
*Associations
**Thyrotoxicosis
**[[Thyrotoxicosis]] (thyrotoxicosis periodic paralysis)
**Steroids
**[[Steroids]]
**ETOH
**[[ETOH]]
**Renal disease
**Renal disease


==Clinical Features==
==Clinical Features==
===Symptoms===
===Symptoms===
*Muscle weakness or paralysis with associated hypokalemia (though potassium levels can be normal)
*Muscle [[weakness]] or paralysis with associated hypokalemia (though potassium levels can be normal)
*Sometimes painful though often painless
*Sometimes [[myalgia|painful]] though often painless
*Weakness can be from hand to leg to complete paralysis
*Weakness can be from hand to leg to complete paralysis
===History===
===History===
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{{Weakness DDX}}
{{Weakness DDX}}


==Diagnosis==
==Evaluation==
===Labs===
===Labs===
*Chemistry (potassium)
*Chemistry (potassium)
*Magnesium
*Thyroid function tests for first presentation


===EKG Findings===
===ECG Findings===
*Sinus bradycardia
*Sinus [[bradycardia]]
*Electrocardiographic (ECG) signs of hypokalemia may be present but not always diagnostic<ref>Hypokalemic Periodic Paralysis. Periodic Paralysis International. http://hkpp.org/physicians/hypokalemic_pp</ref>
*[[ECG]] signs of hypokalemia may be present but not always diagnostic<ref>Hypokalemic Periodic Paralysis. Periodic Paralysis International. http://hkpp.org/physicians/hypokalemic_pp</ref>
**U waves in leads II, V-2, V-3, and V-4
**U waves in leads II, V-2, V-3, and V-4
**Progressive flattening of T waves and depression of ST segment
**Progressive flattening of T waves and depression of ST segment
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==Management==
==Management==
*Replace potassium appropriately - do not try to correct to normal level as once the muscles release potassium you will likely overcorrect
*Replace potassium appropriately - do not try to correct to normal level as once the muscles release potassium you will likely overcorrect
*Consider magnesium
*Consider [[propranolol]] 3 mg/kg PO, expect to see rise in potassium within 2 hours<ref>Lin SH and Lin YF. Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis. Am J Kidney Dis. 2001 Mar;37(3):620-3.</ref>
**Only in hemodynamically stable patients without significant conduction block
**Beta blockers particularly helpful in thyrotoxicosis variant
*Long Term Treatment:  
*Long Term Treatment:  
**Should be initiated by primary physician but often includes eating a low carbohydrate diet and avoiding alcohol
**Should be initiated by primary physician but often includes eating a low carbohydrate diet and avoiding alcohol

Latest revision as of 05:27, 20 August 2022

Background

  • Autosomal dominant channelopathy[1]
  • Acquired hypokalemia from barium poisoning, hyperthyroidism, renal disorders, and GI losses[2]
  • Most first attacks happen by age 16
  • Young males, Asian
  • There is no decrease in total body potassium. Blood potassium level is normal between attacks.[3]
  • Associations

Clinical Features

Symptoms

  • Muscle weakness or paralysis with associated hypokalemia (though potassium levels can be normal)
  • Sometimes painful though often painless
  • Weakness can be from hand to leg to complete paralysis

History

  • Strenuous exercise
  • High carbohydrate meal
  • High sodium meals
  • Sudden changes in temperature
  • Emotional stress
  • Attacks can last several hours to several days

Physical Exam

  • Reflexes are decreased or absent[4]
  • Shoulders and hips, are involved more often than the arms and legs.[4]
  • There is flaccid paralysis rather than hypertonia
  • There should not be myoclonus or spasticity

Differential Diagnosis

Weakness

Evaluation

Labs

  • Chemistry (potassium)
  • Magnesium
  • Thyroid function tests for first presentation

ECG Findings

  • Sinus bradycardia
  • ECG signs of hypokalemia may be present but not always diagnostic[5]
    • U waves in leads II, V-2, V-3, and V-4
    • Progressive flattening of T waves and depression of ST segment
    • Prolongation of the PR and QT intervals

Management

  • Replace potassium appropriately - do not try to correct to normal level as once the muscles release potassium you will likely overcorrect
  • Consider magnesium
  • Consider propranolol 3 mg/kg PO, expect to see rise in potassium within 2 hours[6]
    • Only in hemodynamically stable patients without significant conduction block
    • Beta blockers particularly helpful in thyrotoxicosis variant
  • Long Term Treatment:
    • Should be initiated by primary physician but often includes eating a low carbohydrate diet and avoiding alcohol
    • Medications to increase potassium: Acetazolamide, Spironolactone, Potassium tablets

Disposition

  • Can be discharged from ED after potassium repletion and resolution of symptoms
  • Consider admission if patient remains symptomatic

See Also

References

  1. ↑ June-Bum Kim, MD, PhD. Channelopathies. Korean J Pediatr. 2014 Jan;57(1):1-18 Full Text
  2. ↑ Ahlawat SK and Sachdev A. Hypokalemic paralysis. Postgrad Med J. 1999; 75(882):193-197.
  3. ↑ Mount DB, Zandi-Nejad K. Disorders of potassium balance. In Taal MW, Chertow GM, Marsden PA, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia, Pa: Elsevier Saunders; 2011:chap 17.
  4. ↑ 4.0 4.1 Chinnery PF. Muscle diseases. In: Goldman L, Schafer AI, eds. Goldman’s Cecil Medicine. 24th ed. Philadelphia, Pa: Elsevier Saunders; 2011:chap 429.
  5. ↑ Hypokalemic Periodic Paralysis. Periodic Paralysis International. http://hkpp.org/physicians/hypokalemic_pp
  6. ↑ Lin SH and Lin YF. Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis. Am J Kidney Dis. 2001 Mar;37(3):620-3.
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