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Challenges in the management of an obstetric patient with familial periodic paralysis-when the story does not match the clinical picture
Abstract Number: SUN-33
Abstract Type: Case Report/Case Series
Periodic paralysis (PP) is a set of genetic conditions characterized by episodes of muscle weakness and potential paralysis in the setting of various triggers. Two subclasses can be distinguished by the serum potassium (K) levels during these attacks: hypokalemic (hypok) PP (estimated prevalence of 1:100,000) and hyperkalemic (hyperk) PP (prevalence of around 1:200,000).
A 36 YO G1P000 was admitted at 39 weeks for scheduled C-section for breech presentation. She stated she has a history of hypokalemic familial PP. She reported daily episodes of upper (UE) and lower extremity (LE) weakness, often resolving with PO intake such as juice or bananas. Once or twice a year she would experience severe paralysis often related to episodes of a respiratory or GI illness. She was prescribed acetazolamide for more severe episodes. On the day of admission she was appropriately NPO, labs were notable for K of 4.6 mmol/L. She had no neurological deficit, strength 5/5 in UEs and LEs.
The patient received a standard spinal (L3-L4 level,1.2 mg hyperbaric bupivacaine +15 mcg fentanyl +100 mcg hydromorphone). T4 sensory level was confirmed. Intra-op she reported feeling weakness in her UEs, and the exam revealed 4+/5 strength in both proximal and distal UEs muscles. As spinal anesthesia was a confounding factor and the patient was stable, labs were sent without starting K supplementation. One hour post-op the patient reported worsening weakness in her UEs and LEs. K came back at 5.5 mmol/L. The exam revealed 3/5 strength in UEs and 2/5 in her LEs, with the weakness more evident in proximal muscle groups. 5 hours post-op her exam showed mildly improved strength and repeat labs revealed a K of 3.8 mmol/L. Per Neurology’s recommendations the patient received acetazolamide 125 mg PO X1.
Upon reviewing her symptoms, labs, and family history, the anesthesia team felt that the patient likely has the hyperk rather than hypok form of PP. The combination of NPO status, peri-operative hypothermia, and the stress of delivery led to symptoms. Our suspicion was shared with the patient during her episode and was confirmed on POD 1 after the she contacted another family member with the condition who stated they indeed have the hyperk form.
Of note, acetazolamide has been reported as treatment in both hypo and hyperkalemic PP.
On POD 1 she was tolerating POs and reported increased strength. She had 5/5 strength in her LEs and 4+/5 in UEs. K was 3.4 mmol/L. She had an otherwise uneventful post-operative course leading to discharge on POD 4.
In conclusion, we report a case of obstetric anesthetic management in a patient with hyperkalemic PP, although she reported a history of hypokalemic PP. A thorough history and knowledge of the subtle differences in these two subtypes, as well as vigilant monitoring of symptoms and electrolytes lead us to avoid unnecessary and potentially dangerous K supplementation, establish the diagnosis and redirect treatment