Perioperative Management of a Patient with Hypokalemic Periodic Paralysis: A Case Report

Potassium imbalances can be life-threatening and must be identified and corrected prior to surgery. Patients with hypokalemic periodic paralysis (hypoKPP) experience recurrent muscle weakness or paralysis due to hypokalemia. We present the management of a rare case of hypoKPP during surgery and discuss the general complications and perioperative management of the condition. A 70-year-old man with hypoKPP visited the emergency room with abdominal pain requiring a cholecystectomy. He had not experienced hypoKPP since 1993, 1 year after diagnosis. Preoperative examinations were normal, with a serum potassium level of 4.5 mEq/L. Surgery and recovery were uneventful, with potassium levels ≥ 3.3 mEq/L. The post-surgery serum potassium level was 4.3 mEq/L. The patient had no signs of hypokalemia until 1-week post-surgery. Thorough preoperative preparation, careful assessment of serum potassium levels, avoidance of triggering factors, and appropriate postoperative pain relief can help prevent a hypokalemic attack in patients with hypoKPP.

Perioperative Management of a Patient with Hypokalemic Periodic Paralysis: A Case Report

Potassium imbalances can be life-threatening and must be identified and corrected prior to surgery. Patients with hypokalemic periodic paralysis (hypoKPP) experience recurrent muscle weakness or paralysis due to hypokalemia. We present the management of a rare case of hypoKPP during surgery and discuss the general complications and perioperative management of the condition. A 70-year-old man with hypoKPP visited the emergency room with abdominal pain requiring a cholecystectomy. He had not experienced hypoKPP since 1993, 1 year after diagnosis. Preoperative examinations were normal, with a serum potassium level of 4.5 mEq/L. Surgery and recovery were uneventful, with potassium levels ≥ 3.3 mEq/L. The post-surgery serum potassium level was 4.3 mEq/L. The patient had no signs of hypokalemia until 1-week post-surgery. Thorough preoperative preparation, careful assessment of serum potassium levels, avoidance of triggering factors, and appropriate postoperative pain relief can help prevent a hypokalemic attack in patients with hypoKPP.

Bupivacaine-induced Vasodilation Is Mediated by Decreased Calcium Sensitization in Isolated Endothelium-denuded Rat Aortas Precontracted with Phenylephrine

BACKGROUND: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endotheliumdenuded rat aortas precontracted with phenylephrine. METHODS: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ([Ca2+]i) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. RESULTS: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100 mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced [Ca2+]i decrease in the aortas precontracted with phenylephrine. CONCLUSIONS: Taken together, these results suggest that toxic-dose bupivacaine-induced vasodilation appears to be mediated by decreased calcium sensitization in endothelium-denuded aortas precontracted with phenylephrine. In addition, potassium channel inhibitors had no effect on bupivacaine-induced relaxation. Toxic-dose bupivacaine- induced vasodilation may be partially associated with the inhibitory effect of voltage-operated calcium channels.

Dexmedetomidine-induced contraction of isolated rat aorta is dependent on extracellular calcium concentration / 대한마취과학회지

BACKGROUND: Dexmedetomidine is a highly selective alpha2-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine induces transient hypertension due to vasoconstriction via the activation of the alpha2-adrenoceptor on vascular smooth muscle. The goal of this in vitro study is to investigate the calcium-dependent mechanism underlying dexmedetomidine-induced contraction of isolated endothelium-denuded rat aorta. METHODS: Isolated endothelium-denuded rat thoracic aortic rings were suspended for isometric tension recording. Cumulative dexmedetomidine concentration-response curves were generated in the presence or absence of the following inhibitors: alpha2-adrenoceptor inhibitor rauwolscine; voltage-operated calcium channel blocker verapamil (5 x 10(-7), 10(-6) and 5 x 10(-5) M); purported inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenylborate (5 x 10(-6), 10(-5) and 5 x 10(-5) M); phospholipase C inhibitor U-73122 (10(-6) and 3 x 10(-6) M); and store-operated calcium channel inhibitor gadolinium chloride hexahydrate (Gd3+; 5 x 10(-6) M). Dexmedetomidine concentration-response curves were also generated in low calcium concentrations (1 mM) and calcium-free Krebs solution. RESULTS: Rauwolscine, verapamil, and 2-aminoethoxydiphenylborate attenuated dexmedetomidine-induced contraction in a concentration-dependent manner. Low calcium concentrations attenuated dexmedetomidine-induced contraction, and calcium-free Krebs solution nearly abolished dexmedetomidine-induced contraction. However, U-73122 and Gd3+ had no effect on dexmedetomidine-induced contraction. CONCLUSIONS: Taken together, these results suggest that dexmedetomidine-induced contraction is primarily dependent on extracellular calcium concentrations that contribute to calcium influx via voltage-operated calcium channels of isolated rat aortic smooth muscle. Dexmedetomidine-induced contraction is mediated by alpha2-adrenoceptor stimulation. Dexmedetomidine-induced contraction appears to be partially mediated by calcium release from the sarcoplasmic reticulum.