Prolonged neuromuscular block associated with cholinesterase deficiency.

RATIONALE: Hereditary genetic mutations may cause congenital cholinesterase deficiency. When succinylcholine and mivacurium are applied on cholinesterase-deficient patients during general anesthesia, prolonged postoperative asphyxia occurs, which is an uncommon but very serious complication. PATIENT CONCERNS: A previously healthy 30-year-old female presented prolonged spontaneous breathing recovery after general anesthesia. DIAGNOSES: After the patient's postoperative spontaneous breathing recovery delayed, the plasma cholinesterase was found to be 27 U/L, which was far below the normal level (4000 U/L to 13500 U/L). This patient had no disease that can cause plasma cholinesterase deficiency and was therefore diagnosed as congenital cholinesterase deficiency. INTERVENTIONS AND OUTCOMES: The patient was sent to the intensive care unit (ICU) intubated for mechanical ventilator support, and on the next day the tracheal tube was removed without any complications when her spontaneous respiration resumed. LESSONS: Cholinesterase is an enzyme secreted by the liver involved in many physiological processes in human body. Plasma cholinesterase commonly contains acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). When succinylcholine and mivacurium are applied on patients with cholinesterase-deficiency during general anesthesia, prolonged postoperative asphyxia occurs, which is an uncommon but very serious complication. Lately, new evidences have suggested that hereditary genetic mutations may be responsible for congenital cholinesterase deficiency.

[Hyperlactatemia in surgical ablation of atrial fibrillation and cardiac surgery. Is it a predictive factor of postoperative morbidity?]. / Hiperlactatemia en la ablación quirúrgica de la fibrilación auricular y cirugía cardiaca. ¿Es un factor predictivo de morbimortalidad posoperatoria?

INTRODUCTION: Increased serum lactate in postoperative cardiac surgery is very common and its pathogenesis is due to multiple factors. The elevation of serum lactate is associated with tissue hypoxia (hyperlactatemia type A) and non-hypoxic (hyperlactatemia type B) metabolic disorders. The aim of the study was to assess the evolution of postoperative lactate in surgical atrial fibrillation ablation during cardiac surgery, and to determine whether lactate levels could be predictors of morbimortality. MATERIAL AND METHODS: A case-control study was conducted on 32 patients undergoing surgical atrial fibrillation ablation and cardiac surgery (Maze group) and 32 matched patients (Control group), operated on between 2011 and 2012. An analysis was made of the levels of postoperative lactate, perioperative morbimortality and hospital length of stay. A univariate and multivariate study was performed for a composite endpoint of morbimortality, and prolonged length of stay. RESULTS: Lactate levels were significantly higher at 6, 12 and 24h in the Maze group. The univariate analysis showed that being in the Maze group (OR 3.88; 95% CI 1.3-11.1; P=.01) and an elevated lactate at 12h (OR 1.33; 95% CI 1.01-1.7; P=.04) were significant predictors of major complications, mortality, and longer hospital stays. In the multivariate analysis, surgical atrial fibrillation ablation (Maze group) was an independent predictor of major complications (OR 4.13; 95% CI 1.312.9; P=.015) for the morbimortality composite endpoint (OR 3.9; 95% CI 1.3-11.6; P=.01), and prolonged length of stay in the Intensive Care Unit (OR 5.7; 95% CI 2.01-15.7; P=.01). CONCLUSIONS: The atrial fibrillation surgical ablation may be a not-yet-described cause of type B hyperlactatemia, with serum peak values being reached between 4-24h after cardiac surgery. The predictive value of this elevation, its correlation with morbimortality, its sensitivity and specificity to discriminate the significant thresholds needs to be defined.