[Anesthetic Management of Three Patients with Chronic Inflammatory Demyelinating Polyradiculoneuropathy].

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a chronically progressing or relapsing disease caused by immune-mediated peripheral neuropathy. We report the anesthetic management of three CIDP patients who underwent elective orthopedic surgeries. Owing to the risk of neuraxial anesthetics triggering demyelination, general anesthesia was selected to avoid epidural or spinal anesthesia or other neuraxial blockade. It was also judged prudent to avoid prolonged perioperative immobilization, which might compress vulnerable peripheral nerves. For Patient 1, general anesthesia was induced with propofol, remifentanil, and sevoflurane, and was maintained with sevoflurane and remifentanil. For Patients 2 and 3, general anesthesia was induced and maintained with propofol and remifentanil. For tracheal intubation, under careful monitoring with peripheral nerve stimulators, minimal doses of rocuronium (0.6-0.7 mg x kg(-1)) were administered. When sugammadex was administered to reverse the effect of rocuronium, all patients rapidly regained muscular strength. Postoperative courses were satisfactory without sequelae.

[Successful management of a patient with rhabdomyolysis and marked elevation of serum creatine kinase level].

We experienced successful management of a patient with severe rhabdomyolysis by conservative treatment. A 41-year-old man developed Stanford-A-type acute aortic dissection and underwent an emergent replacement of the aortic root and arch. After the weaning from cardiopulmonary bypass, his left femoral artery was found non-pulsatile, probably due to extension of the aortic dissection, and femoro-femoral artery bypass surgery was added. Estimated ischemia time of the lower extremities was 7 hours. On admission to the intensive care unit (ICU), his left lower extremity showed signs of reperfusion injury accompanied with marked elevation of serum creatine kinase (12,397 IU x l(-1)) and myoglobin (19,980 ng x ml(-1)), and impaired oxygenation (a ratio of PaO2 to FIO2, 130 mmHg). We performed (1) moderately aggressive infusion treatment, (2) maintenance of hyperdynamic states using catecholamine, (3) diuresis therapy using atrial natriuretic peptide and furosemide, and (4) lung protective strategy. Although serum creatinine increased to 2.0 mg x dl(-1) on postoperative day (POD) 1, diuresis was maintained and the level of creatinine returned to normal on POD 6. He was extubated on POD 6 and discharged on POD 7. The early start of these combined therapies seems to have prevented acute renal failure without blood purification.

[Exhaled tidal volume is overestimated due to cardiogenic oscillation: effects of ventilator and mode].

BACKGROUND: We investigated effects of cardiogenic oscillation on overestimation of tidal volume using a lung model, with three ventilators and two ventilatory modes. METHODS: We simulated cardiogenic oscillation at a rate of 90 breaths x min(-1) by ventilating one bellow of a two-bellow-type lung model. The magnitude of cardiogenic oscillation was defined as peak expiratory flow fluctuation when the airway was opened to the atmosphere. The lung model was mechanically ventilated with three ventilators (Bird 8400 STi, Servo-300, and Nellcor Puritan-Bennett 840), two ventilatory modes (volume- and pressure-controlled ventilation), and two respiratory rates (5 and 10 breaths x min(-1)) in random order. We recorded tidal volume on a ventilator monitor and calculated the discrepancy from the set tidal volume. RESULTS: With Bird 8400 STi, monitored tidal volume exceeded set tidal volume, regardless of volume- or pressure-controlled ventilation. The overestimation in tidal volume was larger with smaller respiratory rate and with larger cardiogenic oscillation. In contrast, with the other ventilators, the discrepancy was small. CONCLUSIONS: Exhaled tidal volume is overestimated during mechanical ventilation when cardiogenic oscillation is large.

[Intensive care management of acute pulmonary thromboembolism].

Three patients with acute pulmonary thromboembolism, who had fallen into cardiopulmonary arrest or severe respiratory failure, were treated and saved in our intensive care unit. Two patients were resuscitated with percutaneous cardiopulmonary support device. Two patients underwent surgical embolectomy and we carefully applied positive pressure ventilation to prevent postoperative reperfusion pulmonary edema. Early diagnosis and treatment are essential for saving critically ill patients with acute pulmonary embolism. However, cardiopulmonary resuscitation is often difficult and unsuccessful. Therefore prophylaxis is strongly recommended especially in patients with known risk factors of venous thrombosis. Since reperfusion pulmonary edema is a serious complication after surgical pulmonary embolectomy, careful postoperative respiratory care is needed.