Excessive dynamic airway collapse during general anesthesia: a case report.

BACKGROUND: Excessive dynamic airway collapse (EDAC) is an uncommon cause of high airway pressure during mechanical ventilation. However, EDAC is not widely recognized by anesthesiologists, and therefore, it is often misdiagnosed as asthma. CASE PRESENTATION: A 70-year-old woman with a history of asthma received anesthesia with sevoflurane for a laparotomic cholecystectomy. Under general anesthesia, she developed wheezing, high inspiratory pressure, and a shark-fin waveform on capnography, which was interpreted as an asthma attack. However, treatment with a bronchodilator was ineffective. Bronchoscopy revealed the collapse of the trachea and main bronchi upon expiration. We reviewed the preoperative computed tomography scan and saw bulging of the posterior membrane into the airway lumen, leading to a diagnosis of EDAC. CONCLUSIONS: Although both EDAC and bronchospasm present as similar symptoms, the treatments are different. Bronchoscopy proved useful for distinguishing between these two entities. Positive end-expiratory pressure should be applied and bronchodilators avoided in EDAC.

[Case of electrocardiogram showing ST depression after nonionic contrast media (iopromide) administration].

A 77-year-old man with coronary artery stenosis underwent the left limb artery bypass grafting. When the contrast media was administered on intraoperative limb reperfusion after revascularization, electrocardiogram showed ST depression without skin symptoms and blood pressure decline. The change was not in the right coronary artery area (99% stenosis), but in the left coronary artery area (50% stenosis). The nonionic contrast media may elicit coronary artery vasoconstriction, although there are few side effects including anaphylactic in comparison with the ionic contrast media. In administration of the nonionic contrast media to the patient with coronary artery stenosis (50% or more), it is important to examine electrocardiogram, and is advisable to administer coronary artery dilating drug before-hand.

Tight glycemic control by insulin, started in the preischemic, but not postischemic, period, protects against ischemic spinal cord injury in rabbits.

BACKGROUND: It is not well established whether insulin protects against ischemic spinal cord injury. We examined the effects of a single dose of insulin that corrects mild hyperglycemia on the outcome after transient spinal cord ischemia in rabbits. METHODS: We assigned rabbits to four groups (n = 8 in each); untreated control (C) group, preischemic insulin (Pre-I) group, preischemic insulin with glucose (GI) group (glucose concentrations were maintained at levels similar to the C group by the administration of glucose), and postischemic insulin (Post-I) group. Insulin (0.5 IU/kg) was administered 30 min before ischemia in the Pre-I and GI groups, and just after reperfusion in the Post-I group. Spinal cord ischemia was produced by occluding the abdominal aorta for 13 min. Neurologic and histopathologic evaluations were performed 7 days after ischemia. RESULTS: The mean blood glucose concentration before ischemia in the Pre-I group (118 mg/dL) was significantly lower than in the other three groups (158-180 mg/dL) and those of 30 min after reperfusion in the Pre-I (92 mg/dL) and Post-I (100 mg/dL) groups were significantly lower than in the C (148 mg/dL) and GI (140 mg/dL) groups. The motor function score and number of normal neurons in the anterior lumbar spinal cord in the Pre-I group were significantly greater than in the other three groups. CONCLUSIONS: These results suggest that a relatively small dose of preischemic insulin protects against ischemic spinal cord injury, and that the protective effects result from tight glycemic control before ischemia.

The effects of cyclosporin A and insulin on ischemic spinal cord injury in rabbits.

We examined the effects of cyclosporin A (CsA), a drug that inhibits mitochondrial permeability transition pore, and insulin on ischemic spinal cord damage in rabbits. We assigned rabbits to 5 groups (n = 6 in each); sham barrier-opened group (sham BO), barrier-opened group (BO), barrier-opened-CsA group (BO-CsA), barrier-opened-insulin group (BO-I), and barrier-opened-CsA-insulin group (BO-CsA-I). The blood-spinal cord barrier was opened to facilitate drug penetration by a mild injury to the lumber spinal cord on day 1. CsA (10 mg/kg per day IV) was administered on day 3 to day 5 (total 30 mg/kg). Insulin was administered 30 min before ischemia. In all groups, spinal cord ischemia was produced on day 5 by occluding the abdominal aorta for 13 min. Neurological and histopathological evaluations were performed 4 days after ischemia. In group BO-CsA, blood glucose concentrations were significantly larger compared with the other four groups, and no protection was observed. In contrast, hindlimb motor function in groups BO-I and Bo-CsA-I and histopathology in group BO-CsA-I were significantly better than in groups sham BO, BO, and BO-CsA. The results indicate that insulin protects against ischemic spinal cord injury, whereas the effect of CsA is, at best, minimal.

The effects of an AMPA receptor antagonist on the neurotoxicity of tetracaine intrathecally administered in rabbits.

We have reported that large concentrations of intrathecal local anesthetics increase glutamate concentrations in the cerebrospinal fluid (CSF) and cause neuronal injury in rabbits. In the current study we determined whether an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist, YM872, administered intrathecally, reduces neuronal injury caused by tetracaine. We first examined the effects of intrathecal YM872 10, 30, 100, or 300 mug in rabbits (n = 3 in each). YM872 produced reversible motor and sensory block in a dose-dependent manner. Then, we evaluated modulatory effects of YM872 (300 mug) on tetracaine-induced glutamate release and neuronal injury. Pretreatment of YM872 did not attenuate 1% or 2% tetracaine-induced increases in cerebrospinal fluid glutamate concentrations (n = 3 in each). For evaluation of neuronal injury, rabbits were assigned to 4 groups (n = 6 in each) and intrathecally received 1% tetracaine and saline (1%T), 1% tetracaine and YM872 (1%TY), 2% tetracaine and saline (2%T), or 2% tetracaine and YM872 (2%TY). The volume of saline, YM872, and tetracaine was 0.3 mL. Saline or YM872 was administered 30 min before tetracaine administration. Neurological and histopathological assessments were performed 1 wk after the administration. Two and 1 animals respectively, showed motor and sensory dysfunction in 1%T, whereas 5 animals showed both motor and sensory dysfunction in 2%T. YM872 improved 2% tetracaine-induced motor dysfunction and neuronal damage (chromatolytic neurons, identified by round-shaped cytoplasm with loss of Nissl substance from the central part of the cell and eccentric nuclei). In 2%TY, 3 animals showed normal motor function and 3 showed mild dysfunction (ability to hop, but not normally), whereas 4 animals showed moderate dysfunction (inability to hop) in 2%T (P = 0.042). Only 2 animals showed one chromatolytic neuron in 2%TY, whereas 5 animals showed 4-16 chromatolytic neurons in 2%T (P = 0.020). These results suggest that AMPA receptor activation is involved, at least in part, in the tetracaine-induced neurotoxicity in the spinal cord.

[Anesthetic management with propofol for pheochromocytoma resection under monitoring of bispectral index and blood volume].

In two patients, pheochromocytoma resection was performed under propofol/fentanyl anesthesia, while bispectral index (BIS) monitoring and blood volume measurement using pulse spectrophotometry were done. In one patient (Case 2), arterial blood concentrations of propofol were measured by high performance liquid chromatography (HPLC), and compared with those of the estimated blood concentrations. Continuous infusion of nitroprusside and bolus infusion of nicardipine and/or diltiazem were used when hypertension and tachycardia occurred. After resection of the tumor, propofol dosage was reduced keeping the BIS values around 60. In both patients, blood volume was maintained higher than normal value (Case 1: 79-101, and Case 2: 91-112 ml x kg(-1)) during operation. After tumor resection, the blood pressure was maintained well without rapid infusion of fluid or vasopressor. Arterial blood concentration of propofol was lower than the estimated blood concentration during operation in high blood volume case (Case 2). BIS monitoring and blood volume measurement are useful for adjustment of propofol dosage and for avoidance of hypotension after pheochromocytoma resection.

The nerve root entry zone is highly vulnerable to intrathecal tetracaine in rabbits.

It has been speculated that the nerve root entry zone in the spinal cord, known as the Obersteiner-Redlich zone, may be more sensitive to large concentrations of local anesthetics administered intrathecally. However, there has been no morphological evidence for this. In the present study, we examined morphological changes of nerve fibers at the nerve root entry zone after administration of intrathecal tetracaine in rabbits. Rabbits were assigned to 4 groups (n = 6 in each) and received intrathecal 0.3 mL saline (control), or 1%, 2%, or 4% tetracaine. Neurological and histopathological assessments were performed 1 wk after the administration. Tetracaine 1% selectively injured the myelin sheaths made by oligodendrocytes at the nerve root entry zones of both ventral and dorsal roots, although neurological dysfunction could not be detected. With tetracaine 2% and 4%, histopathological damage extended to the dorsal funiculus, distal part of roots, and cauda equina and neurological dysfunction became apparent. These results demonstrate that the myelin sheaths made by oligodendrocytes at the nerve root entry zone are highly vulnerable to large concentrations of tetracaine given intrathecally.

Is intrathecal magnesium sulfate safe and protective against ischemic spinal cord injury in rabbits?

We performed three sets of experiments to investigate the safety of intrathecal magnesium and to determine its optimal dose for protection, if any, against ischemic spinal cord injury in rabbits. First, we examined neurotoxicity of 0.3, 1, 2, or 3 mg/kg of magnesium sulfate (n = 6 each). Significant sensory dysfunction was observed in the 3-mg/kg group 7 days after administration. Motor dysfunction was found in two rabbits in both the 2- and 3-mg/kg groups. The area of destruction in laminae V-VII was observed in one, two, and one rabbit in the 1-, 2-, and 3-mg/kg groups, respectively. Second, we investigated the temporal profile (6 h, 48 h, and 96 h [n = 3 each]) of histopathologic changes after 3 mg/kg of magnesium sulfate and confirmed similar changes in the rabbits with motor dysfunction at 48 and 96 h. Third, we evaluated the effects of 0.3 mg/kg or 1 mg/kg of magnesium sulfate or saline (n = 6 each) administered before ischemia on hindlimb motor function and histopathology after spinal cord ischemia (15 min). Magnesium did not improve neurologic or histopathologic outcome 96 h after reperfusion. The results indicate that intrathecal magnesium has a risk of neurotoxicity and shows no evidence of protective effects against ischemic spinal cord injury.