[Cranial subdural hematoma with intracranial hypotension related to epidural anesthesia and Trendelenburg position: a case report].

We report a case of cranial subdural hematoma with intracranial hypotension. A 34-year-old woman had laparoscopic ovarial cysterectomy under general anesthesia combined with epidural anesthesia. Two days later, she developed a severe headache and nausea. She underwent cranial magnetic resonance imaging (MRI) scanning, and was diagnosed with cranial subdural hematoma with intracranial hypotension. The patient had had no anticoagulant therapy before the surgery. She was managed conservatively with bed rest and additional intravenous infusion. Her symptoms gradually improved except a slight headache, and she was discharged on the 38th postoperative day. Intracranial hypotension is a syndrome characterized by orthostatic headaches and hypovolemia of cerebrospinal fluid (CSF). There were typical findings on MRI, which include linear enhancement of the pachymeninges, pituitary hyperemia and subdural hemorrhage. We thought that these were due to epidural anesthesia first, but there was no evidence of dural puncture. It was also considered that it is influenced by change in CSF pressure, and intracranial venous engorgement may be due to Trendelenburg position for several hours. Because cranial subdural hematoma is a life-threatening complication, it is necessary to reconsider application of epidural anesthesia for laparoscopic surgery with Trendelenburg position.

Low-dose but not high-dose prostaglandin E(1) improves the histological outcome of severe forebrain ischemia in rats.

PURPOSE: Prostaglandin E(1) (PGE(1)) has been shown to provide short-term neuroprotection against various types of brain ischemia in a dose-dependent manner in mice. However, these findings were obtained from experiments performed without any control over physiological parameters. We performed an outcome study where physiological parameters were controlled in an attempt to confirm the dose-dependant neuroprotective effects of PGE(1). METHODS: A rat model of severe forebrain ischemia was used. Two doses of PGE(1) were administered during the pre-ischemic period, a low dose (LowPG group) and a high dose (HighPG group). Normotension was maintained in the LowPG group, while hypotension was induced in the HighPG group. In separate groups, normal saline (Control) or sodium nitroprusside (SNP) were infused to compare outcomes under similar blood pressure conditions. Histological outcomes in the hippocampal CA1 and entorhinal cortex were evaluated 5 days post-ischemia. RESULTS: HighPG resulted in hyperglycemia. The percentage of dead neurons in the hippocampal CA1 and entorhinal cortex were similar in the Control, SNP, and HighPG groups, the percentage being significantly attenuated in the LowPG group (CA1: Control = 92.8 +/- 2.4%, LowPG = 85.0 +/- 8.5%, HighPG = 95.3 +/- 2.4%, and SNP = 96.4 +/- 0.7%, P < 0.01; entorhinal cortex: Control = 73.8 +/- 4.0%, LowPG = 53.2 +/- 12.3%, HighPG = 72.1 +/- 12.6%, and SNP = 76.5 +/- 4.1%, P < 0.01). CONCLUSION: Pre-ischemic administration of low-dose PGE(1) in rats provided neuroprotection against severe forebrain ischemia. A dose dependency was not observed with PGE(1) dose and outcome.

[Four cases of latent aortic aneurysm--preoperative screening of aortic pathology is necessary for elderly patients].

We report four cases of latent aortic aneurysm revealed by contrast computed tomography (CT) before operations. The incidence of aortic diseases has not been publicized in Japan. However, the report of autopsies demonstrated that the elderly has a high incidence of aortic aneurysm and aortic dissection. Preoperative screening of aortic disease is necessary for elderly patients in order to perform appropriate perioperative managements. At present, contrast CT is the most reliable method for rapid detection of the complicated aortic disease.

[Awake intubation using lightwand technique under conscious sedation with remifentanil].

We experienced two cases of difficult airway due to deformities in the oral cavities. The first patient was a 62-year-old woman with a large benign soft palate tumor and the second was a 64-year-old woman with macroglossia secondary to acromegaly. Both patients were evaluated difficult to ventilate via face mask and presenting serious risks for tracheal intubation under general anesthesia. The tracheal intubation was planned using the lightwand (Trachilight) under conscious sedation with continuous administration of remifentanil. Remifentanil (0.1-0.25 microg x kg(-1) x min(-1)) maintained the patients' spontaneous ventilation and increased their tolerance to the pain and discomfort caused by insertion of the lightwand. In both patients, remifentanil mildly suppressed the coughing reflex as well as the autonomic responses to stimuli to the airway. Tracheal intubation was managed successfully in both cases and the operations were completed under general anesthesia. Although the patients were aware of being intubated, they could not recall the procedures postoperatively. The awake intubation technique using the lightwand under conscious sedation with remifentanil can be safely applied to a patient with difficult airway.

[Case of postoperative pulmonary embolism after tonsillectomy in a healthy young woman].

An 18-year-old healthy woman with no previous history of coagulation disorders underwent general anesthesia for tonsillectomy. The procedure was uneventful. After the surgery, she was ordered to rest on bed overnight. The next day, the patient experienced transient syncope followed by hypotension (< 60 mmHg) and severe dyspnea. Epinephrine 2 mg administration restored the blood pressure promptly, yet dyspnea persisted. The lung-perfusion scintigraphy showed upper-lobe perfusion defect in the left lung and she was diagnosed as having pulmonary embolism. She received low-molecular-weight heparin and warfarin therapy and recovered fully. The postoperative laboratory analysis did not show thrombophilic disorders or prothrombotic state. The pulmonary embolism was speculated to have occurred due to deep vein thrombosis which developed after postoperative immobilization. The prophylactic maneuvers such as elastic stockings were not applied to the patient preoperatively, who had been considered unlikely to develop deep vein thrombosis. Although deep vein thrombosis in children and adolescence are rare, postoperative children should be monitored carefully for thrombotic complications. Postoperative bed rest should be minimized in terms of prevention of thrombosis.

Pulmonary atelectasis manifested after induction of anesthesia: a contribution of sinobronchial syndrome?

A 31-year-old man underwent general anesthesia for sinus surgery. Anesthesia was induced with midazolam and butorphanol, and an endotracheal tube was orally placed with a bronchoscope, due to difficulty with temporomandibular joint opening. Ventilation difficulty and increased peak inspiratory pressure were noticed shortly after tracheal intubation, and bronchoscopy was performed for diagnosis. The bronchi were filled with a clear mucous secretion. Removal of the secretion improved respiration and decreased the peak inspiratory pressure. A chest roentgenogram taken prior to extubation showed right upper lobe atelectasis. A diagnosis of sinobronchial syndrome was made postoperatively. The etiology of the acutely developed atelectasis was unclear. However, the latent syndrome may have induced excessive airway secretion with stimuli such as endotracheal intubation.

The dose-dependent effects of isoflurane on outcome from severe forebrain ischemia in the rat.

Isoflurane improves outcome against cerebral ischemia in the rat. However, the optimal neuroprotective concentration has not been defined. We examined the effects of different isoflurane concentrations on outcome from severe forebrain ischemia in the rat. Fasted rats were subjected to 0.5, 1.0, 1.5, 2.0, or 2.5 minimum alveolar concentration (MAC) isoflurane during 10 min bilateral carotid occlusion plus systemic hypotension. Each isoflurane concentration was administered only before ischemia. Arterial blood pressure was not pharmacologically manipulated. After ischemia, the anesthetic regimen was changed to fentanyl/nitrous oxide and maintained for 2 h. Pericranial temperature was maintained normothermic during the experiment. Neuromotor score, % dead hippocampal CA1 neurons, and cortical injury were measured 5 days postischemia. Preischemic arterial blood pressure decreased as MAC was increased. Animals administered >1.0 MAC frequently exhibited postischemic seizures resulting in increased mortality. There was no difference among MAC conditions for % dead CA1 neurons (93 approximately 95%). In the cortex, neuronal necrosis was less severe with 0.5 MAC and 1.0 MAC isoflurane relative to >1.0 MAC values. The neuromotor score in the 1.0 MAC isoflurane group was superior to the 2.5 MAC group. Dose-dependent effects of preischemic administration of isoflurane on histologic and behavioral outcome after severe forebrain ischemia were observed. Isoflurane MAC values <1.5 provided superior overall outcome relative to larger isoflurane concentrations.

Intraischemic nitrous oxide alters neither neurologic nor histologic outcome: a comparison with dizocilpine.

N-Methyl-D-aspartate receptor antagonism contributes to the anesthetic action of nitrous oxide (N(2)O). We examined the effects of the N-methyl-D-aspartate antagonists N(2)O and dizocilpine on outcome from filament occlusion of the middle cerebral artery (MCAO). Rats breathed 70% nitrogen/30% oxygen or 70% N(2)O/30% oxygen during MCAO. A third group breathed 70% nitrogen/30% oxygen and was given dizocilpine (0.25 mg/kg IV). After 75 min of MCAO, the rats recovered for 3 or 14 days. Pericranial temperature was maintained at 37.5 degrees C +/- 0.2 degrees C during ischemia and for 20 h postischemia. N(2)O did not alter neurologic scores at 3 days (N(2)O, 21 +/- 6; nitrogen, 22 +/- 8; P = 0.95; 0 = normal; 48 = maximal deficit; mean +/- sd; n = 15) or 14 days (N(2)O, 13 +/- 6; nitrogen, 12 +/- 6; P = 0.93; n = 15-16) postischemia. N(2)O had no effect on infarct size at 3 days (N(2)O, 162 +/- 45 mm(3); nitrogen, 162 +/- 61 mm(3); P > 0.99) or 14 days (N(2)O, 147 +/- 56 mm(3); nitrogen, 151 +/- 62 mm(3); P = 0.99) postischemia. Dizocilpine treatment caused smaller infarcts (3 days: 66 +/- 49 mm(3), P < 0.0001 versus nitrogen; 14 days: 84 +/- 50 mm(3), P < 0.006 versus nitrogen) and reduced the neurologic deficit (3 days: 10 +/- 10, P = 0.002 versus nitrogen; 14 days: 6 +/- 7, P = 0.006 versus nitrogen). N(2)O (70%) had no effect on either behavioral or histologic outcome from transient focal cerebral ischemia when compared with results in rats breathing 70% nitrogen. These results indicate that normobaric N(2)O does not alter the response of rat brain to a focal ischemic insult.

The neuroprotective effect of xenon administration during transient middle cerebral artery occlusion in mice.

BACKGROUND: Xenon has been shown to be neuroprotective in several models of in vitro and in vivo neuronal injury. However, its putative neuroprotective properties have not been evaluated in focal cerebral ischemia. The purpose of this study was to determine if xenon offers neuroprotection in a mouse model of middle cerebral artery occlusion. METHODS: C57BL/6 mice underwent 60 min of middle cerebral artery occlusion. The animals (n = 21 per group) were randomized to receive either 70% xenon + 30% O2, 70% N2O + 30% O2, or 35% xenon + 35% N2O + 30% O2. After 24 h, functional neurologic outcome (on three independent scales: four-point, general, and focal deficit scales) and cerebral infarct size were evaluated. RESULTS: The 70% xenon + 30% O2 group showed improved functional outcome (median [interquartile range], four-point scale: 2 [2], 70% xenon + 30% O2 versus 3 [2], 70% N2O + 30% O2, P = 0.0061; general deficit scale: 9 [6], 70% xenon + 30% O2 versus 10 [4], 70% N2O + 30% O2, P = 0.0346). Total cerebral infarct volumes were reduced in the 70% xenon + 30% O2 group compared with the 70% N2O + 30% O2 group (45 +/- 17 mm3 versus 59 +/- 11 mm3, respectively; P = 0.0009). CONCLUSIONS: In this model of transient focal cerebral ischemia, xenon administration improved both functional and histologic outcome.