Successful removal of a potentially lethal left atrial thrombus detected by transesophageal echocardiography following the removal of a left ventricular assist device inflow cannula.

The left ventricular assist device (LVAD) is a battery-operated, mechanical pump-type device that helps in maintaining the pumping ability of a failing heart. Thromboembolism poses a significant risk during and after LVAD implantation. It occurs in up to 35% of patients with adverse sequelae. We present the case of a 75-year-old man who underwent coronary artery bypass graft surgery and LVAD implantation for acute myocardial ischemia and severe left ventricular dysfunction. However, subsequent transthoracic echocardiographic examination revealed an LVAD thrombus, and LVAD removal was suggested following the failure of thrombolytic therapy. After the LVAD cannula was removed, transesophageal echocardiography (TEE) revealed a residual thrombus in the left atrium. Thrombectomy was successfully performed by opening the left atrium with cardiopulmonary bypass. We believe that TEE monitoring aided the implantation and removal of the LVAD device. In this case, we found that TEE not only helped in monitoring the ventricular function but also in detecting other problems such as the residual thrombus. We strongly recommend TEE monitoring during the entire LVAD-removal procedure, particularly for patients who need to undergo LVAD removal because of thrombosis formation.

Generalized depletion of free nerve endings and decrease of cutaneous nervous innervation in streptozotocin-induced painful and painless diabetic rats.

BACKGROUND: The loss of peripheral nerve fiber is evident in chronic painful diabetic neuropathy. However, the correlation between peripheral fiber loss and the genesis of pain is unclear. Using the streptozotocin-induced diabetic rat model and focusing on free nerve endings, we attempted to investigate the peripheral changes that elicit pain syndromes in diabetes. METHODS: Diabetes was induced in rats using 75 mg/kg streptozotocin, while controls received saline solution. "Painful" rats with thermal or mechanical hypersensitivity and "painless" rats (without significant threshold changes) were enrolled. The peripheral nerve endings were immunostained using protein gene product 9.5 in footpad skin sections. The peripheral nerve densities in each behavior group were calculated and averaged. RESULTS: A progressive loss of protein gene product 9.5-blotted nerve fibers was noted after diabetes was induced and as the duration of hyperglycemia proceeded. Painful and painless diabetic rats have similar histological nerve fiber loss including depleted epidermal free nerve endings. CONCLUSION: The results indicated that there are undiscovered pathological changes that are sensitizing the injured nerve fiber in periphery.

Persistent systemic air embolism and delayed pulmonary hemorrhage after weaning from cardiopulmonary bypass--a case report.

Systemic air embolism (SAE) occurring during cardiac surgery is usually associated with high morbidity and mortality. We present a fatal case of persistent SAE identified by transesophageal echocardiography (TEE) after weaning from cardiopulmonary bypass (CPB). Perplexities in identification of a bronchovascular fistula and hesitation in aggressive management to arrest the resultant continuous air entry into systemic circulation caused death as an aftermath. Related instances in literature have been reviewed and appropriate managements are herein discussed.

Intravenous propofol precipitates the hypotension induced by inadvertent epidural thiopental injection.

Administration of improper drugs into epidural space is occasionally present in anesthetic practice. In most instances it would not contribute to significant neurological complications. There had not been severe hypotension reported in the literature in consequence of inadvertent epidural thiopental administration. Here we describe our experience in a case of inadvertent epidural administration of thiopental coinciding with induction of anesthesia with propofol, as a consequence of which profound hypotension was induced, necessitating aggressive inotropic and vasopressive agents to maintain blood pressure. Rapid vascular uptake of thiopental in the epidural space and synergistic action of propofol jointly contributed to the development of the hypotension. Attempts to forestall neurological sequela after the inadvertence seem unnecessary unless apparent symptoms or signs of neurological injury have come upon.

Recurrent life-threatening bradycardia in a child with retained tracheal stent.

We report a child with a retained welded tracheal stent scheduled for removal developing refractory bradycardia and cardiac arrest during attempt to remove the stent. Cardiac massage and pacing were necessary to reestablish circulation. The same type of arrhythmia occurred three times in the postanesthetic care unit after tracheal suction or coughing.

Unusual cause of esophageal perforation during intraoperative transesophageal echocardiography monitoring for cardiac surgery--a case report.

Although esophageal perforation after transesophageal echocardiographic (TEE) examination is rare yet the occurrence of this life-threatening complication is increasing. We report an unusual esophageal perforation occurring 4 days after coronary artery bypass graft surgery and Bentall's procedure. The perforation was due to inadvertent injury of the esophagus that was deformed and distorted by a large calcified lymph node in the mediastinum during intraoperative TEE instrumentation. We suggest that careful preoperative radiological examination of the mediastinum should be done to recognize the anatomical pathology in patient whose routine chest X-ray has disclosed a large calcified lymph node in the mediastinum, if he happens to undergo TEE, so as to avoid disastrous esophageal perforation.

Comparison of the recovery from isoflurane anesthesia with or without fentanyl infusion in patients undergoing elective supratentorial craniotomy.

BACKGROUND: Several anesthetic agents have been used successfully to provide optimal anesthetic maintenance in neurosurgery for supratentorial tumors. Due to longer surgical time that these procedures demand and thoughout avoidance of intracranial bleeding from a hastened emergence of anesthesia in the operating room, the neurosurgeons in our hospital favor a placid late emergence from anesthesia in the neurosurgical intensive care unit (NCU). Accordingly, we designed this clinical trial to compare the effects of volatile general anesthesia with or without fentanyl infusion on postoperative hemodynamics, Glasgow coma scale (GCS) score, extubation time, as well as neurological outcome in patients after craniotomy. METHODS: Forty-two patients undergoing elective surgery for supratentorial lesions were randomly divided into two anesthetic groups. In isoflurane group, after induction, anesthesia was maintained with isoflurane up to 1.2% end-tidal concentration. In fentanyl-isoflurane group, an infusion of fentanyl was started at a rate of 3 micrograms/kg/h after induction, and anesthesia was maintained with isoflurane up to 0.6% end-tidal concentration. All the anesthetics were discontinued once the surgical wound was dressed. We studied the postoperative hemodynamics and several recovery variables for 48 h after completion of anesthesia. RESULTS: The time from completion of surgery to extubation was shorter in isoflurane group (9.3 +/- 6.6 h) as compared with fentanyl-isoflurane group (14 +/- 3.5 h, P < 0.05). Better GCS score was seen in isoflurane group in the early recovery period. However, both groups did not differ in both average postoperative blood pressure and heart rate and there was no significant difference between 2 groups in total duration of the postoperative NCU stay. CONCLUSIONS: In pursuance of the policy of late emergence, we are of the opinion that isoflurane anesthesia offers an earlier recovery than fentanyl-isoflurane anesthesia in patients undergoing supratentorial craniotomy.

Oral clonidine reduces myocardial ischemia in patients with coronary artery disease undergoing noncardiac surgery.

BACKGROUND: To access the clinical effect of clonidine on reduction of myocardial ischemia events in patients with history of coronary artery disease undergoing noncardiac surgeries. METHODS: Sixty ASA class III patients with coronary artery disease were allotted at random to two groups in a prospective, double-blind study to receive either clonidine (3 micrograms/kg) or placebo (control group) 90 minutes before arrival at the operating room. Continuous EKG monitoring (Holter monitor) was performed to analyze the ST segment in lead II, V2 and V5 during the preoperative (since late hours the night before operation), intraoperative and early postoperative periods (total monitoring time = 24 hours). The episode of myocardial ischemia defined as the magnitude of ST segment depression of at least 1 mm, occurring 60 ms after the J point and persisting for three minutes or more was recorded. Perioperative hemodynamic data were analyzed with two-way ANOVA with repeated measures. Student's t-test for unpaired data was used for analysis of demographics. Chi-square test was used for ST segment changes. Results are expressed as mean +/- SD and P < 0.05 was considered to be statistically significant. RESULTS: In the control group, 9 patients (30%) were noted to have episodes of ischemia preoperatively, 7 patients (23.3%) intraoperatively, and 12 patients (40%) postoperatively. The occurrence of myocardial ischemia peaked in the early postoperative period (P < 0.05). On the contrary, in the clonidine group, 10 patients (33.3%) saw ischemic episodes preoperatively, 3 patients (10%) intraoperatively and 5 patients (16.7%) postoperatively. The incidence of myocardial ischemia in clonidine group was significantly lower than that in placebo group in intraoperative and postoperative periods. The mean arterial pressure was significantly lower in some clonidine-treated patients during perioperative periods (P < 0.05). A number of patients in clonidine group suffered from drowsiness (66.7%) after operation (P < 0.05), but they could be easily aroused. In regard to dryness of mouth, nausea and vomiting clonidine and control groups did not differ much (P > 0.05). Demerol consumption was significantly lower in clonidine group (43.7 +/- 4.6 mg) than in control group (76.3 +/- 3.7 mg, P < 0.05). CONCLUSIONS: We conclude that premedication with oral clonidine can significantly reduce the incidence of perioperative myocardial ischemia in patients with CAD undergoing noncardiac surgeries. The incidence of myocardial ischemia in these patients is rather high during perioperative period, which deserves our exceptional caution.