Kidney Preservation for Transportation: IV. Eight-Thousand-Mile International Air Transport1

Eleven do kidneys were removed in Los Angeles, preserved, and air-freighted in small insulated boxes to London, Tel Aviv and Sydney. They were allografted into bilaterally nephrectomized dogs after storage periods of 14 to 23 hours. Except in the case of one technical failure, the rise in serum creatinine in the recipients was minimal, reaching on the average 2.2 ± SD 0.5 mg/100 ml. This simple method of preservation, involving flushing with a new perfusate and storage in ice, could provide a solution to the problem of transporting cadaver kidneys to histocompatible recipients. Survival of two out of three kidneys stored for 48 hours was also obtained.     

Predictive value of HLA antibodies and serum creatinine in chronic rejection: results of a 2-year prospective trial

In this large collaborative study, 2,231 transplanted patients with functioning kidneys were tested for HLA antibodies, then examined 2 years later for graft survival. Among 478 patients with antibodies, 15.1% failed in 2 years, compared to 6.8% failure in 1,753 patients without antibodies (P=0.00000002). Cytotoxicity testing correlated better with outcome than flow cytometry or ELISA testing on HLA coated beads, possibly because it detected non-HLA antigens. When the patients were further broken down into those with serum creatinine at the time of testing of 0.5-1.9, 4.4% of antibody patients failed at 2 years, compared to 4.3% of patients without antibodies. This 0.1% difference increased among patients with serum creatinine values of 2.0-2.9 to 17.9%, and among those with 3.0-3.9 to 16.3%. We conclude that HLA antibodies posttransplantation is predictive of subsequent graft failure, and its predictive value can be enhanced among patients with higher serum creatinine values.     

Presensitization and kidney transplant failures

Over 1000 kidney transplant patients were tested for cytotoxic antibodies before transplantation.     

Cerebral hyperperfusion following carotid endarterectomy: diagnostic utility of intraoperative transcranial Doppler ultrasonography compared with single-photon emission computed tomography study

BACKGROUND AND PURPOSE: Cerebral hyperperfusion syndrome is a rare but serious complication of carotid endarterectomy (CEA). The aim of the present study was to determine whether intraoperative blood flow velocity (BFV) monitoring in the middle cerebral artery (MCA) by using transcranial Doppler ultrasonography (TCD) could be used as a reliable technique to detect cerebral hyperperfusion following CEA by comparing findings with those of brain single photon emission CT (SPECT). METHODS: Intraoperative BFV monitoring was attempted in 67 patients undergoing CEA for treatment of ipsilateral internal carotid artery (ICA) stenosis (> or =70%). Cerebral blood flow (CBF) was also assessed using SPECT, which was performed before and immediately after CEA. RESULTS: Intraoperative BFV monitoring was achieved in 60 patients. Of the 60 patients, post-CEA hyperperfusion (CBF increase > or =100%, compared with preoperative values) was observed in six patients. The sensitivity, specificity, and positive predictive value of the BFV increases immediately after declamping of the ICA for detecting post-CEA hyperperfusion was 100%, 94% and 67%, respectively, with a cut-off point 2.0-fold that of preclamping BFV. The sensitivity and specificity of the BFV increases at the end of the procedure for detecting post-CEA hyperperfusion were 100% for both parameters, with cut-off points of 2.0- to 2.2-fold BFV of preclamping value. Hyperperfusion syndrome developed in two patients with post-CEA hyperperfusion, but intracerebral hemorrhage did not occur. In one of these two patients, BFV monitoring was not possible because of failure to obtain an adequate bone window. CONCLUSION: Intraoperative MCA BFV monitoring by using TCD is a less reliable method to detect cerebral hyperperfusion following CEA than postoperative MCA BFV monitoring, provided adequate monitoring can be achieved.     

CT findings of surgically resected large cell neuroendocrine carcinoma of the lung in 38 patients

OBJECTIVE: We sought to assess the CT features of surgically resected large cell neuroendocrine carcinoma of the lung. MATERIALS AND METHODS: The cases of all patients who underwent surgical resection for primary lung cancer in a single institution from 1993 to 2000 and who received an initial diagnosis of poorly differentiated non-small cell lung carcinoma, small cell carcinoma, carcinoid tumor, and large cell neuroendocrine carcinoma were histologically reviewed. The findings for 43 patients were histologically reclassified and confirmed as large cell neuroendocrine carcinoma. The CT scans available for 38 patients were evaluated by two observers. RESULTS: In the 38 patients, six central tumors and 32 peripheral tumors, with diameters ranging from 12 to 92 mm (mean +/- SD, 32 +/- 19 mm), were identified. None of the tumors had air bronchograms or calcification in the mass or nodule. Of the 19 patients with thin-section CT scans, 14 (74%) showed the tumor-lung interface as well defined and five (26%) showed the interface to be ill defined. Lobulation was identified on 15 scans (79%) and spiculation was evident on six scans (32%). On contrast-enhanced CT scans, inhomogeneously enhanced tumors appeared to be larger (51 +/- 18 mm) than homogeneously enhanced tumors (25 +/- 10 mm; p < 0.001). At histopathologic examination, gross necrosis was noted in 20 of 28 patients who had undergone contrast-enhanced CT, and the cause of inhomogeneous enhancement on CT scans was determined to be intratumoral necrosis. Multiple microscopic necroses were present in all 28 patients. CONCLUSION: Large cell neuroendocrine carcinoma usually appears as a well-defined and lobulated tumor with no air bronchograms or calcification. The inhomogeneous enhancement (caused by necrosis) seen in large cell neuroendocrine carcinomas with large diameters is not necessarily apparent in small-diameter (< 33 mm) large cell neuroendocrine carcinomas, even if the tumor contains necrosis.     

Anesthetic management for a patient with platypnea-orthodeoxia syndrome

We experienced anesthetic management for a patient with platypnea-orthodeoxia syndrome. This syndrome is relatively uncommon and accompanies dyspnea and hypoxemia on changing to a sitting or standing from recumbent position. A 75-year-old man with the syndrome underwent atrial septal defect closure on cardiopulmonary bypass. General anesthesia was induced and maintained with midazolam, propofol, fentanyl and vecuronium bromide. During the induction, Spo2 decreased suddenly from 100% to 70%, Spo2, however, recovered to 97% immediately after changing to Trendelenburg position. The perioperative and postoperative course was uneventful, except for hypoxemia during induction. Although the exact mechanisms of platypneaorthodeoxia remains to be solved, right-to-left shunt by an anatomical abnormality and by change of the atrial septum is considered one of the hypoxic mechanisms. We suggest that it is necessary to prevent right-to-left shunt and hypoxemia in anesthetic management of a patient with platypneaorthodeoxia syndrome.     

Brain and heart specific alteration of methamphetamine (MAP) distribution in MAP-sensitized rat

The repeated administration of methamphetamine (MAP) causes behavioral sensitization in animals. We previously reported that the high accumulation of MAP was observed in the MAP-sensitized animal brain, which suggested that this phenomenon is an important factor in the development or expression of behavioral sensitization. The purpose of the present study is to elucidate the MAP distribution in the MAP-sensitized rat using gas chromatography/mass spectrometry (GC/MS). As a result, the MAP distribution in the heart at 10 min when showing a high accumulation of MAP in the MAP-sensitized rat brain was significantly higher than that of the control rat, whereas no significant differences in the liver, kidney, abdominal muscle, femoral muscle and blood were observed. In the brain and heart, there was no different distribution at 1 min, reflecting only the influx process from blood to brain and heart. On the contrary, there was the significant difference at 10 min, reflecting both the influx and efflux process, suggesting that the efflux process of MAP from brain or heart to blood may be slow due to MAP sensitization. In conclusion, it was clear that the brain and heart specific alteration of the MAP distribution occurred in the MAP sensitization. It was considered that the high accumulation of MAP in the MAP-sensitized rat brain may be related to the expression of behavioral sensitization and that the delayed efflux of MAP in the MAP-sensitized rat heart may be connected with the cardiac toxicity.