Evaluation and management of longitudinally extensive transverse myelitis: a guide for radiologists.

Longitudinal extensive transverse myelitis (LETM) is defined as an intramedullary spinal cord T2 signal abnormality extending craniocaudally over at least three vertebral bodies on an MRI study. Timely and appropriate diagnosis greatly facilitates patient management. The radiologist should review the relevant clinical information and determine the patient demographics and acuity of symptoms. Herein, we review the spectrum of diseases causing LETM and propose interpretation to guide the radiologist when presented with the MRI finding of LETM.

Induction of intracellular glutathione in alveolar type II pneumocytes following BCNU exposure.

N,N'-bis(2-chloroethyl)-N-nitro-sourea (BCNU) is a potent inhibitor of glutathione reductase (GSSG-Red) activity in both tissues and cells. We examined the effects of treating alveolar type II cells with BCNU and found that a marked decrease in cellular GSSG-Red activity occurred in these cells associated with a time-dependent increase in cellular glutathione (GSH) concentrations. The increase in GSH was not found to be related to changes in cellular gamma-glutamyl transpeptidase activity, gamma-glutamylcysteine synthetase activity, nor increased intracellular transport of cystine. When the BCNU-exposed cells were incubated with hydrogen peroxide to produce oxidant stress, the cells exhibited increased susceptibility to oxidant damage when compared with controls, despite the fact that cellular concentrations of GSH were markedly elevated.

Thromboxane contributes to pulmonary hypertension in ischemia-reperfusion lung injury.

Exposure of isolated perfused rabbit lungs (IPL) to ischemia-reperfusion causes a transient increase in pulmonary arterial (PA) pressure at the onset of reperfusion. Because thromboxane A2 (TxA2) is a potent vasoconstrictor, we hypothesized that it may contribute to the ischemia-reperfusion-induced pressor response. To evaluate this hypothesis, we exposed IPL perfused with a cell-free solution to 40 min of warm ischemia followed by reperfusion and measured perfusate immunoreactive thromboxane B2 (iTxB2) and 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha). We observed that ischemia-reperfusion IPL compared with controls had an increase in PA pressure (40.2 +/- 4.8 vs. 9.3 +/- 0.3 mmHg, P < 0.05), lung edema (29.3 +/- 6.3 vs. -0.2 +/- 0.2 g, P < 0.05), iTxB2 perfusate levels (155 +/- 22 vs. < 50 pg/ml, P < 0.05), and i6-keto-PGF1 alpha (436 +/- 33 vs. 61 +/- 16 pg/ml, P < 0.05). In ischemia-reperfusion IPL, infusion of SQ 29548 (10(-6) M), a specific TxA2/prostaglandin H2 receptor antagonist, attenuated the PA pressor response and the degree of edema. We conclude that pulmonary hypertension associated with ischemia-reperfusion results in part from pulmonary release of TxA2. Furthermore, TxA2 directly through membrane effects or indirectly through hydrostatic mechanisms increases the severity of ischemia-reperfusion-induced lung edema.

Ventilation-perfusion inequalities during graft rejection in patients undergoing single lung transplantation for primary pulmonary hypertension.

We report herein data on single lung transplant (SLT) recipients with primary pulmonary hypertension (PPH). One patient did well following surgery but died on the 30th postoperative day due to cytomegalovirus pneumonia. The remaining two patients initially did well with unlimited exercise tolerance following transplantation, but then developed marked dyspnea on exertion and hypoxemia on postoperative days 144 and 120, respectively. Pulmonary function testing showed marked deterioration of function and transbronchial lung biopsy specimens revealed acute graft rejection in one patient and evidence of chronic graft rejection in the second patient. Quantitative ventilation-perfusion lung scanning demonstrated a marked decrease in ventilation to the transplanted lung in both cases associated with only a mild decrease in perfusion. This V/Q mismatch resulted in markedly decreased arterial oxygen saturations, widened alveolar-arterial oxygen gradients, and clinically debilitating dyspnea. We conclude that rejection may result in significant V/Q mismatch and hypoxemia in PPH patients undergoing SLT, which may limit the use of this specific type of surgery for PPH.

Single lung transplantation. Factors in postoperative cytomegalovirus infection.

Thirty-one single lung transplantations were performed between March 17, 1988, and November 1, 1990. Postoperative infection, especially with cytomegalovirus, has been the major cause of morbidity and mortality. Eighteen of the 31 patients were receiving prednisone before transplantation. Every patient was prepared preoperatively with oral cyclosporine 5 mg/kg and azathioprine (Imuran) 2 mg/kg. Every patient received methylprednisolone for 3 days postoperatively, followed by prednisone 1.0 mg/kg/day, oral cyclosporine, and azathioprine. Ten patients additionally had cytolytic therapy with OKT3 and 12 with antilymphocyte globulin. Nine patients had no cytolytic therapy. Cytolytic therapy was chronologic, not randomized. Postoperative infection occurred in 20 patients, 13 of whom had cytomegalovirus infection. Preoperative use of prednisone did not correlate with postoperative infection, cytomegalovirus, or death. Postoperative infection occurred in 17 of 22 patients with cytolytic therapy compared with three of nine without cytolytic therapy (p = 0.035). Cytomegalovirus infection occurred in 13 of 22 with cytolytic therapy and in none of the nine without cytolytic agents (p = 0.003). Therefore preoperative prednisone does not appear to be a contraindication to single lung transplantation. Cytolytic therapy with either OKT3 or antilymphocyte globulin increases the prevalence of postoperative infection with cytomegalovirus and should not be used in patients undergoing lung transplantation.

Washed human platelets prevent ischemia-reperfusion edema in isolated rabbit lungs.

Washed human platelets prevent edema formation in isolated rabbit lungs infused with xanthine oxidase, an enzyme that injures endothelial membranes by generating extracellular oxidants. We hypothesized that platelets would similarly preserve membrane permeability in isolated lungs exposed to ischemia-reperfusion injury, a model that perturbs endothelial cells by the generation of intracellular oxidants. Isolated perfused rabbit lungs (IPL) were exposed to warm ischemia-reperfusion to cause lung edema. The infusion of washed human platelets (1.05 +/- 0.02 x 10(10) cells) prevented edema formation as measured by lung weight gain, wet-to-dry lung weight ratios, histological edema, and preservation of paraendothelial cell tight junctions. Inhibition of the platelet glutathione redox cycle with 1,3-bis(2-chloroethyl)-1-nitrosourea, dehydroepiandrosterone, or 1-chloro-2,4-dinitrobenzene interfered with platelet protective effects. In contrast, inhibition of platelet catalase with aminotriazole and H2O2 had no effect on platelet protection. Lung tissue malonyldialdehyde concentrations were similar in isolated lungs exposed to ischemia-reperfusion with or without the infusion of platelets. These results indicate that platelet attenuation of ischemia-reperfusion lung edema depends on platelet glutathione redox cycle antioxidants but not platelet catalase.

Clinical predictors of prolonged translaryngeal intubation in patients with the adult respiratory distress syndrome.

This study was designed to determine if clinical features apparent after seven days of mechanical ventilation predict long-term intubation beyond 14 days and subsequent need for tracheotomy in patients with ARDS. Twenty-four patients were entered into the study. Group 1 patients were successfully extubated in less than or equal to 14 days after onset of ARDS and group 2 patients remained intubated greater than 14 days. On day 7 of ARDS, group 1 had a higher PaO2/PAO2 ratio, a lower PEEP requirement, less severe chest radiographic abnormalities and a greater likelihood of an improved radiograph from the baseline study. None of group 1 and 11 group 2 patients eventually underwent tracheotomy. Clinical features apparent after seven days of mechanical ventilation in patients with ARDS suggest the likelihood of prolonged intubation beyond 14 days and eventual tracheotomy. Recognition of these features may allow more timely conversion of endotracheal intubation to tracheotomy.