Recently, Burgess et al. (1) documented the incidence and severity of ipsilateral shoulder pain after thoracotomy, a particularly difficult problem to treat. Although they examined several possible mechanisms for such pain, which included thoracic somatic and visceral as well as phrenic nerve nociception, none of their proposed explanations seemed tenable to them. The following case report demonstrates that such shoulder pain may be mediated by the sympathetic nervous system.

The authors studied 12 patients who required deliberate hypotension for spinal fusion operations in order to investigate the efficacy of captopril for reducing dose requirement for sodium nitroprusside (SNP). Six patients, selected at random, were pretreated with captopril, 3 mg/kg po, and the remaining six patients served as controls. All patients received a similar anesthetic technique, consisting of thiopental 3 mg/kg, pancuronium 0.1 mg/kg, morphine 0.5 mg/kg, plus nitrous oxide 70% in oxygen. SNP was used to maintain mean arterial pressure (MAP) at 50-55 mmHg during deliberate hypotension lasting 140 +/- 13 minutes (mean +/- SE). Patients who received captopril required less SNP than untreated patients both early during hypotension (1.4 +/- 0.5 micrograms X kg-1 X min-1 vs. 4.8 +/- 0.8 micrograms X kg-1 X min-1, P less than 0.05), as well as late during hypotension (2.2 +/- 0.2 micrograms X kg-1 X min-1 vs. 5.6 +/- 0.6 micrograms X kg-1 X min-1, P less than 0.05). Whole blood cyanide was significantly lower in the patients pretreated with captopril than the untreated controls both early in the hypotensive period (2.7 +/- 0.6 mumol/l vs. 13 +/- 4 mumol/l, P less than 0.05) and also late in the hypotensive period (3.7 +/- 0.8 mumol/l vs. 30 +/- 10 mumol/l, P less than 0.05). MAP was reduced by captopril pretreatment both following induction of anesthesia (64 +/- 4 mmHg captopril vs. 80 +/- 4 mmHg control, P less than 0.05) and during surgery before deliberate hypotension (86 +/- 5 mmHg captopril vs. 100 +/- 4 control, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

A case of fatal myeloencephalopathy secondary to accidental intrathecal administration of vincristine is reported in a 16-year-old boy. He underwent a progressive ascending chemical meningoencephalitis leading to coma, and died 36 days after the injection. Multiple samples of cerebrospinal fluid (CSF) and serum were assayed for vincristine sulfate. CSF levels of vincristine were consistently much higher than serum levels. At autopsy, all regions of the brain that had been in direct contact with the CSF were necrotic. The spinal cord was likewise necrotic throughout its length. Microscopically there was total neuronal loss with tissue destruction in the affected regions. The presence of numerous gemistocytic astrocytes, some in arrested mitosis, was a conspicuous feature in these areas. Three previous reports of intrathecal vincristine instillation are reviewed. No treatment for this devastating iatrogenic error exists, underscoring the importance of preventive measures in chemotherapy administration.