Blood pressure and adverse perioperative neurologic outcomes: an uncomfortable position.

—Donald Rumsfeld, 2002 In the era of evidence-based medicine, case reports, presenting anecdotal experience of a practitioner, are a vanishing entity in medical journals. It is even more unusual to write an editorial on a case report. But 2 case reports in this issue of the Journal by Drummond et al. touch on the important issue of the role of intraoperative hypotension in the development of neurologic injury and, in doing so, raise a question about whether case reports can or should affect clinical practice. The common theme for the 2 cases reported is that systemic hypotension resulted in devastating central nervous system (CNS) injury (spinal cord and brain, respectively). Systemic hypotension, as a cause of CNS injury, is not a novel concept. What is unusual is the apparent lack of major preoperative risk factors in these patients, other than the operating position (Trendelenburg position in the first case, and beach chair position [BCP] in the second case). The authors propose that the presence of an anatomic variant in the vascular supply of the respective patient (no corroborative evidence of vascular anomaly in the spinal cord in the first case, but a common variant of the circle of Willis in the second case), in conjunction with the systemic hypotension, resulted in a devastating injury. Perhaps more importantly, the question is whether this represents a cause and effect or simple association. The first is a case report of a 19-year-old woman who developed a spinal cord infarction after an ileoanal pullthrough performed under combined general and epidural anesthesia. The epidural catheter was inserted at L3-4 and the infarction involved T9 to conus, which was discovered on day 4 postoperatively, and the actual time of onset of injury was uncertain. Other than the initial test dose, the epidural infusate contained no epinephrine. The hypothesis was that the patient developed spinal cord infarction secondary to induced mild systemic hypotension to control blood loss, with the mean arterial blood pressure (MAP) maintained between 50 to 55 mm Hg for 2.5 hours. (There was some discrepancy between the systolic/diastolic blood pressure and MAP, with the former values lower than the recorded corresponding MAP.) The degree of hypotension was mild, and the authors speculated that the lumbosacral segment of the spinal cord may experience a lower blood pressure than was indicated by the cuff because of the hydrostatic gradient due to the Trendelenburg position, that local pressure within the neuraxis was higher, and/or that the patient may have a “normal congenital” vascular anatomic variation that made her spinal cord vulnerable. The second case involved an otherwise healthy 50-year-old man who underwent a shoulder procedure under general anesthesia in the BCP and subsequently developed a stroke within the distribution of the left middle cerebral artery. Risk factors included hyperlipidemia and history of smoking. Systolic blood pressure, as measured from the arm, was maintained between 95 to 100 mm Hg with a 10minute period at 90 mm Hg. Total anesthesia duration was 137 minutes. Postoperatively, the patient remained unresponsive and a magnetic resonance angiography obtained 4.5 hours later showed ischemic changes in left anterior and middle cerebral artery distribution. Computed tomography angiogram did not reveal any stenosis or occlusion in any of the cerebral arteries. Subsequent magnetic resonance imaging confirmed infarctions in the left frontal, temporal, and parietal lobes. Time-of-flight magnetic resonance angiography demonstrated a predominantly fetal posterior cerebral artery in the right hemisphere with a small proximal segment, absent anterior communicating artery, and the left posterior communicating artery could not be visualized. The authors concluded that a combination of relative systemic hypotension due to the BCP and the anatomic variant of the circle of Willis caused the ischemic infarction. The problem is this: despite a time-honored, tantalizing association between hypotension and adverse neurologic outcome, evidence linking hypotension of this degree and duration to infarction of the CNS is weak and reports of single cases do not make it stronger. In the spinal injury case, there is no indication of “anatomic variation” and the patient underwent a similar surgical procedure (colectomy) 3 months before, with a similar degree of hypotension (by MAP) of uncertain duration, with no neurologic sequelae. Furthermore, a cardiac echo revealed the presence of a patent foramen ovale, and there was evidence of a clot in From the Physician Anesthesia Service, Swedish Neuroscience Institute, Swedish Medical Center, Seattle, Washington.