Journal: Anesthesiology 108(5):858-863, 2008
Reprint: Dept of Anesthesiology, Chonnam National University Medical School, 8 Hak-dong, Gwangju 501-757, South Korea (KY Yoo, MD)
Faculty Disclosure: Abstracted by S. Ouellette, who has nothing to disclose.
Autonomic hyperreflexia (AHR) is a life-threatening emergency during which uncontrolled sympathetic hyperactivity occurs in patients with spinal cord injury (SCI) above the splanchnic outflow, usually at the level of T6. Various noxious and non-noxious stimuli below the level of injury, such as distention of the bladder or bowel, uterine contractions during delivery, and surgery, may trigger the development of AHR. The hypertension associated with AHR may lead to intracranial and retinal hemorrhage, seizures, myocardial infarction, coma, and death. This event may also lead to atrial fibrillation and cardiac arrest. Several pharmacological agents such as IV gan¬glionic blocking drugs, hydralazine, alpha-adrenergic receptor blockers, calcium channel blockers, or nitrates have been used in the prevention or control of AHR. They are not always safe, convenient or predictable.
The development of AHR may be prevented either by general anesthesia, which blunts autonomic reflexes, or regional anesthesia such as spinal or epidural, which blocks afferent and autonomic efferent impulses. The depth of inhalation anesthesia required to block this reflex has not been determined.
This study was conducted to determine the end-tidal concentration of sevoflurane needed to block AHR in SCI patients undergoing transurethral litholapaxy. This study involved 28 patients with chronic, complete SCI; 9 patients without SCI served as control. Anesthesia was induced with thiopental and sevoflurane concentrations in 50% nitrous oxide adjusted to maintain a Bispectral Index of 40-50. When a patient developed AHR during bladder distention, the target sevoflurane concentration was maintained for at least 10 minutes, and then the procedure was resumed. Systolic blood pressure, heart rate, and BSI as well as plasma concentrations of catecholamines and arginine vasopressin were measured before and during the bladder distention. Each target concentration was determined by the up-and-down method based on changes of systolic blood pressure in response to bladder distention.
In SCI, systolic blood pressure increased 67±33 mmHg whereas heart rate decreased by 13±8 beats/ min during the first trial. The hypertensive event was associated with increases in norepinephrine concentrations but not of vasopressin or epinephrine concentrations. Systolic blood pressure, heart rate and norepinephrine concentrations did not change significantly in the control patients. The end-tidal concentrations of sevoflurane to prevent AHR were EC50 of 3.12% and EC95 of 3.83%. The EC95 for sevoflurane in 50% nitrous oxide to block AHR during litholapaxy in patients with SCI was 3.83%. |
