Modulation of Cerebral Function by Muscle Afferent Activity, with Reference to Intravenous Succinylcholine.

Cerebral Function and Muscle Afferent Activity Following Intravenous Succinylcholine in Dogs Anesthetized with Halothane: The Effects of Pretreatment with a Defasciculating Dose of Pancuronium. By WL Lanier, PA Iaizzo, and JH Milde. Anesthesiology 1989; 71:87-95. Reprinted with permission. By the mid-1980s, it was widely assumed that if the depolarizing muscle relaxant, succinylcholine, given IV, produced increases in intracranial pressure, it did so because fasciculations produced increases in intrathoracic and central venous pressures that were transferred to the brain; however, there was no direct evidence that this was true. In contrast, we explored the possibility that the succinylcholine effect on the brain was explained by the afferentation theory of cerebral arousal, which predicts that agents or maneuvers that stimulate muscle stretch receptors will tend to stimulate the brain. Our research in tracheally intubated, lightly anesthetized dogs discovered that IV succinylcholine (which does not cross the blood-brain barrier) produced a doubling of cerebral blood flow that lasted for 30 min and corresponded to activation of the electroencephalogram and increases in intracranial pressure. Later, in our Classic Paper, we were able to assess simultaneously cerebral physiology and afferent nerve traffic emanating from muscle stretch receptors (primarily muscle spindles). We affirmed that the cerebral arousal response to succinylcholine was indeed driven by muscle afferent traffic and was independent of fasciculations or increases in intrathoracic or central venous pressures. Later research in complementary models demonstrated that endogenous movement (e.g., coughing, hiccups) produced a cerebral response very similar to IV succinylcholine, apparently as a result of the same muscle afferent mechanisms, independent of intrathoracic and central venous pressures. Thus, the importance of afferentation theory as a driver of the cerebral state of arousal and cerebral physiology during anesthesia was affirmed.

Disseminated intravascular coagulation after craniotomy.

Disseminated intravascular coagulation (DIC) is reported in neurosurgical patients; however, the incidence of DIC after craniotomy procedures is unknown. Using a surgical database, we identified 3164 patients who underwent primary craniotomy at Mayo Clinic Rochester between January 1, 2000 and December 31, 2004. Potential cases of DIC in this population were identified using 3 search triggers, patients: (1) in whom the diagnosis of DIC was noted on their hospital discharge summary, (2) who received red blood cell-free blood products, or (3) in whom a blood fibrinogen or d-dimer concentration was assessed. Using criteria based on laboratory values, we estimated the incidence of DIC developing within 72 hours of primary craniotomy to be between 13 and 44 per 10,000 patients. Despite a low incidence of DIC, the associated mortality rate was 43% to 75%. Traumatic head injury was a significant risk factor for the development of DIC [odds ratio of trauma was in the range of 16 (95% confidence interval (CI)=5.3-49) to 29 (CI=4.0-204)]. Autologous salvaged blood was administered intraoperatively to 44 patients, and 1 of these developed DIC. Although this small sample of patients receiving salvaged blood requires caution in interpreting the results, the risk of DIC seemed to be greater with salvaged blood than without [odds ratio 24 (CI=2.5-237)]. In children, 2 of 3 patients who developed DIC had congenital malformations of the brain. Findings from this study suggest that DIC is rare after craniotomy, but is often associated with mortality.

Hemodynamic responses to epinephrine-containing local anesthetic injection and to emergence from general anesthesia in transsphenoidal hypophysectomy patients.

Patients undergoing transsphenoidal pituitary surgery may experience hypertensive episodes during the intranasal injection of vasoconstrictor-supplemented local anesthetics or emergence from general anesthesia. The present research characterized the blood pressure responses during transsphenoidal surgery and tested the hypothesis that the underlying pituitary disease influences the incidence and magnitude of the blood pressure responses. The records of 100 patients were retrospectively reviewed. All had direct blood pressure measurements recorded using a computer-based anesthesia recording system. Mean age was 49 +/- 17 years (+/- SD) and 52% were male. Blood pressure increased by 60 +/- 37 mm Hg systolic and 23 +/- 22 mm Hg diastolic with intranasal injection and 42 +/- 24 mm Hg systolic and 23 +/- 16 mm Hg diastolic during emergence from general anesthesia. Systolic blood pressure increased by greater than 50% in 58% of patients following intranasal injection and in 33% of patients upon emergence from anesthesia. Blood pressure responses did not differ with respect to endocrinopathy type (Cushing's disease, acromegaly, or other pathology), gender, age, surgeon, history of prior transsphenoidal surgery, history of either hypertension or diabetes, or preoperative use of either beta-adrenergic or calcium channel-blocking drugs. There was poor correlation between the epinephrine dose injected (range 30-220 microg) and systolic blood pressure response (r = 0.24; r2 = 0.06; P = 0.031). Blood pressure increases were not associated with cardiac arrhythmias, persistent myocardial ischemia, or myocardial infarction. The authors conclude that in transsphenoidal hypophysectomy patients, large blood pressure increases are common with intranasal injection and upon awakening from general anesthesia. However, the authors were not able to find a variable that might enable the prediction of which patients are most likely to experience the most intense blood pressure elevations.