Michele D. Szabo

Exacerbation or unmasking of focal neurologic deficits by sedatives.

Background Transient focal neurologic deficits have been observed in patients emerging from brain tumor or carotid surgery, and a pharmacologic effect of anesthetic agents has been proposed as the cause of such neurologic dysfunction. Therefore, the effect of sedation with midazolam or fentanyl on motor neurologic function was studied prospectively and preoperatively in patients with carotid disease or mass lesions of the brain. Methods Fifty-four unpremedicated adult patients with carotid disease or a brain tumor were given small intravenous doses of either 2.8 +/-1.3 mg midazolam or 170+/-60 micro gram fentanyl in the preoperative period. A thorough motor examination was performed at baseline and after sedation by an individual who was unaware of the details of the patients disease or symptoms. A mental status examination also was performed to control for the effects of inattentiveness or lack of cooperation during the neurologic examination. Results Patients were sedated mildly but were fully cooperative. Focal motor deterioration occurred after sedation in 30% of patients, and the incidence was similar in patients in the fentanyl and midazolam groups. Among patients with a focal motor abnormality on baseline examination or a resolved prior motor deficit, 73% had exacerbation or unmasking of these signs by sedation, whereas no patient without a prior history of motor dysfunction had a sedative-induced change. Sedative-induced changes in neurologic function ranged from unilateral mild weakness to complete plegia, but appeared to be transient in nature. Conclusions Sedation with midazolam or fentanyl can transiently exacerbate or unmask focal motor deficits in patients with prior motor dysfunction.

Myocardial perfusion following acute subarachnoid hemorrhage in patients with an abnormal electrocardiogram.

&NA; To test the hypothesis that acute subarachnoid hemorrhage is associated with abnormal myocardial perfusion, we assessed myocardial blood flow with thallium scintigraphy in 19 patients with a confirmed subarachnoid hemorrhage and an abnormal electrocardiogram. A thallium scan was performed at the bedside of each patient 3 ± 2 days (mean ± SD) after subarachnoid hemorrhage and subsequently was analyzed both qualitatively and quantitatively. Patients averaged 58 ± 13 yr of age and 68% had one or more cardiac risk factors The neurologic condition of patients on the day of the scan was II (median; range I‐V) on the standard 5‐point scale of Botterell. Abnormalities on a standard 12‐lead electrocardiogram obtained on the same day as the scan consisted of repolarization changes in most patients; 10 had T wave inversions and 8 had nonspecific ST segment changes. Thirty‐two percent (n = 6) of patients had an abnormal thallium scan. There were, however, no features of the clinical history, electrocardiogram pattern, or neurologic condition that were associated with a positive scan. For instance, 2 of 4 patients with diffuse deeply inverted T waves had a normal thallium scan, whereas the scan was abnormal in 2 of 8 patients with minor nonspecific electrocardiographic abnormalities. The thallium scan was also positive in neurologically intact (grade I) as well as severely injured (grade V) patients. Thus, abnormal myocardial perfusion and possibly myocardial ischemia occur frequently following subarachnoid hemorrhage, but no specific electrocardiographic characteristic identifies patients with a perfusion abnormality.

Subarachnoid Clonidine Reduces Spinal Cord Blood Flow and Glucose Utilization in Conscious Rats

The authors investigated the spinal blood flow and metabolic effects of subarachnoid clonidine in conscious rats prepared with chronically implanted subarachnoid catheters. For the blood flow experiments, rats received saline (n = 7) or clonidine 20 nmol (7 micrograms; n = 6), 100 nmol (27 micrograms; n = 5), or 400 nmol (107 micrograms; n = 7) intrathecally. Another group of rats received clonidine 400 nmol intravenously (n = 4). Spinal glucose utilization was measured in rats that received either saline (n = 5) or clonidine 100 nmol (n = 5) intrathecally. Spinal cord blood flow (SCBF) and glucose utilization were measured in five gray and three white matter areas of lumbar spinal cord 15 min after drug administration with the autoradiographic iodo-[14C]-antipyrine and 2-[14C]-deoxyglucose methods, respectively. Physiologic differences between the groups were minor. Rats in the blood flow experiments that received clonidine 100 nmol had a slightly lower arterial PO2 level (70 +/- 1 vs. 82 +/- 3 mmHg; P less than 0.05), whereas those in the glucose utilization group were mildly hypocarbic (PCO2 27 +/- 1 vs. 32 +/- 2 mmHg; P less than 0.01) relative to control animals. Only animals that received 400 nmol clonidine intrathecally had significant analgesia, as assessed by the tail-flick test. One control animal for the metabolism experiments was technically unsatisfactory and was excluded from data analysis. Subarachnoid clonidine reduced both SCBF and glucose utilization. In spinal gray matter, the largest decreases in flow (32-44%; P less than 0.01) occurred with 20 nmol clonidine, whereas flow decreased least (12-27%) with the 400-nmol dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension Does Not Cause Spontaneous Hemorrhage of Intracranial Arteriovenous Malformations

The authors measured blood pressure changes non-invasively in 56 conscious, unpremedicated patients with cerebral arteriovenous malformations (AVMs) during preparation for proton beam therapy. The procedure requires six injections of local anesthetic and application of a stereotactic frame by fixation into the outer table of the skull, and has been used during the past 20 yr to treat over 1,000 patients with cerebral AVMs. No effort was made to control blood pressure. Blood pressure increased during administration of the local anesthetic and application of the frame. Maximum systolic and mean arterial pressures averaged 160 +/- 17 and 118 +/- 7 mmHg (mean +/- SD), respectively. This represented an average increase of 44 mmHg (38%) in systolic pressure and 32 mmHg (37%) in mean blood pressure at some point during the procedure (P less than 0.01 compared with pretreatment control pressures). Systolic pressure increased more than 60 mmHg in 21% of patients. Nevertheless, none of these 56 patients nor any of the more than 1,000 patients treated in similar fashion suffered a clinically evident AVM hemorrhage during the procedure. Since the treatment protocol has not changed materially during the past 20 yr, the authors assume that most patients treated in this fashion developed a similar degree of hypertension and conclude from this large clinical experience that moderate arterial hypertension does not precipitate spontaneous hemorrhage of intracranial AVMs.

Effect of profound hypermagnesemia on spinal cord glucose utilization in rats.

The purpose of our study was to investigate the effect of hypermagnesemia on spinal metabolic rate. The 2-[14C]deoxyglucose technique was used to measure regional glucose utilization in the lumbar spinal cord of paralyzed, mechanically ventilated rats receiving 70% nitrous oxide and an intravenous infusion of either saline (n = 5) or magnesium sulfate (n = 5). Plasma magnesium concentrations were 6.75 +/- 0.5 and 0.9 +/- 0.5 mM (p less than 0.01) in hypermagnesemic and control rats, respectively. Hypermagnesemic rats were hypotensive (88 +/- 1 vs. 130 +/- 4 mm Hg, p less than 0.01) but blood pressure remained within the autoregulatory range. Glucose utilization was reduced 26-45% in spinal gray matter and 53-63% in spinal white matter during hypermagnesemia. We conclude that magnesium is a potent spinal metabolic depressant and that this action, which is unusually prominent in spinal white matter, is a plausible explanation for the recently reported beneficial effect of magnesium therapy during spinal cord ischemia.

Case report: profound hypotension after anesthetic induction with propofol in patients treated with rifampin.

Rifampin is commonly used for the treatment of tuberculosis and staphylococcal infections, as well as for prevention of infection in cardiac valve and bone surgeries. We report a case of profound hypotension after anesthesia induction with propofol in a patient who was treated with two 600 mg doses of rifampin for prophylaxis of infection before surgery. In a retrospective case-control study of 75 patients, we confirmed this potentially serious drug-drug interaction. After rifampin, there was a significant and prolonged arterial blood pressure reduction when patients received propofol, but not thiopental.

Excessive atlanto-occipital flexion as a cause of complete airway obstruction following anterior cervical spine fusion

This report describes complete airway obstruction following anterior cervical fusion caused by extreme, fixed flexion of the neck in a halo device. The causes and treatment of such an airway complication are reviewed.

Excess Mg 2+ and Central Nervous System Metabolism

There is perhaps no more dramatic evidence for a depressant effect on the central nervous system (CNS) than the ability of a drug or compound to produce a state of general anesthesia. Mg2+ was at one time thought to have such marked effects on the CNS that early in this century Peck and Meltzer (1916) reported performing surgery on humans under Mg2+ “anesthesia.” Less profound CNS signs and symptoms, ranging from drowsiness to light coma, have also been reported in hypermagnesemic individuals (Randall et al. 1964; Mordes and Wacker 1978; Paymaster 1976).

Autologous transfusion of a neurosurgical patient with sickle cell disease.

To JNA Readership: We report the autologous transfusion of a neurosurgical patient with sickle cell disease. A 29-year-old woman with Arab-haplotype homozygous-S sickle cell disease presented for resection of a frontoparietal meningioma. During an airplane flight to our hospital, she developed splenic infarction. Work-up revealed 63% hemoglobin-S and 37% hemoglobinF expression, and antiJk e+ and anti-Jk antibodies associated with prior transfusion. She was transfused with 3 units of crossmatched packed red blood cells. Seven days later, she developed fever, jaundice, dark urine, and pain in the left upper abdomen, left humerus, and both tibias. Her hematocrit fell from 31.3% to 11%, with the expression of 2 new antibodies, anti-Fy +, and anti-M. A diagnosis of delayed hemolytic transfusion reaction was made. Weekly treatment of 30,000 units of erythropoeitin was initiated. One month later, the patient donated a total of 3 units of blood on a weekly basis. This blood was stored in a standard blood-bank fashion, in a citratephosphate-dextrose-adenine solution at 41C. Hematocrit on repeat admission was 26%. A radiologic embolization of her tumor was carried out to decrease vascularity and intraoperative blood loss. The next day the meningioma was excised under a nitrous-narcotic anesthetic. She was transfused with 3 units of autologous blood over 3 hours for ongoing blood loss. There was no visible hemolysis in the donor blood packs. No homologous blood was transfused. On conclusion of the procedure, arterial blood analysis on facemask oxygen showed: pH 7.44, pCO2 45mm Hg, pO2 158mm Hg, hematocrit 26.1%. The following day she had a single grand-mal seizure with subtherapeutic levels of antiepileptic medications. No intracranial bleed or infarctions were seen on a computerized tomography scan. Postoperative course was otherwise uneventful. Hematocrit on discharge 6 days postoperatively was 23.5%. Transfusion reactions can trigger life-threatening or fatal hemolytic reactions. Red cell alloimmunization, the development of non-ABO antigens, has a reported incidence of 8% to 35% in sickle cell patients. Alloantibodies may fall to levels undetectable on subsequent pretransfusion screening, with severe hemolysis arising from a delayed or ‘‘anamnestic’’ response, repeat expression of these antibodies after recurrent antigen exposure during transfusion. Autologous transfusion avoids this problem, but is apparently rarely used in sickle cell disease. This may be owing to perceived dangers of sickling. Although autologous transfusion has been reported, hemoglobin-A units were transfused concurrently, diluting the sickle cells. Fox et al bubbled oxygen through the units to minimize sickling. However, additional pathophysiology of the disease includes chronic inflammation, nitric oxide dysregulation, and vascular endothelial damage. Acute complications may arise from these pathologic pathways, rather than from isolated changes in hemoglobin polymerization and red cell sickling. Although our patient developed complications associated with sustained exposure to hypobaric hypoxia, these may have been related to adaptive stresses to nitric oxide and vascular endothelial biology associated with acclimatization. Autologous transfusion of deoxygenated sickle cell blood may not be contraindicated, and can avoid the dangers of homologous transfusion. Further reports of this technique would be helpful in confirming its safety.