Daniel K. Reasoner

The incidence of pneumocephalus after supratentorial craniotomy. Observations on the disappearance of intracranial air.

Background:Pneumocephalus occurs in a variety of clinical settings and has important anesthetic implications, particularly if N2O is used. One common cause of pneumocephalus is a craniotomy or craniectomy, and therefore patients undergoing these neurosurgical procedures may be at increased risk for the development of tension pneumocephalus if N2O is used during a subsequent anesthetic. However, because the rate at which a postoperative pneumocephalus resolves has not been well denned, the duration of this risk period is unknown. Methods:Department of Anesthesia billing codes were used to identify all patients undergoing supratentorial craniotomy between 1986 and 1990. This list was cross-indexed with Department of Radiology data to generate a list of patients who had had a computed tomographic scan of the head performed on or after the day of their surgery. From this list, 240 scans were examined for the presence of intracranial air. The magnitude of pneumocephalus, if present, was ranked as large, moderate, small, or trace. Results:Air was seen in all scans obtained in the first 2 postoperative days. Sixty-six percent of these pneumocephali were judged to be moderate or large. The incidence of pneumocephalus decreased to 75% by postoperative day 7. During the 2nd and 3rd postoperative weeks, the incidence of pneumocephalus decreased to 59–6 and 26.3%, respectively. The size of the pneumocephali also decreased. Still, 11.8% of the scans obtained during the 2nd postoperative week had pneumocephali that were judged to be moderate or large. Conclusions:These data indicate that all patients have pneumocephalus immediately after a supratentorial craniotomy. Although the incidence and size of pneumocephali decrease over time, a significant number of patients have an intracranial air collection large enough to put them at risk for complication if N2O is used during a second anesthetic in the first 3 weeks after the first procedure. This information should be considered in the evaluation of the patient and in the selection of anesthetic agents.

Heparin Reduces Neurological Impairment After Cerebral Arterial Air Embolism in the Rabbit

BACKGROUND AND PURPOSE Neurological injury after cerebral air embolism may be due to thromboinflammatory responses at sites of air-injured endothelium. Because heparin inhibits multiple thromboinflammatory processes, we hypothesized that heparin would decrease neurological impairment after cerebral air embolism. METHODS To first establish a dose of air that would cause unequivocal neurological injury, anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 microL/kg of air into the internal carotid artery (n = 5 in each group). One hour later, anesthesia was discontinued. Animals were neurologically evaluated at 24 hours with the use of a scale ranging from 0 (normal) to 97 (coma) points. In a subsequent experiment, anesthetized rabbits received either heparin (n = 17) or saline (n = 15) 5 minutes before air injection (150 microL/kg). Heparin was given as a 200-IU/kg bolus and followed by a constant infusion of 75 IU.kg-1.h-1 for 2 hours. Equal volumes of saline were given to control rabbits. Two hours later, anesthesia was discontinued. Animals were neurologically evaluated 24 hours after air embolism. RESULTS There was a monotonic relationship between dose of air and severity of neurological impairment at 24 hours (P = 1.1 x 10(-7)). Animals receiving 150 microL/kg of air were unequivocally injured (score, 60 +/- 16). In the second experiment, heparin animals had significantly less neurological impairment at 24 hours (34 +/- 14) than saline controls (52 +/- 8) (P = .0013). CONCLUSIONS When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.

Marked Hemodilution Increases Neurologic Injury After Focal Cerebral Ischemia in Rabbits

Moderate hemodilution (hematocrit approximate 30%) reduces neurologic injury after focal cerebral ischemia.In contrast, both clinical and experimental studies suggest that marked hemodilution (hematocrit <30%) may exacerbate neurologic injury. We compared the effect of marked versus minimal hemodilution on cerebral infarct volume after focal cerebral ischemia in rabbits. Anesthetized New Zealand White rabbits underwent hemodilution by exchange of arterial blood with 6% high molecular weight hydroxyethyl starch. In the marked hemodilution group (n = 15) the target hemoglobin concentration was 6 g/100 mL. In the minimal hemodilution group (n = 15) the target hemoglobin concentration was 11 g/100 mL. After hemodilution, middle cerebral artery occlusion was achieved by embolizing an autologous blood clot via the internal carotid artery. Four hours after embolization, the animals were killed and their brains removed. Brains were sectioned, stained with 2,3,5-triphenyltetrazolium chloride, and infarct volumes determined via quantitative image analysis. Systemic physiologic variables were similar between groups, except for arterial hemoglobin concentration. The percentage of hemispheric infarct was significantly larger in the marked hemodilution group as compared to the minimal hemodilution group, 70% +/- 19% vs 51% +/- 23%, respectively (mean +/- SD); P = 0.02. Similarly, the percentage of infarct was greater in the hemodilution group as compared to the minimal hemodilution group in both cortex (73% +/- 18% vs 54% +/- 23%, respectively; P = 0.02) and subcortex (62% +/- 25% vs 44% +/- 23%, respectively; P = 0.04). These findings indicate that marked hemodilution exacerbates neurologic injury resulting from permanent focal ischemia. Although some degree of hemodilution may improve neurologic outcome, the advantage is lost at an extreme level of therapy. (Anesth Analg 1996;82:61-7)

Theoretical Assessment of Normobaric Oxygen Therapy to Treat Pneumocephalus: Recommendations for Dose and Duration of Treatment

Background Pneumocephalus has been linked to several clinical conditions, including headache, lethargy, and even brain herniation or death. The effects of different normobaric oxygen concentrations and durations of therapy on the rate of air absorption were examined. Methods An existing mathematical model of inert gas absorption was used. The model accounts for the major phenomena that determine absorption of bubbles, including surface tension, pressure dependence of bubble size, and removal of gases to the surrounding tissue. Sensitivity analysis tested reliability of our results. Results Times for a 50-ml air collection to have been absorbed were 5.8, 1.9, and 0.6 weeks at an FIO2 of 0.21, 0.4, and 1.0, respectively. Thirty percent and 72% of the air was absorbed in 2 days at an FIO2 of 0.4 and 1.0, respectively. The percent decrease in time for absorption achieved by increasing the FIO2 from 0.21 was nearly identical for different volumes of air. The benefit of increasing the FIO2 decreased with progressive increases in the FIO2. Increasing the FIO2 from 0.21 to 0.4 caused the time to total air absorption to decrease by 67%. In contrast, increasing the FIO2 from 0.8 to 1.0 caused the time to total air absorption to decrease by an additional 3%. Conclusions Based on mathematical model predictions, an FIO2 of 0.4 or 1.0 for at least 1 week or 2 days, respectively, will significantly decrease the time for absorption of a pneumocephalus.

A Comparison of Anesthetic Techniques for Awake Intubation in Neurosurgical Patients

Two different methods of achieving upper airway anesthesia for awake fiberoptic intubation were prospectively compared in patients undergoing surgery for cervical spine instability. Forty patients were randomized to either topical anesthesia or nerve block groups. Topical anesthesia patients were administered nebulized 4% lidocaine (approximately 20 ml) via the oropharynx plus a transtracheal injection of 4% lidocaine (3 ml). Nerve block patients underwent bilateral glossopharyngeal and superior laryngeal nerve blocks with 2% lidocaine (0.5-2 ml per injection site) plus a transtracheal injection of 4% lidocaine (3 ml). The quality of anesthesia for intubation was graded by observers blinded to group assignment. Mean arterial pressure, heart rate, Pao2, Paco2, pHa, SpO2, and plasma lidocaine concentrations were measured during the intubation sequence. Patient recall of intubation and discomfort were assessed during the postoperative period with visual analog scales. Time required for successful intubation and quality of intubation were not different between groups. Physiologic values for the two groups were similar. The mean total dose of lidocaine in the topical anesthesia group was approximately 2 times greater than that in the nerve block group (815 versus 349 mg; p < 0.0001). In contrast, mean plasma lidocaine concentration at initiation of intubation in the topical anesthesia group was half that of nerve block group (2.16 versus 4.23 micrograms/ml; p < 0.0001). Ten minutes later there was no difference for plasma lidocaine concentration between groups. No patients had evidence of seizures or neurologic change during the procedure. There was no difference in patient perception of discomfort during the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Doxycycline Reduces Early Neurologic Impairment after Cerebral Arterial Air Embolism in the Rabbit

Background Previous studies indicate leukocytes play a role in the pathogenesis of cerebral arterial air embolism. Because doxycycline inhibits numerous leukocyte activities, the authors hypothesized doxycycline would decrease neurologic impairment after cerebral arterial air embolism. Methods New Zealand White rabbits anesthetized with methohexital received either intravenous saline (n = 7) or 10 mg/kg doxycycline (n = 7) 1 h before administration of 100 micro liter/kg of air into the internal carotid artery. Somatosensory-evoked potentials (SSEPs) were recorded at 30-min intervals for the next 2 h. After the final recording, the anesthetic was discontinued, and animals recovered. Animals were neurologically evaluated 4 h after air embolism on a scale of 0 (normal) to 99 (coma) points. Results At 4 h, doxycycline animals had lesser neurologic impairment (46 +/- 23; median, 41) than animals that received saline (77 +/- 20; median, 81); P = 0.007. SSEP amplitude was greater in the doxycycline group at 60, 90, and 120 min after air embolism; P = 0.001, 0.006, 0.026, respectively. SSEP amplitudes at 30, 60, 90, and 120 min inversely correlated with 4 h neurologic impairment; tau = -0.43, -0.75, -0.85, -0.79, respectively. Conclusions Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism. Because groups could be distinguished electrophysiologically as soon as 1 h after air embolism and because SSEP amplitude inversely correlated with neurologic impairment, doxycycline appears to inhibit a key early ([approximately] 1 h) process in the pathophysiology of cerebral air embolism.

Somatosensory Evoked Potentials Correlate With Neurological Outcome in Rabbits Undergoing Cerebral Air Embolism

BACKGROUND AND PURPOSE Somatosensory evoked potentials (SSEPs) have been used as an outcome measure in models of cerebral air embolism despite the lack of studies correlating SSEPs with other measures of neurological injury. We examined the relationship between SSEPs and neurological impairment in the setting of cerebral air embolism. METHODS Anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 microL/kg of air into the internal carotid artery. SSEPs were recorded at intervals for the subsequent 2 hours. After the final recording the anesthetic was discontinued, and the animals recovered. Animals were neurologically evaluated at 3 and 24 hours after cerebral air embolism on a scale of zero (normal) to 97 (coma) points. RESULTS There was a clear relationship between the dose of air and 2-hour SSEP amplitude (P = .00003). SSEP amplitudes at 2 hours were inversely correlated with neurological impairment scores at 3 hours (r = -0.71, P < .0001). SSEP amplitudes at 2 hours were less in animals that died (11 +/- 16%; n = 9) than in those that survived to 24 hours (53 +/- 20%; n = 9) (P = .0008). CONCLUSIONS These results support SSEPs as an index of neurological impairment in this model of cerebral air embolism.

Secondary hypotensive insults in a rat forebrain ischemia model

Previous studies have shown that the recently injured brain has an increased sensitivity to subsequent brief episodes of severe ischemia. This investigation was designed to assess whether less severe secondary insults, which alone would be incapable of producing injury, exacerbate brain damage resulting from a primary episode of global ischemia. Rats were subjected to either 10 min of 2-vessel forebrain ischemia (primary insult alone), 20 min of hypotension (mean arterial pressure, MAP = either 40 or 25 mmHg) without vessel occlusion (secondary insult alone), or 10 min ischemia followed 1 h later by the hypotensive challenge (primary + secondary insult). Seven days later, the animals were neurologically evaluated and the brains then prepared for histologic analysis. Neither magnitude of secondary insult alone was found to produce injury. In contrast, the primary insult alone caused moderate damage in the hippocampus, caudoputamen and neocortex. With the exception of increased neuronal necrosis in the hippocampal CA1 sector in rats receiving the primary + secondary insult (MAP = 25 mmHg), no worsening of outcome could be attributed to the secondary insults. These results indicate that the recovering brain may not be as sensitive to hypoperfusion as has previously been suggested.