Visual disturbance and residual paralysis.
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Atracurium↗
Biomedical subjects
A M Lam
Publications and source records attributed to A M Lam.
Thrombotic, infectious, and procedural complications of the jugular bulb catheter in the intensive care unit.
OBJECTIVE: An assessment of the thrombotic, infectious, and technical complications of continuous jugular bulb catheter monitoring in the intensive care unit (ICU) was made. METHODS: Over a 1-year period, 44 patients suffering from traumatic brain injury, subarachnoid hemorrhage, or stroke received jugular bulb catheter monitoring in the ICU. They were followed for catheter insertion complications and the development of bacteremia. In 20 patients chosen randomly, an ultrasonographic evaluation was performed after removal of the catheter for an assessment of internal jugular vein thrombosis. RESULTS: Of the 44 patients, 1 became bacteremic; the source was identified as a thoracostomy site. Among the complications related to the 44 catheter insertions, there were 2 instances of carotid artery puncture (4.5%), 1 misplaced catheter (thoracic placement), and 1 clinically insignificant hematoma. Of the 20 patients investigated with ultrasonography, 8 (40%) had nonobstructive, subclinical internal jugular vein thrombi after jugular bulb catheter monitoring (95% confidence interval, 19-61%). The median monitoring duration was 3 days (range, 1-6 d). No clinical factor was identified to be associated with thrombus formation. CONCLUSION: We conclude the following: 1) the risk of bacteremia related to the jugular bulb catheter was negligible; 2) complications related to catheter insertion were rare and clinically insignificant; and 3) the incidence of subclinical internal jugular vein thrombosis after jugular bulb catheter monitoring is considerable. Although it is worthy to note this complication, no patient with a thrombus became symptomatic in the present series. The risk-benefit assessment of this monitoring technique must include consideration of subclinical thrombosis.
Adolescent↗
Influence of closed head injury on isoflurane MAC in the rat.
We designed the present study to determine whether the minimum alveolar concentration (MAC) for isoflurane is decreased after closed head trauma (CHT) in rats and, if so, whether the decrease of MAC is related to the severity of neurological impairment following CHT. Isoflurane MAC was determined in 36 Sprague-Dawley rats. Then, at time = 0 h, animals were grouped. Group 1 (n = 8) received no CHT, group 2 (n = 14) received moderate CHT, and group 3 (n = 14) received severe CHT. Neurological severity score (NSS, 0 = no deficit and 25 = maximal impairment) and MAC were determined at 1, 4, 24, and 48 h. In groups 1 and 2, isoflurane MAC at 1, 2, 24, and 48 h (1.0-1.1 +/- 0.8-1.2%, median +/- range) was not significantly different from baseline (1.0-1.1 +/- 1.0-1.1%). In group 3, isoflurane MAC at 1, 2, 24, and 48 h (0.4 +/- 0.2-0.5%) was decreased as compared to baseline (1.1 +/- 1.0-1.1%). In group 2, NSS at 1 h was 18 +/- 11-21 and improved by 48 h to 9 +/- 4-15. In group 3, NSS at 1 h was 24 +/- 22-25 and was not significantly different from NSS at 48 h (24 +/- 24-25). Thus, moderate CHT does not significantly alter isoflurane MAC, whereas severe CHT equivalent to a Glasgow Coma Scale score of 3 to 6 significantly decreases isoflurane MAC.
Anesthetics, Inhalation↗
The influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats.
The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. Four groups (E-H) received the same treatment; in addition, head trauma was delivered using a weight-drop device to the left cranium (2 h after ethanol treatment in the acute ethanol groups). To assess the influence of acute plus chronic alcohol and whether the glutamate antagonist ketamine can modify the neurologic outcome following head trauma, two additional head trauma groups were studied: group I received both acute and chronic ethanol treatment and group J received acute ethanol (1.5 g/kg) IP plus ketamine (180 mg/kg). Neurologic assessment was performed at 1, 2, 4, 8, 10, and 24 hours after head trauma or sham trauma in all animals who survived the treatment (omitted in group J animals while still under the anesthetic influence of ketamine). At the end of 24 hours, or at the time of death, the animals were decapitated. Specific gravity was determined from brain tissues adjacent to the injury and the contralateral hemispheres and the volume of hemorrhagic necrosis was quantified. None of the rats in the sham trauma groups died or had neurologic deficits. Of the head trauma groups, the mortality in animals that received 3 g/kg of ethanol and the animals that received acute plus chronic ethanol treatment was 100% before the end of 24 hours. Fifty percent of the animals receiving low-dose acute ethanol treatment (1.5 g/kg) died before 24 hours. In contrast, the mortality in the other groups was only 30% (p < 0.05). The neurologic severity score was significantly higher (greater neurological deficit) in the surviving animals that received acute ethanol treatment at 10 and 24 hours than in rats receiving no ethanol or chronic ethanol treatment. Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.
Administration, Oral↗
Cerebral autoregulation following minor head injury.
The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI). Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.
Adolescent↗
Pentobarbital and venous oxygenation.
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Acute Disease↗
Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury.
Jugular bulb oxygen monitoring can be used to estimate the adequacy of cerebral blood flow to support cerebral metabolism after severe head injury. In the present study, the authors studied the cerebral arteriovenous oxygen difference (AVDO[2]) before and after treatment in 32 head-injured patients (Glasgow Coma Scale scores < or = 8) to examine the relationships among AVDO and cerebral perfusion pressure (CPP), delayed cerebral infarction, and outcome. Fifteen patients (Group A) underwent craniotomy for hematoma evacuation and 17 (Group B) received mannitol for sustained intracranial hypertension (intracranial pressure > 20 mm Hg, > 10 minutes). Radiographic evidence of delayed cerebral infarction was observed in 14 patients. Overall, 17 patients died or were severely disabled. Cerebral AVDO(2) was elevated before craniotomy or mannitol administration; the mean AVDO(2) for all patients before treatment was 8.6 +/- 1.8 vol%. Following craniotomy or mannitol administration, the AVDO(2) decreased in 27 patients and increased in five patients (mean AVDO(2) 6.2 +/- 2.1 vol% in all patients; 6 +/- 1.9 vol% in Group A; and 6.4 +/- 2.4 vol% in Group B). The mean CPP was 75 +/- 9.8 mm Hg and no relationship with AVDO(2) was demonstrated. Before treatment, the AVDO(2) was not associated with delayed cerebral infarction or outcome. By contrast, a limited improvement in elevated AVDO(2) after craniotomy or mannitol administration was significantly associated with delayed cerebral infarction (Group A: p < 0.001; Group B: p < 0.01). Similarly, a limited improvement in elevated AVDO(2) after treatment was significantly associated with an unfavorable outcome (Group A: p < 0.01; Group B: p < 0.001). In conclusion, these findings strongly indicate that, despite adequate cerebral perfusion, limited improvement in elevated cerebral AVDO(2) after treatment consisting of either craniotomy or mannitol administration may be used to help predict delayed cerebral infarction and poor outcome after traumatic brain injury.
Adult↗
Changes in intracranial pressure associated with apneumic retractors.
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Animals↗
Resident education and unreviewed material.
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Anesthesiology↗
The variability of cerebrovascular reactivity with posture and time.
Transcranial Doppler (TCD) ultrasonography has been used in a variety of clinical contexts to assess cerebrovascular reserve by measuring carbon dioxide reactivity. Reproducibility with time and altered position of the patient is examined in the present study. Carbon dioxide reactivity was determined in 10 healthy volunteers using TCD. Hypocarbia was produced by voluntary hyperventilation, and hypercarbia was produced by rebreathing from a circuit primed with 7% carbon dioxide. Each patient was studied in the supine position twice (1 week apart) and once in the seated position. Carbon dioxide reactivity was determined from linear regression analysis of paired middle cerebral artery flow velocity and end-tidal carbon dioxide values. Analysis of covariance for repeated measures was used for statistical analysis. Both the absolute slope and the relative slope (absolute slope expressed as a percentage of flow velocity at 40 mm Hg) were compared. In the supine position, flow velocity, absolute and relative slopes, and mean arterial pressure were similar from one week to the next at all carbon dioxide levels. In contrast, flow velocity, mean arterial pressure (adjusted for hydrostatic gradient), and absolute slope were decreased in the seated position (p < 0.05). No difference was observed when the relative slope was used for comparison. We conclude that absolute carbon dioxide reactivity is reproducible over time but may be influenced by position. Relative reactivity (relative slope), however, was both time and position independent.
Administration, Inhalation↗
Evaluation of impaired cerebral autoregulation by the Valsalva maneuver.
BACKGROUND AND PURPOSE: Transcranial Doppler sonography has recently been used to describe cerebral hemodynamics during the Valsalva maneuver in normal human subjects. Since some changes in flow velocity during the Valsalva maneuver seem to reflect the brain's autoregulatory response to a decrease in cerebral perfusion pressure during the strain, we hypothesized that this method could identify vascular territories with impaired autoregulatory capacity. METHODS: Eight patients with unilateral (n=7) or bilateral (n=1) severe obstruction of the internal carotid artery and impaired vascular responses to the CO2 reactivity test and to dynamic autoregulation testing were studied. We compared changes in flow velocities and blood pressures during defined phases of the Valsalva maneuver in the patients with the results in a group of 17 normal volunteers. We defined two indices to evaluate autoregulatory capacity based on the response to the Valsalva maneuver. RESULTS: During the Valsalva maneuver, changes in flow velocity in the middle cerebral arteries ipsilateral to the lesions showed characteristic abnormalities compared with the normal pattern. Autoregulatory indices of these vessels as defined by the Valsalva maneuver were significantly different from those with normal vascular reactivity to CO2 (P<.0001). There were good correlations between an index based on the changes in flow velocity and blood pressure in phase II and the results of the CO2 test (r=.78; P<.0001) or those of dynamic autoregulatory testing (r=.6; P<.0001). CONCLUSIONS: Vascular territories with severely impaired vasomotor reactivity due to carotid obstruction can be identified by transcranial Doppler sonography by their pattern of flow velocity changes if their autoregulatory capacity is challenged during the Valsalva maneuver.
Adult↗
Intraoperative use of transcranial Doppler ultrasonography.
Transcranial Doppler (TCD) ultrasonography is a diagnostic tool that is well established in the fields of neurology and neurosurgery. There are many potential applications of TCD ultrasonographic monitoring in the perioperative care of the patient at risk of cerebral ischemia, the most important of which are detailed in this article. The introduction of TCD ultrasonography has made it possible to monitor intraoperative CBF changes in a continuous, noninvasive manner. Further refinement in the technology will delineate its appropriate use as an intraoperative monitor.
Brain Ischemia↗
Jugular bulb oximetry for the monitoring of cerebral blood flow and metabolism.
Jugular bulb oximetry can be used to assess the balance between oxygen supply and demand to the brain, measure metabolic byproducts, and determine cerebral blood flow. It has been useful in guiding the management of patients who are at risk of developing global ischemia. In this article, the principles upon which this monitor is based are discussed. Technical considerations such as placement techniques, factors affecting accuracy, limitations of the technique, and proper interpretation of oximetric values are reviewed. Lastly, specific clinical applications are presented.
Brain↗
Laparoscopic Burch colposuspension for stress incontinence: preliminary results.
OBJECTIVE: To assess the safety, effectiveness and potential benefits of laparoscopic Burch colposuspension. DESIGN: Non-randomised prospective study. SUBJECTS: Fifteen women, presenting consecutively with urodynamically confirmed urinary stress incontinence. RESULTS: The operation was successfully completed with no perioperative morbidity in 14 women. One woman subsequently underwent laparotomy after injury to the inferior epigastric artery. The average duration of surgery was 110 minutes, postoperative catheterisation 30 hours, and hospital stay 2.3 days. There was little postoperative discomfort. Most women were able to return to normal activities within one to two weeks. At follow-up (6 weeks-9 months) all the women were continent. CONCLUSION: Laparoscopic Burch colposuspension is a safe and feasible alternative to the open technique. Early results show the benefits of easy access to the cave of Retzius, a clear view of the operating field, minimal intraoperative blood loss, shortened postoperative catheterisation and hospitalisation times, little postoperative pain and early return to normal lifestyle.
Female↗
Change in cerebral blood flow velocity with onset of EEG silence during inhalation anesthesia in humans: evidence of flow-metabolism coupling?
In eight subjects anesthetized with moderate to high doses of inhalation anesthetics (isoflurane or desflurane) during normocapnia, the onset of electrical silence in EEG was associated with a sudden reduction of blood flow velocity monitored from the middle cerebral artery. The magnitude of this reduction was 38 +/- 11% (mean +/- SD; range 24-44%). The change in EEG always preceded the change in flow velocity by 5-7 s. These observations suggest that some flow-metabolism coupling mechanism is preserved during inhalation anesthesia in humans.
Adolescent↗
Cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced EEG suppression.
We studied cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced electrical silence of the electroencephalogram (EEG) in 10 patients. Anaesthesia was induced with propofol 2.5 mg kg-1, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1, and a propofol infusion of 250-300 micrograms kg-1 min-1 was used to induce EEG silence. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by 24 (SEM 5) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler. Carbon dioxide reactivity was tested by varying PaCO2 between 4.0 and 7.0 kPa and recording vmca simultaneously. Although absolute carbon dioxide reactivity was reduced, relative carbon dioxide reactivity was within normal limits for all patients studied (mean 8.5 (SEM 0.8) cm s-1 kPa-1 and 22 (2)% kPa-1, respectively). No significant change in vmca (34 (2) and 35 (2) cm s-1) was observed with the increase in MAP (77 (4) to 101 (4) mm Hg) during autoregulation testing. We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remain intact during propofol-induced isoelectric EEG.
Adult↗
Cerebrovascular response to carbon dioxide during sodium nitroprusside- and isoflurane-induced hypotension.
We have examined the cerebrovascular response to carbon dioxide during normotension, sodium nitroprusside (SNP)-induced hypotension and high dose isoflurane-induced hypotension in 10 patients who received a standardized general anaesthetic. Carbon dioxide reactivity was determined by varying PaCO2 between 3.0 and 8.0 kPa and recording simultaneously blood flow velocity from the middle cerebral artery (vmca). The paired vmca-PaCO2 data were analysed using linear regression to determine carbon dioxide reactivity. During hypotension, both high-dose isoflurane and SNP reduced significantly mean absolute (from 17.4 (SEM 2.3) to 13.0 (1.7) and 8.8 (1.3) cm s-1 kPa-1, respectively; P < 0.05) and relative (from 32.5 (3.8) to 23.6 (2.0) and 15.5 (1.3)% kPa-1, respectively; P < 0.05) cerebrovascular reactivity to carbon dioxide. This reduction was greater during SNP-induced hypotension (P < 0.05). We conclude that cerebrovascular reactivity to carbon dioxide was attenuated during isoflurane and SNP-induced hypotension, and that it was better preserved during isoflurane-induced hypotension.
Adult↗
Ketamine does not increase cerebral blood flow velocity or intracranial pressure during isoflurane/nitrous oxide anesthesia in patients undergoing craniotomy.
Ketamine's effect on cerebral hemodynamics is controversial. We hypothesized that ketamine would not increase intracranial pressure (ICP) and cerebral blood flow (CBF) velocity in anesthetized, ventilated patients. Twenty patients requiring craniotomy for brain tumor or cerebral aneurysm were studied. After induction with thiopental, anesthesia was maintained with isoflurane and nitrous oxide in oxygen. During controlled ventilation (PaCO2 34 +/- 1 mm Hg); middle cerebral artery blood flow velocity (VMCA), mean arterial blood pressure (MAP), bilateral frontooccipital processed electroencephalogram (EEG), and ICP were measured before and for 10 min after intravenous ketamine 1.0 mg/kg. Cerebral arteriovenous oxygen content difference (AVDO2) and cerebral perfusion pressure (CPP) were calculated. After ketamine, MAP, CPP, PaCO2, and AVDO2 were unchanged. ICP decreased from 16 +/- 1 mm Hg to 14 +/- 1 mm Hg (mean +/- SE; P < 0.001) and VMCA decreased from 44 +/- 4 cm/s to 39 +/- 4 cm/s (P < 0.001). Total EEG power decreased (P < 0.02). These results suggest that ketamine can be used in anesthetized, mechanically ventilated patients with mildly increased ICP without adversely altering cerebral hemodynamics.
Anesthesia, Inhalation↗