PubMed Health⌕ Search

Biomedical subjects

A M Lam

Publications and source records attributed to A M Lam.

At least 19 recordsLinked to original sources
PubMed1997

Impaired cerebral autoregulation after mild brain injury.

BACKGROUND: Severe head injury may impair cerebral autoregulation, which can increase the risk of secondary neuronal injury. The likelihood of impairment in autoregulation is assumed to be low with mild head injury. We report here the absence of cerebral autoregulation in a patient who suffered a concussion from an automobile accident 6 days earlier. METHODS: The patient participated in a clinical study approved by the institutional human subjects review committee, investigating the dose-effect relationship of anesthetics on cerebral autoregulation. The patient was scheduled to undergo repair of a knee injury suffered during a motor vehicle accident, during which she had a concussion. The screening evaluation revealed no evidence of neurologic disease. The test was to be performed three times in each patient: baseline autoregulation measurements during stable fentanyl-nitrous oxide anesthesia, second and third measurements during low dose and high dose of the anesthetic to which the patient was assigned. Autoregulation was tested by increasing the mean systemic blood pressure from 80 mm Hg-100 mm Hg using a phenylephrine infusion while simultaneously recording flow velocity from a middle cerebral artery using transcranial Doppler ultrasonography. RESULTS: Static autoregulation testing during baseline testing demonstrated complete absence of this homeostatic mechanism and the study was canceled. Repeated testing in the recovery unit after the patient awoke showed identical results. CONCLUSIONS: Trivial mild head injury may result in loss of cerebral autoregulation. A clinical study of a larger series to document the incidence is warranted.

Adult↗
PubMed1997

Combined hemodilution and hypotension monitored with jugular bulb oxygen saturation, EEG, and ECG decreases transfusion volume and length of ICU stay for major orthopedic surgery.

STUDY OBJECTIVE: To assess the efficacy and safety of hemodilution combined with induced hypotension during surgery. DESIGN: Randomized, nonblinded, controlled study. SETTING: Operating room suite and intensive care unit (ICU) at a university hospital. PATIENTS: 16 ASA physical status I and II patients who underwent general or general plus epidural anesthesia for major orthopedic surgery. INTERVENTIONS: In Group 1 (n = 10), mean arterial blood pressure (MAP) was decreased to 50 mmHg by increasing the inspired concentration of isoflurane and injecting 75 mg of 0.5% bupivacaine into the epidural catheter. Hematocrit was decreased to 20% by phlebotomy and simultaneous infusion of crystalloid and colloid. In Group 2 (n = 6), isoflurane was adjusted to maintain MAP within 20% of baseline values, and no phlebotomy or hemodilution was used. MEASUREMENTS AND MAIN RESULTS: Efficacy of hemodilution combined with induced hypotension (Group 1) was compared to standard management of blood volume and pressure (Group 2) by measuring transfusion volume and length of ICU stay. Safety of hemodilution/hypotension was determined by measuring the electroencephalogram, internal jugular venous oxygen saturation, the electrocardiogram, and central venous oxygen saturation. In Group 1, both the volume of homologous blood (225 +/- 150 ml) and total blood (1440 +/- 286 ml) was significantly less than the volume of homologous blood transfused in Group 2 (2650 +/- 878 ml). No patients in Group 1, but all patients in Group 2 required ICU admission (3.5 +/- 1.6 days) for treatment to prevent sequelae from, or progression of, moderate-severe tissue edema and metabolic acidosis. Cerebral and myocardial measures were not significantly different between groups. CONCLUSIONS: Hemodilution combined with induced hypotension was safe and may reduce the need for transfusion and ICU admission.

Adult↗
PubMed1997

Intracranial pressure, middle cerebral artery flow velocity, and plasma inorganic fluoride concentrations in neurosurgical patients receiving sevoflurane or isoflurane.

UNLABELLED: This study examined the concentration-related effects of sevoflurane and isoflurane on cerebral physiology and plasma inorganic fluoride concentrations. Middle cerebral artery flow velocity (Vmca), intracranial pressure (ICP), electroencephalogram (EEG) activity, and jugular bulb venous oxygen saturation were measured, and cerebral perfusion pressure (CPP) and estimated cerebral vascular resistance (CVRe) were calculated at baseline and at 0.5, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC) sevoflurane (n = 8) or isoflurane (n = 6). Mannitol 0.5-0.75 g/kg was given before dural incision, and blood was sampled for plasma inorganic fluoride during surgery and for up to 72 h postoperatively. Both sevoflurane and isoflurane decreased Vmca (to 31 +/- 12 - 36 +/- 14 cm/s, mean +/- SD), did not significantly alter ICP (13 +/- 9 - 15 +/- 11 mm Hg), and did not cause epileptiform EEG activity. With sevoflurane, decreased Vmca was accompanied by decreased CPP and unchanged CVRe at 0.5 MAC, and unchanged CPP and increased CVRe at 1.0 and 1.5 MAC. Plasma inorganic fluoride was 39.0 +/- 12.9 microM at the end of anesthesia (3.2 +/- 2.0 MAC hours) with sevoflurane, similar to the value (36.2 +/- 3.9 microM) for 3.7 +/- 0.1 MAC hours sevoflurane in patients not receiving mannitol. Decreased Vmca during sevoflurane presumably results from decreased cerebral metabolic rate, with CVRe changing secondarily in accord with CPP. Plasma inorganic fluoride does not seem to be altered by mannitol-induced diuresis. IMPLICATIONS: In neurosurgical patients, sevoflurane decreased middle cerebral artery flow velocity and caused no epileptiform electroencephalogram activity and no increase of intracranial pressure or plasma inorganic fluoride. These effects are suitable for neurosurgery. Two other possible effects of sevoflurane, i.e., increased cerebrospinal fluid volume and/or intracranial elastance, may not be suitable for neurosurgery and warrant further study.

Anesthetics, Inhalation↗
PubMed1997

The rate of blood withdrawal affects the accuracy of jugular venous bulb. Oxygen saturation measurements.

BACKGROUND: Accuracy of jugular venous oxygen saturation (SjvO2) measurement depends on sampling of cerebral venous outflow blood not contaminated by systemic venous blood. The influence of the rate of blood withdrawal has not been determined. METHODS: The authors examined the effect of withdrawing blood at different rates from jugular venous bulb catheters (JVBC) on SjvO2 in 10 mechanically ventilated patients undergoing neurosurgical procedures. All patients received a standardized anesthetic consisting of propofol, fentanyl, vecuronium, and isoflurane. Routine monitors included electrocardiograph (ECG), invasive blood pressure, pulse oximetry, and a JVBC. During a period of stable anesthetic and surgical conditions, JVBC blood samples were drawn at 2, 4, and 10 ml/min using a calibrated pump (Harvard Pump model 900, Harvard Apparatus, South Natick, MA) during mild and moderate hypocapnia (arterial carbon dioxide tension [PaCO2], 26.0 +/- 0.5 and 33.0 +/- 0.5 mmHg). RESULTS: Faster rates of withdrawal (10 and 4 ml/min vs. 2 ml/min) resulted in significantly higher SjvO2 values at both levels of PaCO2 (66.0 +/- 3% and 61.2 +/- 3% vs. 56.9 +/- 3% at PaCO2 = 26.0 +/- 0.5 mmHg, and 75.0 +/- 3% and 71.3 +/- 3% vs. 68.0 +/- 3% at PaCO2 = 33.0 +/- 0.5 mmHg, respectively; P < 0.01). CONCLUSIONS: The authors conclude that the SjvO2 values measured with intermittent sampling are affected by the rate of withdrawing blood from JVBC, probably as a result of extracranial contamination. They recommend blood samples should be drawn slowly.

Adult↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1995

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↗