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Biomedical subjects

J A Myburgh

Publications and source records attributed to J A Myburgh.

At least 19 recordsLinked to original sources
PubMed2005

Crisis management during anaesthesia: sepsis.

BACKGROUND: Anaesthesia with concurrent sepsis is risky, and involves consideration of possible organ dysfunctions-respiratory, cardiovascular, renal, and haematological--as well as ensuring that appropriate antibiotics are given after taking the necessary microbiological specimens. Because prompt attention needs to be paid to so many body systems, the place for a structured approach during anaesthesia for a septic patient was assessed. OBJECTIVES: To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK", supplemented by a specific sub-algorithm for sepsis, in the management of sepsis occurring in association with anaesthesia. METHODS: The potential performance of this structured approach for each of the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved. RESULTS: Sepsis was identified as the primary problem in 13 of the first 4000 reports (<1%) to AIMS. The incidents reported generally occurred in sick patients; 70% were ASA status III or worse. The COVER ABCD algorithm provided a diagnosis and corrective manoeuvre in only 15% (2/13) of reported incidents, and the sepsis sub-algorithm provided adequate therapeutic strategies in a further 38% (5/13) of the incidents. Eight cases required the use of additional sub-algorithms for desaturation (30%), cardiac arrest (15%), hypotension (8%), and aspiration (8%). CONCLUSION: Sepsis involves a serious physiological stress upon multiple organ systems. The use of a structured approach involving a core algorithm and additional sub-algorithms as required provides a series of checklists that can successfully deal with the complex multiple and interrelating problems that these patients present.

Algorithms↗
PubMed2005

Crisis management during anaesthesia: regurgitation, vomiting, and aspiration.

BACKGROUND: Regurgitation, vomiting and aspiration may occur unexpectedly in association with anaesthesia. "Aspiration/regurgitation" was ranked fifth in a large collection of previously reported incidents that arose during general anaesthesia. These problems are encountered by all practising anaesthetists and require instant recognition and a rapid, appropriate response. However, the diagnosis may not be immediately apparent as the initial presentation may vary from laryngospasm, desaturation, bronchospasm or hypoventilation to cardiac arrest. OBJECTIVES: To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK", supplemented by a specific sub-algorithm for regurgitation, vomiting and aspiration, in the management of these complications occurring in association with anaesthesia. METHODS: The potential performance of this structured approach for each of the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved. RESULTS: There were 183 relevant incidents of regurgitation, vomiting and aspiration among the first 4000 reports to the AIMS. Aspiration was documented in 96, was excluded in 69, and in 18 it could not be determined whether or not aspiration had occurred. It was considered that the correct use of an explicit algorithm would have led to earlier recognition and/or better management of the problem in 10% of all cases of regurgitation and vomiting and in 19% of those in which aspiration occurred. CONCLUSION: Regurgitation and/or aspiration should always be considered immediately in any spontaneously breathing patient who suffers desaturation, laryngospasm, airway obstruction, bronchospasm, bradycardia, or cardiac arrest. Any patient in whom aspiration is suspected must be closely monitored in an appropriate perioperative facility, the acuity of which will depend on local staffing and workload. If clinical instability is likely to persist or if there are concerns by attending staff, the patient should be admitted to a high dependency unit or intensive care unit.

Algorithms↗
PubMed2005

Crisis management during anaesthesia: pulmonary oedema.

BACKGROUND: Pulmonary oedema may complicate the perioperative period and the aetiology may be different from non-operative patients. Diagnosis may be difficult during anaesthesia and consequently management may be delayed. OBJECTIVES: To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK", supplemented by a specific sub-algorithm for pulmonary oedema, in its management occurring in association with anaesthesia. METHODS: The potential performance of this structured approach for each of the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved. RESULTS: Pulmonary oedema was identified in 35 (<1%) of the first 4000 reports to AIMS. The most frequent presenting sign was hypoxia (46%) and the most specific sign was the presence of frothy sputum (23%). The core algorithm, although successful in the management of the initial physiological upset, was found to be inadequate for the ongoing management of pulmonary oedema. A specific sub-algorithm for the management of perioperative pulmonary oedema was devised, tested against the reports and would have been effective, if properly applied, in the management of all but one of the reported cases. CONCLUSION: Successful recognition and management of perioperative pulmonary oedema is likely with the application of the structured algorithm and specific sub-algorithm approach outlined in this study.

Algorithms↗
PubMed2005

Driving cerebral perfusion pressure with pressors: how, which, when?

In traumatic brain injury, cerebral hypoperfusion is associated with adverse outcome, particularly in the early phases of management. This has resulted in the increased use of drugs such as adrenaline, noradrenaline, dopamine and phenylephrine to augment or maintain systemic blood pressures at near normal levels. This is now part of standard practice and is endorsed by the Brain Trauma Foundation guidelines. It probably matters little which agent is used, provided appropriate monitoring is in place and those reversible causes of hypotension are promptly excluded and treated. However, blindly applying management guidelines to all patients may negate these early benefits. The time has come move away from artificially separated concepts of "intracranial pressure" versus "cerebral perfusion pressure" based strategies. These should be considered in parallel and applied to an individual patient, rather than making the patient fit into an all-encompassing treatment algorithm. . A paradigm shift from a "set and forget" philosophy to one of "titration against time" to achieve appropriate therapeutic targets is now required. In this context the rational use of vasoactive agents to optimise cerebral perfusion pressure may be employed. On the basis of limited animal and human evidence, noradrenaline appears to be the most appropriate catecholamine for traumatic brain injury, although definitive, targeted trials are required.

Journal Article↗
PubMed2005

"Triple h" therapy for aneurysmal subarachnoid haemorrhage: real therapy or chasing numbers?

Despite technological and medical advances for the treatment of SAH that have had a positive impact on outcomes over the last 20 years, but the all-cause mortality for this often-catastrophic condition remains high at 12 - 15%. Survival will ultimately depend on the severity of the haemorrhage, the subsequent loss of functional neurones and the extracranial reserve of the patient. In this regard, advances in neuroradiology and operative techniques together with expert neurocritical care and rehabilitation provide the best chances of short- and long- term survival respectively. In this context, the contribution of cerebral vasospasm to attributable morbidity and mortality remains conjectural albeit real, and whilst medical anti-vasospastic therapies should be considered in vulnerable patients, they should be used with circumspection and caution. There is little or no evidence to justify the aggressive use of anti-vasospastic therapies as a preventative manner with exception of oral nimodipine in patients with low-grade aneurysmal subarachnoid haemorrhage. Concomitant use of induced hypertension/hypervolaemia/haemodilution cannot be recommended on current evidence, but if employed should be done on an individualised basis, considering the patients underlying neurological condition, cardiopulmonary reserve, adequacy of systemic and neurological monitoring and access to expert neuroradiological, neurosurgical and neurocritical care services.

Journal Article↗
PubMed2004

Quantifying cerebral autoregulation in health and disease.

OBJECTIVE: To review methods of quantifying human cerebral autoregulation in health and disease. DATA SOURCES: Articles and published abstracts on methods to quantify cerebral autoregulation in health and disease. SUMMARY OF REVIEW: Cerebral autoregulation is defined as the relationship between cerebral blood flow and cerebral perfusion pressure. Complex neurohumoral processes are involved in myogenic and metabolic mechanisms to maintain cerebral blood flow at a constant level in the presence of fluctuating systemic and cerebral perfusion pressures. Despite advances in physiological measurement, there is no standard measurement of cerebral blood flow and quantifying cerebral autoregulation remains problematic. Clinical monitors such as transcranial Doppler and jugular bulb oximetry have high levels of error with poor specificity and sensitivity. Cerebral autoregulation is impaired in traumatic brain injury and subarachnoid haemorrhage, so that cerebral blood flow becomes pressure-passive. Hypotension is associated with significant secondary neuronal damage following traumatic brain injury. Hypertensive emergencies represent failure of the upper autoregulatory threshold, often with devastating neurological consequences. The monitoring and treatment of autoregulatory failure remains limited and is essentially directed at maintaining an appropriate systemic blood pressure. Consequently, the use of strategies to manipulate cerebral perfusion requires care and circumspection. CONCLUSIONS: Cerebral autoregulation is impaired with brain injury with cerebral blood flow often becoming pressure-passive. The monitoring and treatment of autoregulatory failure is limited and usually directed at maintaining systemic blood pressure with the effectiveness of this strategy often being unknown.

Journal Article↗
PubMed2003

The effect of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under isoflurane anaesthesia in an ovine model.

The effects of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under steady-state isoflurane anaesthesia were compared with the awake state. Six studies each were conducted in two cohorts of adult ewes: awake sheep and those anaesthetized with 2% isoflurane anaesthesia. In random order, each animal received ramped infusions of adrenaline, noradrenaline (0-40 micrograms/min) and dopamine (0-40 micrograms/kg/min). Cerebral blood flow was measured continuously from changes in Doppler velocities in the sagittal sinus. Autoregulation was determined by linear regression analysis between cerebral blood flow and mean arterial pressure. Isoflurane did not significantly alter cerebral blood flow relative to pre-anaesthesia values (P > 0.05). All three catecholamines significantly and equivalently increased MAP from baseline in a dose dependent manner in both the awake and isoflurane cohorts. Although adrenaline significantly increased cerebral blood flow from baseline in the awake cohort (P < 0.01), none of the catecholamines significantly increased cerebral blood flow during isoflurane anaesthesia. No significant differences were demonstrated between the slopes and intercepts of regression lines for adrenaline, noradrenaline and dopamine within either cohort (ANCOVA). Inter-cohort comparisons between the two autoregulation curves demonstrated no significant difference between the slopes of the autoregulation curves for the awake (pooled slope = 0.39) and isoflurane cohorts (pooled slope = 0.28) (P > 0.05). Over a specific dose range, systemic hypertension induced by adrenaline, noradrenaline and dopamine did not significantly increase cerebral blood flow under 2% isoflurane anaesthesia. The concomitant administration of isoflurane and the catecholamines was not associated with altered autoregulatory function compared to the awake state.

Anesthesia, Inhalation↗
PubMed2003

Recombinant activated factor VII for exsanguinating haemorrhage post bilateral lung transplantation for extra-corporeal lung support-dependent respiratory failure.

Following three weeks of extracorporeal lung support for acute respiratory distress syndrome, a 15-year-old male underwent bilateral lung transplantation. This procedure was complicated by massive postoperative haemorrhage. The administration of recombinant activated Factor VII was associated with improved haemostasis. However, development of cardiac tamponade soon after injection required emergency exploration and evacuation of a large mediastinal clot.

Adolescent↗
PubMed2003

Antibiotic prophylaxis for external ventricular drains in neurosurgical patients: an audit of compliance with a clinical management protocol.

OBJECTIVE: To examine the clinical impact of a management protocol for external ventricular drains (EVD). PATIENTS AND METHODS: All patients with EVDs over a six-month period were reviewed retrospectively. Data concerning the indications for EVD placement, antibiotics and cerebrospinal fluid (CSF) analyses were collected. A restrictive antibiotic protocol (e.g. intravenous cephalothin 1g 6-hourly for 24 hours, unless other antibiotics were prescribed for a documented pre-existing infection) was introduced for all patients requiring placement of an EVD during the following six months and all patients were observed prospectively. Daily CSF samples were collected under sterile conditions and examined for organisms, cells, glucose and protein and sent for microbiological culture. External ventricular drains were removed after five days and replaced if further monitoring or CSF drainage was required. Adherence to the protocol and the incidence of ventriculitis was determined. RESULTS: Twelve patients with EVDs were identified during the 6 month pre-protocol period and 15 patients with EVDs were identified during the 6 month post-protocol period. There was no significant difference between the total (72 vs 88 days) and mean (6 vs 5.9 days) drain placement times between the two groups. There was no significant difference between the mean numbers of CSF samples in the two groups. CSF aspirates were not analysed in 35/72 samples (49%) in the pre-protocol group compared with 45/88 (51%) samples in the post-protocol group. Positive CSF Gram-stains were found in 3/12 (25%) patients in the pre-protocol group and in 0/15(0%) in the post-protocol group. Positive CSF cultures decreased significantly in the post-protocol group (17 vs 5, p = 0.0009). Prophylactic antibiotics were prescribed in 5/12 (42%) patients in the pre-protocol group compared with 12/15 (80%) patients in the post-protocol group. CONCLUSIONS: The protocol was associated with a statistically significant improvement in compliance with antibiotic prescription and reduction in the incidence of positive CSF cultures.

Journal Article↗
PubMed2002

Cerebrovascular carbon dioxide reactivity in sheep: effect of propofol or isoflurane anaesthesia.

Propofol and isoflurane are commonly used in neuroanaesthesia. Some published data suggest that the use of these agents is associated with impaired cerebral blood flow/carbon dioxide (CO2) reactivity. Cerebrovascular CO2 reactivity was therefore measured in three cohorts of adult merino sheep: awake (n=6), anaesthetized with steady-state propofol (15 mg/min; n=6) and anaesthetized with 2% isoflurane (n=6). Changes in cerebral blood flow were measured continuously from changes in velocities of blood in the sagittal sinus via a Doppler probe. Alterations in the partial pressure of carbon dioxide in arterial blood (PaCO2) over the range 18-63 mmHg were achieved by altering either the inspired CO2 concentration or the rate of mechanical ventilation. Cerebral blood flow/CO2 relationships were determined by linear regression analysis, with changes in cerebral blood flow expressed as a percentage of the value for a PaCO2 of 35 mmHg. Propofol decreased cerebral blood flow by 55% relative to pre-anaesthesia values (P=0.0001), while isoflurane did not significantly alter cerebral blood flow (88.45% of baseline, P=0.39). Significant linear relationships between cerebral blood flow and CO2 tension were determined in all individual studies (r2 ranged from 0.72 to 0.99). The slopes of the lines were highly variable between individuals for the awake cohort (mean 4.73, 1.42-7.12, 95% CI). The slopes for the propofol (mean 2.67, 2.06-3.28, 95% CI) and isoflurane (mean 2.82, 219-3.45, 95% CI) cohorts were more predictable. However, there was no significant difference between these anaesthetic agents with respect to the CO2 reactivity of cerebral blood flow.

Anesthetics, Inhalation↗
PubMed2002

The cerebrovascular effects of adrenaline, noradrenaline and dopamine infusions under propofol and isoflurane anaesthesia in sheep.

Infusions of catecholamines are frequently administered to patients receiving propofol or isoflurane anaesthesia. Interactions between these drugs may affect regional circulations, such as the brain. The aim of this animal (sheep) study was to determine the effects of ramped infusions of adrenaline, noradrenaline (10, 20, 40 micrograms/min) and dopamine (10, 20, 40 micrograms/kg/min) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR) and cerebral metabolic rate for oxygen (CMRO2). These measurements were made under awake physiological conditions, and during continuous propofol (15 mg/min) or 2% isoflurane anaesthesia. All three catecholamines significantly and equivalently increased mean arterial pressure from baseline in a dose-dependent manner in the three cohorts (P < 0.001). In the awake cohort (n = 8), dopamine (P < 0.01) significantly increased CBF from baseline whilst adrenaline and noradrenaline did not (P > 0.05). Under propofol (n = 6) and isoflurane (n = 6), all three catecholamines significantly increased CBF (P < 0.001). Dopamine caused the greatest increase in CBF, and was associated with significant increases in ICP (awake: P < 0.001; propofol P < 0.05; isoflurane P < 0.001) and CVR (isoflurane P < 0.05). No significant changes in CMRO2 were demonstrated. Under propofol and isoflurane anaesthesia, the cerebrovascular effects of catecholamines were significantly different from the awake, physiological state, with dopamine demonstrating the most pronounced effects, particularly under propofol. Dopamine-induced hyperaemia was associated with other cerebrovascular changes. In the presence of an equivalent effect on mean arterial pressure, the exaggerated cerebrovascular effects under anaesthesia appear to be centrally mediated, possibly induced by propofol- or isoflurane-dependent changes in blood-brain barrier permeability, thereby causing a direct influence on the cerebral vasculature.

Anesthesia↗
PubMed2001

Tolerance in baboon kidney transplantation with total lymphoid irradiation (TLI) and anti-CD3/CD4-idarubicin conjugates.

BACKGROUND: We previously reported the induction of transplantation tolerance by a modified wide field method of pretransplant total lymphoid irradiation (TLI), cumulative dose 800 cGy, given as 80 or 100 cGy fractions twice/week, in approximately one-third of chacma baboons receiving liver or kidney allografts (1-4) and in vervet monkeys receiving baboon kidney xenografts (5). In this study, the effects of the administration of brief courses of anti-CD3 or CD4-Idarubicin conjugates on the frequency and predictability of tolerance induction by TLI were examined. METHODS: TLI was administered pretransplant in doses of 800, 600, or 400 cGy. The conjugates were administered either after transplantation in doses of 0.25 mg/kg body weight, 3 times/week for 2 weeks, or as a single dose of 1.0 mg/kg body weight 24 hr before transplantation. RESULTS: Operational tolerance, defined as normal graft function >1 year after transplantation, was obtained in one-half of six baboons receiving the single dose of 1 mg/kg of Idarubicin conjugate pretransplant after 800 cGy of TLI and also in one of four baboons treated with 400 cGy of TLI and a single dose of anti-CD3 conjugate before transplantation. By contrast, administration of the conjugated antibodies 3 times/week for 2 weeks after transplantation prevented tolerance induction in all animals, providing further evidence for the involvement of active mechanisms, capable of inhibition by immunosuppressive agents, in tolerance induction with TLI, and of relevance to our reported clinical experience with TLI (6). CONCLUSIONS: These promising findings invite further studies with a larger number of animals and additional brief regimens of irradiation and antibody dosages and specificities.

Animals↗
PubMed2001

Epinephrine, norepinephrine and dopamine infusions decrease propofol concentrations during continuous propofol infusion in an ovine model.

OBJECTIVE: To determine the effects of exogenous ramped infusions of epinephrine, norepinephrine and dopamine on arterial and effluent brain blood concentrations of propofol under steady state intravenous anesthesia. DESIGN: Prospective, randomized animal study. SETTING: University research laboratory. SUBJECTS: Five adult female merino sheep. INTERVENTIONS: Induction (5 mg/kg) and continuous infusion of propofol (15 mg/min) with controlled mechanical ventilation to maintain PaCO2 40 mmHg. After 1 h of continuous anesthesia, each animal randomly received ramped infusions of epinephrine, norepinephrine (10, 20, 40 microg/min) and dopamine (10, 20, 40 microg x kg x min) in 3 x 5 min intervals followed by a 30-min washout period. MEASUREMENTS: Arterial and sagittal sinus whole blood for determination of propofol concentrations using high-pressure liquid chromatography. Cardiac output using a thermodilution method. Level of consciousness using an observational scale. MAIN RESULTS: All three drugs significantly and transiently increased cardiac output in a dose-dependent fashion to a maximum of 146-169% of baseline. Baseline arterial and sagittal sinus propofol concentrations were not statistically different prior to catecholamine infusions. All three drugs significantly reduced mean arterial propofol concentrations (95 % CI, p < 0.05): epinephrine to 41.8% of baseline (11.4-72), norepinephrine to 63 % (27-99) and dopamine to 52.9 % (18.5-87.3). There were parallel reductions of concentrations in sagittal sinus blood leaving the brain. The lowest blood concentrations were associated with emergence from anesthesia. Arterial concentrations were inversely related to the simultaneously determined cardiac output (r2 = 0.74, p < 0.0001). Comparison of the data with the predictions of a previously developed recirculatory model of propofol disposition in sheep showed the data were consistent with a mechanism based on increased first pass dilution and clearance of propofol secondary to the increased cardiac output. CONCLUSIONS: Catecholamines produced circulatory changes that reversed propofol anesthesia. These observations have potential clinical implications for the use of propofol in hyperdynamic circulatory conditions, either induced by exogenous catecholamine infusions or pathological states.

Anesthetics, Intravenous↗