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Biomedical subjects

M E Kerr

Publications and source records attributed to M E Kerr.

At least 19 recordsLinked to original sources

The impact of cardiac complications on outcome in the SAH population.

OBJECTIVES: To determine the impact of cardiac complications (CdCs) on outcomes in patients with acute subarachnoid hemorrhage (SAH). PATIENTS AND METHODS: Eighty-one adult aneurysmal SAH patients with a fisher grade >1 and/or a Hunt and Hess grade >2 were recruited for this study. CdCs were defined as electrocardiogram (ECG) changes, myocardial necrosis, arrythmias, or pulmonary edema. Outcomes were assessed at 3, 6 and 12 months by telephone interview using the Modified Rankin Scale (MRS), Glasgow Outcome Scale (GOS), Barthel Index and Medical Outcome study Short Form-36 (SF-36). RESULTS: The CdCs occurred in 33% of patients. The most common CdCs were arrythmias and pulmonary edema (30%). There was no significant difference in mortality between the two groups. At 3 months there was a significant difference in the Barthel (P = 0.007) and the SF-36 (P = 0.014) with trends in the GOS (P = 0.049) and the MRS (P = 0.063). At 6 months a significant difference remained in the SF-36 (P = 0.028) and a trend in the Barthel (P = 0.069). CONCLUSION: Results show that CdCs may negatively impact outcomes in SAH patients up to 6 months following hemorrhage.

Adolescent↗

Dose response to cerebrospinal fluid drainage on cerebral perfusion in traumatic brain-injured adults.

OBJECT: Intracranial hypertension remains a common complication of traumatic brain injury (TBI). Ventriculostomy drainage is a recommended therapy to decrease intracranial pressure (ICP), but little empirical evidence exists to guide treatment. The authors conducted a study to examine systematically the effect of cerebral spinal fluid (CSF) drainage on ICP and indices of cerebral perfusion. METHODS: Intracranial pressure, cerebral perfusion pressure (CPP), cerebral blood flow velocity (CBFV), and near-infrared spectroscopy-determined regional cerebral oxygenation (rSO2) were measured in 58 patients (with Glasgow Coma Scale scores < or = 8) before, during, and after ventriculostomy drainage. Three randomly ordered CSF drainage protocols varied in the volume of CSF removed (1 ml, 2 ml, and 3 ml). Physiological variables were time averaged in 1-minute blocks from baseline to 10 minutes after cessation of ventricular drainage. There was a significant dose-time interaction for ICP with the three-extraction volume protocol, with incremental decreases in ICP (F [20, 1055] = 6.10; p = 0.0001). There was a significant difference in the CPP depending on the amount of CSF removed (F [2, 1787] = 3.22; p = 0.040) and across time (F [10, 9.58] = 11.9; p = 0.0003) without a significant dose-time interaction. A 3-ml withdrawal of CSF resulted in a 10.1% decrease in ICP and a 2.2% increase in CPP, which were sustained for 10 minutes. There was no significant dose, time or dose-time interaction with CBFV or rSO2. CONCLUSIONS: Cerebrospinal fluid drainage (3 ml) significantly reduced ICP and increased CPP for at least 10 minutes. Analysis of these findings supports the use of ventriculostomy drainage as a means of at least temporarily reducing elevated ICP in patients with TBI.

Adolescent↗

Effects of S-nitrosation of hemoglobin on hypoxic pulmonary vasoconstriction and nitric oxide flux.

Free hemoglobin (Hb) augments hypoxic pulmonary vasoconstriction (HPV), ostensibly by scavenging nitric oxide (NO). However, recent evidence suggests that Hb that is S-nitrosated may act as an NO donor and vasodilator. We studied the effects of oxyHb, Hb that is chemically modified to prevent heme binding or oxidation of NO (cyanometHb), and Hb that is S-nitrosated (SNO-Hb and SNO-cyanometHb) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused rabbit lungs. Perfusate containing either 4 microM oxyHb or SNO-Hb increased normoxic pulmonary artery pressure (Ppa), augmented HPV dramatically, and resulted in an 80% fall in eNO in comparison to perfusion with buffer, whereas 4 microM cyanometHb or SNO-cynanometHb had no effect on these variables. Excess glutathione (GSH) added to perfusate containing SNO-Hb resulted in a 20 to 40% fall in the perfusate SNO concentration, with a concomitant increase in metHb content, without affecting Ppa, HPV, or eNO. In conclusion, free Hb augments HPV by scavenging NO, an effect that is not prevented by S-nitrosation. NO released from SNO-Hb in the presence of GSH does not produce measurable vascular effects in the lung or changes in eNO because of immediate oxidation and metHb formation.

Analysis of Variance↗

Acetazolamide reduces hypoxic pulmonary vasoconstriction in isolated perfused rabbit lungs.

Carbonic anhydrase (CA) may modulate regional blood flow by mediating changes in extra- and intracellular pH. We hypothesized that CA inhibition with acetazolamide would inhibit the kinetics and magnitude of hypoxic pulmonary vasoconstriction (HPV). Isolated rabbit lungs were ventilated and perfused in situ at constant flow, with buffer containing red blood cells. Preparations were sequentially challenged with hypoxic (FI(O(2)) 0.05) and/or hypercapnic (FI(CO(2)) 0.10) gas mixtures for 5 or 10 min. In the experimental groups, acetazolamide (33 microM) was added to the perfusate after establishing baseline responses, and gas challenges were repeated; control groups were studied without acetazolamide. Acetazolamide reduced the increase in pulmonary artery pressure (DeltaPAP) and the rate of pressure rise by approximately 30-50% during hypoxia and combined hypoxia/hypercapnia. The reduction in DeltaPAP occurred for both 5 and 10 min challenges. Acetazolamide did not affect expired nitric oxide concentrations. We conclude that acetazolamide reduces both the magnitude and kinetics of HPV by a mechanism that does not involve nitric oxide.

Acetazolamide↗

Hemoglobin and red blood cells alter the response of expired nitric oxide to mechanical forces.

Expired nitric oxide (NO(e)) varies with hemodynamic or ventilatory perturbations, possibly due to shear stress- or stretch-stimulated NO production. Since hemoglobin (Hb) binds NO, NO(e) changes may reflect changes in blood volume and flow. To determine the role of blood and mechanical forces, we measured NO(e) in anesthetized rabbits, as well as rabbit lungs perfused with buffer, red blood cells (RBCs) or Hb following changes in flow, venous pressure (P(v)), and positive end-expiratory pressure (PEEP). In buffer-perfused lungs decreases in flow and P(v) reduced NO(e), but NO(e) rose when RBCs and Hb were present. These findings are consistent with changes in vascular NO production, whose detection is obscured in blood-perfused lungs by the more dominant effect of Hb NO scavenging. PEEP decreased NO(e) in all perfused lungs but increased NO(e) in live rabbits. The NO(e) fall with PEEP in isolated lungs is consistent with flow redistribution from alveolar septal capillaries to extra-alveolar vessels and decreased surface area or a direct, stretch-mediated depression of lung epithelial NO production. In live rabbits, increased NO(e) may reflect blood flow reduction and decreased Hb NO scavenging and/or autonomic responses that increase NO production. We conclude that blood and systemic responses render it difficult to use NO(e) changes as an accurate measure of lung tissue NO production.

Animals↗

Effects of the RBC membrane and increased perfusate viscosity on hypoxic pulmonary vasoconstriction.

Red blood cells (RBCs) augment hypoxic pulmonary vasoconstriction (HPV) in part by scavenging of nitric oxide (NO) by Hb (Deem S, Swenson ER, Alberts MK, Hedges RG, and Bishop MJ, Am J Respir Crit Care Med 157: 1181-1186, 1998). We studied the contribution of the RBC compartmentalization of Hb to augmentation of HPV and scavenging of NO in isolated perfused rabbit lungs. Lungs were initially perfused with buffer; HPV was provoked by a 5-min challenge with hypoxic gas (inspired O(2) fraction 0.05). Expired NO was measured continuously. Addition of free Hb to the perfusate (0.25 mg/ml) resulted in augmentation of HPV and a fall in expired NO that were similar in magnitude to those associated with a hematocrit of 30% (intracellular Hb of 100 mg/ml). Addition of dextran resulted in a blunting of HPV after free Hb but no change in expired NO. Blunting of HPV by dextran was not prevented by NO synthase inhibition with N(omega)-nitro-L-arginine and/or cyclooxygenase inhibition. RBC ghosts had a mild inhibitory effect on HPV but caused a small reduction in expired NO. In conclusion, the RBC membrane provides a barrier to NO scavenging and augmentation of HPV by Hb. Increased perfusate viscosity inhibits HPV by an undetermined mechanism.

Animals↗

Effect of endotracheal suctioning on cerebral oxygenation in traumatic brain-injured patients.

OBJECTIVE: In patients with severe head injuries, brain damage occurs not only from the primary trauma but also secondarily from a reduction in cerebral oxygenation as a result of brain swelling, ischemia, and elevated intracranial pressure (ICP). However, routine interventions designed to maintain oxygenation, such as endotracheal suctioning (ETS), also may negatively affect the cerebrovascular status by increasing the ICP. The purpose of this study was to determine whether ETS influences cerebral oxygenation in patients with traumatic brain injury. DESIGN: Descriptive, prospective, with repeated assessments within each patient. SETTING: Ten-bed trauma intensive care unit in a university Level I trauma center. SUBJECTS: Nineteen patients who were 16 yrs or older, had acute head injury, a Glasgow Coma Scale score < or =8; external ventricular drain and arterial pressure devices in place, and were intubated and mechanically ventilated. INTERVENTIONS: ETS protocol consisting of administration of four ventilator-delivered breaths at 135% of the patients' actual tidal volume, 100% F(IO)2, before and after suctioning with a standardized catheter at a 16-L flow rate. MEASUREMENTS AND MAIN RESULTS: This study examined cerebrovascular responses as measured by the traditional measures of ICP and cerebral perfusion pressure, as well as middle cerebral artery velocity and jugular venous oxygen tension that occurred during ETS in head-injured adults. The results of this study show that both ICP and cerebral perfusion pressure are increased during ETS. In the majority of patients (84%), the ICP returned to baseline values within 2 mins. CONCLUSIONS: The increase in jugular venous oxygen tension associated with increases in middle cerebral artery velocity and mean arterial pressure suggests that cerebral oxygen delivery was maintained during ETS. Cerebral changes associated with ETS using the described protocol are consistent with the preservation of cerebral oxygenation.

Adolescent↗

Factors that contribute to complications during intrahospital transport of the critically ill.

Transporting patients from the protective environment of the intensive care (ICU) unit to other areas of the hospital has become increasingly common since high technologic testing has become an integral part of health care assessment. The hazards of moving critically ill patients by ambulance or air transport are well recognized and standards of care have been developed based on delineation of these risks. Despite the existing evidence of hazards of interhospital hospital transport, less attention has been given to the potential hazards associated with the intrahospital transport of critically ill patients. A high incidence of serious hemodynamic or respiratory alteration is associated with the intrahospital transport of critically ill patients. In one third of critically ill intrahospital transports, technical mishaps (eg, i.v. disconnects, which could potentially lead to deleterious physiologic outcomes) may occur. As patient acuity increases, there is a greater risk of hemodynamic instability. The purpose of this study was to further investigate the patient complications during transportation to and from the ICU to a diagnostic or treatment site. The sample consisted of thirty-five critically ill patients from the Neuro/Trauma ICU who required continuous physiological monitoring and had an arterial catheter in place. The systemic blood pressure, heart rate and peripheral oxygen saturation were monitored at nine time points throughout the transport process. The incidence of defined technical mishaps that occurred when the patient was off the unit were also recorded. Transport factors examined included the length of time spent off the unit and the number and level of personnel accompanying the patient. A within-subject repeat measure design was used to examine the physiologic changes and mishaps that occurred. Results indicate that while the majority of patients experienced some physiologic responses as a result of transport, the responses were not of sufficient magnitude to be classified as a deleterious. Twenty-three technical mishaps, which included inadvertent ventilator and electrocardiogram disconnects, power failures, interruption of medication administration and disconnection of drainage devices were observed. Factors related to these occurrences of technical mishaps were the number of intravenous solutions and infusion pumps and the time spent outside of the ICU environment.

Adolescent↗

Effect of therapeutic hypothermia on the incidence and treatment of intracranial hypertension.

Therapeutic hypothermia initiated immediately after a severe head trauma holds promise for improving outcomes. However, the effect of hypothermia on intracranial pressure (ICP) is not yet known. This study was a secondary analysis, conducted within a National Institutes of Health clinical trial on the efficacy of therapeutic hypothermia, to determine the effects of therapeutic hypothermia on ICP and of interventions (i.e., cerebrospinal fluid drainage and mannitol administration) on intracranial hypertension. There were no significant differences in the overall incidence or treatment of intracranial hypertension between patients who were treated with therapeutic hypothermia and normal controls. Therapeutic hypothermia maintained the ICP at lower levels during the cooling phase, but once patients were rewarmed, the ICP elevated to the levels of normothermic patients.

Adolescent↗

Genetics and the central nervous system: apolipoprotein E and brain injury.

Apolipoprotein E (apoE), a protein produced by glial cells, is responsible for maintenance of the structural integrity of the microtubules within the axon of the neuron. The gene associated with apolipoprotein E, APOE, influences the construction and regeneration of the microtubules in an APOE allele-specific manner: APOE 2/2 may be neuroprotective, whereas APOE 4/4 may be neurodestructive. Thus, APOE appears to be one genetic factor that modifies the brain's response to insult, and therefore may modify the severity of neuropsychologic deficits. This article presents an overview of the genetic relation between APOE and neuropsychological function in Alzheimer disease and proposes a relation between APOE and recovery after head injury.

Apolipoproteins E↗

Effect of neuromuscular blockers and opiates on the cerebrovascular response to endotracheal suctioning in adults with severe head injuries.

BACKGROUND: Intracranial hypertension occurs in response to routine procedures such as endotracheal suctioning in patients with severe head injuries. In some patients, the intracranial pressure does not immediately return to baseline levels. OBJECTIVES: To examine the effect of drug administration on cerebrovascular response to endotracheal suctioning in adults with severe head injuries. METHODS: Seventy-one subjects were divided into 3 groups: those who received no drugs, those treated with opiates only (morphine sulfate and fentanyl citrate), and those treated with a neuromuscular blocking agent (vecuronium bromide) plus opiates. A controlled protocol involving 2 sequences of endotracheal suctioning that included hyperoxygenation, hyperinflation, and suctioning was used for all subjects. Two-way repeated-measures analyses of variance were done with type of drug as the between-subject factor and phase of suctioning as the within-subject factor. Survival analysis was used to compare the return of intracranial pressure to baseline levels among the 3 groups. RESULTS: Changes in intracranial pressure were significantly smaller in subjects who received a neuromuscular blocking agent plus opiates than in subjects who did not receive any drugs or received opiates only. The greatest increase in intracranial pressure from baseline was in the first and second phases of suctioning. The 3 groups showed no significant difference in the return of intracranial pressure to baseline level. CONCLUSIONS: Neuromuscular blockers attenuate the increases in intracranial pressure that occur with endotracheal suctioning. It is not known whether control of procedurally induced elevations in intracranial pressure affects long-term outcomes in adults with severe head injuries.

APACHE↗

Evaluation of three pancreas specific protein assays, TLI(trypsin-like immunoreactivity), PASP (pancreas specific protein) and CA 19-9 (glycoprotein) for use in the diagnosis of canine pancreatitis.

Three radioimmunoassays (RIA) for the pancreas specific proteins TLI, PASP and CA 19-9 were evaluated in serum from normal control dogs (n = 40) and dogs with pancreatitis (n = 20). Statistically significant differences (P < 0.05) were found for serum TLI and PASP levels between the control and pancreatitis groups. However, only 3/20 dogs with pancreatitis had serum TLI concentrations greater than the highest concentration in control dogs. Concentrations of PASP in serum were higher in 15/20 dogs with pancreatitis than in the control dogs. The magnitude of the increase in concentrations of PASP in pancreatitis was small in the majority of cases. Thus these assays are of limited clinical value in the diagnosis of pancreatitis. There was no cross-reactivity with dog serum in the CA 19-9 assay.

Amylases↗

Relationship between arterial carbon dioxide and end-tidal carbon dioxide in mechanically ventilated adults with severe head trauma.

OBJECTIVE: To examine the agreement and association of a noninvasive method of measuring CO2 (using end-tidal PCO2) with PaCO2 in mechanically ventilated adults with severe head trauma. DESIGN: A prospective, quasi-experimental, repeated-measures study was used to compare end-tidal PCO2 and PaCO2 at two time points: before and after a standardized endotracheal suctioning procedure. INTERVENTIONS: Controlled intervention of endotracheal suctioning. SETTING: The study was conducted at two intensive care units designated as Level 1 trauma centers. PATIENTS: A consecutive sample of 35 severe head-injured patients with a Glasgow Coma Scale score of < or = 8. MEASUREMENTS AND MAIN RESULTS: End-tidal PCO2 and PaC02 values were simultaneously obtained and compared. End-tidal PCO2 was measured, using a sidestream sensor placed in line of the ventilator circuit's deadspace. Arterial gases were drawn from an indwelling arterial catheter. No relationship was found between arterial and end-tidal measures (range r2 = .09 to r2 = .11). Using the Bland-Altman technique, agreement decreased as the amount of positive end-expiratory pressure increased. When a subset of patients (mechanically ventilated, with positive end-expiratory pressures of < 5 cm H2O, paralyzed, and sedated) were examined (n = 12), the correlation between the CO2 measures improved (r2 = .77). CONCLUSIONS: This study indicated that end-tidal PCO2 monitoring correlated well with PaCO2 in patients without respiratory complications or without spontaneous breathing, resulting in rebreathing of gases. However, its clinical validity is questionable in patients who have the greatest need for end-tidal PCO2 monitoring (i.e., patients who have respiratory distress or who are breathing spontaneously and overriding the ventilator.

Adult↗