Biomedical subjects
Publications and source records attributed to John A Ulatowski.
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Modified Hb solutions have been developed as O(2) carrier transfusion fluids, but of concern is the possibility that increased scavenging of nitric oxide (NO) within the plasma will alter vascular reactivity even if the Hb does not readily extravasate. The effect of decreasing hematocrit from approximately 30% to 18% by an exchange transfusion of a 6% sebacyl cross-linked tetrameric Hb solution on the diameter of pial arterioles possessing tight endothelial junctions was examined through a cranial window in anesthetized cats with and without a NO synthase (NOS) inhibitor. Superfusion of a NOS inhibitor decreased diameter, and subsequent Hb transfusion produced additional constriction that was not different from Hb transfusion alone but was different from the dilation observed by exchange transfusion of an albumin solution after NOS inhibition. In contrast, abluminal application of the cross-linked Hb produced constriction that was attenuated by the NOS inhibitor. Neither abluminal nor intraluminal cross-linked Hb interfered with pial arteriolar dilation to cromakalim, an activator of ATP-sensitive potassium channels. Pial vascular reactivity to hypocapnia and hypercapnia was unaffected by Hb transfusion. Microsphere-determined regional blood flow indicated selective decreases in perfusion after Hb transfusion in the kidney, small intestine, and neurohypophysis, which does not have tight endothelial junctions. Administration of a NOS inhibitor to reduce the basal level of NO available for scavenging before Hb transfusion prevented further decreases in blood flow to these regions compared with NOS inhibition alone. In contrast, blood flow to skeletal and left ventricular muscle increased, and cerebral blood flow was unchanged after Hb transfusion. This cross-linked Hb tetramer is known to appear in renal lymph but not in urine. We conclude that cell-free tetrameric Hb does not scavenge sufficient NO in the plasma space to significantly affect baseline tone in vascular beds with tight endothelial junctions but does produce substantial constriction in beds with porous endothelium. The data support increasing the molecular size of Hb by polymerization or conjugation to limit extravasation in all vascular beds to preserve normal vascular reactivity.
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PURPOSE OF REVIEW: Hypertonic saline solutions have received renewed attention as effective agents for the treatment of cerebral edema and in brain resuscitation in a variety of brain injury paradigms. Although evidence of the beneficial action of hypertonic saline solutions in traumatic brain injury is robust, data supporting use in other conditions are only now mounting. RECENT FINDINGS: Osmotic properties of hypertonic saline solutions have been well studied in laboratory-based studies in animal models and in patients with acute brain injury. There are, in addition, emerging data on the extraosmotic actions on brain pathophysiology. This review cites baseline literature and provides new evidence of actions of hypertonic saline solutions: (a). in augmenting cerebral blood flow after subarachnoid hemorrhage, (b). as an antiinflammatory adjunct, and (c). utility in chemonucleolysis for intervertebral disc disease and treatment of seizures associated with severe hyponatremia. SUMMARY: Brain injury from diverse etiologies including trauma, ischemic stroke, global cerebral ischemia from cardiac arrest, intraparenchymal or subarachnoid hemorrhage, infection, or toxic-metabolic derangements are commonly encountered in the clinical setting. Many of these conditions are associated with cerebral edema with or without elevated intracranial pressure. Osmotherapy constitutes the cornerstone of medical therapy for such patients. Hypertonic saline solutions have received renewed attention in clinical practice as osmotic agents for cerebral resuscitation. This article reviews experimental and clinical evidence of the efficacy of hypertonic saline solutions and elaborates on their use in patients with acute neurologic injury. Important areas for current and future research are highlighted before the use of hypertonic saline solutions can be accepted for widespread use.
BACKGROUND: Although respiratory failure commonly occurs during the course of myasthenia gravis (MG), it is rarely described at presentation in patients with previously unrecognized MG. MATERIAL/METHODS: We determined the prevalence and clinical characteristics of patients with respiratory failure associated with undiagnosed MG by review of the medical records of all patients who were diagnosed with MG related respiratory failure at four University hospitals. Respiratory failure was defined on the basis of a forced vital capacity < or =1 liter, negative inspiratory force < or =20 cm H2O, or requirement of mechanical ventilation. RESULTS: Out of 51 MG patients with respiratory failure, 7(14%) patients had no previous diagnosis of MG. Another patient was identified after the review. The mean age of these 8 patients was 56 years (range 23-76 years); six were women. Five had previous episodes of unexplained respiratory failure. On initial evaluation, ocular or bulbar signs were present in 7 patients. The diagnosis of MG was made by edrophonium test (n=3), edrophonium test with positive acetylcholine antibody levels or repetitive nerve stimulation (n=2), repetitive nerve stimulation with positive acetylcholine antibody levels (n=2), and positive acetylcholine antibody levels alone (n=1). Seven patients required mechanical ventilation. Plasma exchange (n=7) or intravenous immunoglobulins (n=1) resulted in successful extubation or resolution of symptoms in all patients. CONCLUSIONS: Respiratory failure can occur at presentation in MG. A high index of suspicion should be maintained in patients with previous history of unexplained respiratory failures.
BACKGROUND AND PURPOSE: It has been reported that National Institutes of Health Stroke Scale (NIHSS) scores correlate poorly with hypoperfused tissue measured by perfusion-weighted imaging (PWI) in nondominant hemisphere stroke. We conducted 2 studies to determine whether tests of hemispatial neglect provide a better measure of hypoperfusion and reperfusion than NIHSS in nondominant hemisphere stroke. METHODS: In study 1, 74 patients with acute ischemic, supratentorial stroke were administered the NIHSS, tests of neglect or aphasia, and diffusion-weighted imaging (DWI) and PWI on day 1 (<24 hours from onset) of stroke. Pearson correlations between volumes of PWI/DWI abnormality and functional tests were calculated. In study 2, 10 patients with acute, nondominant hemisphere stroke who were candidates for intervention to restore perfusion underwent PWI, DWI, NIHSS, and a line cancellation test on days 1 and 3. Correlations between change in volumes of PWI/DWI abnormality and change in functional tests were calculated. RESULTS: In study 1, in nondominant hemisphere stroke, volume of PWI abnormality correlated significantly with neglect scores (r=0.71; P<0.002) but not with NIHSS scores (r=0.39; P=NS). In dominant hemisphere stroke, volume of PWI abnormality correlated better with aphasia scores (r=0.50; P=0.0001) than with NIHSS scores (r=0.45; P=0.001). In study 2, change in volume of hypoperfused tissue on PWI correlated with change in line cancellation performance (r=0.83; P=0.003) but not with change in NIHSS score (r=0.26; P=NS). CONCLUSIONS: Tests of hemispatial neglect may better reflect dysfunction and reperfusion than NIHSS for patients with nondominant hemisphere stroke.
The effect of transfusing a nonextravasating, zero-link polymer of cell-free hemoglobin on pial arteriolar diameter, cerebral blood flow (CBF), and O2 transport (CBF x arterial O2 content) was compared with that of transfusing an albumin solution at equivalent reductions in hematocrit (approximately 19%) in anesthetized cats. The influence of viscosity was assessed by coinfusion of a high-viscosity solution of polyvinylpyrrolidone (PVP), which increased plasma viscosity two- to threefold. Exchange transfusion of a 5% albumin solution resulted in pial arteriolar dilation, increased CBF, and unchanged O2 transport, whereas there were no significant changes over time in a control group. Exchange transfusion of a 12% polymeric hemoglobin solution resulted in pial arteriolar constriction and unchanged CBF and O2 transport. Coinfusion of PVP with albumin produced pial arteriolar dilation that was similar to that obtained with transfusion of albumin alone. In contrast, coinfusion of PVP with hemoglobin converted the constrictor response to a dilator response that prevented a decrease in CBF. Pial arteriolar dilation to hypercapnia was unimpaired in groups transfused with albumin or hemoglobin alone but was attenuated in the largest vessels in albumin and hemoglobin groups coinfused with PVP. Unexpectedly, hypocapnic vasoconstriction was blunted in all groups after transfusion of albumin or hemoglobin alone or with PVP. We conclude that 1) the increase in arteriolar diameter after albumin transfusion represents a compensatory response that prevents decreased O2 transport at reduced O2-carrying capacity, 2) the decrease in diameter associated with near-normal O2-carrying capacity after cell-free polymeric hemoglobin transfusion represents a compensatory mechanism that prevents increased O2 transport at reduced blood viscosity, 3) pial arterioles are capable of dilating to an increase in plasma viscosity when hemoglobin is present in the plasma, 4) decreasing hematocrit does not impair pial arteriolar dilation to hypercapnia unless plasma viscosity is increased, and 5) pial arteriolar constriction to hypocapnia is impaired at reduced hematocrit independently of O2-carrying capacity.
OBJECTIVE: Greater demand and limited resources for intensive care monitoring for patients with neurologic disease may change patterns of intensive care unit utilization. The necessity and duration of intensive care unit management for all neurosurgical patients after brain tumor resection are not clear. This study evaluates a) the preoperative and perioperative variables predictive of extended need for intensive care unit monitoring (>1 day); and b) the type and timing of intensive care unit resources in patients for whom less intensive postoperative monitoring may be feasible. DESIGN: Retrospective chart review. SETTING: A neurocritical care unit of a university teaching hospital. PATIENTS: Patients were 158 consecutive postoperative brain tumor resection patients admitted to a neurocritical care unit within a 1-yr period (1998-1999). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Twenty-three patients (15%) admitted to the neurocritical care unit for >24 hrs were compared with 135 (85%) patients admitted for <24 hrs. Predictors of >1-day stay in the neurocritical care unit in a logistic regression model were a tumor severity index comprising radiologic characteristics of tumor location, mass effect, and midline shift on the preoperative magnetic resonance imaging scan (odds ratio, 12.5; 95% confidence interval, 3.1-50.5); an intraoperative fluid score comprising estimated blood loss, total volume of crystalloid, and other colloid/hypertonic solutions administered (odds ratio, 1.8; 95% confidence interval, 1.2-2.6); and postoperative intubation (odds ratio, 67.5; 95% confidence interval, 6.5-702.0). Area under the receiver operating characteristic curve for the model of independent predictors for staying >1 day in the neurocritical care unit was 0.91. Neurocritical care unit resource use was reviewed in detail for 134 of 135 patients who stayed in the neurocritical care unit for <1 day. Sixty-five (49%) patients required no interventions beyond postanesthetic care and frequent neurologic exams. A total of 226 intensive care unit interventions were performed (mean +/- sd, 1.7 +/- 2.6) in 69 (51%) patients. Ninety (67%) patients had no further interventions after the first 4 hrs. Neurocritical care unit resource use beyond 4 hrs, largely consisting of intravenous analgesic use (72% of orders), was significantly associated with female gender, benign tumor on frozen section biopsy, and postoperative intubation (chi-square, p <.05). CONCLUSIONS: A small fraction of patients require prolonged intensive care unit stay after craniotomy for tumor resection. A patient's risk of prolonged stay can be well predicted by certain radiologic findings, large intraoperative blood loss, fluid requirements, and the decision to keep the patient intubated at the end of surgery. Of those patients requiring intensive care unit resources beyond the first 4 hrs, the interventions may not be critical in nature. A prospective outcome study is required to determine feasibility, cost, and outcome of patients cared for in extended recovery and then transferred to a skilled nursing ward.
INTRODUCTION: Intracerebral hemorrhage (ICH) associated with pregnancy commonly occurs in the postpartum period in the setting of preeclampsia/eclampsia. We describe the clinical course of two patients with ICH due to postpartum cerebral vasculopathy in the absence of toxemia. METHODS: We reviewed two cases with ICH and postpartum vasculopathy in our hospital (1996-2001) and compared them with seven similar case reports from the literature. RESULTS: Mean age of all patients is 28.7+/-5.6 years (mean+/-S.D.). Toxemia of pregnancy was absent in all cases. ICHs were cortical in eight and putaminal in one patient. Erythrocyte sedimentation rate was elevated in two. Two cases rehemorrhaged during the same admission. No cerebral infarctions were reported. All patients had diffuse vasculopathy on conventional catheter angiography, with no clinical manifestations or laboratory data supportive of extracerebral or systemic vasculitis. Eight patients were treated with corticosteroids, two with additional cytotoxic agents and one with nimodipine alone. Improvement on follow-up cerebral angiography (catheter or MRA) and transcranial Doppler ultrasonography (TCD) was noted in eight cases. One did not have follow-up cerebral imaging but had an excellent clinical outcome. All cases had good to excellent functional recovery. CONCLUSIONS: Postpartum ICH in the absence of toxemia may be associated with isolated cerebral vasculopathy. The clinical course and functional outcome is good to excellent. This entity appears to be distinct from cerebral vasculitis, which is usually associated with poor outcome.
OBJECTIVE: To evaluate the reliability of transcranial Doppler ultrasound in detecting symptomatic vasospasm in patients after aneurysmal subarachnoid hemorrhage and monitoring response after hypertensive and endovascular treatments. DESIGN: Retrospective chart review. SETTING: Neurosciences critical care unit in a tertiary-care university hospital. PATIENTS: All patients admitted to a neurosciences critical care unit with the diagnosis of subarachnoid hemorrhage between January 1990 and June 1997. INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: We reviewed transcranial Doppler ultrasound data of 199 patients; 55 had symptomatic vasospasm. Clinical symptoms and corresponding vascular distributions were identified, as was angiographic vasospasm (n = 35). The sensitivity and specificity of transcranial Doppler ultrasound for anterior circulation vessels were calculated by using a mean cerebral blood flow velocity criterion of >120 cm/sec. Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitivity and specificity of transcranial Doppler ultrasound and cerebral angiography. The sensitivity of transcranial Doppler ultrasound for anterior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%. The sensitivity of cerebral angiography was 80%. For individual vessels, the sensitivity and specificity of transcranial Doppler ultrasound were middle cerebral artery, 64% and 78%; anterior cerebral artery, 45% and 84%; and internal carotid artery, 80% and 77%, respectively. The mean times for symptomatic and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days, respectively. In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow velocities >120 cm/sec was 7.0 +/- 3 days (p <.05). Symptomatic vasospasm also was associated with thickness of clot on head computed tomography scan and rapidly increasing mean cerebral blood flow velocities. Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 patients. CONCLUSIONS: The reliability of transcranial Doppler ultrasound was better at detecting high mean cerebral blood flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal carotid artery distributions than for anterior cerebral artery distribution. Transcranial Doppler ultrasound was as sensitive as cerebral angiography at detecting symptomatic vasospasm. High mean cerebral blood flow velocities can be apparent before the presence of symptomatic vasospasm. Daily transcranial Doppler ultrasound monitoring could provide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of endovascular treatment.
The beneficial effect of hemodilution on cerebral blood flow (CBF) during focal cerebral ischemia is mitigated by reduced arterial oxygen content (CaO2). In anesthetized cats subjected to permanent middle cerebral artery occlusion, the time course of regional CBF was evaluated after isovolemic exchange transfusion with either albumin or a tetrameric hemoglobin-based oxygen carrier. The transfusion started 30 min after arterial occlusion. We tested the hypothesis that bulk oxygen transport (CBF x CaO2) to ischemic tissue is increased by hemoglobin transfusion at a hematocrit of 18% compared with albumin-transfused cats at a hematocrit of 18% or control cats at a hematocrit of 30% and equivalent arterial pressure. In the nonischemic hemisphere, CBF increased selectively after albumin transfusion, and oxygen transport was similar among groups. In the ischemic cortex, albumin transfusion increased CBF, but oxygen transport was not increased above that of the control group. Hemoglobin transfusion increased both CBF and oxygen transport in the ischemic cortex above values in the control group, but the increase was delayed until 4 h of ischemia. Consequently, acute injury volume measured at 6 h of ischemia was not significantly attenuated. In contrast to the cortex, CBF in the ischemic caudate nucleus was not substantially increased by either albumin or hemoglobin transfusion. Therefore, in a large animal model of permanent focal ischemia in which transfusion starts 30 min after ischemia, tetrameric cross-linked hemoglobin transfusion can augment oxygen transport to the ischemic cortex, but the increase can be delayed and not necessarily provide protection. Moreover, an end-artery region such as the caudate nucleus is less likely to benefit from hemodilution.