Marek A. Mirski

Diagnosis and Treatment of Vascular Air Embolism

Vascular air embolism is a potentially life-threatening event that is now encountered routinely in the operating room and other patient care areas. The circumstances under which physicians and nurses may encounter air embolism are no longer limited to neurosurgical procedures conducted in the “sitting position” and occur in such diverse areas as the interventional radiology suite or laparoscopic surgical center. Advances in monitoring devices coupled with an understanding of the pathophysiology of vascular air embolism will enable the physician to successfully manage these potentially challenging clinical scenarios. A comprehensive review of the etiology and diagnosis of vascular air embolism, including approaches to prevention and management based on experimental and clinical data, is presented. This compendium of information will permit the healthcare professional to rapidly assess the relative risk of vascular air embolism and implement monitoring and treatment strategies appropriate for the planned invasive procedure.

Anticonvulsant effect of anterior thalamic high frequency electrical stimulation in the rat

Evidence suggests that a specific subcortical pathway synaptically linking the anterior thalamic nuclear complex (AN) to the hypothalamus and midbrain is important in the expression of pentylenetetrazol (PTZ) seizures. Perturbation of neuronal activity along this path via focal disruption or chemical inhibition significantly raises seizure threshold. Recent data has demonstrated that focal electrical stimulation within the hypothalamic component of this pathway inhibited seizure expression in a current and frequency dependent fashion. Similar experiments were conducted in the AN to investigate the hypothesis that stimulation of this thalamic nuclear region can prevent the propagation of PTZ seizures between cortical and subcortical regions. Our results indicate that high frequency (100 Hz) stimulation of AN did not alter the expression of low dose PTZ induced cortical bursting but did raise the clonic seizure threshold compared to naive animals or those stimulated at sites near, but not in AN (P < 0.01). Low frequency stimulation (8 Hz) was in contrast, proconvulsant and could induce behavioral arrest responses accompanied by rhythmic high voltage EEG even without PTZ challenge. This data further highlights the role of AN in mediating the expression of seizures and provides experimental support for the concept that this thalamic region may be a promising target for focal stimulation to treat intractable seizures in humans.

Treatment of refractory intracranial hypertension with 23.4% saline.

ObjectiveTo evaluate the effect of intravenous bolus administration of 23.4% saline (8008 mOsm/L) on refractory intracranial hypertension (RIH) in patients with diverse intracranial diseases.DesignRetrospective chart review.SettingA neurosciences intensive care unit in a university hospital.Patients

Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema : Effect on intracranial pressure and lateral displacement of the brain

OBJECTIVE To determine the effect of continuous hypertonic (3%) saline/acetate infusion on intracranial pressure (ICP) and lateral displacement of the brain in patients with cerebral edema. DESIGN Retrospective chart review. SETTINGS Neurocritical care unit of a university hospital. PATIENTS Twenty-seven consecutive patients with cerebral edema (30 episodes), including patients with head trauma (n = 8), postoperative edema (n = 5), nontraumatic intracranial hemorrhage (n = 8), and cerebral infarction (n = 6). INTERVENTION Intravenous infusion of 3% saline/acetate to increase serum sodium concentrations to 145 to 155 mmol/L. MEASUREMENTS AND MAIN RESULTS A reduction in mean ICP within the first 12 hrs correlating with an increase in the serum sodium concentration was observed in patients with head trauma (r2 = .91, p = .03), and postoperative edema (r2 = .82, p = .06), but not in patients with nontraumatic intracranial hemorrhage or cerebral infarction. In patients with head trauma, the beneficial effect of hypertonic saline on ICP was short-lasting, and after 72 hrs of infusion, four patients required intravenous pentobarbital due to poor ICP control. Among the 21 patients who had a repeat computed tomographic scan within 72 hrs of initiating hypertonic saline, lateral displacement of the brain was reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SEM]) and in patients with postoperative edema (3.1 +/- 1.6 to 1.1 +/- 0.7). This effect was not observed in patients with nontraumatic intracranial bleeding or cerebral infarction. The treatment was terminated in three patients due to the development of pulmonary edema, and was terminated in another three patients due to development of diabetes insipidus. CONCLUSIONS Hypertonic saline administration as a 3% infusion appears to be a promising therapy for cerebral edema in patients with head trauma or postoperative edema. Further studies are required to determine the optimal duration of benefit and the specific patient population that is most likely to benefit from this treatment.

Impact of a Neuroscience Intensive Care Unit on Neurosurgical Patient Outcomes and Cost of Care: Evidence-based Support for an Intensivist-directed Specialty Icu Model of Care

Analysis of patient data from a new neuroscience intensive care unit (NSICU) permitted evaluation of whether such a specialty ICU favorably altered clinical outcomes in critically ill neuroscience patients, and whether such a care model produced an efficient use of resources. A retrospective review was performed to compare (1) the clinical outcomes, as defined by percent mortality and disposition at discharge, between patients with a primary diagnosis of intracerebral hemorrhage treated in 1995 in medical or surgical ICUs and those treated in the same medical facility in an NSICU in 1997; and (2) the efficiency of care, as defined by length of ICU stay, total cost of care, and specific resource use, between patients treated in the NSICU and national benchmark standards for general ICUs during the 1997 fiscal year (FY). In the latter, extracted patient population data on neurosurgery patients requiring ICU treatment during FY 1997 were used with the following adjacent-disease related group (A-DRG)-coded diseases: craniotomy with and without coma or intracerebral hemorrhage, and skull fracture with and without coma lasting longer than 1 hour. Outcome measures of percent mortality and disposition at discharge in patients with intracerebral hemorrhage were significantly improved (P < .05), compared with those in a similar cohort treated 2 years earlier in a general ICU setting. Also, patients treated in the NSICU had shorter hospital stays (P < .01) and lower total costs of care (P < .01) than a national benchmark. The data suggest that a neuroscience specialty ICU arena staffed by specialty-trained intensivists and nurses is beneficial.

Electrical Stimulation of the Mammillary Nuclei Increases Seizure Threshold to Pentylenetetrazol in Rats

Summary: High‐frequency electrical stimulation of mammillary nuclei (MN) of rat posterior hypothalamus resulted in a significant increase in seizure threshold induced by pentylenetetrazol (PTZ). The anticonvulsant effect was frequency and intensity specific. Stimulation at 100 Hz (1–5V, 30–200 μA) afforded protection against EEG and behavioral manifestations of PTZ seizures. Stimulation of either low frequency (5 Hz), high intensities (8–20 V, 300–800 μA), or outside the histologically verified MN target region did not increase seizure threshold. In some instances, high‐intensity stimulation of MN alone elicited spike‐wave epileptiform EEG activity accompanied by either arrest of behavior or myoclonic seizures. In animals with ongoing seizure activity, electrical stimulation of MN disrupted the high‐voltage synchronous wave forms on cortical EEG. These data support the concept that electrical perturbation of MN in hypothalamus may functionally inhibit generalization of paroxysmal activity required for expression of the EEG and, in particular, the behavioral component of PTZ seizures. These studies provide additional insight into forebrain‐brainstem interactions mediating generalized seizure expression.

Glucocorticoid therapy in neurologic critical care

Background:The pivotal role of inflammation and edema across the spectrum of central nervous system injury has driven extensive investigation into the therapeutic potential of glucocorticoids. Objective:To review the experimental and clinical data relating to the efficacy and adverse effects of glucocorticoids in conditions encountered in critical neurologic and neurosurgical illness. Data Source:Search of MEDLINE and Cochrane databases, manual review of article bibliographies. Data Synthesis and Conclusions:The efficacy of glucocorticoids is well established in ameliorating edema associated with brain tumors and in improving outcome in subsets of patients with bacterial meningitis. Despite frequently encouraging experimental results, clinical trials of glucocorticoids in ischemic stroke, intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage, and traumatic brain injury have not shown a definite therapeutic effect. The evidence supporting glucocorticoid therapy for spinal cord injury is controversial; however methylprednisolone continues to be widely employed in this setting.

Controversies in the management of aneurysmal subarachnoid hemorrhage

Background:The care of patients with aneurysmal subarachnoid hemorrhage has evolved significantly with the advent of new diagnostic and therapeutic modalities. Although it is believed that these advances have contributed to improved outcomes, considerable uncertainty persists regarding key areas of management. Objective:To review selected controversies in the management of aneurysmal subarachnoid hemorrhage, with a special emphasis on endovascular vs. surgical techniques for securing aneurysms, the diagnosis and therapy of cerebral vasospasm, neuroprotection, antithrombotic and anticonvulsant agents, cerebral salt wasting, and myocardial dysfunction, and to suggest venues for further clinical investigation. Data Source:Search of MEDLINE and Cochrane databases and manual review of article bibliographies. Data Synthesis and Conclusions:Many aspects of care in patients with aneurysmal subarachnoid hemorrhage remain highly controversial and warrant further resolution with hypothesis-driven clinical or translational research. It is anticipated that the rigorous evaluation and implementation of such data will provide a basis for improvements in short- and long-term outcomes.

Sedation for the critically ill neurologic patient.

OBJECTIVE To review the scientific basis for sedation of critically ill neurologic patients by summarizing the distinct neurophysiologic disturbances present in this population and presenting the central nervous system effects of sedative agents to permit optimal drug therapy. DATA SOURCES Review of the English language clinical and scientific literature using MEDline data search. STUDY SELECTION Literature references were selected through a key word search of sedative therapy, drugs used for sedation, and specific neurologic disorders and processes to provide an in-depth overview of sedative drug mechanisms of action, effects on neurophysiology and intracranial dynamics, pharmacokinetics, and toxicity profile. Special emphasis was placed on neurologic side effects. DATA EXTRACTION Clinical and scientific literature was reviewed and data relevant to neurophysiologic effects of sedative drug therapy were summarized. Recommendations for institution of sedative therapy and of particular agents were made as a result of analysis of all pooled data. DATA SYNTHESIS Critically ill patients with neurologic pathology present as a unique subset of individuals cared for in an acute care setting. Because monitoring of neurologic patients requires frequent assessment of the neurologic examination, the goal of sedative therapy should be to enhance, or to minimally perturb elicitation of the examination. Neurophysiologic disturbances introduce distinct risks for sedation and require their identification and understanding before the initiation of any sedative therapy. Sedative drugs, in particular, act to disturb central nervous system function and their effects may result in diagnostic confusion and further neurologic deterioration. The pharmacokinetic and neurophysiologic actions of the common classes of sedative agents, such as benzodiazepines, opioids, barbiturates, and neuroleptics, as well as ketamine, propofol, and clonidine are discussed. Recommendations are presented based on the specific type of sedation required and the underlying neurologic disturbance. Several specific examples, including head trauma, neuromuscular disease, and alcohol withdrawal, are provided. CONCLUSIONS Preservation of the neurologic examination is paramount in documenting clinical improvement or deterioration in the critically ill neurologic patient. Pharmacologic sedation in this unique population of acute care patients requires careful consideration of the underlying neurophysiologic disturbances and potential adverse effects introduced by sedative drugs.

Critical care and perioperative management in traumatic spinal cord injury

&NA; Traumatic spinal cord injury is frequently associated with brain injury and with alterations in respiratory and cardiovascular function that require critical care management. Complications include respiratory failure, atelectasis, pneumonia, neurogenic shock, autonomic dysreflexia, venous thromboembolism, and sepsis. While complications may be managed with supportive care, the goal of ameliorating neurologic outcome has proved elusive. Methylprednisolone, when instituted <8 hours after traumatic spinal cord injury, was associated in two clinical trials with statistically significant improvements in motor scores at 6 months and 1 year; however, critical reappraisal of these data raises questions about their validity and clinical relevance. Until more evidence of clinically effective therapies is available, acute management must be driven by pathophysiologic principles, with emphasis on interventions that attenuate secondary neurologic injury; these include the rational use of immobilization, cautious airway management, and promotion of cord perfusion and oxygenation with the appropriate level of hemodynamic and respiratory support. Clinical trials of pharmacologic neuroprotection have yielded disappointing results, but the ongoing elucidation of spinal cord repair and regenerative mechanisms suggests new therapeutic prospects.