Predictive model of length of stay and discharge destination in neuroscience admissions.

BACKGROUND: The purpose of this study was to try and determine the best predictors of hospital length of stay and discharge destination in patients admitted to a neuroscience service. METHODS: Valid data was collected for 170 patients. Variables included age, gender, location prior to admission, principle diagnosis, various physiological measurements upon admission, comorbidity, independence in various activities of daily living prior to admission, length of stay, and disposition upon discharge. Study design was a correlational descriptive study performed through the analysis of data and the development and validation of statistically significant factors in determining the length of stay. RESULTS: All factors with a strong (P < 0.05) relationship with the length of stay were entered into a forward stepwise linear regression with length of stay as the dependent variable. The three most significant variables in predicting length of stay in this study were admission from an outpatient setting, modified Rankin score on admission, and systolic blood pressure on admission. CONCLUSIONS: Functional status at admission, specifically, a higher modified Rankin score and a lower systolic blood pressure along with the acquisition of deep vein thrombosis, catheter associated urinary tract infections, intubation, and admission to an intensive care unit all have a statistically significant effect on the hospital length of stay.

Anoxia-induced changes in optimal substrate for peripheral nerve.

Hyperglycemia accentuates the injury produced by anoxia both in the central and peripheral nervous system. To understand whether this is a consequence of changes in metabolic pathways produced by anoxia, the effect of the metabolic substrate used by the rat peripheral nerve on the nerve action potential (NAP) was studied in the presence and absence of anoxia. In the continuously oxygenated state, the NAP was well preserved with glucose, lactate, as well as with high concentrations of sorbitol and fructose but not ß-hydroxybutyrate, acetate or galactose. With intermittent anoxia, the pattern of substrate effects on the NAP changed markedly so that low concentrations of fructose became able to support neurophysiologic activity but not high concentrations of glucose. These alterations occurred gradually with repeated episodes of anoxia as reflected by the progressive increase in the time needed for the NAP to disappear during anoxia when using glucose as substrate. This "preconditioning" effect was not seen with other substrates and an opposite effect was seen with lactate. In fact, the rate at which the NAP disappeared during anoxia was not simply related to degree of recovery after anoxia. These are distinct phenomena. For example, the NAP persisted longest during anoxia in the setting of hyperglycemia but this was the state in which the anoxic damage was most severe. Correlating the results with existing literature on the metabolic functions of Schwann cells and axons generates testable hypotheses for the mechanism of hyperglycemic damage during anoxia and lead to discussions of the role for a metabolic shuttle between Schwann cells and axons as well as a potential important role of glycogen.

Peripheral nerve at extreme low temperatures 2: pharmacologic modulation of temperature effects.

Changes in temperature have profound and clinically important effects on the peripheral nerve. In a previous paper, the effects of temperature on many properties of the peripheral nerve action potential (NAP) were explored including the NAP amplitude, conduction velocity and response to paired pulse stimulation. In this paper, the effects of pharmacologic manipulations on these parameters were explored in order to further understand the mechanisms of these effects. The reduction in conduction velocity with temperature was shown to be independent of the ionic composition of the perfusate and was unaffected by potassium or sodium channel blockade. This implies that the phenomenon of reduced conduction velocities at low temperature may be related to changes in the passive properties of the axon with temperature. Blockade of sodium channels and chronic membrane depolarization produced by high perfusate potassium concentrations or high dose 4-aminopyridine impair the resistance of the nerve to hypothermia and enhance the injury to the nerve produced by cycles of cooling and rewarming. This suggests the possibility that changes in the sodium inactivation channel may be responsible for the changes in the NAP amplitude with temperature and that prolonged sodium inactivation may lead more permanent changes in excitability.

Peripheral nerve at extreme low temperatures 1: effects of temperature on the action potential.

Hypothermia is an important means of neuroprotection. Understanding the effects of temperature on a physiologic measurement such as the nerve action potential (NAP) is important in monitoring its effects. The effects of hypothermia on the NAP amplitude, conduction velocity, and response to paired pulse stimulation were quantified in a rat sciatic nerve preparation from 37 to 10 degrees C. The time course of temperature related changes and the effect of repeated cycles of cooling and rewarming are explored using the following measures of the NAP: peak-to-peak amplitude, conduction velocity, duration, area under the curve and response to paired pulse stimuli. The NAP amplitude initially increases as temperature is reduced to 27 degrees C and then drops to roughly 50% of its baseline value by 16 degrees C while the area under the curve increases gradually until it begins to decline at 16 degrees C. Permanent loss of the NAP appears only after cooling below 10 degrees C for extended periods. Although the dependence of amplitude on temperature is approximately sigmoidal, the conduction velocity declines linearly at a rate of 2.8m/s/ degrees C. The response to paired pulse stimulation is strongly dependent on both temperature and the interstimulus interval with the responses at shorter interstimulus intervals being more temperature sensitive. With repetitive cycles of cooling and rewarming, the NAP amplitude declines by roughly 4% with every cycle without changes in the temperature at which the NAP amplitude reaches 50% of baseline. Only minor differences in conduction velocity are seen during cooling and rewarming.

Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials.

BACKGROUND: Deep hypothermia is an important cerebral protectant and is critical in procedures requiring circulatory arrest. The purpose of this study was to determine the factors that influence the neurophysiologic changes during cooling before circulatory arrest, in particular the occurrence of electrocerebral silence. METHODS: In 109 patients undergoing hypothermic circulatory arrest with neurophysiologic monitoring, five electrophysiologic events were selected for detailed study. RESULTS: The mean nasopharyngeal temperature when periodic complexes appeared in the electroencephalogram after cooling was 29.6 degrees C +/- 3 degrees C, electroencephalogram burst-suppression appeared at 24.4 degrees C +/- 4 degrees C, and electrocerebral silence appeared at 17.8 degrees C +/- 4 degrees C. The N20-P22 complex of the somatosensory evoked response disappeared at 21.4 degrees C +/- 4 degrees C, and the somatosensory evoked response N13 wave disappeared at 17.3 degrees C +/- 4 degrees C. The temperatures of these various events were not significantly affected by any patient-specific or surgical variables, although the time to cool to electrocerebral silence was prolonged by high hemoglobin concentrations, low arterial partial pressure of carbon dioxide, and by slow cooling rates. Only 60% of patients demonstrated electrocerebral silence by either a nasopharyngeal temperature of 18 degrees C or a cooling time of 30 minutes. CONCLUSIONS: With the high degree of interpatient variability in these neurophysiologic measures, the only absolute predictors of electrocerebral silence were nasopharyngeal temperature below 12.5 degrees C and cooling longer than 50 minutes.

Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming.

BACKGROUND: Electrophysiologic studies during rewarming after deep hypothermic circulatory arrest probe the state of the brain during this critical period and may provide insight into the neurological effects of circulatory arrest and the neurologic outcome. METHODS: Electroencephalogram (EEG) and evoked potentials were monitored during rewarming in 109 patients undergoing aortic surgery with hypothermic circulatory arrest. RESULTS: The sequence of neurophysiologic events during rewarming did not mirror the events during cooling. The evoked potentials recovered first followed by EEG burst-suppression and then continuous EEG. The time to recovery of the evoked potentials N20-P22 complex was significantly correlated with the time of circulatory arrest even in patients without postoperative neurologic deficits (r = 0.37, (p = 0.002). The nasopharyngeal temperatures at which continuous EEG activity and the N20-P22 complex returned were strongly correlated (r = 0.44, p = 0.0002; r = 0.41, p = 0.00003) with postoperative neurologic impairment. Specifically, the relative risk for postoperative neurologic impairment increased by a factor of 1.56 (95% CI 1.1 to 2.2) for every degree increase in temperature at which the EEG first became continuous. CONCLUSIONS: No trend toward shortened recovery times or improved neurologic outcome was noted with lower temperatures at circulatory arrest, indicating that the process of cooling to electrocerebral silence produced a relatively uniform degree of cerebral protection, independent of the actual nasopharyngeal temperature.

Acute type A aortic dissection: retrograde perfusion with left superior vena cava.

Retrograde cerebral perfusion with hypothermic circulatory arrest confers additional cerebral protection during repair of type A aortic dissection. We present a 42-year-old man with acute type A aortic dissection and a persistent, left superior vena cava. Cannulation of the right and left superior vena cava is used for retrograde perfusion of both hemispheres with bilateral monitoring of electroencephalogram and somatosensory-evoked potentials during and after the hypothermic circulatory arrest interval.

Generalized averaging and noise levels in evoked responses.

A formal relationship between the mean square noise level in an evoked potential experiment, the number of averages and the autocorrelation function of the noise is derived. The generalized averaging process is recast as a filter applied to the noise signal. This filter is computed for a number of different types of evoked potential experiments in which various weighting factors and stochastic stimulation times are allowed. Although the variance in noise level estimates can be large, there is a general trend for noise reduction to occur more slowly than the expected 1/N when the total time over which averaging occurs is small in comparison to the correlation time of the noise. When the total averaging time exceeds the temporal extent of the autocorrelation function, the expected 1/N behavior is observed.

Fatal hyperammonemia after orthotopic lung transplantation.

BACKGROUND: A case of fatal hyperammonemia complicating orthotopic lung transplantation was previously reported. OBJECTIVE: To describe the incidence, clinical features, and treatment of hyperammonemia associated with orthotopic lung transplantation. DESIGN: Retrospective cohort analysis. SETTING: Academic medical center and lung transplantation center in Philadelphia, Pennsylvania. PATIENTS: 145 sequential adult patients who underwent orthotopic lung transplantation. MEASUREMENTS: Plasma ammonium levels. RESULTS: Six of the 145 patients who had had orthotopic lung transplantation developed hyperammonemia, all within the first 26 days after transplantation. The 30-day post-transplantation mortality rate was 67% for patients with hyperammonemia compared with 17% for those without hyperammonemia (P = 0.01). Development of major gastrointestinal complications (P = 0.03), use of total parenteral nutrition (P < 0.001), and lung transplantation for primary pulmonary hypertension (P = 0.045) were associated with hyperammonemia. CONCLUSIONS: Hyperammonemia is a potentially fatal event occurring after orthotopic lung transplantation. It is associated with high nitrogen load, concurrent medical stressors, primary pulmonary hypertension, and hepatic glutamine synthetase deficiency.

Postoperative neurologic assessment and management of the cardiac surgical patient.

The neurologic evaluation of patients in the immediate postoperative period and postanesthetic state is unique and challenging. Neurologic assessment is complicated by the lingering residual effects of anesthetics as well as by the effects of narcotic analgesics, anxiolytics, and muscle relaxants, especially in ventilated patients. In this review we examine the suspected causes, clinical manifestations, diagnostic options, and intervention schemes for the common neurologic syndromes seen after cardiac operations.

Ventricular asystole during vagus nerve stimulation for epilepsy in humans.

Electrical stimulation of the vagus nerve, a recently available option for patients with refractory epilepsy, has demonstrated safety and efficacy. We report four patients with refractory epilepsy who experienced ventricular asystole intraoperatively during initial testing for implantation of the vagus nerve stimulator. Acute intraoperative vagus nerve stimulation may create ventricular asystole in humans. Extracorporeal cervical vagus nerve stimulation testing with continuous EKG monitoring intraoperatively before generator implantation is warranted.

Oxygen delivery during retrograde cerebral perfusion in humans.

UNLABELLED: Retrograde cerebral perfusion (RCP) potentially delivers metabolic substrate to the brain during surgery using hypothermic circulatory arrest (HCA). Serial measurements of O2 extraction ratio (OER), PCO2, and pH from the RCP inflow and outflow were used to determine the time course for O2 delivery in 28 adults undergoing aortic reconstruction using HCA with RCP. HCA was instituted after systemic cooling on cardiopulmonary bypass for 3 min after the electroencephalogram became isoelectric. RCP with oxygenated blood at 10 degrees C was administered at an internal jugular venous pressure of 20-25 mm Hg. Serial analyses of blood oxygen, carbon dioxide, pH, and hemoglobin concentration were made in samples from the RCP inflow (superior vena cava) and outflow (innominate and left carotid arteries) at different times after institution of RCP. Nineteen patients had no strokes, five patients had preoperative strokes, and four patients had intraoperative strokes. In the group of patients without strokes, HCA with RCP was initiated at a mean nasopharyngeal temperature of 14.3 degrees C with mean RCP flow rate of 220 mL/min, which lasted 19-70 min. OER increased over time to a maximal detected value of 0.66 and increased to 0.5 of its maximal detected value 15 min after initiation of HCA. The RCP inflow-outflow gradient for PCO2 (slope 0.73 mm Hg/min; P < 0.001) and pH (slope 0.007 U/min; P < 0.001) changed linearly over time after initiation of HCA. In the group of patients with preoperative or intraoperative strokes, the OER and the RCP inflow-outflow gradient for PCO2 changed significantly more slowly over time after HCA compared with the group of patients without strokes. During RCP, continued CO2 production and increased O2 extraction over time across the cerebral vascular bed suggest the presence of viable, but possibly ischemic tissue. Reduced cerebral metabolism in infarcted brain regions may explain the decreased rate of O2 extraction during RCP in patients with strokes. IMPLICATIONS: Examining the time course of oxygen extraction, carbon dioxide production, and pH changes from the retrograde cerebral perfusate provided a means to assess metabolic activity during hypothermic circulatory arrest.

Physiologic study of pressure point techniques used in the martial arts.

BACKGROUND: Study physiologic changes occurring during "knockouts" produced by application of pressure point techniques during martial arts demonstrations. EXPERIMENTAL DESIGN: prospective analysis of physiologic variables during and immediately following an acute event. SETTING: martial arts demonstration carried out at a medical center hospital. SUBJECTS: 12 normal volunteers participating in a martial arts demonstration. INTERVENTIONS: application of various pressure point techniques that have been observed to produce states of unresponsiveness in volunteers. MEASURES: continuous ECG and video/EEG monitoring with measurements of blood pressure and oxygen saturation. Qualitative analysis of EEG and ECG recordings and quantitative comparison of heart rate, blood pressure, and oxygen saturation measurements before during and after the period of induced unconsciousness. RESULTS: No significant changes in blood pressure, oxygen saturation, cardiac rate or rhythm, or electroencephalogram are noted during the knockouts produced by application of pressure point techniques. There was only variable inability for subjects to remember words spoken to them during the episode of apparent unresponsiveness. CONCLUSIONS: The mechanism for the state of unresponsiveness produced by application of pressure point techniques is not related to a significant cardiac or pulmonary process. There is no evidence of reduced cerebral blood flow during this time or of other dangerous physiologic changes. The exact mechanism for this phenomenon remains uncertain.

Paradoxical response to valproic acid in a patient with a hypothalamic hamartoma.

OBJECTIVE: To report a patient who developed the paradoxical effect of increasing electrical seizure activity and confusion with initiation of valproic acid therapy. CASE SUMMARY: A 25-year-old African-American woman with a hypothalamic hamartoma had an electroencephalogram (EEG) that demonstrated frequent bursts of generalized spike and wave activity. The prevalence of spike and wave activity increased dramatically and the patient became increasingly somnolent as valproic acid was added to carbamazepine and phenobarbital therapy. Her EEG and mental status changes resolved when the valproic acid was discontinued. There was a strong positive correlation between the prevalence of spike and wave activity and the valproic acid concentration, but not between spike and wave activity and the concentrations of carbamazepine or phenobarbital. DISCUSSION: Although this is a complex case, it is clear that the addition of valproic acid produced an increase in spike and wave activity. Possible mechanisms and pathophysiologic significance of this paradoxical effect are discussed in light of the differences between this epileptic syndrome and the primary generalized epilepsies.

Neurophysiologic effects of retrograde cerebral perfusion used for aortic reconstruction.

OBJECTIVE: The results of neurophysiologic monitoring using somatosensory evoked potentials (SSEPs) and electroencephalography (EEG) were analyzed to determine if retrograde cerebral perfusion (RCP) supported central nervous system electrical function during surgery that required temporary interruption of antegrade cerebral perfusion (IACP). DESIGN: A prospective, observational study. SETTING: A university hospital. PARTICIPANTS: Fifteen adult patients who underwent aortic reconstruction using RCP and three patients who underwent thoracic aortic operations using hypothermic circulatory arrest without RCP. INTERVENTIONS: SSEPs and EEG were monitored continuously throughout the operation. Regression analysis was performed to determine the factors that affected the rate of decrease in SSEP amplitudes during IACP and the time required for SSEP and EEG activity to recover after antegrade cerebral perfusion (ACP) was restored. MEASUREMENTS AND MAIN RESULTS: The amplitude of SSEPs that were elicited decreased over time after IACP. The mean +/- standard deviation (SD) time required for the brachial plexus (Erb's point), cervicomedullary junction (N13), and brainstem (N18) SSEPs to decrease to 0.5 of their original amplitude after IACP were 30 +/- 2, 19 +/- 2, and 16 +/- 2 minutes, respectively. The rate of decrease in the N18 SSEP amplitude after IACP correlated positively to the fraction of no-flow time (p = 0.01). CONCLUSION: RCP attenuated the rate of decay in SSEP amplitudes during IACP. This suggested that RCP had a measurable physiologic effect on central nervous system function and may increase the time that ACP can be safely interrupted.

Treatment of refractory status epilepticus with propofol: clinical and pharmacokinetic findings.

PURPOSE: We compared propofol with high-dose barbiturates in the treatment of refractory status epilepticus (RSE) and propose a protocol for the administration of propofol in RSE in adults, correlating propofol's effect with plasma levels. METHODS: Sixteen patients with RSE were included; 8 were treated primarily with high-dose barbiturates and 8 were treated primarily with propofol. RESULTS: Both groups of patients had multiple medical problems and a subsequent high mortality. A smaller but not statistically significant fraction of patients had their seizures controlled with propofol (63%) than with high-dose barbiturate therapy (82%). The time from initiation of high-dose barbiturate therapy to attainment of control of RSE was longer (123 min) than the time to attainment of seizure control in the group receiving propofol (2.6 min, p = 0.002). Plasma concentrations of propofol associated with control of SE were 14 microM +/- 4 (2.5 microg/ml). Recurrent seizures were common when propofol infusions were suddenly discontinued but not when the infusions were gradually tapered. CONCLUSIONS: If used appropriately, propofol infusions can effectively and quickly terminate many but not all episodes of RSE. Propofol is a promising agent for use in treating RSE, but more studies are required to determine its true value in comparison with other agents.

Relationships between cerebral blood flow velocities and arterial pressures during intra-aortic counterpulsation.

OBJECTIVE: To determine the effects of intra-aortic counterpulsation (IABP) on cerebral blood flow velocity. DESIGN: Prospective self-controlled study. SETTING: University hospital surgical intensive care unit. PARTICIPANTS: Nineteen cardiac surgical patients requiring perioperative IABP assistance. INTERVENTIONS: Simultaneous recording of transcranial Doppler middle cerebral artery blood flow velocity and arterial pressure in response to changes in the magnitude of augmentation and trigger ratio. MEASUREMENTS AND MAIN RESULTS: Instantaneous cerebral blood flow velocities correlated with arterial pressures during IABP (r = 0.650) at different magnitudes of augmentation and trigger ratios. The increase in arterial pressure during balloon inflation was associated with an increase in cerebral blood flow velocity, and the decrease in arterial pressure in response to balloon deflation was associated with a decrease in cerebral blood flow velocity that was dependent on the magnitude of augmentation. Different magnitudes of augmentation or trigger ratios had no effect on peak systolic cerebral blood flow velocity, mean cerebral blood flow velocity, mean arterial pressure, or the mean velocity-to-pressure ratio. Instantaneous cerebral blood flow velocity to arterial pressure ratios were lowest in response to balloon deflation at the time of pre-ejection. CONCLUSIONS: IABP modified the phasic profile of cerebral blood flow to reflect the arterial pressure waveform without affecting mean cerebral blood flow velocity. Peak systolic cerebral blood flow velocity was maintained in augmented beats despite the decreased systolic arterial pressure associated with afterload reduction. The acute decrease in cerebral blood flow velocity at pre-ejection was balanced by increased cerebral blood flow velocity during balloon inflation in diastole.