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Biomedical subjects

L F Marshall

Publications and source records attributed to L F Marshall.

At least 91 records · Page 5Linked to original sources
PubMed1982

The neurologic effects of thiopental therapy following experimental cardiac arrest in cats.

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.

Animals↗
PubMed1982

EEG monitoring of clinical coma: the compressed spectral array.

Twenty-four comatose patients were studied by 16-hour compressed spectral array (CSA), made from four-channel portable EEG recordings. Causes of coma included head injury (15), anoxia (6), and brainstem strokes (3). CSA was classified on the basis of frequency and alternating or nonalternating patterns. Alternating CSA was significantly associated with survival (p less than 0.005) in the head-injured and anoxic group combined, and in the head-injured subgroup (p less than 0.013). The prognostic value of CSA equaled the Glasgow Coma Scale or neurologic examination and occasionally added prognostic information.

Adult↗
PubMed1982

Localizing and prognostic value of auditory evoked responses in coma after closed head injury.

We studied brainstem auditory evoked responses (BAERs) in 26 comatose patients after head injury, and long-latency auditory evoked responses (AERs) in 24 patients. BAERs-AERs were graded for abnormality to evaluate graded outcome. Only six patients had central BAER abnormalities. AERs were abnormal in 21, and all patients with abnormal BAER had abnormal AER, implying that the major site of injury affected the cerebral hemispheres. BAER was abnormal in only 5 of 12 with decerebration, suggesting that decerebration may occur with diffuse hemispheric injury. BAER (p less than 0.01) and AER (p less than 0.01) strongly correlated with outcome. Preservation of AER and normal BAER indicated good quality of survival; absent AER and normal BAER, survival; and absent AER and abnormal BAER, severe disability or death. BAER-AER predicted outcome as accurately as the detailed neurologic examination and occasionally added predictive power.

Adult↗
PubMed1982

Acute dimethyl sulfoxide therapy in brain edema. Part 3: effect of a 3-hour infusion.

Albino rabbits with experimental brain edema produced by a combined cryogenic left hemisphere lesion and metabolic 6-aminonicotinamide lesion were administered a 3-hour intravenous infusion of dimethyl sulfoxide (DMSO). Simultaneous recording of intracranial pressure (ICP), systolic arterial pressure (SAP), and central venous pressure (CVP) and electroencephalography were performed while the animals were being ventilated mechanically to produce a constant Pa CO2 value (38-42 torr). At the end of the infusion, the brain water and electrolyte contents were measured. There was a persistent and progressive reduction of ICP during the infusion, the nadir occurring at 3 hours (p less than 0.005 from zero time), with no change in SAP or CVP. There was a reduction of brain water in both hemispheres when compared to untreated controls, but this was significant for the right hemisphere only (p less than 0.005). There was a significant reduction of the brain sodium content for both hemispheres, but no significant change occurred in brain potassium content. The DMSO infusion was effective not only in reducing ICP, but also in sustaining this reduction for 3 hours.

Animals↗
PubMed1982

Neurological monitoring.

Intensive care of the patient who has acute brain injury has undergone major changes. Neurologic monitoring, particularly continuous recording of the intracranial pressure, appears to have contributed to an improved outcome in head-injured patients. Computerized axial tomographic scanning has revolutionized the diagnosis and serial assessment of the patient. Other techniques such as cerebral blood flow measurements, reflectance spectrophotometry, and sophisticated electrophysiologic recording are being utilized in the laboratory and in man as monitoring techniques. There utility and potential applications are discussed, and the present role of monitoring reviewed.

Brain Injuries↗
PubMed1981

The epidemiology of head injury: a prospective study of an entire community-San Diego County, California, 1978.

In 1978, a prospective study of all deaths from head injury and of all patients admitted to hospitals with a diagnosis of head injury was conducted in San Diego County, California. The overall incidence of head injury was nearly 0.3%; the highest rate was seen at ages 10-29 years. At all ages, head injury rates were higher in males than in females, and the death rate in males was 2.6 times that in females. The overall case fatality ratio was 7.5%, and 65% of all deaths occurred prior to hospitalization. Among those who survived to hospitalization, the case fatality ratio was less than 3%. Motor vehicle accidents caused 53% of all head injuries and 73% of all deaths. Although other causes of head injury showed seasonal variation, the frequency of motor vehicle head injuries did not vary by month.

Accidents, Traffic↗
PubMed1981

Prospective study of patients hospitalized with head injury in San Diego County, 1978.

The characteristics of 1311 head-injured patients admitted to 10 selected San Diego hospitals are detailed. Fifty patients who subsequently died are included. Glasgow coma scale scores were strongly related to survival. After adjustment for the Glasgow coma scale score, there was an independent association between age and survival, but not between sex and survival. The four characteristics associated with head injury that bore the highest case fatality ratios (all greater than 30%) in descending order were spinal cord injury, obstructed airway, difficulty breathing, and shock. Previous unconsciousness and transport by private vehicle were predictive of survival. None of the four adverse predictors or multiple injury showed an independent association with mortality when the Glasgow coma scale score was taken into account.

Adolescent↗
PubMed1980

Cerebral circulatory and metabolic responses to intravenously administered lorazepam.

Cerebral vascular and metabolic effects of lorazepam were evaluated in ten awake monkeys by use of a modification of the Kety-Schmidt technique. Five received ketamine, 10 mg/kg, im, five to eight hours prior to the study, but all animals were otherwise treated identically. Monkeys receiving ketamine had significantly greater (P < 0.05) cerebral blood flow (CBF) values before lorazepam was given (46 +/- 1 ml/100 g/min) than did monkeys not receiving ketamine (41 +/- 1 ml/100 g/min), but in all other respects, premedicated and unpremedicated animals did not differ. Lorazepam administration did not significantly alter systemic arterial blood pressure or blood-gas values. However, it did decrease CBF by 26 per cent and increase cerebral vascular resistance (CVR) by approximately 25 per cent (P < 0.01). The cerebral metabolic rate for glucose (CMRg) decreased 42 per cent (P < 0.05). Following lorazepam administration, the cerebral metabolic rate for oxygen (CMRO2) decreased by 21-30 per cent. When combined CMRO2 data for the two anesthetic groups are pooled, this decrease is significant (P < 0.05). This study indicates that sedative doses of lorazepam decrease cerebral blood flow and metabolism with minimal effects on blood pressure and blood-gas values. Lorazepam administration did not produce any change in cerebral metabolism indicative of brain hypoxia or ischemia.

Anesthesia, Intravenous↗
PubMed1980

Treatment of brain swelling and brain edema in man.

Despite our relative lack of understanding of how many agents work to improve brain edema states, the ability to treat patients empirically has improved dramatically over the last 10 years. The armamentarium of the treating clinician has been aided by the availability of the nonosmotic diuretics, by the more rational use of mannitol therapy, by the availability of higher doses of dexamethasone, and perhaps by the availability of barbiturates. What is required and what is now under way is the testing of various combinations of drugs and therapeutic regimens in laboratory models, which then can be applied to the treatment of cerebral edema in man. We must learn, for example, whether the use of certain agents during the first 24 to 48 hr in patients should be supplanted by the use of other drugs at a later time. We need to know the doses, as well as the value and risks of multiple drug modalities. If such information is forthcoming, we must continue to use the potent agents that we have without losing sight of the fact that they have side effects which may only exacerbate the clinical problem. Significant progress has been made in defining the process called "cerebral edema" and those factors responsible for its resolution. Now that this information has become available, the development of more specific antiedema therapy appears more likely. There are encouraging reports that such agents might be available in the near future.

Barbiturates↗
PubMed1979

High-dose barbiturate therapy in humans: a clinical review of 60 patients.

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.

Adolescent↗