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Cerebral hemodynamic effects of pentobarbital coma in head-injured patients.

The purpose of this study was to examine the changes in cerebral hemodynamics of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variables were measured in 67 severely head-injured patients at the following times: before the loading dose of pentobarbital; after the loading dose of pentobarbital (average pentobarbital level 28.1+/-8.3 microg/mL); and 3 days later, when the peak pentobarbital level averaged 42.5+/-17.2 microg/mL. Intracranial pressure (ICP) and mean arterial blood pressure (MAP) were decreased by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, respectively. Cerebral perfusion pressure (CPP) was unchanged when the entire group was analyzed together. CBF, cerebral oxygen consumption (CMR(O)2), and arteriovenous oxygen difference (AVD(O)2) were significantly decreased after the loading dose of pentobarbital, by 20%, 31%, and 11%, respectively. The average cerebrovascular resistance (CVR) was increased by 20%. The change in CMR(O)2 with the loading dose of pentobarbital was closely related to the pretreatment value (n = 67, r2 = 0.65, p < .001). Thirty (45%) of the patients had a "good ICP response," with a reduction in ICP from 34+/-9 to 15+/-5 mm Hg after the initial loading dose of pentobarbital. Twenty-seven (40%) of the patients had a "partial ICP response," with ICP decreasing but still remaining above 20 mm Hg after the loading dose of pentobarbital. In the remaining 10 patients, ICP did not change or even increased after pentobarbital. In the 30 patients with a good ICP response, pretreatment CMR(O)2 and AVD(O)2 were greater before administration of pentobarbital, and CMR(O)2 and AVD(O)2 decreased more with the loading dose of pentobarbital, than in the patients with partial or no ICP response. The outcome was significantly better in the patients with a good or partial ICP response to pentobarbital, with 21% of these patients having a good recovery or moderate disability at 3 months after injury, compared with 100% persistent vegetative state or death in the nonresponders. In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, partly because their CMR(O)2 is already markedly reduced by the injury and partly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because hypotension limits the amount of barbiturates that can be given.

Adult↗

Physician knowledge of the Glasgow Coma Scale.

Appropriate triage is critical to optimizing outcome from battle related injuries. The Glasgow Coma Scale (GCS) is the primary means by which combat casualties, who have suffered head injury, are triaged. For the GCS to be reliable in this critical role, it must be applied accurately. To determine the level of knowledge of the GCS among military physicians with exposure and/or training in the scale we administered a prospective, voluntary, and anonymous survey to physicians of all levels of training at military medical centers with significant patient referral base. The main outcome measures were correct identification of title and categories of the GCS along with appropriate scoring of each category. Overall performance on the survey was marginal. Many were able to identify what "GCS" stands for, but far fewer were able to identify the titles of the specific categories, let alone identify the specific scoring of each category. When evaluated based on medical specialties, those in surgical specialties outperformed those in the medical specialties. When comparing the different levels of training, residents and fellows performed better than attending staff or interns. Finally, those with Advanced Trauma Life Support (ATLS) certification performed significantly better than those without the training. Physician knowledge of the GCS, as demonstrated in this study, is poor, even in a population of individuals with specific training in the use of the scale. It is concluded that, to optimize outcome from combat related head injury, methods for improving accurate quantitation of neurologic state need to be explored.

Certification↗

Factors associated with mortality of myxedema coma: report of eight cases and literature survey.

High-dose thyroid hormone replacement has been recommended for treatment of myxedema coma (MC) while questions of safety of the therapy and of efficacy of low-dose thyroid hormone replacement have not been systematically addressed. We treated 8 patients with MC in a period of 18 years, the first 3 with high-dose intravenous injections of levotriiodothyronine (LT3) and the other 5 patients with a smaller amount of either LT3 or levothyroxine (LT4). Two of the first 3 patients died of pneumonia and the other 5 recovered despite pulmonary abnormalities at the outset. To find factors associated with fatal outcome after treatment, the MEDLINE database was searched for MC cases with data of thyroid hormone replacement and outcome within 1 month of therapy. Clinical data for our 5 patients and 82 cases from the MEDLINE search were pooled and factors associated with mortality were sought among age, gender, presence of cardiac or pulmonary complications, and doses of thyroid hormone by multiple logistic regression analysis. It revealed that greater age, cardiac complications, and high-dose thyroid hormone replacement (LT4 > or = 500 microg/d or LT3 > or = 75 microg/d) were significantly associated with a fatal outcome within 1 month of treatment. Elderly MC patients can be treated with low-dose hormone replacement. A bolus of 500 microg LT4, especially by mouth or via nasogastric tube, appears to be tolerated by younger patients (< 55 years) without cardiac complication. The conclusion remains to be confirmed in more patients.

Adult↗

Unusual presentation of myxoedema coma in the elderly.

Seven patients were found to be suffering from myxoedema coma over a two-year period in this geriatric department. The majority presented with unusual clinical features. Generalized convulsions were particularly common, occuring in five patients. Four patients were previously diagnosed as suffering from myxoedema, but thyroxine therapy had been discontinued. These findings would suggest that this condition is not unusual in the elderly; but it could easily be missed on account of its atypical presentation.

Aged↗

Cerebral electrical activity influences the effects of etomidate on cerebral perfusion pressure in traumatic coma.

The effects of 124 boluses of etomidate 0.2 mg kg-1 i.v. on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) were studied in eight patients with severe head injury (Glasgow coma score less than 8). The data were divided into two groups based on the minimum voltage of the cerebral function monitor (CFM) recording before the bolus. In group A this was less than 5 microV (representing profound cortical electrical depression), while in group B the minimum voltage was greater than 5 microV. The mean decrease in ICP following etomidate was significantly greater in group B (mean +/- SEM: -8.6 +/- 0.7 mm Hg) than in group A (-3.8 +/- 0.6 mm Hg) (P less than 0.0001). The decrease in arterial pressure was similar in both groups. Consequently, there was a small mean increase in CPP in group B (2.2 +/- 0.9 mm Hg), whereas in group A CPP decreased (-4.7 +/- 1.5 mm Hg) (P less than 0.001). There was a strong correlation between the decreases in ICP and MAP in group A (r = 0.70, P less than 0.01), but not in group B (r = 0.05). Thus, when cortical electrical activity was already maximally suppressed, further administration of an i.v. anaesthetic agent produced only relatively small decreases in ICP, largely as a passive response to decreases in MAP. CPP was therefore usually reduced. Conversely, in the absence of such depression larger decreases in ICP, unrelated to hypotension, occurred and these were usually associated with increases in CPP. However, even under these circumstances, potentially dangerous decreases in CPP may be seen.

Adolescent↗

Performing a cure for schizophrenia: insulin coma therapy on the wards.

Most historians of psychiatry regard insulin coma therapy (ICT) either as an embarrassing stumble on the path to modern biological psychiatry or as one member of a long line of somatic therapies used to treat mental illness in the mid-twentieth century. This article explores the ICT era, roughly 1933-60, as a key moment in the development of American psychiatry. Developed only ten years after insulin had been embraced as a "miracle drug" for the treatment of diabetes, ICT was perceived by psychiatrists as a means of bringing their field closer to mainstream medicine, particularly to neurology. In addition, the story of ICT reveals how a treatment never quite proven on paper was unquestionably efficacious in the local world in which it was performed. An institutionally-based treatment, ICT was administered in a specific area of the mental hospital deemed the insulin unit, a room with its own staff, practices, and attitudes toward mental illness. There, psychiatrists often experienced wondrous recoveries of individual, formerly intractable patients. These intense personal experiences allowed psychiatrists to feel truly efficacious, enabling them to reinvent themselves as medical doctors rather than behavioral and disciplinary supervisors. The confidence they derived from this capacity, along with the operating room-like setting of the insulin unit, the unit's specialized staffing and group bond, and the availability of both risk-assessment tests and a medley of treatments that countered side effects and complications, allowed ICT to be understood as an efficacious treatment for schizophrenia within the local world in which it was administered.

History, 20th Century↗

Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition.

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.

Animals↗

The prognostic value of the components of the Glasgow Coma Scale following acute stroke.

BACKGROUND: The Glasgow Coma Scale (GCS) is widely used in assessing level of consciousness. The GCS verbal component may be misleading in acute stroke: a focal neurological deficit leading to dysphasia could affect the score, independently of level of consciousness. AIM: To investigate the relationship, in all strokes and in dysphasic patients, between stroke outcome and total GCS (with and without the verbal score) and its components, to assess their relative values. STUDY DESIGN: Retrospective analysis following prospective data collection in an acute stroke unit and follow-up. METHODS: Outcomes studied were 2-week mortality and 3-month recovery (survival, subject living at home). We used area under the receiver operating characteristic curve (AUC) to compare versions of the GCS and multivariate logistic regression to identify which subset of GCS components best predicted outcome. RESULTS: Of 1517 patients with acute stroke, 1217 had complete clinical and follow-up data; 349 were dysphasic. Total GCS had greater AUC than the GCS without the verbal score, for mortality (all patients 0.78 vs. 0.76, p=0.021; dysphasics 0.72 vs. 0.71, p=0.52) and recovery (all patients 0.71 vs. 0.67, p=0.0001; dysphasics 0.74 vs. 0.70, p=0.055). Verbal and eye scores independently provided prognostic information, for each patient group and outcome measure. CONCLUSIONS: The GCS contains valuable predictive information. Regardless of whether dysphasia is present, the verbal score should be assessed since it adds prognostic information to that from the eye component, and has greater value than the motor score.

Aged↗

Coma in Mozambican gravidas: causes and perinatal outcome.

Ninety-one consecutive cases of coma were identified among gravidas at Maputo Central Hospital. The commonest causes were eclampsia (70 cases), cerebral malaria (six cases), and meningitis (five cases). Fetal mortality in eclampsia was 23 per cent and maternal mortality 10 per cent. There was a markedly higher incidence of eclampsia during the colder months.

Adolescent↗

Lipids in the proximal tubules of the kidney in diabetic coma.

Vacuolization of the renal tubular epithelial cells (the Armanni-Ebstein lesion) associated with diabetic hyperglycemia is usually regarded as an accumulation of glycogen. In a case of death of diabetic coma, the vacuoles were stained strongly for lipids. This observation may have both clinical and therapeutic consequences, and may increase our knowledge of the metabolism in diabetes.

Diabetic Coma↗

Coma blisters in a case of fatal theophylline intoxication.

A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.

Adult↗

Coma due to hypercalcemia in a patient with Paget's disease and multiple parathyroid adenomata.

A patient with histologically proven coexistent Paget's disease of the bone and parathyroid adenomatosis is described. She developed coma associated with hypercalcemia and underwent successfully surgical removal of two parathyroid adenomata. The differential diagnosis of hypercalcemia in patients with this rare association is discussed and the importance of early surgical treatment is stressed. A review of similar reported case is presented.

Adenoma↗

Improved brain metabolism with fructose 1-6 diphosphate during insulin-induced hypoglycemic coma.

The effect of fructose 1-6 diphosphate (FDP) on brain metabolism and brain function was investigated in hypoglycemic rabbits. The electroencephalogram and differences in oxygen content of arterial and cerebral venous blood were used as indicators for brain metabolic activity. Hypoglycemic coma was induced and maintained for 1 hour by insulin administration. At the onset of isoelectric EEG, six rabbits were treated with FDP and five rabbits received 0.9% saline. The animals were killed by an overdose of barbiturate 60 minutes after hypoglycemic recovery with glucose. FDP-treated rabbits had lower arterial glucose concentration after 40 minutes of treatment (p less than .05) and a significantly greater difference between the oxygen content of arterial and venous blood after 40 minutes (p less than .01), and after 60 minutes (p less than .025) of FDP infusion than saline-treated rabbits. FDP-treated rabbits also had a lower cerebral glucose-oxygen index than did saline-treated rabbits (p less than .005, after 20 and 40 minutes of FDP infusion). FDP administration was followed by a return of EEG activity during hypoglycemia, whereas saline produced no such effect. After glucose infusion, EEG activity was improved in FDP-treated rabbits; in saline-treated rabbits, minimal or no EEG activity was observed. The data suggest the possibility that, at the doses given in this study, FDP is taken up and used as a metabolic substrate by the brain.

Animals↗

Relationship between Glasgow coma scale and functional outcome.

The Glasgow Coma Scale (GCS) is routinely used in the acute care setting after traumatic brain injury (TBI) to guide decisions in triage, based on its ability to predict morbidity and mortality. Although the GCS has been previously demonstrated to predict mortality, efficacy in prediction of functional outcome has not been established. The purpose of this study was to assess the value of the acute GCS in predicting functional outcome in survivors of TBI. This study used the Multicenter National Institute on Disability and Rehabilitation Research TBI Model Systems database of 501 patients who had received acute medical care and inpatient rehabilitation within a coordinated neurotrauma program for treatment of TBI. Initial and lowest 24 hr GCS scores were correlated with the following outcome measures: the Disability Rating Scale (DRS), Rancho Los Amigos Levels of Cognitive Functioning Scale (LCFS), and cognitive and motor components of the Functional Independence Measure (FIM(SM)-COG and FIM(SM)-M). Outcome data were collected at admission to and discharge from the inpatient TBI rehabilitation unit. Correlation analysis revealed only modest, but statistically significant, relationships between initial and lowest GCS scores and outcome variables. Initial and lowest GCS score comparison with outcome demonstrated the following correlation coefficients: admission DRS, -0.25 and -0.28; discharge DRS, -0.24 and -0.24; admission LCFS, 0.31 and 0.33; discharge LCFS, 0.27 and 0.25; admission FIM-COG, 0.36 and 0.37; discharge FIM-COG, 0.23 and 0.23; admission FIM-M, 0.31 and 0.31; discharge FIM-M, 0.25 and 0.21. The GCS as a single variable may have limited value as a predictor of functional outcome.

Adolescent↗

The history of the Glasgow Coma Scale: implications for practice.

The Glasgow Coma Scale (GCS) has been the gold standard of neurologic assessment for trauma patients since its development by Jennett and Teasdale in the early 1970s. The GCS was found to be a simple tool to use. It became the method of choice for trauma care practitioners to document neurologic findings over time and predict functional outcome. Although the scale has been shown to be effective, many authors have cited weaknesses in the scale including the inability to predict outcome, variation in inter-rater reliability, and the inconsistent use by caregivers in the prehospital and hospital settings. This article outlines the components of the GCS and how practitioners can best use the scale, particularly in patients whose injuries and treatments make them difficult to assess.

Adult↗

Reversible coma caused by risperidone-ritonavir interaction.

Medications that act on the central nervous system are frequently used in people infected with human immunodeficiency virus (HIV). Actually, drug interactions are an important factor in the treatment of patients with (HIV) infection and because of the complexity of the current drug regimens, clinicians should be trained in order to recognize and manage drug interactions. Herein, we present an HIV infected male admitted for manic behavior and treated with risperidone who developed a profound coma secondary to increased levels of risperidone because of a possible drug interaction with ritonavir and indinavir. Subsequently, we discuss this interaction, rarely described in the literature. Risperidone is a cytochrome P450 (CYP2D6) enzyme substrate and weak inhibitor and a CYP3A4 substrate. Possible interactions with CYP2D6 inhibitors (amiodarone, fluoxetine or ritonavir) and CYP3A4 inhibitors (indinavir and ritonavir) can increase its serum concentrations and produce significant adverse effects. In conclusion, this drug combination should be administered with caution and routinely examined for signs and symptoms of risperidone toxicity. Dosages should be reduced as needed. Finally, we think that in patients taking multiple medications, plasma levels of risperidone should be monitored especially if drug interactions are possible.

Antipsychotic Agents↗

Operative treatment of heterotopic hip ossification in patients with coma after brain injury.

In 13 joints of 12 patients who sustained traumatic brain injury, heterotopic ossifications of the hip were surgically excised at an average of 15 months after the patients' recovery from coma. All of the patients were referred by neurologists of the postcoma unit who deemed surgery necessary to speed up the rehabilitation program of the patients. Before surgery, three patients were able to ambulate, whereas nine were not ambulatory. Eight hips were ankylosed, whereas five had a severe painful limitation of joint motion. All of the patients were checked at regular intervals after the operation, and the final followup averaged 38 months. In an attempt to prevent postoperative recurrence of ossification, 100 mg of indomethacin was administered daily after surgery for 6 weeks. At followup, 10 patients could ambulate, and two were able to sit in a wheelchair. Patients with poor neuromuscular control tended to lose part of their postoperative range of motion, and heterotopic periarticular ossification recurred in two of them (three hips). No correlation was found between recurrence and the time that elapsed from head injury to the operation, but old ossifications continued to show osteogenic activity at the histologic level.

Adolescent↗