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PubMed1986

Coma.

The preceding discussion is an attempt to stress anatomy in the diagnosis of coma. By localizing the offending lesion, the physician can apply the appropriate diagnostic and therapeutic measures more adeptly. Because physicians are also frequently asked to prognosticate, I have tried to summarize the work of Plum and Posner in their study of the outcome of patients presenting in coma. The primary care physician is encouraged to plan at least for the basics in case he or she is faced with a comatose patient.

Coma↗

PubMedDate not supplied

Acute renal failure due to atraumatic rhabdomyolysis in coma diabeticum.

A case report of a twelve year old boy with coma diabeticum and atraumatic rhabdomyolysis is presented. At admission the patient was comatose. Hyperglycemia and hyperosmolarity were the main metabolic disorders. 32 hours after admission marked myoglobinuria due to atraumatic rhabdomyolysis led to acute renal failure. At first uremia was compensated by arteriovenous hemofiltration and later by conventional hemodialysis. During the sixth week after admission urinary output started and serum creatinine and urea levels gradually declined to normal. Special attention should be paid to atraumatic rhabdomyolysis in patients with coma diabeticum. Continuous arteriovenous hemofiltration is an effective extracorporal therapeutic technique to compensate uremia in critically ill patients.

Acute Kidney Injury↗

PubMedDate not supplied

Neuropsychological sequelae after head injury with mesencephalic coma in childhood.

Eleven children aging between 4 years 11 months and 12 years 6 months were examined periodically over five years following closed head injury with mesencephalic coma (Plum and Posner's definition). It was found that although transient sequelae (neurological and cognitive) on coma resolution were severe, long-term recovery was generally good. The subjects had drug, neurological and psychological treatment during the 2-5-years period and showed apparently better recovery than reported in literature for trauma in adults. This suggests that the mildly controversial "age" variable is highly important in long-term prognosis of impairments following head injury. Further studies will be necessary; with the systematic use of the same standardised testing procedures in all studies, we suggest to obviate the problems in collation arising from discrepancies in methodological, neurological and psychological techniques.

Age Factors↗

PubMed1985

Prevalence of coma in black subjects.

Coma, commonly known as "being unconscious" or "out cold," is a state of consciousness characterized by a total inability to perceive incoming stimuli. A retrospective phenomenologic study found that 10 of 36 control, 19 of 36 precare, and 20 of 36 aftercare subjects (49 of 108, or 45.4 percent) had experienced coma at least once during their lives. The implications of these findings are discussed.

Black People↗

PubMed1985

[Recovery of consciousness after prolonged coma in patients with severe craniocerebral injuries].

The authors specify and describe 7 stages of regaining consciousness by patients who had been in coma from 11 to 180 days, including opening of the eyes; fixation of the eyes on an object; recognition of close relatives; understanding of directly addressed speech; patient's own speech; amnestic confusion; consciousness with all formal signs of being clear. The condition of the patients at these stages is compared with EEG findings suggestive of the functional disintegration of the brain as a system in comatose patients, the vegetative status and the restoration of connections between different departments of the brain corresponding to the recovery of long absent consciousness of patients. It is concluded that at the current stage of medical sciences the maximum duration of coma compatible with the subsequent full recovery of mental activity of the patient under 30 years does not exceed 11 days.

Adolescent↗

PubMed1979

[Oral automatism in acute coma].

Of 98 patients in ai acute state of coma different etiology, 18 (or 18.4 percent) showed series of rhythmic oral motions ("chewing automatisms"). Only one of these patients was observed to develop an apallic syndrome. The characteristic features of chewing automatisms and their concomitant symptoms are described, and the need for delimiting them from more differentiated oral-motor patterns is emphasized. Both forms are of different importance to an assessment of the respective course of disease. The observation of chewing automatisms in acute states of coma does not allow the incipient development of an apallic syndrome to be inferred.

Acute Disease↗

PubMed1979

Hypoglycemic coma with ketoacidosis in nondiabetic alcoholics.

Five nondiabetic, chronically alcoholic patients presented in a comatose state during a two month prospective study and were found to be ketoacidotic. All of the patients were men, 28 to 59 years old. The usual history was one of chronic heavy, daily alcohol consumption until one to three days before presentation, when persistent anorexia, abdominal distress, nausea and vomiting commenced, with abstention from food thereafter. The patients were found to be in hypoglycemic coma, with diaphoresis, tachypnea and tachycardia, and immediately awoke when intravenous infusion of glucose was started. Serum glucose ranged between 19 and 27 mg per dl, the average arterial pH was 7.19 and the mean anion gap was 25 mEq per liter. Reaction with Acetest tablets was positive for ketones in both serum and urine in three of the patients. Serum beta-hydroxybutyrate was elevated in the four patients in whom it was measured. Lactic acidosis was not present. All patients were managed with prolonged intravenous infusions of glucose and saline solutions, and within 12 to 18 hours they were feeling well and findings on serum chemistry studies were normal. Follow-up after three months showed no repeated difficulties. The combination of alcoholic ketoacidosis and hypoglycemic coma in nondiabetic persons has not been described in the literature as a clinical entity; it may, however, represent a common but unrecognized syndrome. Therefore, because of its potentially serious consequences and because treatment is simple and effective, this entity must be thought of in alcoholic patients with altered mental status.

Acidosis↗

PubMed1979

[Mortality from diabetic coma at the Basle Cantonal Hospital during 2 consecutive observation periods 1968-1973 abd 1973-1978, using conventional insulin therapy and treatment with lose dose insulin].

163 patients were admitted to the Cantonal Hospital, Basel, during the decade 1968--1978 with severe diabetic ketoacidosis or non-ketotic coma. The hospital mortality rate was 28% in the first period (1968--1973) but decreased to 14% (p less than 0.025) in the second period (1973--1978). The lower mortality rate in the second period was due to diminished early mortality within 3 days after admission. The decline in the mortality rate during the second period was assumed to be due to a general improvement of treatment and possibly to a direct effect of low-dose insulin therapy. The latter conclusion followed from the fact that the remaining recompensation therapy, such as fluid and electrolyte replacement, was similar during both periods. However, in the non-ketotic patients low-dose insulin therapy resulted in a delayed fall in blood glucose and distinctly diminished potassium retention. The fatalities in the second period of treatment were mainly due to thromboembolic complications. This points to the need for a search for preventive measures against thromboembolism in order to resuce mortality in severe diabetic coma further.

Blood Glucose↗

PubMed1984

The radiology of nontraumatic coma.

This article describes a logical approach to the neuroimaging evaluation of patients with coma. The decision tree analysis provides an efficient method and attempts to convey the logical sequential concepts of analysis of CCT findings in patients presenting in stupor or coma. The sequential approach tabulated serves as a good mnemonic for clinicians faced daily with decisions to be made in the evaluation and management of comatose patients. The approach also provides a framework for subsequent statistical (Bayesian or other) analysis of efficacy, cost effectiveness, and impact on clinical practice and health care delivery.

Atrophy↗

PubMed1978

Diagnosing and treating myxedema and myxedema coma.

Every patient with myxedema has hypothyroidism, but not every hypothyroid patient has myxedema. It often is possible to diagnose myxedema on clinical grounds alone. Characteristic symptoms are weakness, cold intolerance, mental and physical slowness, dry skin, typical facies, and hoarse voice. Results of the total serum thyroxine and free thyroxine index tests usually will confirm the diagnosis. L-thyroxine is the treatment of choice for myxedema, but it must be given to elderly patients with extreme caution. The transition from the hypothyroid to the euthyroid state brings about changes that put an added burden on the heart. The patient's clinical status and results of thyroid function tests determine the proper maintenance dose. Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group. Primary treatment is prompt administration of adequate doses of thyroid hormone--either l-throxine given intravenously of L-triiodothyronine given by nasogastric tube. It also is essential to identify and treat the condition precipitating the coma.

Coma↗

PubMed1984

[Myxedema coma: myth or reality? Discussion apropos of 7 recent cases].

The authors, in reporting 7 personal cases, confront their findings with previously published data. The study of cases presented as myxedema comas consistently demonstrates a precipitating cause, which in itself can produce a low T3 and T4 syndrome. The occurrence of such a cause in a patient with hypothyroidism can lead to acute decompensation, but should such conditions be considered as myxedema comas since treatment is above all aimed against the acute aggression?

Aged↗

PubMed1984

[Variability of the EEG in the acute period of comas resulting from cerebral circulatory disorders].

Up to now there has been a general consensus in the literature that the development of the comatose state is attended with the appearance on the EEG of high amplitude slow activity. The article shows that the acute period of coma is not always associated with this regularity. A large part of the EBG presents low amplitude irregular activity with occasional rapid fluctuations. In some cases there are phenomena characteristic of the physiological nocturnal sleep. The data obtained make it possible to consider the role of different synchronizing and desynchronizing cerebral systems in the genesis of electrical activity in the period of coma and are of certain interest in terms of studying the neurophysiological mechanisms of comatose states.

Adult↗

PubMed1981

Treatment of ketoacidosis and diabetic coma by continuous intravenous administration of water, glucose, regular insulin and electrolytes.

The therapeutical scheme prescribed for the treatment of ketoacidosis and diabetic coma before the 1970s is quite stereotyped and inflexible in regard to the routes of administration and doses of insulin, as well as the management of dehydration and metabolic acidosis. This paper reports the experience of the Endocrinology Service of the General Hospital of the "La Raza" Medical Center for over 10 years. 35 patients with diabetic ketoacidosis were included in a treatment by continuous intravenous administration of glucose, water, insulin and potassium. These patients were programmed in a 12 hour study. The dose of insulin was estimated at a ratio of 1 IU per 1 gm of excess glucose over 2.0 gm/l. The amount of glucose administered was in ratio to the caloric requirements per kilo of bodyweight of the individual patient. The volume of water was administered on the basis of the degree of dehydration estimated. The potassium was prescribed at a ratio of 20 mEq/l of solution, or more if necessary. The patient's recovery was observed during a period of from 7 to 10 hours, with improvement of the hyperglycemia, dehydration and metabolic acidosis. The method has allowed us to observe the diabetic patient's rapid recovery when he has been in ketoacidosis or coma, without complications such as hypoglycemia. No mortality was observed.

Diabetic Coma↗

PubMed1982

Coma as a complication of total parenteral nutrition. Clinical case.

We report a case of coma occurring during the onset of anabolism and which was concomitant of the perfusion of an aminoacids solution. The neurological problem vanished when we stopped aminoacids perfusion. It is stressed that the perfusion of a non-physiological aminoacids spectrum distribution might lead to metabolic abnormalities resembling hepatic comas.

Acid-Base Equilibrium↗

PubMed1983

Similarity between tyramine-induced neurotoxicity and the coma of Reye's syndrome.

The objective of the present investigation was to determine whether or not tyramine induces coma in experimental animals with impaired mitochondrial monoamine oxidase function, and whether the coma in these animals was a function of increased cerebrospinal fluid (CSF) pressure. Ten mongrel dogs were treated (orally) daily with the monoamine oxidase-inhibiting drug, phenelzine (4.5 mg/kg), over a period of 1 month. The present studies indicated that in phenelzine-treated animals with liver disease and behavioral side effects (n = 4), the i.v. administration of tyramine (1 mg/kg) caused substantial elevation in CSF pressure that exceeded 30 mm Hg (initial pressure 12.5 +/- 2.1). This was followed by substantial accumulation of tyramine, dopamine and norepinephrine concentrations in CSF of these animals. The animals became comatose soon afterward. The administration of tyramine to pretreated (n = 10) or phenelzine-treated animals without liver disease (n = 6) caused only the expected transient increase in blood pressure but with no significant effect on CSF pressure of these animals. These animals recovered fully from the experiment without any ill effect. These studies suggest that tyramine may have obvious implications in the development of intracranial hypertension in Reye's syndrome.

Animals↗

PubMed1981

[Ocular signs in coma caused by cranial injury].

Following a short introduction on the value of ocular symptoms in traumatized patients based upon the literature, the A. describes his case material comprising 10 cases of severe cranial-encephalic traumatisms with coma. According to the A., the investigation in patients with cranial traumatisms in coma of the reflex eye motility (research of statokynetic movements) and of the movements obtained by vestibular stimulation with cold water offers useful elements for localization of the lesion and for prognosis.

Adolescent↗

PubMedDate not supplied

[Coma in myxedema. Clinical contribution].

Coma due to myxoedema was first reported in 1879, and recent surveys have shown that only 150 cases are mentioned in the literature. Two cases successfully treated in a resuscitation department over the last six years are presented. The problems presented by patients of this type are discussed, and stress is laid on the importance of resuscitatory and intensive management, at least until resolution of the coma.

Aged↗

PubMed1981

[Treatment of head injury coma with prolonged pentobarbital anaesthesia (author's transl)].

Forty-five patients in deep coma resulting from head injury were treated with pentobarbital in doses adjusted to maintain serum barbiturate levels between 15 and 25 mg/l and short burst suppression phases on EEG. Brain death occurred in 20%. The overall mortality rate was 60%, no death being attributable to treatment; 24% of the patients were able to resume active life. Patients with non-reactive pupils during the early phase of coma were compared with patients of similar ages and neurological symptoms non treated with pentobarbital. In treated patients the incidence of brain death was reduced by 50% and the mortality rate by 25% (p less than 0.05), without increase in deaths from intercurrent complications and in severe sequelae among survivors.

Adolescent↗