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A 10-year-old, intact male, cocker spaniel was presented with hypothermia, without shivering, and progressive stupor leading to coma. Myxedema coma, potentially precipitated by diuretic therapy, was tentatively diagnosed and treatment initiated, but progressive respiratory depression led to the decision to euthanize. Postmortem findings supported the diagnosis of myxedema coma.
The hypoglycaemic coma is a severe complication for type 1 diabetic patients. Rarely fatal it may be associated with various paroxysmal accidents, potentially harmful, especially during driving. Hypoglycaemia certainly alters the quality of life because it markedly increases the anxiety of both the patient and his/her family. It is considered as a major limiting factor in the glycaemic management of type 1 diabetic patients. Being the consequence of numerous causal factors, hypoglycaemic coma is not always easy to prevent and may occur as a paroxysmal phenomenon, sometimes without obvious contributing circumstances. After having defined the various hypoglycaemic thresholds, we will analyse the pathophysiology of insulin-induced hypoglycaemia and of its hormonal counterregulation, and we will describe the hypoglycaemia unawareness phenomenon. These elements should help to better understand why a hypoglycaemic coma may suddenly occur in a diabetic patient. Some advices will also be given to reduce the risk of such a paroxysmal complication in patients with type 1 diabetes.
With a few very rare exceptions, hypoglycemia and diabetic coma almost always occur in patients with diabetes mellitus, and are among the most common emergencies in children. For the emergency physician, it is important, on the basis of a specific history-taking and information from, for example, family members, supplemented by a clinical examination done in the light of knowledge of the typical symptoms of each of the entities, to determine whether hypoglycemia or diabetic coma is presenting. The most important technical examination is the measurement of blood glucose. In the event of hypoglycemia, the first therapeutic measure is the administration of sugar--in the case of a comatose patient via a venous line. The s.c. or i.m. administration of glucagon to achieve short-term improvement might be considered. In the event of a diabetic coma, abundant electrolyte solution is initially needed, followed by i.v. insulin. Referral to hospital is mandatory.
In this paper we describe a successfully treated case of hyperosmolar hyperglycemic non ketotic coma (HHNC). The HHNC was observed in a patient affected by Waldenström's macroglobulinemia, associated with type II diabetes and complicated by pulmonary tuberculosis. Hyperosmolar hyperglycemic nonketotic coma is a clinical condition with a high mortality rate associated with a severe increase in blood viscosity. This increase in blood viscosity justifies several clinical manifestations of the HHNC. We believe that an increase in the blood viscosity produced by the simultaneous presence of the single diseases mentioned above may have encouraged the development of hyperosmolar coma in the case reported.
The authors present two cases of chronic alcoholism in two female patients aged 41 and 52 years without diabetes mellitus, in whom hypoglycaemic coma occurred during the abstinence period. Hypoglycaemia in one patient occurred suddenly as a result of fasting within 24 hours following the last alcohol intake, whereas a severe hypoglycaemia in the second patient was developing progressively during 72 hours; patient did not eat much and the last meal took 24 hours before the onset of hypoglycaemic coma. Diagnosis of hypoglycaemic coma was suspected because as no alcohol or acetic acid smell were felt, no alcohol or methanol was detected in blood (tested only in one patient). Adrenergic reactions were not distinct (no excessive sweating, convulsions, tachycardia). The authors suggest, that a severe hypoglycaemia should be considered in patients suspected of alcoholism, and the treatment should start earlier with intravenous glucose administration.
OBJECTIVE: To find out efficacy and benefits of early starting of stimulation therapy in coma patients. DESIGN: Randomized controlled trial. METHOD: Sixty children admitted to the Department of Pediatrics, having coma due to non-traumatic neurological insult were randomly selected. Both study and control groups had 30 patients each. Children in the study group were given stimulation therapy while those in control group received no stimulation. The level of consciousness was assessed before and two weeks after giving stimulation therapy. RESULTS: Improvement in level of consciousness was better in study group as compared to control after two weeks of stimulation therapy. CONCLUSION: Stimulation therapy was found to be highly effective in coma patients.
INTRODUCTION: hyroid dysfunction is common in Down's syndrome, most common being hypothyroidism. Longstanding, untreated hypothyroidism can lead to myxedema coma. METHODS: Here we report a patient with Down's syndrome who presented with myxedema coma. DISCUSSION: The three essential elements for the diagnosis of myxedema coma include altered mental status, defective thermoregulation and a precipitating event or illness; all of these were present in our patient. Also, very high TSH, low T3 and T4, and the rapid response to the treatment with levothyroxine confirmed the diagnosis. CONCLUSION: Patients with Down's syndrome should have regular screening for thyroid dysfunction.
The variation in time of some blood biochemical parameters was investigated in 100 patients with acute head injury and coma of variable duration, in parallel with the clinical course. The purpose of this study was to establish possible correlations between the severity of the trauma (assessed according to the coma classification proposed by C. Arseni) and the variation of the parameters studied. The results show complex correlations between the biochemical events in the patient and the degree of brain function impairment initially and after some time. Long lasting coma (over 14 days) is associated with complex biochemical alterations representing an additional element for defining the clinical condition.
Clinique Saint Martin is a specialized center for neurologic rééducation which disposes since the month of May 1989 of a ten beds unit intended to receive head injury during coma awakening stage (as soon as possible after intensive care). Effectively important clinical troubles are in relation with traumatism and coma but also secondary effects seems to be due to a long stay in Intensive Care Unit (in spite of all qualities of the medical team). Every patient has a room which can be personified and become very familiar for purpose to create a safe surrounding, without movement limitation and rich in sensorial stimulations and human contacts. Team for each patient is very numerous. In very intensive and permanent way the first period is distinguished by the need of a presence. Repeated calls "for nothing" are characteristic of coma awakening and must count in the unit working.
The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
Coma blisters are self-limited lesions that occur in the setting of coma of various causes, but are most commonly associated with barbiturate overdose. Examination of a skin biopsy specimen demonstrates the characteristic presence of eccrine sweat duct necrosis. Although the exact cause of coma blisters remains unknown, they are not related to underlying infections or rheumatologic disorders, and do not contraindicate the continued therapeutic use of barbiturates.
Three cases of coma occuring during parenteral alimentation are presented. The common factor was that they occurred during the phase of realimentation in patients with severely impaired nutrition. In two cases out of three, the coma marked the beginning of the absolute or relative anabolic period. They were studied clinically, biologically and electrically. In one case only, major hypophosphataemia was discovered (2mg/l). Of the three patients, one only died 4 days after the onset of coma, whilst clinical and biological characteristics had returned to normal.
Many possible complications are associated with cardiopulmonary bypass. They are similar to the risks accompanying most surgical procedures and include stroke, renal failure, and death. This potential for complication increases when bypass exceeds 2 hours and rises sharply when pump time is prolonged more than 3 to 4 hours. One group of serious complications is major neurologic disorders. The risk of significant cerebral dysfunction, that is, severe focal stroke or coma, is about 1%, and this risk increases with age and coexistent cardiovascular disease. This article focuses on the complication of coma and the possible role cardiopulmonary bypass plays in improving survival rates. A case study is presented illustrating the potential role of cardiopulmonary bypass in the unexpected neurologic recovery from coma.
As desirable as it might be to predict early in the course of coma whether a patient will do well or poorly, all studies of coma prognosis are plagued by inherent methodologic problems that tend to diminish the utility of the derived criteria: especially the tendency of poor prognoses to be self-fulfilling, the rapid drop-off in patient population due to death from nonneurologic causes, and the need to lump, for the sake of statistical significance, outcome categories that ought to be kept distinct for purposes of ethical decision making. Even for a methodologically ideal study, if 100 per cent of the N patients fulfilling a particular criterion experienced the same poor outcome, the probability of a false prediction of poor outcome in the next patient meeting that criterion is approximately 1/(N + 2), which is hardly negligible for a realistically sized study. Moreover, there is a 50 per cent chance of at least one false-positive prediction among the next (N + 1) patients fulfilling the criterion. Given this inherent unreliability of early predictors for individual patients, given that decisions to continue life support are reversible, whereas decisions to withdraw it are usually not, and given that the death of a patient with potential for recovery is a more serious error than the (typically) transient prolongation of life of a patient destined soon to die anyway or (much less commonly) to remain in a chronic vegetative state, it would seem prudent to continue life support for all patients during the first few weeks or months of coma or vegetative state, regardless of early indicators of poor outcome. Early prognostication can still serve other useful purposes, however, including the counseling of families, triage and DNR decisions, and future clinical investigations of brain-resuscitative measures.
The occurrence of coma betrays a deficiency of the ascending reticular activating system (ARAS) of the brain stem, which constitutes the neurophysiological support of wakefulness. Multiple factors, acting separately or jointly, may be responsible for coma. They include diffuse lesions or circumscribed lesions with repercussions on the ARAS metabolic and toxic factors, intracranial hypertension, cerebral oedema, epileptic activity, and so forth. Owing to the influence it exerts on the management of coma, the physiopathological approach is as necessary as the aetiological approach.
Imaging has become one of the main methods to diagnose and monitor coma. CT is the technique of choice in the exploration of traumatic coma or spontaneous intracerebral haemorrhage, but MRI is better than CT to explore comas of ischaemic, infective, tumoral or toxic origin, as it provides earlier and more precise images.
In 34 comatose patients in the acute phase, the mean hemispheric CBF is lowered as well as the CMRO2, with a quite good relation between these values and the coma level and prognostic so. The cerebral response to a PaCO2 range indicates a quite good relation with the coma level (the lowest value in the most severe comas). The cerebral autoregulation study, using Aramine induced hypertension, can separate the cases with a present autoregulation and the cases with a loss of autoregulation (the most severe and the poorest prognosis). In dynamic conditions (variation of the PaCO2 or Aramine induced hypertension), the change in CMRO2 is interesting : rather good prognosis among the patients with a normal metabolic autoregulation - poor prognosis among those whose metabolic autoregulation is lost.
The EEGs of 26 patients who remained at least 6 hours in coma after cardiovascular arrest were analyzed. The first EEG was recorded within few days after reanimation, classified in a 5-grade scale of increasingly severe impairment and compared with the final clinical outcome. On the basis of the present study and of a review of 408 EEG findings reported in similar investigations in the literature we conclude that the EEG can be useful in predicting the outcome of patients in postanoxic coma states: the EEG should be recorded at earliest 8-12 hours but within 2 days after reanimation, a barbiturate intoxication and hypothermia should be excluded. The classification of the recordings in a 5-grade scale has proven to be helpful and accurate in predicting the outcome: Grade I EEG findings imply a very good prognosis, a complete remission can be expected in most cases. Grade II and III findings have no definite prognosis: the EEG should be repeated one or two days later, a favorable outcome is to be expected only with rapid improvement of the tracing. Grade IV and Grade V findings have a very serious prognosis: complete recovery has been described episodically, most in the pediatric population and with findings of alpha-coma.