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PubMed1989

Studies of ammonia loading: effects of rate of delivery and enhanced removal of NH4 on blood levels of ammonia and coma induction.

Using dose-response curves, the dose of NH4Ac inducing coma in one-half of the animals was increased by 60 to 80% after 1 mmol of arginine. The larger increase occurred in larger rats but was not proportional to the increase in weight. Incremental subcoma doses of NH4 raised the amount of NH4 required for inducing coma and the brain level of ammonia at the point of coma. After a portacaval shunt the results were similar, although lower doses of NH4 were required from the beginning. Blood ammonias after a loading dose (1.25 mmol) of NH4 were influenced by the duration of a preinfusion of NH4 and by the preinjection of various amino acids involved in the disposal of NH4 in the urea cycle. The amount of reduction in blood ammonia by ornithine and arginine compounds was less the longer the preinfusion of NH4. Blood ammonia was not lowered by glutamate at any time but was increased with longer preinfusion periods. Hepatectomy (Hx) reduced the removal of an NH4 load. After a modest load (0.85 mmol) of NH4, blood ammonia increased 5-fold, over that of sham-operated rats, with 70% Hx and 15-fold with 90% Hx. Ornithine reduced these blood ammonias by about 50%. Arginine had no effect. These studies indicate ways of reducing toxicity of NH4 and factors that predispose to or enhance toxicity.

Amino Acids↗

PubMed1992

Clinical outcome and cognitive impairment in patients with severe head injuries treated with barbiturate coma.

This study reports on clinical outcome in 38 patients with severe head injuries (posttraumatic coma for 6 hours or more) treated with barbiturate coma because of intracranial hypertension. Eighteen patients died, 4 patients remained in a severely disabled or a chronic vegetative state, and 16 patients reached the levels good recovery/moderate disability. Six of these patients returned to work or school full time, 4 for half time and 3 were in a rehabilitation program. Fourteen patients were subjected to a comprehensive neuropsychological assessment. All patients except one exhibited varying degrees of cognitive dysfunction and 6 patients had signs of personality change. The quality of life for the majority of surviving patients was relatively good but the positive effects of barbiturate coma therapy in the age groups over 40 years appeared to be limited.

Adult↗

PubMed1976

Classification of coma.

By order of the Head Injuries Committee of the W.F.N.S. the author and his coworkers give definitions of consciousness, clouding of consciouness and unconciousness or coma. Furthermore, they suggest a definition of the termination of unconsciousness, with particular reference to the transition into a stage of clouding of consciousness. Any statistical evaluation and comparison of different materials depend on the use of identical definitions. As an example, it has been shown that the duration of aa uninterrupted coma, which can be survived, becomes relatively short if in accordance with the proposed definitions the various stages of clouding of consciousness are excluded from "coma".

Brain Injuries↗

PubMed1996

Fulminant malignant hyperthermia associated with ketoacidotic diabetic coma.

Malignant hyperthermia (MH) in humans is usually triggered by volatile anaesthetics and depolarizing muscle relaxants. However, other factors or drugs (e.g. cresol) are thought to induce MH. We report a case of fulminant MH associated with a ketoacidotic diabetic coma. After therapy for diabetic coma with insulin (containing the preservative cresol) and electrolyte solutions was started, the patient complained of increasing myalgia, developed a high fever and respiratory and metabolic acidosis and lost consciousness. MH was treated immediately with dantrolene; the patient recovered within 14 days. Five months later the patient was diagnosed as MH-susceptible by the in vitro caffeine and halothane contracture test. This case supports the assessment that MH and diabetes are associated diseases and that cresol could possibly trigger MH. Furthermore, therapy with dantrolene has been demonstrated to be beneficial in the treatment of MH associated with diabetic coma.

Adult↗

PubMed1978

Postbulbar duodenal ulcer occurring in a patient of diabetic coma.

Duodenal ulcer beyond the bulb occurred in a diabetic patient when he was in ketoacidotic coma causing serious anemia. Early investigation of the stomach and duodenum by endoscope was quite valuable for evaluating this bleeding complication and the healing process of the lesion was serially recorded. Since several cases of diabetic coma have been reported to die from gastrointestinal bleeding, this report presents the important aspect in the management of diabetic coma, and usefulness of emergency endoscope.

Adult↗

PubMedDate not supplied

Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: case report.

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA1c) 8%, C peptide <0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.

Adult↗

PubMedDate not supplied

Lack of correlation between plasma 4-hydroxyglutethimide and severity of coma in acute glutethimide poisoning. A case report and brief review of the literature.

Glutethimide poisoning is characterised by coma, anticholinergic poisoning syndrome, hypotension, and other complications. Previous studies have shown that the severity of intoxication does not correlate with plasma glutethimide concentrations in individual patients. Glutethimide is partly converted to 4-hydroxyglutethimide, a metabolite which accumulates in the plasma of humans, and which has been thought to contribute to coma after plasma glutethimide concentrations have fallen. We followed plasma concentrations of glutethimide and 4-hydroxyglutethimide in a man who overdosed with glutethimide. Plasma 4-hydroxyglutethimide concentrations did not correlate with the degree of coma in our patient, and actually rose as the patient awakened. Other studies also indicate that 4-hydroxyglutethimide may not play an important role in glutethimide poisoning.

Coma↗

PubMed2001

Peritoneal dialysis in an infant with type 1 diabetes and hyperosmolar coma.

Hyperosmolar coma which is characterized by severe hyperglycemia in absence of chetosis is very rare in pediatric age with only 11 cases reported in the literature. The outcome of the condition is usually poor with mental retardation being the most common event. Here a case of hyperosmolar coma is described in a female of three months of age who was treated with peritoneal dialysis 11 hours after admittance to hospital. This female patient has been receiving insulin from three months of age and today at the age of 10 years she leads a normal life despite being on insulin therapy. A very low level of C-peptide (<0.3 ng/ml) clearly confirms she is affected by Type 1 diabetes. To our knowledge this is the first case report of hyperosmolar coma in a neonate with Type 1 diabetes who survived this condition without late neurological consequences.

Acidosis, Lactic↗

PubMed2003

[Hypophyseal coma].

Pituitary coma is a rare case of emergency and primarily due to ACTH and TSH deficiency. Pituitary coma occurs more often in patients with well-known pituitary deficiency than in patients with intrasellar tumor. Clinical manifestations are hypotonia, bradycardia, decreased skin and nipple pigmentation, muscle weakness, vomitus, nausea, obstipation, hypothermia, and hypoventilation. A postpartal agalactia is often the first sign of Sheehan's syndrome. Unlike primary adrenal insufficiency (Addison's disease) ACTH deficiency does not cause hyperpigmentation, hyperkalemia, or salt loss. The suspicion of pituitary coma requires replacement with 100 mg hydrocortisone iv, 200 mg hydrocortisone iv/24 h, 500 micro g levothyroxine iv and fluid substitution. Since thyroxine accelerates the degradation of cortisol and can precipitate adrenal crisis in patients with limited pituitary reserve, hydrocortisone replacement should always precede levothyroxine therapy. ACTH stimulation test, CRH stimulation test and insulin tolerance test (optional) should be performed after therapeutic compensation to determine pituitary function.

Adrenal Insufficiency↗

PubMed2002

[Myxedema coma as a rare differential diagnosis of severe consciousness disturbance].

Myxedema coma is a rare and life-threatening complication of untreated hypothyroidism. Therefore, it must be part of the differential diagnosis in comatose patients. We report one patient who presented with CO(2) narcosis,hypothermia, bradycardia,hyporeflexia, tetraparesis, ascitis, pleural effusions, and heart insufficiency. Examination of the CSF, cranial CT, MRI, and MR angiography were normal. In suspicion of myxedema coma,the patient was treated with high dose L-thyroxine and hydrocortisone for preventing secondary adrenal insufficiency. A fast clinical recovery, decreased T4 (7.2 ng/l) and T3 (0.93 ng/l), and increased TSH (20.19 mU/l) together with the following anamnesis of radio iodine therapy and insufficient thyroxine intake confirmed the diagnosis. In conclusion, treatment of the myxedema coma must be started as soon as the laboratory results are confirmatory, since its course depends on the time of initiation of treatment.

Adrenal Insufficiency↗

PubMed1999

Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma.

Critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery.

Aged↗

PubMed1985

Frequency of diabetic ketoacidosis and hypoglycemic coma during treatment with continuous subcutaneous insulin infusion. Audit of medical care.

The frequency of diabetic ketoacidosis and hypoglycemic coma in a large series of patients with insulin-dependent diabetes treated by long-term continuous subcutaneous insulin infusion was compared with the frequency of these events in a matched group of patients treated by conventional insulin injections at the same hospital over the same period of time. Ketoacidosis and hypoglycemic coma occurred no more frequently in continuous subcutaneous insulin infusion-treated patients. Therefore, intensified insulin therapy achieved by continuous subcutaneous insulin infusion does not appear to be associated with a greater risk of ketoacidosis or hypoglycemic coma than does conventional insulin therapy.

Adult↗

PubMed1975

"Alpha-pattern coma" in high voltage electrical injury.

Two cases are reported in which reversible deep coma subsequent to high voltage electrical injury occurred in association with alpha frequencies in the EEG. The EEG pattern differs from the alpha rhythm of the normal awake patient by its diffuse distribution and unresponsiveness to a variety of stimulation. The term "alpha-pattern coma" is introduced to designate the occurrence of this pattern in comatose patients. The EEG in the cases described initially demonstrated activity in the alpha frequency which occurred in a generalized distribution and was unresponsive to stimulation. During the early stages of recovery an increased incidence of theta and delta activity was observed. The recovery records contained a low voltage alpha rhythm and responded to photic stimulation. The literature on this subject is reviewed and the possible modes of pathogenesis are discussed. The authors conclude that such examples of alpha-pattern coma are the result of diffuse cerebral damage and might be detected more frequently in comatose patients who survive if these patients are studied earlier in their clinical course with EEGs.

Adult↗

PubMed1988

Short latency somatosensory evoked potentials and brain-stem auditory evoked potentials in coma due to CNS depressant drug poisoning. Preliminary observations.

In patients in coma due to severe CNS depressant drug overdose the central somatosensory conduction time (CCT) after median nerve stimulation is prolonged and N20 is dispersed. Brain-stem auditory evoked potentials demonstrate delayed interpeak latencies (IPLs) I-III, III-V and I-V. This was observed in 4 out of 5 patients investigated after intake of an overdose of amitriptyline (2 cases), barbiturates, meprobamate and nitrazepam (one case each). Toxic levels of drug overdose were related to prolonged CCT and IPLs, whereas normal CCT and IPLs were found at therapeutic drug plasma levels. CCT, IPLs and dispersion of N20 decreased during the course of coma. All patients were successfully treated. It appeared that SSEP and BAEP investigations could make a distinction between a 'toxic' and a 'therapeutic' coma level in severe drug overdose. It further appeared that normalization of CCT and IPLs preceded clinical improvement.

Adult↗

PubMed1991

Terminal coma affects messenger RNA detection in post mortem human temporal cortex.

In situ hybridization histochemistry has been used to study the amount of M1 muscarinic receptor mRNA in temporal cortex from subjects with Alzheimer's disease and other neurodegenerative disorders, where the duration of terminal coma was known. Total polyadenylated mRNA and glutamate decarboxylase activity were also measured. Both muscarinic receptor mRNA and enzyme activity showed a significant decline with increasing duration of terminal coma, but were not related to diagnosis. Polyadenylated mRNA signal did not show an association with coma. These data indicate the need to consider the nature of the terminal illness in post mortem studies of mRNA as well as for neurochemical research.

Alzheimer Disease↗

PubMed1975

Concentrations of free amino acids in plasma, erythrocytes and cerebrospinal fluid in coma.

The concentrations of free amino acids were measured in plasma and erythrocytes in 15 patients, and in cerebrospinal fluid in eight patients, who were in coma. Although there was a variety of causes of coma, there seemed to be a characteristic pattern of the concentrations of amino acids for coma, and the plasma/cerebrospinal fluid ratios also showed constant patterns.

Amino Acids↗

PubMed1984

Thyroid crisis presenting as coma.

Coma is a rare complication of thyrotoxicosis. A patient with coma due to a thyroid crisis is reported. The EEG showed extremely slow and low voltage activity, which gradually returned to normal. Coma as a presenting symptom of thyroid crisis has not been reported before.

Adult↗

PubMedDate not supplied

Two roads to coma: the Scottish hypothesis.

Clinical experience seems to indicate two separate types of entry to coma. Some patients follow a pathway characterized by confusion, hallucinations, mumbling delirium, myoclonic jerks, and seizures. The author has called this sequence of symptoms the high road to coma and hypothesized that its basic underlying pathophysiology involves increased neuronal firing rates. Other patients develop somnolence, lethargy, obtundation, and unresponsiveness without seizures or muscle twitches. This low road to coma involves either anatomical compression of the midbrain reticular formation or a metabolic or toxic disorder characterized by membrane stabilization and decreased neuronal excitability.

Coma↗