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Acyclovir induced coma in the intensive care unit.

A 73-year-old man with multiorgan failure requiring mechanical ventilation and haemodialysis developed herpes labialis infection during his stay in the ICU. This was treated with enteral acyclovir. He developed persistent neurologic impairment soon after acyclovir administration, which, over the course of seven days, progressed to coma, the aetiology of which was unclear. The computed tomograph (CT) of the brain and the cerebrospinal fluid (CSF) examination was normal. The electroencephalogram (EEG) showed generalized slowing. The possibility of acyclovir neurotoxicity was considered and the drug was discontinued. Haemodialysis was instituted and the patient made a complete neurological recovery. We believe that this is the first reported case of coma due to enteral acyclovir.

Acyclovir↗

Coma and metabolic acidosis early in severe acute paracetamol poisoning.

Coma and profound metabolic acidosis early in acute paracetamol poisoning have been described in three patients. Of five further patients (four female, one male, aged 17-80 years) with severe poisoning (plasma paracetamol concentration greater than 800 mg/l, 4-12 h postingestion), four were deeply unconscious on admission and two had a severe metabolic acidosis. Signs of hepatorenal damage were minimal and no additional poisons were detected except salicylates (plasma concentration 290 mg/l) in one instance. Plasma paracetamol half-lives were prolonged (median 9.4 h, range 4.8-39 h) and one patient sustained massive hepatic damage and a further patient died despite treatment with intravenous acetylcysteine. Paracetamol poisoning, when associated with exceptionally high plasma concentrations, can give rise to coma and metabolic acidosis in the absence of hepatic failure or other drugs. Although unusual, other such presentations may not have been recognized because a toxicology screen was not performed.

Acetaminophen↗

Shock, metabolic acidosis, and coma following ibuprofen overdose in a child.

OBJECTIVE: To report a child who developed shock, loss of consciousness, and metabolic acidosis following an ibuprofen overdose. CASE SUMMARY: A 6-year-old boy with no prior medical problems ingested approximately thirty 200-mg tablets of ibuprofen. The patient developed shock, coma, and metabolic acidosis. He was treated successfully with intubation and mechanical ventilation, fluid resuscitation, and decontamination with activated charcoal. The patient was discharged without any clinical sequelae. DISCUSSION: Serious adverse complications following ibuprofen overdose have been reported rarely in children. We reviewed literature pertaining to the etiology, pharmacology, pathophysiology, and management of complications following ibuprofen overdoses, as well as other case reports. CONCLUSIONS: Coma, metabolic acidosis, and shock were noted in a child who ingested a large quantity of ibuprofen. These complications have been described rarely in children. We attribute his favorable clinical outcome to early and aggressive intervention consisting of tracheal intubation, fluid resuscitation, and decontamination with activated charcoal. Although ibuprofen overdoses are usually benign, healthcare professionals should be aware of the various potentially serious complications that may occur.

Acidosis↗

Alpha rhythm and alpha-like activity in coma.

A normal waking EEG was obtained on a 22 year old man four days prior to cardiopulmonary arrest. Three days after resuscitation the EEG showed the pattern of alpha-like activity while the patient remained in deep coma. Since the EEGs were recorded by the same technician using the same 16 channel electroencephalograph and montages, it is possible to compare in the same individual these alpha-frequency activities before and after arrest. The alpha-like activity of coma does not resemble the waking alpha rhythm in amplitude, frequency, spatial distribution, variability and reactivity.

Adult↗

Epileptiform discharges in presence of continuous background activity in anoxic coma.

The EEGs of a group of patients in anoxic coma following cardiorespiratory arrest were retrospectively studied. Twelve of 70 patients had at least one EEG recorded during the acute period which consisted of epileptiform discharges in the presence of continuous diffuse background activity. Nine of the patients died while three made a generally favorable recovery. The analysis confirms the prediction of a recent revision of EEG grades in coma that this particular pattern of activity is of uncertain prognostic significance. This is in contrast to the occurrence of epileptiform discharges during discontinuous "burst suppression" activity which generally indicates a fatal outcome.

Aged↗

Triphasic waves in myxedema coma.

Triphasic waves occur in metabolic and nonmetabolic encephalopathies. We report an elderly patient in whom triphasic waves were associated with myxedema coma and disappeared after thyroid replacement therapy was initiated. The association between myxedema coma and triphasic waves has not been previously reported.

Aged↗

Diffuse theta activity and spindle-like bursts during coma after cardiac arrest.

An usual combination of diffuse theta activity with intermittent bursts of spindle-like activity, followed by 2-3 Hz rhythmic discharges and lasting about 7 seconds, was noted in a coma patient after cardiac arrest. We speculate that the theta pattern coma and spindle-like bursts originated in the pontine region, and that those bursts in turn triggered or recruited rhythmic slow-wave complexes similar to absence discharges.

Aged↗

Case report: coma due to oxytetracycline.

An unusual case is reported of coma of gradual onset in a 67-year old woman being treated with oxytetracycline. Ten hours after the last dose, the patient regained consciousness but remained confused with hallucinations for another 24 hours. The possibility of side-effects should be borne in mind in any patient who develops coma whilst on oxytetracycline.

Aged↗

Neuroleptic malignant syndrome presenting as hyperosmolar non-ketotic diabetic coma.

A 50-year-old man presented with hyperosmolar non-ketotic diabetic coma associated with the neuroleptic malignant syndrome (NMS) after intramuscular treatment with haloperidol. It is suggested that NMS may occur as a complication of uncontrolled diabetes mellitus with dehydration. Conversely, NMS might precipitate diabetic coma in patients with previously well controlled blood glucose.

Body Temperature Regulation↗

SSEPs and prognosis in postanoxic coma: only short or also long latency responses?

BACKGROUND: Short latency somatosensory evoked potential (SSEP) (N20) is a good predictor of poor outcome in postanoxic coma. It has been suggested that the long latency response (N70) may increase the sensitivity of SSEPs for predicting poor outcome. METHODS: As part of a prospective cohort study in 407 adult patients unconscious 24 hours after cardiopulmonary resuscitation (CPR), N20 was recorded 24, 48, and 72 hours after CPR, and N70 was recorded at least once in 319 patients. Poor outcome was defined as death or persistent vegetative state 1 month after CPR. RESULTS: Absent N20 had a 0% false positive test rate at all time intervals, with prevalence of poor test result varying from 37 to 48%. Addition of abnormal N70 (absent or delayed > 130 msec) with present N20 as poor test result added 21 to 28% to this prevalence, but at the cost of a false positive test rate of 4 to 15%. Good outcome could not be predicted reliably with either of the tests, as only 28% of patients with normal N20 and N70 had a good outcome. CONCLUSION: Determination of presence or absence of the N70 in patients with postanoxic coma gives additional information about the likelihood of poor outcome, but it is not precise enough to base treatment decisions solely on its absence.

Cohort Studies↗

Recovery from drug-induced alpha coma.

A 41-year-old man in deep coma after drug overdosage showed electroencephalographic activity of alpha frequency. He remained comatose for 20 hours, and assisted ventilation was required for 28 hours, but he eventually recovered. Alpha coma has generally been considered to have grave prognostic implications, but acute drug intoxication is an exception to this rule. Intensive supportive therapy is important.

Adult↗

Nontraumatic "spindle coma": clinical, EEG, and prognostic features.

"Spindle coma" denotes the association of alteration of consciousness with electroencephalographic (EEG) activity resembling slow-wave sleep. Clinical, EEG, and pathologic data were reviewed for 36 patients with this syndrome, who were divided into two groups, based on the level of consciousness at the time of the initial neurologic evaluation. Fifteen patients were stuporous or semicomatose; none exhibited abnormalities of brainstem motor function, and 14 survived. Twenty-one patients were comatose; 20 had abnormalities of brainstem motor function, and only 4 survived. The outcome of nontraumatic spindle coma is unfavorable when the patient is fully comatose and brainstem motor function is impaired.

Adolescent↗

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↗

Coma with triphasic wave pattern in EEG as a complication of temporal arteritis.

Coma is rare in temporal arteritis (TA). We describe a patient with TA who suddenly developed coma with a triphasic EEG pattern that resolved after initiation of steroid treatment. Although the arterial lesions in TA are segmental in nature, TA may present with signs of diffuse neurologic deficit; early treatment can result in complete resolution.

Aged↗

Evaluation of level of consciousness by the Glasgow coma scale in children with Reye's syndrome.

The Glasgow Coma Scale, which was designed to evaluate level of consciousness after head trauma, has been compared to the Lovejoy scale in 21 patients with Reye's syndrome. Like other investigators, we have noted a poorer prognosis in those patients with higher peak NH3 levels and rapid progression of disease. However, we have also noted that the Glasgow coma scale provides a better, earlier indicator of progressive central nervous system disease than the Lovejoy scale and, therefore, helps physicians caring for such patients to institute intracranial pressure (ICP) monitoring and vigorous measures for the control of elevated ICP earlier than they might otherwise.

Child↗

Spontaneous intracranial hypotension resulting in coma: case report.

OBJECTIVE: Spontaneous intracranial hypotension is a potentially severe condition characterized by a distinct clinical picture caused by low cerebrospinal fluid pressure. Although coma has been reported previously as a presentation of this condition, this is the first report in which misdiagnosis of this condition and unwarranted surgery led to coma. CLINICAL PRESENTATION: A 62-year-old man presented with a history of headache, and cranial magnetic resonance imaging showed bilateral chronic subdural hematomas. After evacuation of the hematoma, the patient's condition deteriorated into a state of profound depression of consciousness. Repeated cranial computed tomographic scans showed intracranial air, and intracranial pressure monitoring showed negative recording. Spinal magnetic resonance imaging demonstrated epidural cerebrospinal fluid leaks at the middle and lower thoracic levels. INTERVENTION: Epidural blood patch resulted in almost immediate improvement in the patient's condition, and he was fully awake 24 hours later. CONCLUSION: This case report expands the presently known clinical spectrum of this uncommon and generally benign illness.

Blood Patch, Epidural↗

Olanzapine-lnduced hyperglycemic nonketonic coma.

OBJECTIVE: To report a case of olanzapine-induced hyperglycemia leading to a hyperosmolar, hyperglycemic, nonketonic coma. CASE SUMMARY: A 51-year-old, 85.5-kg (ideal body weight 79.9 kg), white man presented to a Veterans Affairs hospital with a serum glucose concentration of 1596 mg/dL. Soon thereafter, he went into a hyperosmolar, hyperglycemic, nonketonic coma. Olanzapine therapy had been instituted less than six months prior to this event; approximately two months before this event, his blood glucose was 108 mg/dL. Eight days after stopping olanzapine, the glucose concentration returned to normal, and the patient no longer required insulin nor any other glucose-lowering agents. DISCUSSION: The insulin resistance caused by olanzapine is normally attributed to the weight gain associated with the drug. In this patient, it appears that olanzapine caused hyperglycemia by a mechanism other than weight gain. CONCLUSIONS: This case report and others from the literature suggest that olanzapine therapy may induce hyperglycemia in some patients.

Antipsychotic Agents↗

Reversible coma secondary to cefepime neurotoxicity.

OBJECTIVE: To describe a case of cefepime neurotoxicity associated with acute renal failure that resulted in nonconvulsive status epilepticus. CASE SUMMARY: A 66-year-old woman with acute myeloid leukemia had fever on the third day of the initial chemotherapy cycle. Empiric antibiotic treatment with cefepime 2 g every 8 hours was started; fluconazole and vancomycin were subsequently added due to the persistence of fever. Ten days after initiation of cefepime, the patient developed acute renal failure followed by altered consciousness (Glasgow coma scale 6) associated with nonconvulsive status epilepticus. Cefepime was discontinued. Epileptiform activity in the electroencephalogram disappeared with clonazepam, and the patient regained consciousness 48 hours after cefepime withdrawal. DISCUSSION: Acute renal impairment combined with the use of cefepime may account for nonconvulsive status epilepticus. An objective causality assessment revealed that the adverse event was probably due to cefepime. Cefepime's neurotoxic effects derive from high serum concentrations resulting from decreased renal clearance, increased unbound antibiotic, and blood-brain barrier dysfunction during uremia. CONCLUSIONS: The combination of cefepime treatment and acute renal failure may induce drug-related neurotoxicity. Nonconvulsive status epilepticus frequently passes unnoticed in severely ill patients without a history of epilepsy. This disorder should be included in the list of potential causes of coma. In this patient, early detection of nonconvulsive status epilepticus and withdrawal of the antibiotic resulted in full recovery.

Acute Kidney Injury↗