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PubMedDate not supplied

Hyperosmolar nonketotic coma: prevention, diagnosis, and treatment.

With the multi-faceted approach to head and neck cancer today, maintaining caloric intake by long-term enteral hyperalimentation is commonplace. Along with the tremendous advantages of this form of nutrition, the disadvantage of hyperosmolar nonketotic diabetic acidotic coma is present. Mortality rates are quoted from 40% to 70% according to the literature reviewed. Therefore, prevention is the best form of treatment. The cause, diagnosis, and treatment will be discussed.

Carcinoma, Squamous Cell↗
PubMed2004

Diabetic keto-acidotic (DKA) coma following olanzapine initiation in a previously euglycaemic woman and successful continued therapy with olanzapine.

We report the case of a euglycaemic woman whose glucose control rapidly decompensated following olanzapine initiation leading to diabetic coma. Hyperglycaemia has been associated with chronic psychotic disorders and antipsychotics for many years. However, it is unusual to see such rapid and life-threatening changes associated with treatment. The case highlights that changes in antipsychotic treatment may be associated with large changes in glucose tolerance, and that it is possible to continue antipsychotic treatment with appropriate diabetic care.

Adult↗
PubMed2005

Seizures, metabolic acidosis and coma resulting from acute isoniazid intoxication.

Isoniazid is an anti-tuberculosis drug, used commonly for treatment and prophylaxis of tuberculosis. Acute isoniazid intoxication is characterized by a clinical triad consisting of metabolic acidosis resistant to treatment with sodium bicarbonate, seizures which may be fatal and refractory to standard anticonvulsant therapy, and coma. Treatment requires admission to the intensive care unit for ventilatory support, management of seizures and metabolic acidosis. Pyridoxine, in a dose equivalent to the amount of isoniazid ingested, is the only effective antidote. We report the successful treatment of two isoniazid intoxication cases: the case of a child developing an accidental acute isoniazid intoxication and an adult case of isoniazid intoxication with the intent of suicide.

Acidosis↗
PubMed1984

Hypoglycemic coma induced by inadvertent administration of glyburide.

A 79-year-old nondiabetic woman was inadvertently given a 5-mg tablet of glyburide. Blood glucose concentration was 2.6 mmol/L three hours after ingestion. The patient was discharged 9 hours after ingestion and readmitted 10 1/2 hours after ingestion, in a hypoglycemic coma (blood glucose, 0.65 mmol/L). She was treated with two bolus doses of dextrose and intravenous dextrose. Her blood glucose was abnormal until hospital day 3. On hospital day 4, she was discharged with no apparent sequelae. This patient's severe reaction may have been due to mild renal insufficiency or concurrent use of timolol. Should inadvertent administration of glyburide occur in a patient with impaired renal function, the patient should be monitored for at least 24 hours.

Aged↗
PubMed1991

Important abnormalities in recordings of somatosensory evoked potentials in coma.

We have chosen six illustrations showing how much vital information can be obtained from median nerve SEPs during the first 24 hours in coma. With avulsion of brachial plexus roots there was loss of SEPs at the cervical cord and the scalp from the affected side. In a severe injury of the cervical cord there was preservation of brachial plexus potentials, while SEPs at the cervical cord were absent. After critical deterioration in a case of repeated subarachnoidal hemorrhage, scalp SEPs with very short latency occurred, which is a finding suggestive of destruction of cortical SEP generators heralding a fatal outcome. In a case of brain injury combined with central hyperthermia, there was initially a loss of scalp SEPs probably due to the combined effect of these factors. In a case of brain injury there were bifid peaks at the scalp level. It is important to assess central sensory conduction time only to the first scalp SEP, otherwise an erroneously abnormal state may be inferred. In a patient with clinical and EEG evidence of brain death there was a loss of far-field thalamic potentials at the neck. It is important to be aware of such presentations to be able to provide corroborative assurance for the assessment of prognosis.

Adult↗
PubMed1993

Episodic coma due to acute basilar artery migraine: correlation of EEG and brainstem auditory evoked potential patterns.

Our patient presented with three episodes of deep coma in 5 weeks, followed by a complete recovery. The neuroradiological tests and spinal fluid analysis excluded structural lesions, including subarachnoid hemorrhage, from the diagnosis. A nonconvulsive status was excluded by 24-hour EEG monitoring. The EEGs and brainstem auditory evoked responses were abnormal during ictus, but they reversed to normal with the clinical recovery. Timely neurophysiological tests helped in the diagnosis of basilar artery migraine.

Basilar Artery↗
PubMed2001

Cisternal MHPG level inversely correlates with Glasgow coma scale after aneurysmal subarachnoid hemorrhage.

We measured the concentrations of monoamines and amino acids in the cisternal cerebrospinal fluid obtained from 15 patients after aneurysmal subarachnoid hemorrhage. Based on the Glasgow Coma Scale (GCS), the patients were divided into two conscious (GCS always 14 or better from the third post-operative day to Day 12; n = 8) and unconscious groups (n = 7). We examined the concentrations of monoamines and amino acids between the two groups and evaluated the correlation between the concentrations and the GCS at CSF sampling. The concentration of MHPG was significantly higher in the unconscious than in the conscious group from Days 4 to 12. A significant inverse correlation was observed between the MHPG concentration and the GCS (r = approximately 0.635, p < 0.0001). Measuring the cisternal MHPG concentration may be useful for estimating convalescence after subarachnoid hemorrhage.

Aged↗
PubMed2004

Reliability of the Glasgow Coma Scale for the emergency department evaluation of poisoned patients.

UNLABELLED: The Glasgow Coma Scale (GCS) was developed for monitoring the mental status of head-injured patients in the intensive care unit. The purpose of this study is to determine the inter-rater reliability of the GCS for poisoning patients in the emergency department. METHODS: This was a prospective, observational study. Two observers used a standard assessment checklist to determine the GCS of suspected poisoning patients. Inter-rater reliability was assessed with a weighted Kappa score. RESULTS: A total of 39 patients were enrolled. Weighted kappa for the total GCS demonstrated excellent agreement. Agreement was also good for each component of the score. CONCLUSION: The GCS is a reliable tool for the evaluation of mental status of poisoning patients in the emergency department.

Adolescent↗
PubMed2004

Glasgow Coma Scale score and QTc interval in the prognosis of organophosphate poisoning.

OBJECTIVES: The aim of this study was to assess the applicability of the Glasgow Coma Scale (GCS) score and the Q-T interval corrected for heart rate (QTc interval) in predicting outcome and complications in patients with organophosphate (OP) poisoning. METHODS: This prospective, observational study included 65 patients older than 18 years. In the out-of-hospital setting, the end-tidal carbon dioxide (ETCO2), oxygen saturation (SaO2), QTc interval, and GCS score were monitored in each patient. A statistical comparison was then made between the group with respiratory failure and the group without this complication. RESULTS: The group with complications had significantly different values of measured parameters--a longer QTc interval and a lower GCS score, a higher number of intubations, and worse outcomes (p < 0.05). The two measures, GCS score and QTc interval, have been shown to be equally good in predicting respiratory failure and hospital mortality in patients with OP poisoning. CONCLUSIONS: In the initial out-of-hospital care of patients with OP poisoning, it is essential to monitor QTc interval and GCS score. These measures help with prognosis, and may suggest when to initiate precautions to prevent complications (i.e., respiratory failure). The simplicity and promptness of these methods allow providers to perform early and effective triage.

APACHE↗
PubMed2005

Performance of the pediatric glasgow coma scale in children with blunt head trauma.

OBJECTIVES: To compare the accuracy of a pediatric Glasgow Coma Scale (GCS) score in preverbal children with blunt head trauma with the standard GCS score in older children. METHODS: The authors prospectively enrolled children younger than 18 years with blunt head trauma. Patients were divided into cohorts of those 2 years and younger and those older than 2 years. The authors assigned a pediatric GCS score to the younger cohort and the standard GCS score to the older cohort. Outcomes were 1) traumatic brain injury (TBI) on computed tomography (CT) scan or 2) TBI in need of acute intervention. The authors created and compared receiver operating characteristic (ROC) curves between the age cohorts for the association of GCS scores and TBI. RESULTS: The authors enrolled 2,043 children, and 327 were 2 years and younger. Among these 327, 15 (7.7%; 95% confidence interval [CI] = 4.4% to 12.4%) of 194 who underwent imaging with CT had TBI visible and nine (2.8%; 95% CI = 1.3% to 5.2%) had TBI needing acute intervention. In children older than 2 years, 83 (7.7%; 95% CI = 6.2% to 9.5%) of the 1,077 who underwent imaging with CT had TBI visible and 96 (5.6%; 95% CI = 4.6% to 6.8%) had TBI needing acute intervention. For the pediatric GCS in children 2 years and younger, the area under the ROC curve was 0.72 (95% CI = 0.56 to 0.87) for TBI on CT scan and 0.97 (95% CI = 0.94 to 1.00) for TBI needing acute intervention. For the standard GCS in older children, the area under the ROC curve was 0.82 (95% CI = 0.76 to 0.87) for TBI on CT scan and 0.87 (95% CI = 0.83 to 0.92) for TBI needing acute intervention. CONCLUSIONS: This pediatric GCS for children 2 years and younger compares favorably with the standard GCS in the evaluation of children with blunt head trauma. The pediatric GCS is particularly accurate in evaluating preverbal children with blunt head trauma with regard to the need for acute intervention.

Adolescent↗
PubMed2006

A comparison of five simplified scales to the out-of-hospital Glasgow Coma Scale for the prediction of traumatic brain injury outcomes.

BACKGROUND: The 15-point Glasgow Coma Scale (GCS) frequently is used in the initial evaluation of traumatic brain injury (TBI) in out-of-hospital settings. We hypothesized that the GCS might be unnecessarily complex for out-of-hospital use. OBJECTIVES: To assess whether a simpler scoring system might demonstrate similar accuracy in the prediction of TBI outcomes. METHODS: We performed a retrospective analysis of a trauma registry consisting of patients evaluated at our Level 1 trauma center from 1990 to 2002. The ability of out-of-hospital GCS scores to predict four clinically relevant TBI outcomes (emergency intubation, neurosurgical intervention, brain injury, and mortality) by using areas under receiver operating characteristic curves (AUROCs) was calculated. The same analyses for five simplified scales were performed, and compared with the predictive accuracies of the total GCS score. RESULTS: In this evaluation of 7,233 trauma patients over a 12-year period of time, the AUROCs for the total GCS score were 0.83 (95% confidence interval [CI] = 0.81 to 0.84) for emergency intubation, 0.86 (95% CI = 0.85 to 0.88) for neurosurgical intervention, 0.83 (95% CI = 0.82 to 0.84) for brain injury, and 0.89 (95% CI = 0.88 to 0.90) for mortality. The five simplified scales approached the performance of the total GCS score for all clinical outcomes. CONCLUSIONS: In the evaluation of injured patients, five simplified neurological scales approached the performance of the total GCS score for the prediction of four clinically relevant TBI outcomes.

Adolescent↗
PubMed2006

Prediction of poor outcome within the first 3 days of postanoxic coma.

OBJECTIVE: To determine the optimal timing of somatosensory evoked potential (SSEP) recordings and the additional value of clinical and biochemical variables for the prediction of poor outcome in patients who remain comatose after cardiopulmonary resuscitation (CPR). METHODS: A prospective cohort study was conducted in 32 intensive care units including adult patients still unconscious 24 hours after CPR. Clinical, neurophysiologic, and biochemical variables were recorded 24, 48, and 72 hours after CPR and related to death or persisting unconsciousness after 1 month. RESULTS: Of 407 included patients, 356 (87%) had a poor outcome. In 301 of 305 patients unconscious at 72 hours, at least one SSEP was recorded, and in 136 (45%), at least one recording showed bilateral absence of N20. All these patients had a poor outcome (95% CI of false positive rate 0 to 3%), irrespective of the timing of SSEP. In the same 305 patients, neuron-specific enolase (NSE) was determined at least once in 231, and all 138 (60%) with a value >33 microg/L at any time had a poor outcome (95% CI of false positive rate 0 to 3%). The test results of SSEP and NSE overlapped only partially. The performance of all clinical tests was inferior to SSEP and NSE testing, with lower prevalences of abnormal test results and wider 95% CI of false positive rates. CONCLUSION: Poor outcome in postanoxic coma can be reliably predicted with somatosensory evoked potentials and neuron-specific enolase as early as 24 hours after cardiopulmonary resuscitation in a substantial number of patients.

Adult↗
PubMed1984

Monitoring by compressed spectral array in prolonged coma.

Compressed spectral array (CSA) transforms the electroencephalogram into a succinct graphic display of changes in frequency and amplitude. We used CSA to monitor 51 comatose patients for at least 15 hours daily for up to 49 days. The crucial CSA feature was the presence or absence of a peak of activity within the theta or alpha frequency range (4.0 to 13 Hz). Persistence or return of this peak in the first 10 days of coma was seen in all patients who made a good recovery; continued absence of the peak for 10 days, or its return and loss, was associated with death or a residual disability.

Adolescent↗
PubMed1986

Compartment syndromes and compression neuropathies in coma.

Eight patients are reported who developed peripheral nerve injuries due to limb compression during unattended coma. In each patient, the site of the peripheral nerve lesion or the unique combination of peripheral nerve lesions and swollen limbs, pressure blisters, or myoglobinuria indicated that compartment syndromes caused the nerve injury. The peripheral nerve injuries were characterized by severe axonal loss with persistent and often disabling sequelae.

Adult↗
PubMed1988

Reversible coma with prolonged absence of pupillary and brainstem reflexes: an unusual response to a hypoxic-ischemic event in MS.

A quadriparetic man with multiple sclerosis became comatose with absent pupillary and brainstem reflexes for 48 hours following a respiratory arrest. A periodic electroencephalographic pattern was recorded 12 hours after arrest suggesting a poor prognosis. Despite the poor prognostic signs, clinical recovery to baseline occurred within 2 weeks. Reversible coma with absent pupillary and brainstem reflexes may occur in MS patients for prolonged periods and lead to potential errors in prognosis if not recognized.

Brain Ischemia↗
PubMed1996

Recovery from coma caused by primary CNS mantle cell lymphoma presenting as encephalitis.

We report a 74-year-old woman with progressive cognitial deterioration and changes in personality. She had no clinical signs of an inflammatory CNS process, but brain CT and MRI scans and cytologic examination of the CSF were initially indicative of encephalitis and ventriculitis. Antiviral and antibacterial therapy had no effect on the course of symptoms, and patient became comatose. We established the diagnosis of a primary CNS mantle cell lymphoma (PCNSL) and began corticosteroids. Within a few days the patient became alert and was able to walk again. Nonenhancing and non-space-occupying PCNSLs are rare but must be considered in the differential diagnosis of coma and encephalitis. Comatose PCNSL patients without radiographic evidence for herniation can be successfully treated with corticosteroids even if the EEG has a burst suppression pattern.

Adrenal Cortex Hormones↗