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Pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils.

Acute clinical deterioration due to infarction or haemorrhage of an existing, often previously unrecognized, pituitary tumour is a rare but well-described complication. It can occur spontaneously or may be caused e.g. by mechanical ventilation, infection or surgical procedures. We report on a case of pituitary apoplexy occurring in a 64-year-old patient 3 weeks after cardiac surgery. The patient presented with deep coma and dilated pupils. Magnetic resonance imaging revealed a haemorrhagic pituitary tumour. After prompt endocrinologic replacement therapy with levothyroxine and hydrocortisone the patient regained consciousness. Neurological examination revealed right oculomotor nerve palsy and bilateral cranial nerve VI palsy. Subsequent trans-sphenoidal removal of a nonfunctional macroadenoma with large necrotic areas was performed. The patient recovered completely. To our knowledge, pituitary tumours presenting with a combination of deep coma and dilated pupils must be considered exceedingly rare. Possible pathophysiologic mechanisms are discussed. As our case illustrates, even in severe cases complete recovery is possible if the diagnosis is suspected, and diagnostic and therapeutic measures are initiated in time.

Coma↗

Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.

A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.

Anti-Inflammatory Agents, Non-Steroidal↗

[Baclofen-intoxication in a child resulting in coma, bradycardia and transitory defect of visual power].

A twelve and a half year old girl of foreign nationality was been found in her domestic environment in unwakeable condition. The emergency was alarmed, and she was transferred to the children's hospital. Her condition at this time: she was unconscious and suffering from cold sweat but her circulation was stable and her respiration sufficient. Because of language barriers it was difficult to find out the antecedence of her state, but an empty box of pills (Amitryptilin) lying next to the patient may serve as a first hint to a intoxication. The father denied that his daughter might have consumed drugs or alcohol and meant that any abuse of medicine was out of the question. First urinary measurements to check if any drugs might be involved remain inconspicuous; in a control measurement of the blood 12 hours later only an elevation of the CPK is noticed as an unusual detail. The CPK-MB remains being according to normal. The native CT of the skull remains inconspicuous as well as the control with contrastation after 12 hours and a MRT-examination after 36 hours. The liquor punction does not give hints to any pathological facts. The EEG shows a high degree of continuous irregular slowe waves over both hemispheres in the delta and theta activity range. This gives reason to assume an encephalitis. The result of an electrocardiogram reveals a sinus bradycardia. The therapy was symptomatically, virustatically with aciclovir, antibiotically with cefotaxim and prophylactically against edema of brain with dexamethason. After 24 hours the patient abruptly awakes from coma and after 36 hours the reason for the coma can be stated: The toxicological examinations of the blood lead to the result: Intoxication with Baclofen. Explantation for the origin of the tablets: The family lives together with an aunt, who, after a cerebrovascular accident, was treated with Baclofen, Amitryptilin and ASA.

Acyclovir↗

[Prolonged coma caused by diazepam sedation in ventilated patients. Diagnostic and therapeutic use of the benzodiazepine antagonist Ro 15-1788].

Repeated administration of diazepam in two ventilated patients had caused drug cumulation and coma over several days. In both cases central nervous depression could be demonstrated by the benzodiazepin antagonist Ro 15-1788 which induced reversal of coma. Estimation of plasma concentrations in a 70-year-old female patient 150 hours after the last administration showed a diazepam concentration of 437 ng/ml and a desmethyl-diazepam concentration of 483 ng/ml. The calculated elimination half-life of these substances were 109 and 403 hours. In the second case benzodiazepin could be demonstrated in urine for 10 days after withdrawal of medication. These observations suggest that diazepam is not a suitable drug for prolonged sedation in artificially ventilated patients. The benzodiazepin antagonist Ro 15-1788 represents a valuable diagnostic aid in ascertained or suspect cases of benzodiazepin intoxications. It can also be used therapeutically for reversal of central nervous depression.

Aged↗

[Paraproteinaemic coma in multiple myeloma (author's transl)].

The diagnosis of paraproteinaemic coma was made in 5 out of 74 patients with plasmocytoma. Compared with the other patients these 5 showed a nearly twofold increase of total serum and CSF protein concentration, a higher percentage of plasma cells in sternal marrow and extreme hypergamma-globulinaemia in the immunoelectrophoresis. In both groups CSF and serum amino acid concentrations showed no pathological changes. Psychopathologically the patients with paraproteinaemic coma showed the picture of an exogenous psychosyndrome. Electroencephalography demonstrated moderate general disturbances.

Aged↗

Computed tomography in the assessment of raised intracranial pressure in non-traumatic coma.

Cranial computed tomography (CT) scans and invasive intracranial pressure (ICP) measurements were reviewed for 34 children with non-traumatic coma from various causes. CT scan features including focal or generalised changes in density were noted and changes in cerebrospinal fluid (CSF) spaces were graded and correlated with the level of maximum ICP in the first 12 hours of treatment and monitoring. Seven patients had normal findings and 27 had abnormal scans. Nineteen of the 27 patients with abnormal scans had generalised abnormalities with varying degrees of loss of CSF space. Seventeen of these 19 patients had pressures greater than 15 mmHg. The highest pressures being found in those with the greatest degree of CSF space obliteration. In the remaining 8 patients, who had focal abnormalities either within the basal ganglia or cerebral hemisphere, there was no relationship between local CSF space obliteration and the level of ICP. In the 7 patients with normal scans three had ICPs of 20 mmHg or greater in the first 12 hours of monitoring and a further two also developed an ICP of this level 13-36 hours after the initiation of monitoring. In non-traumatic coma of various causes there is an association between loss of CSF space and increased ICP. However, there were two important exceptions to this; firstly in patients with focal abnormalities either within the basal ganglia or cerebral hemisphere, in whom the loss of adjacent CSF spaces was not a good indicator of generalised raised ICP; secondly some patients with normal scans, in whom this finding did not indicate normal ICP nor ensure that it remained at this level.

Adolescent↗

Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma.

In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma. Two hours after the ischemic insults, the level of brain-derived neurotrophic factor (BDNF) mRNA was markedly increased in the granule cells of the dentate gyrus, and at 24 h it was still significantly elevated. NGF mRNA showed a pronounced increase 4 h after 2 min of ischemia but had returned to a control level at 24 h. Both 2 and 10 min of ischemia caused a clear reduction of the level of mRNA for neurotrophin 3 (NT-3) in the dentate granule cells and in regions CA2 and medial CA1 of the hippocampus 2 and 4 h after the insults. The increase of BDNF mRNA could be partially blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX but was not influenced by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Both NBQX and MK-801 attenuated the decrease of NT-3 mRNA after ischemia. One and 30 min of hypoglycemic coma also induced marked increases in BDNF and NGF mRNA in dentate granule cells with maximal levels at 2 h. If the changes of mRNA expression lead to alterations in the relative availability of neurotrophic factors, this could influence functional outcome and neuronal necrosis following ischemic and hypoglycemic insults.

Animals↗

Endocrine emergencies. Adrenal crisis, myxedema coma, and thyroid storm.

Each of the endocrine emergencies discussed here--adrenal crisis, myxedema coma, and thyroid storm--represents decompensation of a long-standing endocrine disorder and is precipitated in most cases by some stressful event. Each necessitates immediate, aggressive therapy. Even with such therapy, the mortality rate remains 30% to 50% for myxedema coma and 30% to 40% for thyroid storm. Therapy must be instituted on the basis of strong clinical suspicion, without delay for results of specific hormone assays to confirm the diagnosis. Although some risks may be inherent in this approach, they are minimal compared with the risks of delaying therapy until laboratory confirmation can be obtained. Immediate therapy consists of specific measures to correct the hormone deficit or excess; the precipitating cause should then be sought and treated.

Addison Disease↗

Monitoring emergence from coma following severe brain injury in an octogenarian using behavioural indicators, electrophysiological measures and metabolic studies: a demonstration of the potential for good recovery in older adults.

This case study describes a multi-disciplinary investigation of the emergence from coma of an 80-year old female (KE) following severe traumatic brain injury. The relationship between cognitive/behavioural ability and the integrity of cerebral function was assessed using neuropsychological measures, positron emission tomography, electroencephalography, somatosensory evoked potentials and trans-cranial magnetic stimulation. These investigations were performed as KE was beginning to emerge from coma (4 weeks) and, again, approximately 1 year following brain injury, when she was judged to have achieved her maximum level of recovery. Neuropsychological measures revealed improvement during the first year post-injury in KE's speed of information processing, memory and executive abilities. Electrophysiological and metabolic studies indicated a restoration of functional integrity that was consistent with the gradual recovery in higher brain function documented using behavioural procedures. This case study demonstrates the rehabilitation potential of pre-morbidly healthy older adults following severe traumatic brain injury.

Accidents, Traffic↗

Utility of Glasgow Coma Scale-Extended in symptom prediction following mild traumatic brain injury.

STUDY OBJECTIVE: To examine the efficacy of the Glasgow Coma Scale-Extended (GCS-E) for the prediction of symptoms commonly associated with mild traumatic brain injury (TBI). METHOD: Three hundred and sixty-one participants with a mild TBI were evaluated using the GCS-E and the Standardized Assessment of Concussion. A sub-group of 185 participants took part in a more extensive evaluation, which also included measures of depression and vestibular symptoms. All participants had a Glasgow Coma Scale score of 15, but experienced varying lengths of post-traumatic amnesia (PTA) as measured by the GCS-E. RESULTS: Use of the GCS-E for assessment of PTA duration revealed that longer lengths of amnesia following mild TBI were associated with greater incidence of dizziness, depression and cognitive impairments during the first weeks after injury. CONCLUSION: Results suggest that the GCS-E is a useful tool for the prediction of symptoms associated with mild TBI.

Adult↗

The prognosis of medical coma in Ibadan: results of multivariate analysis.

During a recent prospective investigation of 116 children with medical coma in Ibadan, 52 (45%) survived intact, 23 (20%) developed residual neurological deficits and the remaining 41 (35%) died. This series is concerned with the use of multivariate analysis in predicting outcome of medical coma in an individual patient, based mostly on clinical information (27 variables) obtained within 12 hours of admission. Stepwise logistic regression analysis revealed that only 17 of the 27 variables have independent significance in predicting outcome. When discriminant analysis was performed on these 17 variables so as to obtain a classification function of outcome (survived intact, survived with deficits and dead), 92% of the cases were correctly classified. Eight children were, however, seriously misclassified. These were four intact survivors and four dead cases who were classified as dead and survived without neurological sequelae, respectively. These results suggest that multivariate analysis of clinical and laboratory information obtained in the comatose state can provide predictive information.

Adolescent↗

The JFK Coma Recovery Scale--Revised.

The JFK Coma Recovery Scale (CRS) was developed to help characterise and monitor patients functioning at Rancho Levels I-IV and has been used widely in both clinical and research settings within the US and Europe. The CRS was recently revised to address a number of concerns emanating from our own clinical experience with the scale, feedback from users and researchers as well as the results of Rasch analyses. Additionally, the CRS did not include all of the behavioural criteria necessary to diagnose the minimally conscious state (MCS), thereby limiting diagnostic utility. The revised JFK Coma Recovery Scale (CRS-R) includes addition of new items, merging of items found to be statistically similar, deletion or modification of items showing poor fit with the scale's underlying construct, renaming of items, more stringent scoring criteria, and quantification of elicited behaviours to improve accuracy of rating. Psychometric properties of the CRS-R appear to meet standards for measurement and evaluation tools for use in clinical and research settings, and diagnostic application suggests that the scale is capable of discriminating patients in the minimally conscious state from those in the vegetative state.

Brain↗

Failure of therapeutic coma and ketamine for therapy of human rabies.

The recent success in treating a human rabies patient in Milwaukee prompted the use of a similar therapeutic approach in a 33-year-old male Thai patient who was admitted in the early stages of furious rabies. He received therapeutic coma with intravenous diazepam and sodium thiopental to maintain an electroencephalographic burst suppression pattern, which was maintained for a period of 46 h, as well as intravenous ketamine (48 mg/kg/day) as a continuous infusion and ribavirin (48 to 128 mg/kg/day) via a nasogastric tube. He never developed rabies virus antibodies and he died on his 8th hospital day. At least three other patients have been treated unsuccessfully with a similar therapeutic approach. Because of the lack of a clear scientific rationale, high associated costs, and potential complications of therapeutic coma, the authors recommend caution in taking this approach for the therapy of rabies outside the setting of a clinical trial. More experimental work is also needed in cell culture systems and in animal models of rabies in order to develop effective therapy for human rabies.

Adult↗

Neuropsychological outcome in relation to the traumatic coma data bank classification of computed tomography imaging.

The Traumatic Coma Data Bank (TCDB) classification of CT (computed tomography) scan has been related to the general outcome and intracranial pressure evolution. Our aim was to analyse the relationship of this classification with neuropsychological outcome and late indices of ventricular dilatation. Fifty-seven patients with a moderate or severe head injury (mean admission Glasgow Coma Scale Score, 7.7) were studied from 122 consecutive cases. There were 49 males and 8 females (mean age, 27.7 years). Subjects were classified into TCDB categories on the basis of their most serious acute CT scan finding. From the last control CT scan image, performed at a mean of 6.12 months postinjury, several measures of ventricular dilatation were calculated. Neuropsychological assessment at 6-month included tests of verbal and visual memory, visuoconstructive functions, fine motor speed, and frontal lobe functions. Patients with diffuse injury type I showed better neuropsychological outcome than patients with more severe diffuse injuries and those with mass lesions. Within the diffuse injury groups, the degree of diffuse damage was related to measures of verbal memory and attention and cognitive flexibility. Ventricular enlargement was more evident in patients with mass lesions and it decreased in the remaining groups as the severity of diffuse injury diminished. These results show that there is a relationship between acute intracranial lesion diagnosis according to TCDB classification and neuropsychological results and ventricular dilatation indices at 6 months postinjury.

Adolescent↗

Influence of bolus doses of phenoperidine on intracranial pressure and systemic arterial pressure in traumatic coma.

The effects of bolus doses of phenoperidine 1-2 mg i.v. either alone, or combined with pancuronium 2-4 mg, were investigated in seven patients in traumatic coma. Phenoperidine alone significantly reduced mean arterial pressure (MAP) by a mean (+/- SEM) of 13.2 (+/- 2.8) mm Hg. Overall there was no significant change in intracranial pressure (ICP) despite the decreases in MAP and, consequently, cerebral perfusion pressure (CPP) decreased (14.0 +/- 2.4 mm Hg) on all but one occasion. In some instances these decreases were considerable (maximum 38 mm Hg). Similar results were obtained when phenoperidine was combined with pancuronium. These findings suggest that the bolus administration of phenoperidine and probably other opiates should be avoided in traumatic coma.

Adolescent↗

Migraine coma. Meningitic migraine with cerebral oedema associated with a new form of autosomal dominant cerebellar ataxia.

A family with hemiplegic migraine has been documented for a period of over forty years. From this study and the literature we conclude that (1) migraine is a cause of recurrent coma which may be associated with life-threatening cerebral hemisphere oedema; (2) hyperpyrexia with CSF pleocytosis occurs in hemiplegic migraine, which may thus simulate viral meningoencephalitis; and (3) cerebral angiography is hazardous in hemiplegic migraine and may exacerbate coma and cerebral oedema. In the family reported, cerebellar ataxia was present during recovery from attacks of hemiplegic migraine and affected patients ultimately suffered from persistent ataxia with radiological cerebellar atrophy. This syndrome thus constitutes a distinct form of late-onset autosomal dominant cerebellar ataxia and also of familial periodic ataxia. The status of 'cerebellar migraine' is reviewed.

Adult↗

Neuropsychological outcome in relation to head injury severity. Contributions of coma length and focal abnormalities.

Neuropsychological test performances of 102 consecutive head-injured patients were evaluated at 1 mo and 1 yr after injury. The results of the study indicated that both coma length and the presence of focal abnormalities on computed tomography (CT) scans contribute independently to neuropsychological outcome. The effects of coma length are stronger than the effects of focal abnormalities evident on CT scans and continue to exert a stronger influence on neuropsychological outcome over the year postinjury. These results suggest that the extent of diffuse pathology may be a more important determinant of long-term behavioral outcome than the presence of focal lesions.

Adolescent↗

Predicting mortality of intensive care unit patients. The importance of coma.

Five hundred fifty-eight patients from two general medical/surgical ICUs were studied with respect to the relationship of mortality and length of stay to 18 treatment and condition variables. Two multiple logistic regression models were developed to estimate the probability of mortality. One was a model incorporating main effects only; the other allowed for the interaction of pairs of variables. For ICU mortality, the best predictive variables using the main effects model were coma, cardiopulmonary resuscitation (CPR) in the ICU, and shock. With the interactive model, the variables selected were shock plus coma, and CPR in the ICU.

Coma↗