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Gastrointestinal hemorrhage in long-lasting traumatic coma.

Sixteen cases, aged 19 to 61 years and suffering from traumatic coma were studied for periods varying from 7 to 20 months. Obvious or occult gastrointestinal hemorrhage appeared in every case, the earliest presentation being after a few weeks and the latest at 20 months. Gastric acidity was normal in 15 cases. Five patients had duodenal ulceration in repeated roentgenological examination. Concomitant clinical findings included clubbing and paraarticular new bone formation in 9 patients. In addition, hypoxia with repeated values between 63 and 88 mm was observed in 13 of the 16 patients. The latter observation strongly suggests that hypoxia of gastrointestinal mucosa may, indeed, play a pathogenetic role in gastrointestinal hemorrhage of patients with C.C.I.

Adult↗

Coma and the etiology of violence, Part 1.

Coma and the etiology of violence are explored by the author through a review of the literature. Animal studies, post-traumatic psychic disorder studies, post-traumatic anger and violence studies, tumor and lesion of the limbic system studies, temporal lobe epilepsy studies, and episodic dysfunction syndrome studies, minimal brain studies are reviewed in Part 1 of this article. Part 2, to be published in a later issue of the journal, will conclude the review with clinical surveys on violent individuals and studies on clinical treatment of violence.These studies reveal the etiologic significance of central nervous system dysfunction in the production of violent behavior. Because central nervous system factors are involved in some instances of violent behavior, physicians clearly have a role in the early identification of potentially violent subjects and in the intervention or treatment of individuals who have been violent toward others. Studies have consistently found that lower socioeconomic groups are more predisposed to brain injury from trauma, and several studies have indicated that this is true for segments of the black community. Therefore, investigations in the relationship between central nervous system injury and violence should be a major goal of the black community. Black physicians should assume a lead role in these inquiries and in the prevention and treatment of violence, specifically black-on-black murder.

Adult↗

[Value of early acoustic and somatosensory evoked potentials in monitoring and prognostic assessment of coma in barbiturate therapy--comparison with clinical aspects and EEG].

25 comatose patients suffering from severe cerebral lesions of different etiology were examined during barbiturate-therapy by Glasgow-Pittsburg-Coma-Scoring-System (GPCS), EEG, somatosensory and brainstem acoustic evoked potentials. The findings were correlated in view of prognostic prediction and importance for monitoring. A modified form of the Glasgow-Outcome-Score (GOS; independent-survival, dependent-survival, dead) was used for evaluating the outcome. In case of an initial GPCS less than 10 points none of the patients survived, in case of GPCS greater than 10 points 11 out of 19 patients survived. The latter relation of survival was also found in patients with improving or impairing scores during the observation period. In case of initial burst-suppression pattern in the EEG 7 out of 11 patients survived, in case of diffuse abnormalities with or with-out additional focal signs - 4 out of 10 patients survived, but in the latter there was none with an outcome of independent survival. All patients with an isoelectric EEG died. In case of bilateral recording of scalp- SEP 7 out of 11 patients survived, in case of unilateral loss of scalp-EP 4 out of 8 patients survived, but in the latter cases none with an outcome of independence. All patients with initial bilateral failure of scalp-SSEP or loss during the observation period died. In case of bilateral registrable BAEP (wave I to V) 11 out of 17 patients survived. All patients with initial uni- or bilateral failure of those potentials or loss during the observation period died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Recovery of motor function after severe traumatic coma.

This paper describes the resumption of motor activity during the successive stages of recovery following severe traumatic coma and discusses the likely mechanisms of such resumption. Even in severe brain injury a considerable amount of motor recovery is possible and leads to a normal level of function in half of the cases. The impairment of voluntary movements is often transitory and recovers spontaneously but in cases of persistent deficits probably from direct lesion of the pyramidal tract re-education efforts are relatively inefficient. The disorders of reflex and semi-automatic motor activity subserving tonic adjustments, gait and locomotion are nearly constant and often severe. The recovery of this basal function is the most important to attain and to secure and this can be achieved through extensive and prolonged retraining of reflex activity. Presumably these disorders are not caused by direct lesions of brainstem structures but rather to a functional denervation akin to spinal shock. A resumption of function in the denervated groups of neurons should necessitate the reopening of silent synapses and/or a structural reorganisation of synaptic connections, this dynamic process being highly influenced by retraining.

Coma↗

Transition from alpha to theta pattern coma in fatal cerebral anoxia.

A transition of alpha to theta pattern coma is documented in a case of fatal cerebral anoxia after a cardiac arrest. The patient was a 35-year-old woman who suffered a cardiac arrest due to myocardial ischaemia and ventricular tachycardia. Altogether 6 EEGs showing progressive deterioration were performed during the 11 days of survival. There was histopathological evidence of extensive ischaemic damage involving cerebral and cerebellar cortex, basal ganglia and brainstem structures. Although closed chest cardiopulmonary resuscitation was begun with minimal delay after cardiac arrest, the outcome may reflect the increasingly documented failure of this type of resuscitation to provide adequate organ perfusion during cardiac arrest.

Adult↗

Diazepam-induced coma with bullae and eccrine sweat gland necrosis.

Bullous skin lesions that indicate sweat gland necrosis have been known to occur in drug-induced coma resulting from barbiturates and in carbon monoxide poisoning. To our knowledge, this is the first cases in which diazepam is implicated in causing bullous lesions over pressure points, and the first case showing on biopsy specimen eccrine sweat gland and sweat duct necrosis. Penile and oral lesions are being described here for the first time to our knowledge. The following mechanisms could be responsible for the skin lesions: hypoxia, local pressure, hyperthermia with excessive sweating, and a specific toxic effect on the eccrine gland. With the increasing use of the benzodiazepines, such lesions could be seen more frequently in the future.

Adult↗

The limits of surgical management of traumatic coma.

It appears, on the whole, that the better results we are now able to attain in the treatment of traumatic coma are unrelated to a real improvement in surgical possibilities. The role of surgery seems, conversely, to be more limited than in previous times. Surgical intervention still keeps strictly mandatory whenever intracranial hypertension is related to extracranial effusions while, in brain contusion/lacerations, it is warranted only in selected cases.

Brain Concussion↗

[Toxicity of the cerebrospinal fluid in comas of various etiologies].

The cerebrospinal fluid (CSF) was examined by chromatography-mass spectrometry in 10 normal subjects and 27 patients with comas of different etiology. The findings included detection of a number of highly toxic intermediate metabolites of intra- and extracerebral origin. Their concentration was dependent on the nature of the condition. Maximal toxicity of the CSF was observed in cases of severe craniocerebral trauma and hemorrhagic stroke which were associated with the penetration of blood into the CSF.

Coma↗

Myxoedema coma. A review.

Myxoedema coma is a rare emergency needing prompt recognition and urgent treatment before diagnostic confirmation. The pathyphysiology, clinical features, differential diagnosis, investigations and treatment are described. Triiodothyronine in small doses intravenously with continuous cardiac monitoring is suggested. Slow rewarming, care of the airway and prompt treatment of hypoventilation by assisted ventilation, the use of hydrocortisone and the avoidance of sedatives, vasopressors and overloading are also discussed, as is prevention. This emergency occurs in elderly people often with co-existent disease and thus only close attention to detail will be rewarded with improving results and falling mortality figures.

Acute Kidney Injury↗

Rhabdomyolysis following violent behavior and coma.

An individual suspected of being under the influence of phencyclidine (PCP) exhibited acute psychotic and violent behavior which was followed by cardiac arrest, coma, and renal failure. Sections of the damaged muscle showed rhabdomyolysis, and sections of the kidneys showed myoglonin casts positive for immunoperoxidase stain. Extensive toxicology studies for narcotics, PCP, and cocaine were negative. Therefore, a correlation between PCP and rhabdomyolysis associated with acute psychotic and violent behavior could not be made with certainty. The etiology and pathogenesis of rhabdomyolysis are discussed in depth.

Adult↗

Alpha-coma: clinical and evoked potential studies.

Simultaneous brainstem auditory and somatosensory evoked potential studies to median nerve stimulation were performed in two comatose patients, having diffuse alpha-pattern in their EEGs. CT scan of the brain in both cases did not reveal any mass lesion. In Case 1, the clinical and evoked potential studies suggested a brain stem lesion, and in Case 2 there was diffuse encephalopathy, with asymmetric dysfunction of the brainstem as seen in the evoked potential patterns. The suggested separation of alpha-pattern into two distinct groups, based on the reactivity and the presence or absence of sleep activities, into brainstem and diffuse cortical lesions could not be supported by our evoked potential studies. Our study, based on the observations of the evoked potential studies, indicated that the reactivity to sensory stimulation and intermittent attenuation of diffuse alpha-like activity relate to the integrity of the ascending sensory inputs to the thalamus. In the absence of evoked potential data, the localization of lesion(s) in alpha-coma pattern may be imprecise. Moreover, the circadian sleep rhythms and the presence or absence of "sleep spindles" appeared to depend on the inputs of the ascending sensory pathways to the structures generating the sleep activities. The specific neuronal structures generating the alpha-pattern still remain unidentified; however, this pattern seems to be originating from the structures rostral to the mesencephalon, possibly in the thalamic-thalamocortical circuits.

Adult↗

Suppression-burst pattern associated with generalized epileptiform discharges and alpha-theta pattern coma.

In this paper we reported a patient with multisystem failure, whose EEG immediately preceding death demonstrated a unique combination of suppression-burst pattern, generalized epileptiform discharges, and alpha-theta pattern coma. Post-mortem examination showed ischemic-anoxic lesions involving cortical and sub-cortical gray matter. The lack of white matter pathology in our patient indicates that white matter lesions may not be involved in the pathogenesis of the above EEG patterns in anoxic encephalopathy.

Aged↗

Evolution of cardiorespiratory variables in myxedema coma--a case report.

Normalization of hemodynamic, oxygen transport and oxygen consumption indices occurred within a week of treatment in a patient with myxedema coma. Ventilatory weaning and extubation was achieved using aminophylline, physical therapy and pleural drainage. Before extubation, naloxone was administered without any significant ventilatory improvement or change in endorphin levels.

Coma↗

Cardiac enzyme changes in myxedema coma.

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.

Aged↗

[Use of barbiturates in posttraumatic comas at the mesencephalic level. Apropos of 38 cases].

Thirty-eight patients with brain injury and mesencephalic coma, or a Glasgow score of less than 5, were treated routinely with Thiopental administered by electric syringe for a mean duration of 4 days. Follow up review criteria were based on clinical computed tomography and electroencephalographic data, as well as results of monitoring of intracranial pressure and assay of blood barbiturate levels. Global results indicated a mortality of 55.3% and reintegration of 34.2% of the patients. Results as a function of the different parameters of surveillance are discussed.

Adult↗

Hyponatraemia complicating the treatment of myxoedema coma. A case report.

Hyponatraemia is a common complication of severe hypothyroidism, but is usually readily corrected by administering L-thyroxine. A case of myxoedema coma in which the serum sodium level dropped precipitously when therapy was started is described and it is suggested that this was due to a state of relative hypocortisolism. Serum sodium values should be closely monitored in myxoedema treated with L-thyroxine; their decrease may signal the onset of an Addisonian-like crisis requiring urgent corticosteroid supplementation.

Coma↗

Predicting outcome from hypoxic-ischemic coma.

Outcome from coma caused by cerebral hypoxia-ischemia (eg, cardiac arrest) was compared with serial neurological findings in 210 patients. Thirteen percent of patients regained independent function at some point during the first postarrest year. Computer application of new multivariate techniques to the prospectively observed findings generated easily utilized rules that classified patients by likely outcome. At the time of initial examination, 52 patients (one fourth of the total population) had absent pupillary light reflexes, and none of these patients ever regained independent daily function. By contrast, the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the findings of extensor, flexor, or withdrawal responses to pain identified a smaller group of 27 patients, 11 (41%) of whom regained independence in their daily lives. By 24 hours after onset, 93 poor-outcome patients were identified by motor responses that were absent, extensor, or flexor and by spontaneous eye movements that were neither orienting nor roving conjugate; only one regained independent function. This contrasts with recovery in 19 (63%) of 30 patients who at that time showed improvement in their eye-opening responses and obeyed commands or had motor responses that were withdrawal or localizing. Similarly simple rules distinguished between good- and poor-prognosis patients on postarrest days 3, 7, and 14.

Adult↗