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PubMed1997

Non-traumatic coma--profile and prognosis.

Two hundred consecutive patients of non-traumatic coma, were investigated to establish its aetiology. Neurologic profile of these patients included assessment of Glasgow Coma Scale (GCS) score and evaluation of brainstem reflexes. 102 patients died and only 54 patients could make good recovery. Cerebrovascular diseases (33%), CNS infections (21%), and hepatic encephalopathy (18%) were the frequent causes of non-traumatic coma, with the first two carrying relatively poor prognosis. Poor outcome was also associated with low GCS score and absence of brainstem reflexes specially absent pupillary, oculocephalic and oculovestibular responses and decerebrate posture.

Adolescent↗
PubMedDate not supplied

[Visual constructive deficits and coma depth].

The present study has the purpose of relating the capacities of visual retention with the Benton Visual Retention Test and the level of coma depth, which is measured with the GCS (Glasgow Coma Scale). 31 subject suffering cranioencephalic damage admitted to the intensive care unit (ICU) have been studied. GCS scores were obtained during their stay in the intensive care unit and the Benton Visual Retention Test was administered after hospital discharge. The procedure followed consists in comparing the performance of subjects with higher GCS scores to subjects with lower values when executing administration. A of form C of BVRT. We could conclude as follows: firstly that BVRT is a useful tool to detect the existence of brain damage; secondly, indexes of brain damage presence with BVRT are: a low figure in correct design, more errors, less errors in distortion and rotation; more errors in the left visual hemifield. Thirdly, the depth of coma is a good prognosis index on BVRT execution and in consequence of visuo-constructive abilities.

Brain Injuries↗
PubMed1990

[Hyperglycemic hyperosmolar nonketotic coma].

Ten patients with the syndrome of non-ketotic hyperosmolar coma are described. The mean age of the patients was 62.3 +/- 17.12 years. One patient was 16 years old. In 9 cases the patients had type II diabetes, one had type I diabetes. In 7 cases the coma was the first sign of diabetes. The factor predisposing in most cases was infection. In the treatment-acting insulin and hypotonic solutions were given. In 2 cases clinical signs of the DIS syndrome were observed manifesting themselves with local changes, including mental disturbances. Heparin was given with good effect. Three patients (30%) died in hospital. The cause of death was serious disease associated with this coma: pancreatitis and myocarditis, purulent bronchopneumonia, myocardial infarction.

Adolescent↗
PubMed1986

Nonketotic hyperosmolal diabetic coma in a child: management with low-dose insulin infusion and intracranial pressure monitoring.

Nonketotic hyperosmolal diabetic coma, which is rare in children, is associated with a high mortality in both children and adults. We report a case of nonketotic hyperosmolal diabetic coma in a 3 1/2-year-old child, who was successfully managed with low-dose insulin infusion and invasive intracranial pressure monitoring and recovered without sequelae. Despite severely elevated serum glucose (2,660 mg/dL) and osmolality (435 mosm/kg) levels, there was no elevation of intracranial pressure during her treatment. This case illustrates that insulin should be used cautiously and at low dose in this disease, and that intracranial pressure monitoring is of use in the management of such patients. The pathogenesis and clinical features of nonketotic hyperosmolal diabetic coma are briefly reviewed.

Child, Preschool↗
PubMed1986

Cerebral edema complicating nonketotic hyperosmolar coma.

Cerebral edema as a complication of the therapy of diabetic coma has been described for over 50 years, although modern awareness dates to about 1967. Almost all cases have occurred in patients with diabetic ketoacidosis (DKA). Although a few cases of cerebral edema have been reported in patients with nonketotic hyperosmolar coma (NKHC), these are in general not well documented by either autopsy data of cat scans. Over a period of 9 years, I have encountered 5 patients who developed cerebral edema as a complication of the therapy of NKHC. The initial plasma glucose in these patients was 1,496 +/- (SD) 296 mg/dl and plasma osmolality was 382 +/- 29 mosm/kg. All had depression of sensorium to at least a stupor (stage I coma or greater). All were treated with intravenous insulin and either 77 or 154 mM NaCl, and plasma glucose fell at a mean rate of 38 mg/dl/h. In all patients, plasma glucose fell below 250 mg/dl (mean of 18 +/- 66 mg/dl) and all patients experienced increased depression of sensorium, elevated csf pressure, and brain swelling as diagnosed by cat scanning. Therapy with various combinations of glucose, mannitol and steroids were without effect. In 1 patient, insertion of a subdural intracranial screw lowered intracranial pressure from 24 to 3 cm of H2O. Three of the 5 patients died and 2 remain in a persistent vegetative state, 1 of whom is also quadriplegic.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Nontraumatic coma in extramural practice].

After a short review on pathophysiologic mechanisms of comatose states and their complications, a cohort of 392 comatose patients (Glasgow Coma Scale < or = 8) hospitalized in intensive care is analyzed in order to estimate the relative frequency of the different causes of nontraumatic coma. Depending on pathology, the following practical, sequential procedure is recommended: at first, identification and treatment of disorders of vital functions, objective estimate of the severity of the coma and rapid diagnostic orientation with a targeted neurologic investigation; then, simple therapeutic interventions in order to treat reversible causes of a metabolic encephalopathy as well as immediate measures for neuroprotection (anticonvulsive and antihypotensive therapy, oxygen, etc.). An initial, adequate control of the comatose patient is mandatory in order to limit disabling cerebral complications.

Brain Diseases, Metabolic↗
PubMed1993

[The reactivity of the mesenteric arterioles to adrenaline in metabolic coma].

The reactivity of mesoappendix arterioles to applicated epinephrine application was investigated in 2 models of metabolic coma, hypoglycemic and acetonemic. Hypoglycemic coma (HC) was induced by insulin injection (20 IE/kg) i. m. to rats fasting for 18 hours. Acetonemic coma (AC) was induced by i. v. acetone injection (5.5 mmol). The sensitivity of arterioles to applicated epinephrine did not change in HC and increased twofold in AC vs. the control values (p < 0.01). The reaction of arterioles to injection of double threshold dose of epinephrine in HC developed sooner and the degree of vasoconstriction was 41% higher than in controls. In AC the reaction developed two times sooner and the degree of arterioles constriction was 1.5 times higher vs. the control (p < 0.01).

Acetone↗
PubMed1994

[Assessment of the deepness of coma in children. Evolution of clinical thoughts].

Clinical assessment is an essential fundamental element in the evaluation of comatose states, particularly in children. Paediatricians quickly recognized that the early Glasgow Coma Scale, used for over 20 years in adults, is inadapted for children because it lacks brain stem criteria, involves interpretation of motor response (particularly difficult in infants) and uses verbal response which is of little value before language acquisition. The first attempt at standardized coma assessment in children was the Paediatric Coma Scale, developed in Australia in 1982. This scale improved on the Glasgow scale, removing the motor retraction response, modifying the verbal response scale (normal, words, sounds, crying, or none) and quantifying the best possible score as a function of age. In 1983 a fundamental modification was proposed in the Jacob scale. Besides removing the motor retraction response, this scale replaced the verbal scale with one based on ocular behaviour, thus evaluating consciousness of presence or stimulation. The vestibular response and pupil reactions were also included to assess brain stem activity. In 1987, we introduced the Bicêtre scale which uses ocular behaviour instead of verbal response and separates ocular diameter as a specific criteria. Assessment of four reflexes (mimic, photomotor, cornea and cough) provides precise information on the activities of the different levels of the brain stem. Several comparative studies have been conducted to determine the positive predictive value and interpersonal variability of these scales. In a prospective multicentric study of 277 comatose children aged 6 months to 15 years, we found that the Bicêtre scale had a positive predictive value of 94% for good outcome at 24 hours and that interpersonal disagreement occurred in only 10.1% of 65 cases studied (compared with 13.5% for the Glasgow scale which was studied simultaneously). Paediatricians now have reliable clinical scales for assessing the conscious level in children.

Adolescent↗
PubMedDate not supplied

[The use and the potential of auditory electrophysiology in patients in posttraumatic coma].

21 patients in post-traumatic coma status were submitted to a auditory electrophysiological valuation together with EEG, TC, and "Glasgow Coma Scale" (GCS) with the purpose to obtain the relative prognostic value quoad vitam and quoad valetudinem. In particular it was carried out the brainstem auditory evoked potentials (ABR) and the auditory middle latency potentials (MLR and SSR-40 Hz). 12 patients survived and their clinical conditions were classified according to the "Glasgow Outcome Scale"; 9 of 21 patients died. With the aim of quoad vitam prognosis, the ABR showed a good reliability whereas GCS, EEG, TC and MLR proved not much usefulness. On the contrary the absence of SSR-40 Hz always coincided with the subsequent patients death. With the aim of GOS a meaningful relationship was found between the clinical outcome conditions from coma and the improvement in MLR and EEG.

Adolescent↗
PubMed1993

[Coma from cerebral and metabolic causes].

The medical causes of coma fall into two main categories: intercranial diseases, and metabolic disturbances. The clinical examination should define 1) vital functions, 2) depth of coma, 3) whether cerebral signs are diffuse or local, 4) any signs of organ disease. The blood sugar level must be determined. Hypoglycemia may be the cause even if the signs point to another cause. Head injury and intoxication/poisoning must always be considered, even if a medical cause is suspected. Prolonged coma calls for repeated clinical and laboratory examination. Combinations of causes, e.g. organ disease plus intoxication should be considered.

Brain Diseases↗
PubMed1984

Auditory brain-stem and middle- and long-latency evoked potentials in coma.

Twenty-five patients in coma, each with a Glasgow Coma Scale measure less than or equal to five, were studied within the first three days of hospitalization with auditory brain-stem and middle- and long-latency evoked potentials. Survival was related to the simultaneous preservation of long- and middle-latency and brain-stem evoked potentials. The preservation of just middle-latency and/or brain-stem components did not correlate with survival. However, if the group of patients in coma due to head trauma was analyzed separately, survival could be related to the results of the brain-stem evoked potentials. There was no relationship between survival and the results of the initial clinical neurological examination. In patients who survived, there was no pattern of evoked potential preservation that related to the quality of survival.

Adolescent↗
PubMed1990

Valproate-induced coma with ketosis and carnitine insufficiency.

We observed two patients who developed coma following administration of valproate in dosages of 32 to 40 mg/kg per day. Valproate levels were within the therapeutic range, and results of liver function studies were normal. Both patients had ketosis and adipic aciduria. Plasma free carnitine levels were decreased during coma and after recovery. One patient excreted ethylmalonic acid, butyrylcarnitine, and glutarylcarnitine during and after resolution of coma, suggesting a multiple acyl coenzyme A dehydrogenation defect. Low serum carnitine levels may predispose patients to development of altered consciousness when treated with valproate.

Acids↗
PubMed2004

Outcome and prognostic factors in head injuries with an admission Glasgow Coma Scale score of 3.

HYPOTHESIS: To identify significant risk factors associated with mortality in patients with a Glasgow Coma Scale score of 3. DESIGN: Trauma registry study. SETTING: Level I urban trauma center. PATIENTS: A total of 760 patients with head injury with an admission Glasgow Coma Scale score of 3. Analysis was performed in all patients and in only patients who reached the hospital alive and had no major extracranial injuries (exclusion of patients with a chest or abdominal Abbreviated Injury Score [AIS] >3). MAIN OUTCOME MEASURES: Stepwise logistic regression analysis was used to identify independent risk factors associated with mortality. RESULTS: Blunt trauma accounted for 477 (63%) and penetrating trauma for 283 (37%) of the 760 head injuries. Penetrating trauma was significantly more likely to be associated with a lack of vital signs on admission (15% vs 9%; P = .03). Overall mortality was 76% (94% for penetrating injuries and 65% for blunt injuries; P<.001). Overall, 79% of patients had a head AIS of 4 or greater. Mortality in the subgroup was 64% (320/497) and was significantly higher in penetrating vs blunt trauma (89% vs 52%; P<.001). Penetrating trauma, high head AIS, hypotension on admission, and age older than 55 years were independent significant risk factors associated with mortality. Only 10% of the 177 survivors had good functional outcome at hospital discharge. Eighty-six patients (17% of those with vital signs on admission) became organ donors. CONCLUSIONS: Patients with head injury with an admission Glasgow Coma Scale score of 3 have a poor prognosis. Mechanism of injury, head AIS, hypotension on admission, and age play a critical role in outcome. These patients are an important source of organ donation and should be evaluated and resuscitated aggressively.

Adult↗
PubMed2001

Routine intracranial pressure monitoring in acute coma.

BACKGROUND: Studies in traumatic encephalopathy first led to the insight that the damage seen was not just due to direct consequences of the primary injury. A significant, and potentially preventable, contribution to the overall morbidity arose from secondary hypoxic-ischaemic damage. Brain swelling accompanied by raised intracranial pressure (ICP) resulted in inadequate cerebral perfusion with well-oxygenated blood. Detection of raised ICP could be useful in alerting clinicians to the need to improve cerebral perfusion, with consequent reductions in brain injury. OBJECTIVES: To determine whether routine ICP monitoring in all acute cases of severe coma reduces the risk of all-cause mortality or severe disability at final follow up. SEARCH STRATEGY: We searched MEDLINE, EMBASE, The Injuries Group's specialised register and the reference lists of all relevant articles and review articles. In addition we searched the Index of Scientific and Technical Proceedings using "intracranial pressure" as keyword. SELECTION CRITERIA: All randomised controlled studies of real-time ICP monitoring by invasive or semi-invasive means in acute coma (traumatic or non-traumatic aetiology) versus no ICP monitoring (ie clinical assessment of ICP ) DATA COLLECTION AND ANALYSIS: Primary outcome measures were all-cause mortality and severe disability at the end of the follow up period. MAIN RESULTS: No studies meeting the selection criteria have been identified to date. REVIEWER'S CONCLUSIONS: There are no data from randomised controlled trials that can clarify the role of ICP monitoring in acute coma.

Acute Disease↗
PubMed1975

Can one predict outcome of medical coma?

The combined evaluation of the motor response to stimulation and the oculovestibular (OV) reflex gives useful indicants to the outcome of medical coma. We examined 48 patients during the first 12 h and at 24 h after the onset of medical coma. We excluded patients who had ingested drugs or who had hypothermia. Motor responses to a noxious stimulus were scored on a 6 'best' and 1 'worst' scale, and the presence or absence of oculovestibular responses to icewater irrigations was recorded. Subjects were divided by outcome at three months into three groups: death or persistent vegetative state, severe disability, and moderate disability or good recovery. On the basis of the present series it was often possible to distinguish among the outcomes at or before 24 h. The patient's age and the presence or absence of pupillary responses, spontaneous eye movements and oculocephalic responses were not predictive of outcome, nor were the respiratory pattern, blood gases, blood pressure, heart rate and temperature. A minimal motor score and an absence of oculovestibular responses at 12 h always were assoicated with death. With higher motor scores, the absence of oculovestibular responses at either 12 or 24 h implied an outcome no better than severe disability. The results of the present study imply that early bedside assessments can yield accurate predictive information in medical coma.

Cerebrovascular Disorders↗
PubMed1985

Disruption of the blood-brain barrier in hyperammonemic coma and the pharmacologic effects of dexamethasone and difluoromethyl ornithine.

Both hyperammonemia and blood-brain barrier (BBB) breakdown have been implicated in the evolution of hepatic encephalopathy. To define a possible relationship, Swiss Albino mice were subjected to sublethal encephalopathic doses of ammonium acetate; the integrity of the BBB was determined grossly with Evans blue and quantitatively with [14C]-alpha-aminoisobutyrate (AIB). Some animals were injected with a dose of ammonium acetate sufficient to maintain coma for 1 hr (AC group). One group, termed stuporous (AS), received only enough ammonium acetate to interfere with grooming and exploratory activity; this dosage was insufficient to completely block the righting response, which was absent in the AC group. When compared to that of controls (CON) receiving normal saline instead of ammonium acetate, cerebral tissue from the AC group was stained blue and contained nearly double the amount of AIB; AS group brain tissue was unstained and the AIB content did not differ significantly from normal. Some of the AC group were pretreated with drugs known to retard BBB breakdown; one set received dexamethasone (AC-DXMN), another the ornithine decarboxylase inhibitor difluoromethyl ornithine (AC-DFMO), and a third L-ornithine (AC-ORN). Brain tissue from the AC-ORN group stained blue and AIB content did not differ significantly from that of the untreated AC group. Cerebral tissue of the AC-DXMN pretreatment group stained light blue; AIB content was significantly lower than in the AC group and greater than the CON group. The AC-DFMO brains were unstained and AIB content was significantly lower than in the AC group but did not differ significantly from CON. These results indicate that hyperammonemia may induce BBB breakdown but that the disruption of barrier integrity is not antecedent to the development of coma, although it seems to coincide with coma in time.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1990

Familial migraine coma: a case study.

A family suffering from a rare malignant type of migraine is described. The syndrome is characterized by episodes of coma with meningitic signs and fever and pareses as well as persistent cerebellar signs. Coma attacks last up to several days and can be precipitated by minor head trauma, vigorous work and angiography. From a study of this family and the literature, it is concluded that this syndrome has to be included in the differential diagnosis of coma and that angiography should be avoided in the patients.

Adult↗
PubMed1989

Valproic acid induction of coma in rats: synergism with NH4+ and pentobarbital.

Dose-response curves for the incidence of coma after intraperitoneal injections of various doses of valproic acid (VP) and octanoic acid (OA) showed that, mole for mole, valproic acid was less toxic than octanoic acid. However, a simultaneous subcoma dose of pentobarbital (PB) enhanced the toxicity of VP more than that of OA. The dose-response curve for NH4Cl was affected by simultaneous subcoma doses of VP and OA but not by PB. VP enhanced the toxicity of the NH4+ by 52%; OA enhanced the toxicity by 12%. PB added significantly to the toxicity of VP and NH4+ when the three were given simultaneously. Doses of 0.7 mmol NH4+ and 0.5 mmol VP given separately had little or no encephalopathic effect, with blood ammonias of 250-1250 micrograms/dl. When given simultaneously they induced a deep coma and raised the blood ammonia threefold, to about 3600 micrograms/dl. Similar doses of OA and NH4+, induced a similar deep coma, but blood levels of ammonia were not as high. Simultaneous injections of 250 mg glucose did not alter the results. Thus VP toxicity is enhanced substantially by its synergistic interactions with PB and the NH4+.

Ammonium Chloride↗