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PubMed1983

External ophthalmoplegia, alpha and spindle coma in imipramine overdose: case report and review of the literature.

A 13-year-old boy with imipramine overdose developed seizures, respiratory arrest, and coma. Abnormalities of oculovestibular reflexes, electroencephalograms, and brainstem auditory evoked potentials were monitored in relation to measurements of drug levels. An alpha-coma electroencephalographic pattern evolved into one evidencing spindle coma and eventually into a normal pattern. Prolonged brainstem auditory evoked potentials also normalized as coma and oculocephalic reflex abnormalities resolved. In spite of the history that suggested hypoxic damage, the absence of reflex eye movements in a comatose patient and the presence of alpha- and spindle-coma electroencephalographic patterns, even with prolonged brainstem auditory evoked potentials, are not reliable prognostic indicators in tricyclic drug overdose.

Adolescent↗

PubMed2005

Predictive value of electroencephalography and computed tomography in childhood non-traumatic coma.

OBJECTIVES: To study value of electroencephalogram (EEG) and computed tomography (CT Scan) in predicting outcome of non-traumatic coma in children. METHODS: 100 consecutive children, between 2 months to 12 years, with non-traumatic coma, (Glasgow Coma Scale score < 8). Demographic and clinical data was recorded at admission. EEG and CT scan were done within 24 hours of admission. Etiologic diagnosis was assigned on basis of clinical data and relevant laboratory investigations. The outcome was recorded as survived and died. Among survivors it was graded as no disability, or mild, moderate, or severe disability. Odds ratio and/or relative risk (RR) with 95% confidence interval (C I) were calculated. RESULTS: EEG could be done in 60 patients (43 survived; 7 were normal, 8 had mild, 17 moderate and 11 severe disability) CT scan in 93 patients (60 survived; 11 were normal, 14 had mild, 21 moderate and 14 severe disability). A normal/borderline EEG was associated with good outcome (P = 0.001); 11 of 12 survived and of survivors 55% had no or mild disability. Electrocerebral silence on EEG was a predictor of death (OR = 44 -sub .95% Cl - 1.5-7372; P = 0.01). An abnormal EEG was associated with significant increase in risk of disability among survivors (RR = 2.6, 95% Cl = 1.2-5.4, P = 0.03). Among CT abnormalities intracranial bleed suggested increased risk of death (RR = 2.1; 95% Cl - 0.8-5.3; P = 0.058), while, hydrocephalus was associated with better survival (RR = 0.7; 95% CI - 0.5 to 0.96; P = 0.029). However, hydrocephalus when compared with other abnormal CT scan findings, was associated with higher risk of moderate and severe disability among survivors (P = 0.046) CONCLUSION: A normal CT scan and EEG, and some of the specific findings could be helpful in predicting outcome in children with non-traumatic coma. EEG and CT scan should be done at admission in all patients with non-traumatic coma if feasible.

Child↗

PubMed1999

Barbiturate coma for severe, refractory vasospasm following subarachnoid haemorrhage.

OBJECTIVE: To document the outcome of patients treated with barbiturate coma for severe symptomatic angioplasty-resistant vasospasm. To compare mortality with that predicted by admission APACHE II score, and neurological outcome with that of historical controls treated with barbiturate coma for vasospasm, and with historical controls with delayed ischaemic deficits from vasospasm treated with nimodipine. DESIGN: Cohort study. SETTING: Neurosurgical Intensive Care Unit of tertiary referral university teaching hospital. PATIENTS: Eleven (6.7%) of 164 consecutive patients with aneurysmal SAH managed according to our protocol who were treated with thiopentone-induced burst suppression coma for severe symptomatic, angioplasty-resistant vasospasm. INTERVENTIONS: Chart, database and literature review. MEASUREMENTS AND RESULTS: All 11 patients survived to hospital discharge (mortality 0%) compared with first-day APACHE II predicted mortality of 30.6% (p=0.15). Outcome at 6 months was: good recovery 8/11 (72.7%), moderate disability 2/11 (18.2%), vegetative survival 1/11 (9.1%). Ten of 11 (90.9%) had a good neurological outcome compared with 50.6% of historical controls with delayed ischaemic deficit from vasospasm (odds ratio 9.78, 95% confidence interval 1.24-77.0, p=0.02), and 0% of previously reported patients treated with barbiturate coma for vasospasm (p < 0.01). CONCLUSION: Our results are better than previously published outcomes and suggest formal evaluation of barbiturate coma in the treatment of severe resistant symptomatic vasospasm following SAH is warranted.

APACHE↗

PubMed1998

Barbiturate coma may promote reversible bone marrow suppression in patients with severe isolated traumatic brain injury.

OBJECTIVES: Barbiturate coma is employed in brain-injured patients whenever increases in intracranial pressure remain unresponsive to less aggressive therapeutic regimens. Barbiturate-mediated neuroprotection, however, is weakened by an increased infection rate related to barbiturate-induced immunosuppression. Co-administration of barbiturates with antibiotics known to induce bone marrow suppression could, in turn, potentiate barbiturate-mediated immunosuppression. Adverse drug reactions and interactions of thiopental with antibiotics in terms of leukopenia, infection rate, and bone marrow suppression were investigated. METHODS: White blood cells were measured daily, tracheobronchial secretion and urine were examined for bacterial growth twice a week or if an infection was suspected. RESULTS: A total of 52 patients with severe isolated head injury were consecutively investigated. Due to increased intracranial pressure (ICP), which did not respond to analgosedation, barbiturate coma was performed in 23 cases. The other 29 patients remained analgosedated. Leukocytes and neutrophils were reversibly and significantly decreased in all patients, mostly sustained under thiopental. The pulmonary infection rate due to gram-negative organisms was nearly doubled during barbiturate coma. Reversible agranulocytosis and bone marrow suppression attributed to antibiotics developed in six patients after thiopental administration. Mortality rate, however, was not increased by these adverse effects. CONCLUSIONS: Barbiturate coma may cause reversible leukopenia and an increased infection rate. Long-term administration of thiopental may also promote reversible antibiotic-induced bone marrow suppression. The mechanisms and site of interaction between thiopental and antibiotics cannot be assessed by the present study and remain to be clarified. However, during and after barbiturate coma, close monitoring of leukocytes and infections and careful selection of antibiotics is required.

Adult↗

PubMed1981

Insulin-induced hypoglycemic coma and regional cerebral energy metabolism.

Swiss-Albino female mice weighing 20 g were rendered hypoglycemic by injecting insulin (2 units/kg). Animals were sacrificed at 40 min (pre-coma), 2 h (coma) and 4.5 h (recovery) after insulin injection by rapid submersion in liquid N2. Following sectioning at 20 micrometer, samples from the ascending reticular activating system and the inferior colliculus were freeze-dried and assayed for glucose, lactate, ATP and phosphocreatine (PCr). There was a preferential effect of hypoglycemia on ATP and PCr in cells of the ascending reticular activating system. ATP was depleted 30%, and PCr 55% in the pre-coma stage. ATP and PCr in cells from the inferior colliculus were not decreased. This selective effect on cells of the ascending reticular activating system followed by coma suggests that the coma per se may not represent total failure of the organism, but rather a compensatory mechanism designed to permit the animal to correct its compromised energy status.

Adenosine Triphosphate↗

PubMed1985

Octanoic acid-induced coma and reticular formation energy metabolism.

The medium chain fatty acid octanoic acid was injected i.p. into 20-22 g Swiss-Albino mice at a dose of 15 mumol/g. This dose produced a reproducible response consisting of a 3-4 min period of drowsiness, followed by coma. These mice as well as suitable controls were sacrificed by rapid submersion in liquid N2, or by microwave irradiation in a 7.3 kW microwave oven. Tissue from the reticular formation and the inferior colliculus was prepared for microanalysis of the energy metabolites glucose, glycogen, ATP and phosphocreatine. Results from this study showed a selective effect on energy metabolism in cells of the reticular formation. Both glucose and glycogen were elevated in the coma and precoma state. In addition, ATP and phosphocreatine were decreased in the reticular formation during coma. These results show a selective effect of octanoic acid on energy metabolism in the reticular formation both in the precoma stage, and during overt coma. The selective vulnerability of the reticular formation to metabolic insult may act in a beneficial manner to the animal by inducing coma. This lowers the overall demand for energy, thereby placing the animal in a milieu in which there is an increased chance for correction of the perturbation.

Adenosine Triphosphate↗

PubMed1975

Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain.

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.

Animals↗

PubMed1996

[Auditory P300 in subjects in a post-anoxic coma. Preliminary data].

The first results concerning the role of event related potentials (P300) in assessing a prognosis in comatose patients reported in the literature have been encouraging. The cause of the coma is an important prognostic factor by itself, especially when traumatic and anoxic comas are compared, with a less favorable prognosis in anoxic coma. In our study, only anoxic patients have been investigated using somatosensory evoked potentials, brainstem auditory evoked potentials P300 auditory event-related potentials. Clinical evaluation was performed using Glasgow, Liege and Jouvet coma scales. In twenty patients studied, six had a positive P300 and three of them awake. Out of the 14 patients without a P300 only one awoke (5%), 12 patients died and one is in deep coma. Despite the small number of patients in this study, the first results confirm the interest of auditory P300, in addition to clinical evaluation and evoked potential testing.

Adult↗

PubMed2006

Coma might not preclude emergency operation in acute aortic dissection.

BACKGROUND: Syncope or new onset focal neurologic deficits are described in as many as one fifth of patients with acute aortic dissection referred for surgery. Coma or stroke caused by involvement of the arch vessels and secondary brain malperfusion is considered a major contraindication for emergency aortic repair. Initial experience with emergency operation in selected patients with acute type A aortic dissection complicated by coma is described. METHODS: Five comatose (median Glasgow coma score, 5.5), hemodynamically stable (systolic blood pressure > or = 100 mm Hg) patients with preserved pupillary reactivity and coma duration of less than 12 hours underwent emergency surgical repair. The ascending aorta was always replaced using profound hypothermic circulatory arrest. RESULTS: There were no operative deaths. No hemorrhagic brain infarction developed postoperatively. Ischemic strokes were documented by radiology in 3 patients, and were always right-sided. Four patients returned to normal life with no neurologic sequelae, whereas 1 patient showed partially recovered left hemiparesis and mild cognitive impairment. CONCLUSIONS: Coma may not represent an absolute contraindication for resuscitative surgery in hemodynamically stable patients with acute type A aortic dissection. A larger experience is necessary to draw more definitive conclusions.

Acute Disease↗

PubMed2005

Incomplete alpha coma pattern in a child.

Only 19 cases of alpha coma pattern in the pediatric age group had been reported. Recently the concept of reactivity has been included in the definition of alpha coma. Electroencephalography reveals reactivity to painful stimuli in incomplete alpha coma. In adults, this pattern has a better prognosis than the complete pattern with no reactivity. A 5-year-old child had coma secondary to hypoxic brain damage after surgery. His electroencephalogram documented an incomplete alpha coma pattern. He remained in a vegetative state. This study is the first report of a child with incomplete alpha pattern documented on electroencephalogram.

Alpha Rhythm↗

PubMed2006

Critical score of Glasgow Coma Scale for pediatric traumatic brain injury.

The aim of this study is to determine the predictive critical value of the Glasgow Coma Scale for use as a determinant of outcome for children with traumatic brain injuries. A total of 309 children, aged 2-10 years, were enrolled in this study. Each subject underwent the following assessments: Glasgow Coma Scale; clinical data; brain computed tomography; and Glasgow Outcome Scale assessments. The receiver operating characteristic curve indicated that a critical point of the Glasgow Coma Scale set at 5 was most strongly correlated with outcome of pediatric traumatic brain injury. Subarachnoid hemorrhage with brain swelling and edema, subdural, intracerebral hemorrhage, and basal ganglion lesions were associated with severe injury and poor outcome (P < 0.05). However, cortical lesions did not affect injury severity and outcome. In injuries associated with traumatic brain injuries, only chest trauma had a tendency to be associated with poor outcome (P < 0.05). Of the factors analyzed, the score of the Glasgow Coma Scale was the most effective predictor for outcome in pediatric traumatic brain injury. Furthermore, the predictive critical score of the Glasgow Coma Scale should be set at 5 for pediatric traumatic brain injury. The computed tomographic findings also were important in determining injury severity and predicting outcome.

Accidents, Traffic↗

PubMed2003

Acute postpartum mental status change and coma caused by previously undiagnosed ornithine transcarbamylase deficiency.

BACKGROUND: Acute postpartum mental status change usually represents postpartum blues or depression. Psychosis and coma are rare. This is a case report of a patient with previously undiagnosed ornithine transcarbamylase deficiency presenting as postpartum acute mental status change and coma. CASE: A 28-year-old multipara developed acute mental status change and coma 3 days after cesarean delivery. A metabolic profile and neurologic workup were unrevealing. An electroencephalogram revealed diffusely slow brain activity. She developed hyperammonemia and hyperglutaminemia and was diagnosed with ornithine transcarbamylase deficiency. Her newborn son was diagnosed with ornithine transcarbamylase deficiency on the previous day. Treatment with oral lactulose resulted in normalization of her ammonia level and resolution of her coma within 48 hours. She suffers no long-term sequelae. Dietary avoidance of protein was advised; outpatient treatment with sodium benzoate, sodium phenylacetate, and lactulose was initiated. A pedigree analysis is ongoing. CONCLUSION: Ornithine transcarbamylase deficiency should be included in the differential diagnosis of acute postpartum coma. Hyperammonemia, hyperglutaminemia, and orotic aciduria are diagnostic, facilitate early treatment, and mitigate the risk of permanent neurologic impairment or death.

Acute Disease↗

PubMedDate not supplied

Association between serum levels of reactive nitrogen intermediates and coma in children with cerebral malaria in Papua New Guinea.

Serum levels of reactive nitrogen intermediates (RNI; nitrate plus nitrite) were measured in 92 patients with cerebral malaria in the Madang Province of Papua New Guinea. RNI levels were compared to disease severity and clinical outcome, and correlated with both the depth of coma on admission and its duration. Median levels were higher among children with deeper coma than among those with lighter coma (35.6 microM vs. 16.7 microM; P = 0.008) and also among children with longer duration of coma (72 h; 59.3 microM vs. 19.3 microM; P = 0.004). RNI levels also correlated with clinical outcome, fatal cases having significantly higher RNI levels than survivors (41.2 microM vs. 18.5 microM; P = 0.014). Thus, high RNI levels are associated with indices of disease severity and may predict outcome in children with cerebral malaria. These data are consistent with the hypothesis that nitric oxide is involved in the pathogenesis of coma in human cerebral malaria.

Child↗

PubMed1977

Aspects of coma after severe head injury.

Features of coma during the first week after sever head injury were analysed in 700 patients. Coma is best defined as inability to obey commands, to speak, or to open the eyes. If eye opening is omitted from the definition then some less severly affected patients will be included in the early stages, the duration of coma will be overestimated, and in the later stages the distiction between coma and other unresponsive states may be blurred. Other features which correlate with responsiveness (as judged by motor response, speech, and eye opening) are pupil reactions and eye movements; respiratory abnormalities are less common and less closely related to other aspects of severity. A rigorous fefinition of coma is necessary for valid commparisons between individual patients and between different series of patients with head injury. This is essential for the assessment of alternative management regimens and for establishing predictive criteria.

Adolescent↗

PubMed1982

[Prognostic value of the trigemino-facial reflex in severe post-traumatic comas].

The blink reflex (BR) study has been carried out on 40 severe head injury cases (average age 24.3 years). The recording was conducted several times between the 2nd and the 12th day and was repeated during the first month and beyond in prolonged comas. 23 patients did not respond even to high intensity stimuli. 17 patients displayed delayed and low amplitude latency responses: one of the components, early R1 or late R2 could be missing. The existence of a detectable focalized hemispheric lesion had no effect on the disappearance of the delayed lateral response. No BR was observed in mesencephalic, protubering comas and in 4 cases of subcortical and diencephalic comas. BR was observed in subcortical or diencephalic comas and in 5 cases of mesencephalic comas. The evolution of patients who did not display any electrical response during the first recording was unfavourable in 15 cases. Among the 5/8 remaining comatose cases, the BR was missing on the 2nd day and back on the 7th day. Among the 17 patients who displayed BR their evolution proved to be very favourable or favourable in 13 cases. In all the patients who survived beyond a month the response latencies proved normal, yet their amplitude was considerably lowered. The lack of BR is temporary but it is an element of unfavourable prognosis if it persists beyond a span of 8 days.

Adolescent↗

PubMed2003

Re-evaluation of short latency somatosensory evoked potentials (P13, P14 and N18) for brainstem function in children who once suffered from deep coma.

One of the major clinical features of brain death is deep coma. Therefore, we re-evaluated retrospectively electrophysiological examinations of brainstem function in about 31 children who had once suffered from deep coma in order to reveal its pathophysiological characteristics. The patient age at coma ranged from 1 month to 10 years (mean 2 years 1 month). The electrophysiological examinations were performed, including any of short-latency somatosensory evoked potential (SSEP), brainstem auditory evoked potential (BAEP) and blink reflexes. We first compared results between the fair and poor prognostic groups, and then re-evaluated SSEP results on a few severely impaired patients with persistent vegetative state (PVS). Subsequently, SSEP clarified more specific findings for a deep coma condition than BAEP and blink reflex. A lack of P14, N18 and N20, and an amplitude reduction or vagueness of P13 in SSEP in these children strongly suggested high risk in their future neurological prognosis. In conclusion, electrophysiological examinations, especially SSEP (P13, P14 and N18), might be very useful in obtaining a long-term neurological prognosis after deep coma in children.

Blinking↗

PubMed2000

The Glasgow coma scale.

Teasdale and Jennett first presented the Glasgow Coma Scale in 1974 as an aid in the clinical assessment of unconsciousness. It was devised as a formal scheme to overcome the ambiguities and misunderstandings that arose when information about comatose patients was presented and groups of patients were compared. Since then, the Glasgow Coma Scale has been used extensively, being used to grade individual patients, compare effectiveness of treatments, and as a prognostic indicator. It has been incorporated into numerous trauma and critical illness classification systems. However, a number of competing scales have been developed to overcome its perceived deficiencies. These scales are generally more complex. One of the expressed reservations regarding the Glasgow Coma Scale has been its failure to incorporate brainstem reflexes. The scale also includes a numerical skew toward the motor response. An important current issue is the appropriate application of the Glasgow Coma Scale to intubated patients. A number of approaches have been used to assign the verbal score to such patients. The timing of initial scoring is another area of discussion. Despite its drawbacks, the Glasgow Coma Scale remains the most universally utilized level of consciousness scale worldwide. It seems destined to be used in emergency medicine for some time.

Glasgow Coma Scale↗

PubMed2004

Reversible coma: a rare presentation of spontaneous intracranial hypotension.

BACKGROUND: Spontaneous intracranial hypotension (SIH) is a well-recognized neurologic disorder that typically presents with orthostatic headaches, low cerebral spinal fluid pressures and distinct abnormalities on magnetic resonance imaging. METHODS: We present a case of a rare presentation of SIH. RESULTS: A 49-year-old man presented with a two week history of orthostatic headaches that rapidly progressed to encephalopathy and coma, requiring intubation. Neuroimaging revealed abnormalities typical of SIH; diffusely enhancing pachymeninges, subdural fluid collections, and descent of the brain. Treatment with an epidural blood patch reversed his coma within minutes. Following a second blood patch, the patient became asymptomatic. No cerebral spinal leak could be identified on magnetic resonance imaging or on a nuclear medicine technetium cerebral spinal fluid flow study. At six month follow-up, he remained symptom free. CONCLUSION: The mechanism of coma in SIH is presumed to be compression of the diencephalon from downward displacement of the brain. Although it is very unusual for patients with SIH to present with coma, it is important to recognize since the coma may be reversible with epidural blood patches.

Blood Patch, Epidural↗