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PubMed1997

[Incidence, clinical picture and treatment of hypothyroid coma. Results of a survey].

BACKGROUND: Myxedema coma is a severe life-threatening clinical state with a high mortality rate. Very often symptoms are masked because of concurrent illnesses. There are no data available about the incidence and prevalence of this disease. Therefore we conducted a survey in the Federal Republic of Germany between 1993 and 1995 by a questionnaire on the occurrence of myxedema coma. METHODS: Questionnaires were mailed to 800 departments of medicine. RESULTS: We received 168 questionnaires for further evaluation. Among those, 24 patients were classified as myxedema coma, but according to clinical data we could reclassify 12 patients as myxedema coma and 12 patients as severely hypothyroid but without coma. The mean age of the patients was 73 years. The etiology was Hashimoto's thyroiditis in 16 patients (67%), in 15 patients the thyroid disease was unknown. In 6 patients thyroid hormone therapy was withdrawn after thyroid surgery. One patient became hypothyroid after radioiodine therapy and 1 patient had secondary hypothyroidism. 19 of the 24 patients received i.v. thyroxine therapy and 11 patients received corticosteroids additionally. Six patients (25%) died. CONCLUSION: These data emphasize that myxedema coma is a rare disease (24 patients within two years in Germany) occurring especially in older patients and is associated with a high mortality rate also in non-comatose patients. In the majority of the patients myxedema coma was the first manifestation of thyroid disease.

Aged↗
PubMed1999

Exaggerated vasopressin secretion and attenuated osmoregulated thirst in human survivors of hyperosmolar coma.

AIMS/HYPOTHESIS: To test the hypothesis that subnormal thirst sensation could contribute to the development of the hypernatraemia characteristic of hyperosmolar coma, we studied osmoregulation in survivors of hyperosmolar coma. METHODS: Eight survivors of hyperosmolar coma, eight control subjects with Type II (non-insulin-dependent) diabetes mellitus and eight healthy control subjects underwent water deprivation during which measurements of thirst, plasma osmolality and vasopressin were taken. RESULTS: Water deprivation caused greater peak plasma osmolality in the hyperosmolar coma group (301.7 +/- 2.7 mmol/kg) than in Type II diabetic (294.3 +/- 3.2 mmol/kg, p < 0.01) or control group (296.9 +/- 3.0 mmol/kg, p < 0.01) and a greater increase in plasma vasopressin concentration (hyperosmolar coma, 5.8 +/- 1.3 pmol/l, Type II diabetes, 1.8 +/- 1.3 pmol/l, p < 0.001, control subjects, 2.2 +/- 1.8 pmol/l, p < 0.001). Thirst ratings were lower following water deprivation in the hyperosmolar coma group (3.5 +/- 0.8 cm) than in Type II diabetes (7.7 +/- 1.6 cm, p < 0.001) or control subjects (7.4 +/- 1.3 cm, p <0.001), and the hyperosmolar group patients drank less in 30 min following water deprivation (401 +/- 105 ml) than Type II diabetic (856 +/- 218 ml, p < 0.001) or control subjects (789 +/- 213 ml, p < 0.001). CONCLUSION/INTERPRETATION: Survivors of hyperosmolar coma have subnormal osmoregulated thirst and fluid intake, which might contribute to the hypernatraemic dehydration typical of the condition.

Aged↗
PubMed1982

Some observations on the blink reflex in posttraumatic coma.

Blink reflex studies were carried out on 51 comatose patients with signs of brain stem impairment due to head injury. Twenty-five patients were studied in acute coma on day 1 or 2 after trauma. Twenty-six patients were studied in prolonged coma during days 3-12 after brain injury. Brain stem involvement was divided clinically and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due to direct violence to the brain stem. Further, the comatose states were separated by behavioural and EEG signs of sleep into "sleep' and more "alert' states. The blink reflexes were recorded after mechanical and electrical stimulation. Mechanical stimulation appeared to be more effective in evoking late responses than the electrical stimulus. The elicitability of the late responses was also dependent on the time of stimulation. During "sleep', usually accompanied by a spindle-EEG, the late responses were totally absent after both mechanical and electrical stimulation in acute coma. In more "alert' states, usually accompanied by high voltage delta waves in the EEG, the late responses, especially direct R2, could be frequently elicited by mechanical stimulation. These differences decreased during prolonged coma. All patients with signs of secondary brain stem involvement who had at least one late component in the acute stage of coma recovered well. So did all patients, with one exception, with primary brain stem injuries. Early recovery of the blink reflexes in cases of primary brain stem injury was a further favourable sign. Consistent absence of R2 (and R1) in prolonged coma indicated a bad outcome. The presence of all components in prolonged coma was of less prognostic significance than in the acute stage.

Adult↗
PubMed2006

Electroencephalographic assessment of coma.

SUMMARY: Altered mental status ranging from confusion to deep unresponsiveness can be described as coma. Electroencephalography is an important tool in assessing comatose patients. Some EEG patterns are seen with lighter stages of coma and have a good prognosis, whereas others are seen in deep, often irreversible coma. These EEG patterns carry a much more grave prognosis. This paper discusses the various EEG features seen in coma, ranging from intermittent rhythmic delta activity to electrocerebral inactivity. A discussion regarding etiology and prognosis is presented after the EEG pattern is described in detail. Special EEG features, such as alpha coma, beta coma, spindle coma, etc., are discussed toward the end.

Coma↗
PubMedDate not supplied

Catatonic coma with profound bradycardia.

Catatonia may be monosymptomatic at presentation, with stupor or coma as the cardinal and only manifestation. A case of catatonic coma with profound bradycardia is presented to help clinicians recognize this entity and include catatonia in the differential diagnosis of coma as a rare etiology after other more common causes of coma have been excluded. Cases of catatonic coma are nevertheless important to identify because treatment with intravenous benzodiazepines is simple and highly effective. The authors argue that the descriptive term "catatonic coma" is preferable over terms implying psychogenesis, such as "psychogenic" or "hysterical" coma; for catatonia, the authors have a specific treatment, in the form of benzodiazepines; for "psychogenesis," there is none.

Adult↗
PubMed1991

A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate.

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.

3-Hydroxybutyric Acid↗
PubMed1975

Correlation between brain monoamine levels and postictal coma following electroshock.

Duration of postictal coma following maximal electroshock seizure and monoamine levels in the whole brain were measured in mice. Pretreatment with intraperitoneal alpha-methyl-p-tyrosine (alpha-MT), 5-hydroxytryptophane (5-HTP), or intraventricular 6-hydroxydopamine (6-OHDA) prolonged the coma duration, whereas p-chlorophenylalanine (PCPA) did not affect the coma, and L-DOPA tended to shorten the coma and counteracted the effect of alpha-MT. When the shock was repeated five times with one hour intervals, the duration of coma was progressively increased being accompanied by elevated serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) levels in the brain. In alpha-MT treated group, a striking parallelism was remarked between coma prolongation and norepinephrine (NE) or dopamine (DA) reduction. These data suggest that prolongation of postictal coma is correlated with reduced NE and DA levels and/or with elevated 5-HT and 5-HIAA levels in the brain.

Animals↗
PubMed2003

Severe anaemia in childhood cerebral malaria is associated with profound coma.

BACKGROUND: Severe anaemia in children with cerebral malaria has been associated with respiratory distress secondary to lactic acidosis and/or hypoxia. The ensuing metabolic derangement may further depress the level of consciousness culminating in presentation with profound coma. This association has poorly been studied. OBJECTIVE: To determine the relationship between profound coma at presentation and the presence of severe anaemia in children with cerebral malaria. METHODS: This cross-sectional study involved 100 children with cerebral malaria who were consecutively recruited at admission in the Paediatric emergency unit of Mulago hospital in Uganda from July to December 2000. Clinical and laboratory evaluation was done using the hospital's guidelines for the management of severe malaria. The exposure factor of interest was severe anaemia (Hb < 5.0 g/dl) and occurrence of profound coma (Blantyre coma Scale 0) was the outcome measure. RESULTS: Severe anaemia and profound coma were seen in 20% and 9% of the children respectively. Severe anaemia was independently associated with profound coma, adjusted OR 1.34 (CI 1.17 - 1.95), p = 0. 002 and age < 3 years, adjusted OR 1.42 (CI 1.13 - 1.54), p = 0.001). Thirty percent of those with severe anaemia had deep sighing (acidotic) breathing compared to only 15% of those with haemoglobin (Hb) > 5 g/dl, OR 1.21 (CI 0.90 - 1.64), p = 0.118. There was no association between the malaria parasite density and severe anaemia. A similar proportion of those with severe anaemia regained consciousness within 24 hours compared to those with Hb > 5 g/dl (30 vs 42.5%), OR 1.56 (0.65 - 3.71), p = 0.307. CONCLUSIONS: The findings suggest that profound coma in cerebral malaria may not only result from primary malaria encephalitis but possibly also from a metabolic dysfunction due to severe anaemia.

Anemia↗
PubMed1992

[The type of coma as prognostic indicator in severe cranial trauma in childhood].

Various methods are used by neurologists to evaluate posttraumatic brain damage. The most important and reliable are the length of posttraumatic amnesia and coma. In previous papers we have already described the value of the type of coma in the prognosis of serious head injury in childhood (Baracchini-Muratorio et al. 1985; Pruneti et al. 1985). In this study, 30 children (aged 6-12 years) with serious closed head injury and subsequent coma were evaluated. The children were divided into two groups according to the type of coma, using the Plum and Posner coma classification (1966) modified by Pagni et al. (1974). The children were followed up for at least two years (9 for five years) after the trauma by means of neurological, physical, EEG, CT scan and neuropsychological examinations. The neuropsychological test results confirm the hypothesis of a different evolution of sequelae in relation to the type of coma, independently of length of coma and site of brain damage.

Adolescent↗
PubMedDate not supplied

The EEG in metabolic encephalopathy and coma.

Excellent early work on stupor and coma can be found (particularly with regard to anoxia) in the work of Fischgold and Mathis (1959) in France, and Pamela Prior in England (1973a). These workers correlated deepening levels of coma with particular EEG patterns, and the suppression of EEG reactivity. Alpha frequency patterns in coma (alpha coma), spindle-like sleep patterns in coma (spindle coma) and "triphasic waves" are among the wide variety of endocrine disorders discussed in case reports and series leading to identification of particular EEG patterns. EEG correlations with prognosis are most reliable with cardiorespiratory arrest (CRA) with its consequent anoxic-ischemic insult. If etiology is known, EEG can often be a reliable predictor of outcome. EEG usually has little specificity with regards to etiology, but some patterns do favor particular diagnoses: for example, triphasic waves (TWs) are frequently seen with hepatic and renal insufficiency in young adults; spindle coma patterns are believed to indicate dysfunction at the brainstem level (Chatrian, 1990). EEG is most useful in differentiating organic from psychiatric conditions, in excluding nonconvulsive status epilepticus (NCSE), and in providing a rough guide as to the degree of cortical and subcortical dysfunction.

Alpha Rhythm↗
PubMed2006

[The beginnings of modern biological psychiatry in Hungary: the atropine coma. A historical overview].

In the authors' opinion modern biological psychiatry in Hungary started with the investigations into the biological mechanism of atropine coma therapy. Atropine coma was used in the period between 1950 and 1975 mainly in the treatment of various psychoses and obsessive compulsive disorder. In a previous communication the method, indications and adverse effects of atropine coma were outlined and the professional and broader social reasons for its eventual disappearance were discussed. In this paper the therapeutic effectiveness and research into the biological mode of action of atropine coma are summarized. Although thousands of patients received atropine coma therapy in the United States and in several Central-Eastern European countries including Hungary, this therapeutic modality is hardly ever features even in papers on the history of psychiatry. This is all the more surprising because initial therapeutic results with atropine coma were favourable and it seemed to be a more safe and efficient treatment than the more widely used insulin coma.

Atropine↗
PubMed2007

Analysis on care outcome of patients with polytrauma and coma.

OBJECTIVE: To make further improvement of outcome of patients with polytrauma and coma. METHODS: The data of 3361 patients (2378 males and 983 females, aged from 5-95 years, 38.2 years on average) with severe polytrauma and coma admitted to Chongqing Emergency Medical Center (Level I Trauma Center), Chongqing, China, from November 1978 to December 2004 were analyzed retrospectively in this study. RESULTS: The overall survival rate and mortality were 93.2% (3133/3361) and 6.8% (228/3361), respectively. The mortalities in patients with coma duration less than 1 hour and combined with neural dysfunction and in patients with coma duration larger than or equal to 1 hour and combined with or without neural dysfunction were significantly higher than that of those with coma duration less than 1 hour but without neural dysfunction [39.5% (136/344) vs 3.0% (92/3017), P less than 0.01]. There existed significant differences in GCS, ISS, and revised trauma score (RTS) between the death group and the survival group (P less than 0.01). RTS was in good correspondence with patient's pathophysiological status and outcome in patients with multiple trauma and coma for different groups of systolic blood pressure (SBP). The mortality in patients with SBP less than 90 mm Hg was significantly higher than that of those with SBP larger than or equal to 90 mm Hg [33.3% (68/204) vs 5.1% (160/3157), P less than 0.01]. The mortality in polytrauma patients combined with serious head injury (AIS larger than or equal to 3) was 8.2%, among which, 76.5% died from lung complications. The morbidity rate of lung complications and mortality rate increased in patients with head injury complicated with chest or abdomen injury (23.9%, 61.1% vs 27.3%, 50.0%). The mortality reached up to 61.9% in patients complicated with severe head, chest and abdomen injuries simultaneously. CONCLUSIONS: It plays a key role to establish a fast and effective trauma care system and prompt and definite surgical procedures and to strengthen the management of complications for improving the survival rate of patients with severe polytrauma and coma.

Accidents, Traffic↗
PubMed1995

An assessment of cerebrospinal fluid's total creatine-kinase activity in the differential diagnosis of metabolic and organic causes of coma.

The objective of the study was to assess total cerebrospinal creatinine-kinase activity (CSF-CK) measurement in differential diagnosis of "metabolic" and organic causes of coma. The setting for the study was a tertiary care reference medical center and community general hospital. The design of the study was a series of consecutive patients with profound coma (Glasgow scale ratings between 3 and 6) as the presenting complaint to the emergency room and controls. Measurements and main results were as follows: CSF-CK was measured in 103 consecutive patients including 18 patients with metabolic causes of coma, 27 patients with organic causes of coma, 18 patients scheduled for elective orthopedic surgery with epidural anesthesia and 27 patients with compressive myelopathy and radiculopathy. CSF-CK activities were significantly different between groups (H = 29.48, p < 0.001, Kruskal-Wallis test), controls had a median of 0 mU/ml (range 0-16 mU/ml), patients with metabolic causes of coma had a median of 0 mU/ml (range 0-65 mU/ml), patients with compressive myelopathy or radiculopathy had a median of 19 mU/ml (range 0-80 mU/ml), and patients with organic causes of coma had a median of 20 mU/ml (range 0-400 mU/ml). The test sensitivity was 83% (95% confidence interval (CI 65-100%) specificity 62% (CI 43-80%) positive predictive value 60% (CI 49-79%) and negative predictive value 85% (CI 75-95%). The conclusion of the study was that the test is useful for ruling out metabolic causes of coma when CSF-CK activity is high (i.e., above 16 mU/ml).

Adult↗
PubMed1994

Stimulation programs for coma patients.

The coma stimulation techniques mentioned here are not the only methods that can be used; coma stimulation programs should be individualized. Families should be encouraged to participate even while the patient is in the ICU. Recovery from coma is often long and tedious, but with use of a coma stimulation program, there is hope for recovery from coma. Because the process of coma recovery is unclear, research is still needed. Critical care nurses have an opportunity to participate in coma recovery by incorporating these stimulation techniques into their practice.

Acoustic Stimulation↗
PubMed2006

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster.

Carbon dioxide gas is used as an insect anesthetic in many laboratories, despite recent studies which have shown that CO(2) can alter behavior and fitness. We examine the effects of CO(2) and anoxia (N(2)) on cold tolerance, measuring the rapid cold-hardening (RCH) response and chill coma recovery in Drosophila melanogaster. Short exposures to CO(2) or N(2) do not significantly affect RCH, but 60 min of exposure negates RCH. Exposure to CO(2) anesthesia increases chill coma recovery time, but this effect disappears if the flies are given 90 min recovery in air before chill coma induction. Flies treated with N(2) show a similar pattern, but require significantly longer chill coma recovery times even after 90 min of recovery from anoxia. Our results suggest that CO(2) anesthesia is an acceptable way to manipulate flies before cold tolerance experiments (when using RCH or chill coma recovery as a measure), provided exposure duration is minimized and recovery is permitted before chill coma induction. However, we recommend that exposure to N(2) not be used as a method of anesthesia for chill coma studies.

Acclimatization↗
PubMed2006

Increased levels of pregnenolone and its neuroactive metabolite allopregnanolone in autopsied brain tissue from cirrhotic patients who died in hepatic coma.

It has been suggested that neurosteroids with agonist properties at the central GABA-A receptor are implicated in the pathogenesis of hepatic encephalopathy (HE) in chronic liver disease. In order to address this issue, gas chromatography/mass spectrometry was used to measure the neurosteroids pregnenolone, allopregnanolone, and tetrahydrodeoxycorticosterone (THDOC) in postmortem brain tissue from controls, cirrhotic patients who died without HE, a patient who died in uremic coma, and cirrhotic patients who died in hepatic coma. Exposure of rat cerebral cortical membranes to brain extracts from hepatic coma patients resulted in a 53% (p < 0.001) increase in binding of [3H]muscimol, a GABA-A receptor ligand. Subsequent GC/MS analysis showed that concentrations of the GABA-A receptor agonist neurosteroid allopregnanolone were significantly increased in brain tissue from hepatic coma patients compared to patients without HE or controls (p < 0.001). Brain allopregnanolone concentrations were significantly correlated with the magnitude of induction of [3H]muscimol binding (r2 = 0.82, p < 0.0001). Concentrations of allopregnanolone comparable to those observed in hepatic coma brains are pathophysiologically relevant. Concentrations of the neurosteroid precursor pregnenolone were also increased in brain tissue from hepatic coma patients, while those of a second neurosteroid THDOC were below the levels of detection in all groups. Brain concentrations of benzodiazepine receptor ligands estimated by radioreceptor assay were not significantly increased in cirrhotic patients with or without hepatic coma. These findings suggest that increased levels of allopregnanolone rather than "endogenous benzodiazepines" offer a cogent explanation for the phenomenon of "increased GABAergic tone" previously proposed in HE.

Adult↗
PubMed2002

Compressed spectral arrays of patients with fulminant hepatic failure in hepatic coma undergoing liver transplantation.

Assessing the coma status of patients with fulminant hepatic failure (FHF) is important for determining the reversibility of brain damage and for properly timing liver transplantation. The compressed spectral array (CSA) method is a frequency analysis technique that processes electroencephalogram signals by computer to facilitate on-line interpretation. This method has been used to monitor the consciousness levels of neurointensive care unit patients. In this study, we determined whether CSA could be used to assess the coma status of patients with FHF, and whether CSA provided information that was useful in deciding when to proceed with liver transplantation. CSA recording was carried out in 17 FHF patients with encephalopathy (coma grade III-IV) who underwent living-related liver transplantation between August 1997 and May 1999. Recording was performed with a Neuromonitor OEE-72044 (NIHON KOHDEN, Osaka, Japan) every 24 h before and after transplantation, until the patients regained consciousness. The CSAs of healthy controls were distributed almost equally between 0 and 16 Hz. The CSAs of FHF patients in hepatic coma were classified into three patterns. Eight of the 17 patients showed very prominent slow waves of about 2 Hz (group A), and seven patients showed strongly suppressed rapid waves between 8 and 16 Hz (group B). The remaining two patients showed CSA patterns that were similar to those of healthy controls, even though these patients were comatose (group C). Abnormal CSA patterns were observed in 15 of the 17 patients (88%). Group B patients seemed to have higher coma grades than did group A patients. Sixteen patients underwent liver transplantation, completely recovered from hepatic encephalopathy, and subsequently showed CSA patterns similar to those of healthy controls. One patient died without regaining consciousness. These results suggest that CSA is useful in assessing the coma status of FHF patients and in evaluating electrophysiological recovery from hepatic coma after liver transplantation.

Adolescent↗
PubMed1979

Hyperammonemic coma after hepatectomy in germ-free rats.

Current theories on the pathogenesis of hepatic coma indicate that intestinal bacteria produce cerebral toxins, such as ammonia, mercaptans, and short-chain fatty acids. To test the hypothesis that elimination of anaerobic and aerobic intestinal bacteria retards the onset and alters the biochemical profile of acute hepatic coma, we determined the onset of coma and the ammonia concentration in blood and cecal contents in 7 germ-free and 10 normal dehepatized rats. Ammonia levels were also determined in a further group of 7 germ-free and 12 normal rats 24 hr after hepatic vascular exclusion was accomplished. Onset of coma for germ-free rats (x: 34 hr) was identical to that of normal rats (x: 36 hr). Arterial ammonia was equally elevated in germ-free rats (x: 834 mumol/liter) and in normal rats (x: 854 mumol/liter), although the ammonia concentration in the cecal contents was significantly lower in germ-free rats (x: 1762 mumol/liter) than in normal rats (x: 5572 mumol/liter). In germ-free animals, portal venous blood contained more ammonia than arterial blood (x A-V difference: -87 mumol/liter), indicating nonbacterial intestinal ammonia release. We conclude that intestinal bacteria toxins are of minor importance in the mechanism of acute hepatic coma of the liverless rat and that presumably bacterial toxins, such as ammonia, can be products of nonbacterial metabolism. Since hyperammonemia could be considered an important determinant of coma in our model, prevention of hyperammonemia in functionally anhepatic animals should be the next objective in unraveling the pathogenesis of acute hepatic coma.

Ammonia↗