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A 55-year-old woman with renal tubular acidosis and urinary potassium wasting became comatose and subsequently fitted when her plasma potassium level fell to 0.9 mmol/l. Her neurological state resolved with potassium therapy. She had no other recognised cause for her coma. It appears that coma represents the extreme of the spectrum of neurological change that may occur in association with hypokalaemia.
Some of the immediate cardiovascular changes and alterations in oxygenation occurring in a patient in myxoedema coma following the oral administration of a single dose of triiodothyronine (T3) (2.5 micrograms) are described. These included increases in oxygen consumption, oxygen delivery, cardiac output, heart rate and ventricular stroke work. Low dose oral T3 can be effective in myxoedema coma and these patients may benefit from the continuous, comprehensive monitoring which can be provided in an intensive care unit. Our observations suggest that over-vigorous attempts to reverse the hypothyroid state could precipitate tissue hypoxia and/or myocardial ischaemia.
The Glasgow Coma Scale is widely accepted as a measure of impaired consciousness both in clinical practice and in research. In its standard form, the scale is inapplicable to infants and children below the age of 5 years. We have devised a paediatric coma scale, which recognises that the expected normal verbal and motor responses must be related to the patient's age. This scale has been routinely used in a paediatric teaching hospital over a 10-year period and has appeared to be satisfactory, although it is less sensitive to changes in the conscious level than the adult scale. We have assessed the consistency of observer evaluation, using video tapes of infants and children exhibiting varying levels of consciousness: when conducted after formal instruction, assessments were reasonably consistent.
Necrotizing fasciitis is a rapidly spreading infection of the subcutaneous tissue and fascia; diabetes mellitus appears to be the most frequent underlying disease. Early diagnosis and immediate aggressive surgical therapy are paramount to curtail morbidity and mortality, but diagnosis is often difficult and unnecessarily delayed. We describe a case of necrotizing fasciitis precipitating diabetic ketoacidotic coma where correct diagnosis was not made until the 14th hospital day. We stress the fact that physicians caring for critically ill patients should be keenly aware of the possibility of necrotizing fasciitis when tending diabetic patients with unexplained fever; failure to recognize the disease can have devastating results. Finally, we believe this to be the first reported case of diabetic ketoacidotic coma precipitated by necrotizing fasciitis.
Spontaneous heart rate, respiration rate and electrodermal activity were studied in 32 patients with different grades of severe poisoning by ingestion of various drugs. The degree of their behavioural impairment was determined with the Munich Coma Scale (MCS) which measures stimulus evoked somatomotor responses. There was a significant reduction of spontaneous variations of heart rate and respiration rate with increasing severity of coma. Spontaneous electrodermal fluctuations were present only at the least severe grades of impairment. Thus, cardiorespiratory and electrodermal activity can provide significant information on the level of behavioural impairment in severe poisoning.
A total of 28 patients with non-traumatic coma were studied both with somatosensory- and motor-evoked potentials. While somatosensory-evoked potentials (SEP) have proved to be useful in predicting the outcome in patients with severe brain damage, the aim of this study was to find out whether the additional evaluation of motor-evoked potentials (MEP) could contribute to a better prediction of the outcome than SEP alone. Our results clearly indicate that in terms of prognostic value, SEP are superior to MEP. Nine patients with bilaterally preserved MEP died, while all of the patients with bilaterally preserved SEP and a central conduction time less than or equal to 6.5 ms survived, with a Glasgow outcome score of 1 to 3. Therefore, we cannot recommend the inclusion of MEP in the prognostic evaluation of patients with non-traumatic coma.
Two nephrotic children treated with prednisone developed steroid-induced diabetes and non-ketotic hyperosmolar coma (NKHC). Both patients presented with convulsions, coma and shock. The glucose concentration of the cerebrospinal fluid was 425 mg/dl and 622 mg/dl, respectively. Both patients had no diabetic family history, but had been treated with prednisone for 4 and 8 months, receiving total doses of 6.6 and 10.8 g, respectively. Despite conventional therapy, both patients deteriorated rapidly and died several hours later. Steroid-induced diabetes associated with NKHC is a rare but serious complication of steroid therapy.
The process of coma emergence is defined and important issues are identified. Rehabilitative goals for persons emerging from coma are best served by a focus on their response capabilities, rather than sensory stimulation. A method called "response system analysis" is described to guide assessment and treatment of response capabilities.
We report an endocrine emergency of a 52-year-old woman with chronic anterior-pituitary failure of autoimmune origin who developed hypopituitary crisis with coma and severe hypotension provoked by an intercurrent bronchopneumonia. At admission to the ICU hypopituitarism had not been diagnosed and only Hashimoto's thyroiditis with thyroid replacement therapy could be obtained from the patient's history. Although the patient presented with somatic signs suggestive of hypopituitarism, other causes of coma and hypotension had first to be excluded. In the absence of specific treatment the patient died 18 h later with refractory cardiac arrest. Diagnosis of acute decompensated chronic hypophyseal failure must be considered if hypothermia, refractory hypotension and signs of infection without fever are associated with a short stature and the loss of axillary and public hair. Waiting for laboratory confirmation of the diagnosis must not delay immediate life-saving specific glucocorticoid treatment.
A total of 24 patients with clinical evidence of brain death (n = 17), severe coma (n = 2; GCS approximately 3) and apallic syndrome (n = 4) underwent a comparative investigation with 99mTc-HMPAO brain scintigraphy, EEG, auditory and somatosensory evoked potentials. Accompanied by EEG and evoked potentials, brain scintigraphy enabled confirmation of cerebral death in 15/17 patients. In one case clinical examination and evoked potentials suggest brain death, but cerebral perfusion and EEG were normal ("brain stem death"). One patient with evidence of cerebral death in clinical examination, brain scintigraphy and evoked potentials, showed questionable focal EEG activity; however, autopsy revealed intravital autolysis of the entire brain. All patients with apallic syndrome and deep coma showed a distinct cerebral perfusion, but gross EEG abnormalities; evoked potentials were delayed or absent. Planar scintigraphy with 99mTc-HMPAO appears to be superior to neurophysiological techniques discriminating patients with agonal cerebral dysfunction from those with brain death.
Myxoedema coma is a medical emergency with high mortality. In this study, clinical response and plasma variations of thyroid hormones were analysed in 7 patients, 6 presenting with myxoedema coma and one with myxoedema ileus. These patients were treated with intravenous or oral l-thyroxine (l-T4). 1000 mu l-T4 iv were administered in two patients. Within 3 h, plasma T4 and triiodothyronine (T3) reached a peak upper normal range, then diminished slowly during 5-9 days. The 5 remaining patients were treated with 500 micrograms l-T4 po on the first day, then 100 micrograms l-T4 daily by mouth. Plasma T4 and T3 increased slowly, remaining in hypothyroid range but clinical response (assessed on mental status, pulse rate and body temperature) occurred within 24-72 h. Cortisone therapy was used in 3 patients. Two patients died of myocardial infarction, or septicemia, one while receiving cortisone therapy and i.v. l-T4, another one treated only by oral l-T4. This study suggests: 1) oral absorption of l-T4 is variable, but clinical response occurs quickly even in myxoedema ileus; 2) the intravenous route involves high peaks of plasma T4 and T3; 3) peripheral conversion of T4 to T3 allows gradually T3 delivery to organ systems, even if only l-T4 is used and 4) initial and daily dosage determinations need further studies.
A brief review of some therapy results in 763 episodes of diabetic coma from 1960 to 1973 reveals a significant decrease in lethality after institution of an intensive care unit. Present aspects of management are: intensification of shock therapy, potassium substitution and treatment of cerebral edema. The possibly dangerous role of hypotonic solutions is discussed. The lowering of the as yet high lethality of diabetic coma is an urgent necessity.
OBJECTIVE: To investigate whether accurate prognostic rules can be derived from the combined results of studies concerning prediction of poor prognosis in anoxic-ischaemic coma with biochemical markers of brain damage in cerebrospinal fluid (CSF) or serum. DESIGN: A meta-analysis of prognostic studies in anoxic-ischaemic coma, selected from Medline and EMBASE databases, according to predefined criteria. SUBJECTS: Twenty-eight studies, with a total of 802 unselected, consecutive patients, in which tests, sampling time and outcome measures were described unequivocally and results were described using clear cut-off values or raw data. MAIN OUTCOME MEASURES: Poor outcome, defined as death or vegetative state, versus good outcome, defined as any other outcome state. ANALYSES: The overall prognostic accuracy of these variables was expressed as the 95% CIs of the pooled false-positive test rate and the pooled positive-likelihood ratios. RESULTS: Only markers in CSF (creatine kinase isoenzyme (CKBB) >204 U/l, neuron specific enolase (NSE) >33 ng/ml, lactate dehydrogenase (LDH) >82 U/l and glutamate oxaloacetate (GOT) >62 U/l) reached a 0% false-positive rate. However, due to small sample sizes, the confidence limits were wide. The accuracy of prediction of poor outcome seemed acceptably high for CSF-CKBB (pooled false-positive rate 0% [95% CI 0-2.3%]; pooled positive-likelihood ratio 33.2 [95% CI 4.8-230.2]), but this result was based on two retrospective studies without blinding of the treating physicians for the test result. CONCLUSIONS: Because of small numbers of patients studied and methodological limitations the combined results are not sufficiently accurate to provide a solid basis for non-treatment decisions.
The prognostic significance of post-anoxic-ischemic alpha coma (AC) is controversial. We recorded somatosensory evoked potentials (SEPs) and performed serial electroencephalography (EEG) in a 60-year-old woman in coma after cardiac arrest. The first EEG was recorded after 48 hours (GCS=5; E1-V1-M3); brain-stem reflexes were preserved. The EEG pattern showed monotonous alpha frequencies (10-11 Hz) with posterior predominance; acoustic and noxious stimuli evoked EEG reactivity. Early cortical SEPs (72 h) were normal. On the fifth day (GCS=8; E4-V1-M3), the EEG alpha pattern was replaced by a diffuse delta activity; rhythmic theta changes appeared spontaneously or in response to stimuli. The patient regained consciousness on the tenth day and EEG showed posterior theta activity (6-7 c/s) partially reactive to stimuli. At the 6-month follow-up, cognitive evaluation showed mild dementia. Recent studies identified two forms of AC. Patients with complete AC have an outcome that is almost invariably poor. Conversely, incomplete AC (posteriorly accentuated alpha frequency, reactive and with SEPs mostly normal) reflects a less severe degree of anoxic-ischemic encephalopathy. The case we report should be classified, according to the SEPs and EEG features, as incomplete AC. The fact that the patient has regained consciousness, even if with residual cognitive impairment, confirms the need to distinguish this variant from complete AC.
Multiple therapeutic modalities have been used to treat hepatic encephalopathy. L: -Acetylcarnitine (LAC) is a physiologically active substance that improves both the energetic and the neurotransmission profiles. LAC is able to cross the hematoencephalic barrier and reach the cerebral regions, where the acetylic group may be utilized. The aim of this work was to evaluate the efficacy of LAC in the treatment of hepatic coma in cirrhotic patients. Twenty-four suitably selected patients were enrolled in the study and, following randomization, received either LAC (n=13) or placebo (n=11). Statistically significant differences in neurological findings, as evaluated by the Glasgow Scale, as well as in ammonia serum levels and BUN were found following LAC treatment. In the placebo group we observed two cases of improved neurological findings as well as one case of improved EEG grading. In the other group we observed an improvement of neurological findings and of EEG grade in 10 and 8 subjects, respectively. Noteworthily, seven (54%) patients went from grade 4 down to grade 3, and one from grade 4 down to grade 1. The improvement in the neurological picture was evident at between 1 and 4 hr after the end of treatment, remaining until 24 hr after. No side effects were observed in our study series. Our study demonstrates that LAC administration improved neurological and biohumoral symptoms in selective cirrhotic patients with hepatic coma.
BACKGROUND: Bispectral Index (BIS) derived from electroencephalogram (EEG) is primarily developed to monitor the depth of unconsciousness. Recent evidence suggests that BIS may also help in the detection of cerebral ischemia and prognostication of outcome of traumatic brain injury (TBI). The present study was designed to investigate the correlation between Glasgow Coma Score (GCS) and BIS in mild and moderate head injury. METHODS: In 29 patients with mild (GCS 13-15) and moderate (GCS 9-12) head injuries who underwent craniotomy, GCS and BIS were measured before surgery, after surgery and once a day for the first 10 days. RESULTS: A significant correlation was found between GCS and BIS in the data sets from all the patients (r = 0.67; p < 0.001). Mean BIS values increased with increasing GCS scores. However, the scatter of BIS values for any GCS score was high limiting the value of BIS in predicting GCS. Mean BIS values were significantly different between mild and moderate head injuries [65.7 +/- 16.1 vs. 85.7 +/- 6.1, p = 0.006]. CONCLUSION: In patients with mild and moderate head injury, significant correlation exists between GCS and BIS. But the high degree of scatter of BIS values for any given GCS score limits its use as a monitor of depth of coma in TBI. Further studies are required to understand the relation between BIS algorithm and cerebral electrical activity following TBI to define the role of BIS as an electrophysiological correlate of consciousness in TBI.
Hyperosmolar nonketotic coma occurred in a 29-year-old diabetic man with chronic renal failure after the repeated use of oral glycerol for treatment of acute neovascular glaucoma. Treatment with intravenous hypotonic saline, albumin, and packed red blood cells together with insulin and bicarbonate was successful in overcoming the coma.
Amantadine has found use primarily as an antiviral agent and in the symptomatic treatment of parkinsonism. However, the use of amantadine for the subjective alleviation of fatigue in multiple sclerosis and in the treatment of agitated aggressive behavior in the traumatic brain injured patient has also been described. Side effects of amantadine are primarily related to the central nervous system and include hallucinations, confusion, and nightmares. Toxic manifestations include acute psychosis, coma, cardiovascular toxicity, and death. Amantadine toxicity is a particular problem in patients with renal insufficiency because 90% of an oral dose is excreted unchanged in the urine. We present a case of amantadine-induced coma in a patient with multiple sclerosis and end-stage renal disease. Moreover, this degree of amantadine toxicity was profoundly apparent at a drug level usually not associated with such a severe presentation.