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This article describes the clinical recognition of, and pathophysiological mechanisms underlying the development of, thyroid storm and myxedema coma. Effective therapeutic management of these conditions depends on a clear understanding of the physiological adaptations occurring in hyperthyroidism and hypothyroidism, and of how precipitating events may produce these decompensated states.
Extracranial-intracranial arterial bypass was performed in five baboons to assess the effectiveness of the procedure in preventing acute cerebral ischemia following middle cerebral artery occlusion in our primate model. Thirty minutes following middle cerebral artery occlusion, the animals were placed in barbiturate coma while the extracranial-intracranial artery bypass was being completed. In the three animals with patent extracranial-intracranial arterial bypasses, infarction was prevented. In the two with occluded extracranial-intracranial arterial bypasses, a large infarction in the territory of the middle cerebral artery occurred. In a clinical correlate, postoperative ischemia was presumably prevented in three patients by barbiturate administration and revascularization for unanticipated intracranial vessel occlusion.
Two concepts are advanced to explain some fo the puzzling biochemical features found in nonketotic hyperosmolar diabetic coma. It is firstly suggested that an insulinised liver (reflecting residual beta-cell secretory activity) coexists with a diabetic periphery, thereby inactivating intrahepatic oxidation of incoming free fatty acids, which are directed largly along nonketogenic metabolic pathways such as triglyceride synthesis. This could account for the lack of hyperketonaemia. Secondly, it is hypothesised that within the liver enhanced neoglucogenesis occurs, due to the prevailing portal-vein into ratio of glucagon to insulin, and is mainly responsible for the development of massive hyperglycaemia.
This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.
BACKGROUND: The Glasgow coma scale (GCS) is an objective measurement of a patient's level of consciousness and has prognostic implications in traumatic head injuries. Morbidity and mortality of patients with meningitis have been related amongst others to level of consciousness, hypoglycorrhachia, extremes of age, and high CSF protein values. In this prospective study of 100 patients the correlation between the GCS, age, CSF-neutrophil count and CSF-glucose and protein levels and the eventual outcome of the patients was assessed. METHODS: In 100 consecutive patients with meningitis (bacterial, viral, tuberculous, cryptococcal and other) the GCS, age, CSF-neutrophil count and CSF-protein and glucose levels were determined at admission. After treatment the outcome of the patient was assigned to one of four categories: healthy, minor and severe neurological deficits and death. RESULTS: From a non-parametric one-way analysis of variance it was found that with respect to mean GCS-values significant differences were present among the outcome categories (P < 0.0001). The outcome categories did not differ significantly with respect to age, CSF-neutrophil count or CSF-glucose level, but did differ significantly with respect to the CSF-protein level (P < 0.0025). Additionally, 88% of patients with a GCS value of > 12 had a good neurological outcome, while 88% of those with a GCS value of < or = 8 had a poor outcome. CONCLUSION: A good correlation between both the GCS and CSF-protein level at admission and the outcome of patients with meningitis was found, with the GCS value being a better prognostic indicator than high CSF protein levels.
Coma and stupor are pathologic neural states whose signs arise from either massive cortical or brainstem disease or toxicity. A variety of pathological processes can cause brain disease. Often one has to begin treatment before the diagnosis of the cause of the problem is made. At all stages of treatment, great care must be taken to avoid precipitating an intracranial crisis. The physiological derangements that may aid in the diagnosis include arousability, pupil reactivity, various reflexes, breathing patterns, and cardiovascular function. The treatment needs to be both specific and general; i.e., the condition itself must be treated, if possible, and the intracranial pressure must be lowered if it has been raised by the condition. Treatments for raised intracranial pressure include hyperventilation, diuretics, corticosteroids, avoidance of jugular vein compression, coughing, and any change of the position of the head and neck from normal. When sedating or anesthetizing these patients, one should avoid drugs that increase cerebral blood flow such as ketamine and inhaled anesthetics, using instead drugs that lower cerebral blood flow such as thiopental, lidocaine, and narcotics (with ventilation).
STUDY OBJECTIVE: Emergency physicians often use the Glasgow Coma Scale (GCS) to help guide decisions in patient care, yet the reliability of the GCS has never been tested in a typical broad sample of emergency department (ED) patients. We determined the interrater reliability of the GCS between emergency physicians when adult patients with altered levels of consciousness are assessed. METHODS: In this prospective observational study at a university Level I trauma center, we enrolled a convenience sample of ED patients older than 17 years who presented with an altered level of consciousness. Two residency-trained attending emergency physicians independently assessed and recorded the GCS score and its components (eye, verbal, and motor) in blinded fashion within a 5-minute period. Data were analyzed for interrater reliability by using standard ordinal calculations. We also created scatter plots and Bland-Altman plots for each GCS component and for the GCS score. RESULTS: One hundred thirty-one patients were screened and enrolled in the study, with 15 excluded because of protocol violations. Of the 116 remaining patients, the agreement percentage for exact total GCS was 32% (tau-b=0.739; Spearman rho=0.864; Spearman rho2=75%). Agreement percentage for GCS components were eye 74% (tau-b=0.715; Spearman rho=0.757; Spearman rho2=57%), verbal 55% (tau-b=0.587; Spearman rho=0.665; Spearman rho2=44%), and motor 72% (tau-b=0.742; Spearman rho=0.808; Spearman rho2=65%). Our Spearman's analyses found that only approximately half (44% to 65%) of the observed variance could be explained by the relationship between the paired component measures. For GCS components, only 55% to 74% of paired measures were identical, and 6% to 17% of them were 2 or more points apart. CONCLUSION: We found only moderate degrees of interrater agreement for the GCS and its components.
A 50-year-old man presented to the emergency department in a coma with fixed and dilated pupils. Skin and mucous membranes were noted to be an ashen grey color. Initial vital signs were blood pressure of 104/70 mm Hg; pulse, 110; and respirations, 12. Initial arterial blood gases were pH of 7.25; PaCO2, 26.6 mm Hg; PaO2, 22.1 mm Hg; oxygen saturation, 15.2%; and methemoglobin level, 81.5%. Venous and arterial blood samples were chocolate brown, and it was noted that the color did not change when 100% oxygen was bubbled through the blood. Methylene blue 140 mg was given intravenously, and the patient gradually became more responsive. He was discharged three days later with no neurologic deficits. A comprehensive literature search revealed no reported cases of complete patient recovery with this high a methemoglobin level.
A specific arousal therapy with NAGD (Naloxone, Activated Charcoal, Glucagon, Doxapram) is outlined for victims of drug overdose in comatose and semi-comatose states. Several direct benefits accrue if early awakening or lightening of such patients is safely accomplished. There are: 1) elimination of need for prolonged intubation or tracheostomy; 2) patient's ability to tell which drug(s) were taken; 3) excessively frantic and vigorous supportive treatment is obviated; and 4) the overall hospital stay is shortened. The NAGD regimen has been found to effectively, safely, and predictably reverse coma. Therapy consists of: naloxone 0.8 mg to 1.6 mg intravenously; large-bore orogastric tube instillation of 100 gm to 120 gm activated charcoal slurry; glucagon 1 mg to 2 mg intravenously; and, in selected cases, doxapram 1 mg/kg to 2 mg/kg intravenously.
Reported is a case of ethanol-induced hypoglycemic coma in a 33-month-old boy after accidental ingestion of ethanol. Blood glucose was 10 mg% and blood ethanol was 71 mg%. He responded promptly to an IV bolus of 50% dextrose. The pathophysiology and clinical presentation of this not uncommon metabolic disorder are discussed. A plan for early recognition and management is presented.
Presented is the case of a 32-year-old man admitted with coma, hyperthermia, and tachycardia. The patient had a progressive downhill course and died in the medical ICU ten hours after admission. Autopsy and further investigation revealed thyroid storm as the most likely cause of death.
STUDY OBJECTIVE: Inferential and descriptive statistics continue to be used incorrectly when analyzing biomedical data. Glasgow Coma Score (GCS) and Revised Trauma Score (RTS) data have recently been described and analyzed using parametric statistical methods in several studies despite the ordinal nature of these data scales. The objective of this study was to determine whether GCS and RTS data are normally distributed, despite their ordinal nature. HYPOTHESIS: Neither GCS nor RTS data are normally distributed. DESIGN: A retrospective review of GCS and RTS data obtained at a medical school teaching and county hospital that is a Level I trauma center. PARTICIPANTS: Patients who met criteria for trauma team activation at the hospital. METHODS: GCS and RTS data distributions were compared to a standard normal distribution using the chi 2 goodness of fit test. RESULTS: GCS and RTS data distributions differed significantly from the normal distribution for all data sets examined. CONCLUSION: Parametric statistical descriptors and inferential methods are inappropriate for use with GCS and RTS data. Ordinal data should be tested for normality before statistical analysis with parametric statistical methods.
STUDY OBJECTIVE: To explore how Student's t test, which assumes normal errors, is affected by the nonnormal distribution of Glasgow Coma Scale (GCS) scores. METHODS: A sample of 145,295 GCS scores from the Pennsylvania Trauma Systems Foundation was assumed to represent the true GCS distribution. Four Monte Carlo simulations, each based on 40,000 replications, were conducted to approximate the distribution of t values arising from the samples drawn from the GCS distribution, using sample sizes of 10, 30, 60, and 100 per group. RESULTS: The histograms of t values derived from the GCS distribution resembled the corresponding Student t distributions for sample sizes of 30 or more per group. The t test was conservative in samples of size 10, conservative to acceptable in samples of sizes 30 and 60, and acceptable in samples of size 100. In no case was the t test liberal. CONCLUSION: The t test can be applied to GCS data with a type I error rate that never exceeds the investigator's chosen significance level. However, a sample size exceeding 30 per group is required for the error rate to adequately approximate the chosen significance level.
We present the case of a 21-month-old child with hypoketotic hypoglycemic coma. The differential diagnosis initially included metabolic causes versus a toxicologic emergency (unripe ackee fruit poisoning). Using information obtained from the emergency department, the diagnosis was confirmed as the late-onset form of glutaric acidemia type II. This case illustrates the importance of emergency physicians in the diagnosis and management of children with inborn errors of metabolism.
The acid-base status of the arterial blood, jugular venous blood, peripheral venous blood and lumbar cerebrospinal fluid and the free amino acids in the cerebrospinal fluid have been studied in 12 patients suffering from coma due to head injury. They were given S adenosyl-methionine (10 mg/kg/day). Significant statistical differences of acid-base balance and CSF free amino acids have been obtained after the administration of te compound. The clinical and biochemical significance of the use of S adenosyl-methionine in severe brain injuries is discussed
Foetal hydrops is always a challenge for the clinician. We report a case of tachycardia associated with hydrops and hydramnios in a pregnancy complicated with diabetic coma at 28 weeks gestation. Normal foetal heart rate was recorded immediately after correction of maternal acidotic status and hydrops eventually disappeared. The woman was delivered at 32 weeks and the baby had an uncomplicated postnatal course. We hypothesise that maternal ketoacidosis has been the precipitating factor of tachycardia and congestive heart failure and that this case is conceptually similar to the "late death" phenomenon, reported in cases of poorly controlled maternal diabetes.
Contradictory descriptions exist concerning the fetal heart-rate (FHR) patterns that appear during maternal hypoglycaemia. We report a case of maternal hypoglycaemic coma during which a FHR tracing was obtained showing a normal type D accelerative pattern.
The motor response of the Glasgow 'coma' scale is readily learned by nurses and doctors. It can be used as a reliable indicator of changes in the state of a comatose patient, as there is a high agreement rate between different observers.