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An educational intervention to increase use of the Glasgow Coma Scale by emergency department personnel.

Data from a large series of acutely injured patients revealed the Glasgow Coma Score was acquired in less than one half of those for whom it should have been documented. To improve these statistics, a five-part educational intervention based on an application of the PRECEDE-PROCEED model was developed. The study populations consisted of hospital-based nurse-managers and their emergency department nursing staff. Evaluation of the educational intervention's effectiveness suggested (1) simply conveying benefits of a particular patient care practice is insufficient to bring about immediate and permanent changes and (2) the most significant changes occurred in settings in which a formal policy and formal data collection procedures were established to accompany and reinforce the educational intervention. On-site advocacy and physician support are essential if changes in nursing practice are to occur in hospital emergency departments.

Education, Nursing, Continuing↗

Prognostic value of evoked responses and event-related brain potentials in coma.

The behaviourally unresponsive patient, unable to exhibit the presence of cognition, constitutes a conundrum for health care specialists. Prognostic uncertainty impedes accurate management decisions and the application of ethical principles. An early, reliable prognosis is highly desirable. In this review investigations studying comatose patients with coma of different etiologies were selected. It is concluded that objective prognostication is enhanced by the use of electrophysiological tests. Persistent abnormalities of brainstem auditory evoked potentials and short-latency somatosensory evoked potentials reliably indicate the likelihood of irreversible neurological deficit or death. Meanwhile, the presence of "cognitive" event-related brain potentials (e.g., P300 and mismatch negativity) reflects the functional integrity of higher level information processing and, therefore, the likelihood of capacity for cognition. An approach that combines clinical and electrophysiological values provides optimal prediction of outcome and level of disability.

Acoustic Stimulation↗

Effectiveness of a Glasgow Coma Scale instructional video for EMS providers.

INTRODUCTION: The Glasgow Coma Scale (GCS) is the standard measure used to quantify the level of consciousness of patients who have sustained head injuries. Rapid and accurate GCS scoring is essential. OBJECTIVE: To evaluate the effectiveness of a GCS teaching video shown to prehospital emergency medical services (EMS) providers. METHODS: Participants and setting--United States, Mid-Atlantic region EMS providers. Intervention--Each participant scored all of the three components of the GCS for each of four scenarios provided before and after viewing a video-tape recording containing four scenarios. Design--Before-and-after single (Phase I) and parallel Cohort (Phase II). Analysis--Proportions of correct scores were compared using chi-square, and relative risk was calculated to measure the strength of the association. RESULTS: 75 participants were included in Phase I. In Phase II, 46 participants participated in a parallel cohort design: 20 used GCS reference cards and 26 did not use the cards. Before observing the instructional video, only 14.7% score all of the scenarios correctly, where as after viewing the video, 64.0% scored the scenarios results were observed after viewing the video for those who used the GCS cards (p = 0.001; RR = 2.0; 95% CI = 1.29 to 3.10) than for those not using the cards (p < 0.0001; RR = 10.0; 95% CI = 2.60 to 38.50). CONCLUSIONS: Post-video viewing scores were better than those observed before the video presentation. Ongoing evaluations include analysis of long-term skill retention and scoring accuracy in the clinical environment.

Audiovisual Aids↗

Emergent intubation and CT scan pathology of blunt trauma patients with Glasgow Coma Scale scores of 3-13.

INTRODUCTION: Widely accepted guidelines for use of pharmacologic agents for prehospital intubation have not been fully developed. Toward the goal of formulating specific guidelines, this study sought to determine how well the Glasgow Coma Scale (GCS) score stratifies the need for emergent intubation (within 30 minutes of emergency department arrival or in the prehospital setting). METHODS: A one-year, retrospective review of the charts of blunt trauma patients with presumed head injury who presented to the emergency department of a Level 1 trauma center with a GCS score of less than or equal to 13 was performed. A total of 120 patients met the inclusion and exclusion criteria. RESULTS: A significant number of patients presenting with a GCS score of less than or equal to 9 required emergent intubation. A significant minority of patients presenting with a GCS score of 10-13 required emergent intubation (20%) or had intracranial pathology on head CT scan (23%), and the majority of patients from this subgroup did not require subsequent intubation. Alcohol or substance intoxication and communication barriers such as deafness and language difficulties limited the clinical examination. CONCLUSIONS: Patients with a presenting GCS score of less than or equal to 9 represent candidates for the use of pharmacologic agents to facilitate aggressive airway control by well-trained and supervised emergency medical technicians (EMTs). Emergent intubation of patients with a GCS score of 10-13 is problematic. Patients with a presenting GCS score of 10-13 must be evaluated individually and closely monitored.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Frontal blood flow changes in recovery from coma.

Two-dimensional studies of cortical blood flow were conducted in 20 closed head injury patients in a comatose state and subsequently in 9 patients as they recovered to an awake and responding state. Comatose patients showed a reduction of frontal flow compared to the resting pattern observed in age matched normal volunteers. In most patients the normal anterior-to-posterior flow gradient was reversed. Increases in global flow, while in coma, tended to exaggerate this reversal. Patients who survived showed a normalization of the regional flow pattern as they regained consciousness. The marked reduction of frontal blood flow in the comatose state was independent of locus of injury as determined by computed tomography (CT) scan data. Combined with previous CBF studies of sensory and cognitive activation, these findings suggest that frontal reduction may be a nonspecific effect of any state or condition involving reduced directed mental activity. This, in turn, raises questions about recent interpretations offered for frontal CBF reduction in psychiatric disease.

Adult↗

Recovery of mitochondrial and plasma membrane function following hypoglycemic coma: coupling of ATP synthesis, K+ transport, and changes in extra- and intracellular pH.

The primary objective of the present study was to evaluate the recovery of plasma and mitochondrial membrane functions after 30 min of hypoglycemic coma and to establish whether a lingering accumulation of free fatty acids (FFAs) delays the recovery. A secondary objective was to study whether production of metabolic acids following glucose infusion leads to a fall in intracellular pH (pHi). Phosphocreatine, creatine, ATP, ADP, and AMP, as well as glycogen, glucose, lactate, pyruvate, and FFAs of rat brain cortex and caudoputamen were measured, and "free" ADP was calculated from the creatine kinase equilibrium. Extracellular pH (pHe) and K+ concentration (K+e) were measured with ion-sensitive microelectrodes, and pHi was derived by the CO2 method. Glucose injection was followed by resumption of oxidative phosphorylation within approximately 2 min and by an equally rapid restoration of normal K+e levels. These functions recovered although tissue FFAs remained elevated for at least 7-8 min. Tissue lactate content increased only moderately and production of metabolic acids did not lead to intracellular acidosis. After 15 min of recovery, pHi was moderately increased, although pHe fell toward 7.0. It is speculated that the dissociation between intra- and extra-cellular pH is compatible with an up-regulation of an Na+/H+ antiporter, e.g., by phosphorylation.

Adenosine Triphosphate↗

Bilateral nephrectomy stopped disease progression in plasma-resistant hemolytic uremic syndrome with neurological signs and coma.

Four women were admitted over three years because of anemia and renal failure. They had evidence of hemolytic uremic syndrome (HUS) with severe vascular involvement and glomerular collapse. Despite intensive plasma exchange, all patients developed neurologic signs (with seizures and coma in 2) and papilledema. Three developed refractory hypertension and three required dialysis. All patients had abnormal von Willebrand factor (vWF) fragmentation as reflected by decreased high molecular weight and increased low molecular weight vWF multimers in the circulation. Assuming that the disease was sustained by shear stress-induced abnormal vWF fragmentation in damaged renal microvasculature, bilateral nephrectomy was done. Surgery was followed within two weeks by complete hematologic and clinical remission consistently associated with the restoring of vWF fragmentation pathway to normal. We speculate that in HUS resistant to plasma exchange or infusion, removing the kidneys eliminates a major site of vWF fragmentation, which would limit platelet activation and protect patients from the further spreading of microvascular lesions.

Adult↗

Coma-induced bullae and sweat gland necrosis following clobazam.

Coma-induced bullae and sweat gland necrosis is a rare clinicopathological entity described in association with a variety of aetiopathological conditions all of which have resulted in an impairment of conscious level. We report the first case observed in association with clobazam, used as adjunctive therapy for resistant epilepsy in a 4-year old. The potential underlying mechanisms and previously reported associations are discussed.

Anti-Anxiety Agents↗

Severe non-ketotic hyperosmolar coma--intensive care management.

We report a case of non-ketotic hyperosmolar coma, which presented with blood sugar levels far exceeding any previously recorded in the literature. The patient developed acute renal failure, probably because of rhabdomyolysis, which was successfully managed with continuous veno-venous haemofiltration. He developed blurring of vision resulting from biochemical changes, which was managed conservatively. We discuss the mechanisms of causation of the renal failure and visual blurring.

Acute Kidney Injury↗

The status of the Glasgow Coma Scale.

The Glasgow Coma Scale (GCS) was first introduced in the 1970s to provide a simple and reliable method of recording and monitoring change in the level of consciousness of head injured patients. Since its introduction, the GCS has been widely utilized in the trauma community and its use expanded beyond the original intentions of the score. In the context of traumatic injury, this paper discusses the use of the GCS as a predictor of outcome, the limitations of the GCS, the reliability of the GCS and potential alternatives through a critical review of the literature. The relevance to Australian trauma populations is also addressed.

Emergency Service, Hospital↗

Reversible coma in children after improper baclofen pump insertion.

We report the occurrence of delayed postoperative coma in five of nine consecutive children following surgery for insertion of baclofen infusion pumps. We suspect that improper technique resulted in an inadvertent administration of an intrathecal baclofen bolus. We suggest ways to minimize this risk.

Analgesics, Opioid↗

Increased GABA release in the human brain cortex as a potential pathogenetic basis of hyperosmolar diabetic coma.

Human cerebral cortical slices preincubated with [3H]GABA, [3H]noradrenaline, or 5-[3H]hydroxytryptamine and superfused with Krebs solution or Mg(2+)-free Krebs solution were used to investigate the influence of increased D-glucose concentrations on the release of these [3H]-neurotransmitters evoked by high K+ content or NMDA receptor activation, respectively. An increase in level of D-glucose (normal content, 11.1 mM) by 32, 60, and/or 100 mM (a range characteristic for hyperosmolar diabetic coma) increased the [3H]GABA release and inhibited the [3H]noradrenaline release evoked by both methods of stimulation. The K(+)-induced 5-[3H]hydroxytryptamine release was also inhibited by high D-glucose content. Blockade of GABAB receptors by p-(3-aminopropyl)-p-diethoxymethylphosphinic acid (CGP 35348) attenuated the inhibitory effect of high D-glucose content on the K(+)-evoked release of [3H]noradrenaline and 5-[3H]hydroxytryptamine, suggesting that the effect on monoamine release is, at least to a major part, the result of the increased GABA release and, as a consequence, of an increased GABA concentration at inhibitory GABAB receptors. The membrane-impermeable sorbitol mimicked the increasing effect of D-glucose on [3H]GABA release and its inhibitory effect on 5-[3H]hydroxytryptamine release. However, dimethyl sulfoxide, which is known to permeate rapidly through biological membranes, had no effect at concentrations equiosmolar to D-glucose. It is concluded that a reduction in brain cell volume caused by increased extracellular, compared with cytoplasmic, osmolarity is crucial for the changes in neuronal function observed at high D-glucose and sorbitol content.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Area-selective stimulus-provoked seizures in post-anoxic coma.

We describe the case of a 70-year-old patient in whom hemiconvulsive seizures occurred during metabolic derangement, multiple stroke and post-anoxic coma following cardiac arrest. We employed the methods of clinical and EEG evaluation and CT brain scan. We found that hemiconvulsive seizures were provoked following a light tactile stimulus in the left-trigeminal area and occasionally a strong tapping in the right-trigeminal area. We conclude that this type of stimulus-provoked seizure is extremely rare and could be explained by diffuse and severe brain damage.

Aged↗

Coma probably induced by lorazepam-valproate interaction.

Both valproate (VPA) and lorazepam (LZP) are primarily cleared from the body by glucuronidation. Concomitant administration of VPA has been reported to reduce the elimination of LZP. However, it remains unknown whether this drug interaction is clinically significant. We report a patient with epilepsy who showed that VPA-LZP interaction could result in severe encephalopathy such as coma.

Adult↗

Glasgow Coma Scale predicts coagulopathy in pediatric trauma patients.

The aim of this study was to determine if neurologic findings at the time of initial resuscitation can predict coagulation abnormalities resulting from head injury. Fifty-three children with head injury were reviewed for Glasgow Coma Scale (GCS), prothrombin time (PT), international normalized ratio (INR), partial thromboplastin time (PTT), use of fresh frozen plasma (FFP) and outcome. Twenty-six of the 53 children (49%) presented with a GCS of 15 and 27 (51%) had a GCS less than 14. The incidence of computed tomography (CT)-documented intracranial injury was 12% in those children with a GCS of 15 versus 78% when GCS < or = 14 (P < .05). Abnormal coagulation (PT > 14.5, INR > 1.2, PTT > 38) in children with a GCS = 15 was 7% v 67% when GCS was < or = 14 (P < .05). A mean of 1 unit of FFP per patient was required in children with a GCS of < or = 14. No child with GCS of 15 and CT evidence for intracranial injury had a coagulopathy, and no child with GCS of 15 required FFP. In head injured children, significant coagulation abnormalities requiring treatment are excluded by the presence of a normal GCS at presentation. Children with GCS less than 14 are at risk for intracranial injury and coagulopathy, this risk increases inversely with the GCS. Children who present with a GCS less than 8 should have FFP prepared at the time of admission. These data may guide the use of laboratory tests and blood bank resources during trauma resuscitation.

Blood Coagulation Tests↗

Isolated corticotrophin-deficiency found through alcohol-induced hypoglycemic coma.

A case of hypoglycemic coma after alcohol ingestion was observed in a chronic alcoholic. Upon close examination isolated corticotrophin-deficiency was found. It is suggested that ethanol-induced hypoglycemia may be consistent with dysfunction of mitochondria in hepatic cells and that there may be disorder of the hypothalamus in the chronic drinker.

Adrenocorticotropic Hormone↗

[Treatment of diabetic coma and precoma with continuous low-dose insulin infusions (author's transl)].

13 patients, nine women and four men, aged 22 to 83 years, were treated for diabetic coma or precoma between September 1974 and January 1976. Ten patients were known diabetics and six of them had been treated with insulin. On admission blood sugar was 32.4 +/- 3.3 mmol/l (5.84 +/- 0.6 g/l). The capillary blood pH was 7.15 +/- 0.06 (n = 13). Treatment consisted of continuous insulin infusion (6 IU soluble insulin/hour), physiological saline, potassium substitution and sodium bicarbonate (if the pH was below 7.15). In the first hours of treatment 98 +/- 12IU of insulin, 6.5 +/- 0.5 litres of fluid, 168 +/- 22 mmol of potassium and 237 +/- 55 mmol NaHCO3 were required. During the first 4 hours of the insulin infusion the blood sugar decrease per hour was 3.55 mmol/l (0.64 g/l). Hypokalaemia during treatment occurred in one case, hypoglycaemia was not observed. A preceding treatment with insulin and severe acidosis did not influence therapeutic success. Twelve patients were treated successfully, one patient died 6 hours after admission following mesenteric arterial embolism.

Adult↗