White paper on academic emergency medicine in India: INDO-US Joint Working Group (JWG).

Emergency Medicine (EM) is a new discipline for India. As Medical Council of India (MCI) makes progress in recognizing the need to develop EM residency training programs in India it is important that there exist an established training model for future faculty, residents and medical students. This INDO-US white paper makes a serious attempt to recognize the opportunities and challenges in developing academic emergency medicine in India. The contents of this white paper address the overall scenario and are not targeted towards a person, physician, body, hospital or any other associated entity. This paper emphasizes the importance of MCI recognized training in Emergency Medicine for physicians in India.

Elderly patients with altered mental status.

Mental status changes in the elderly are a source of concern and a challenge for the emergency physician. A variety of medical conditions and psychiatric disturbances are potential causes of those symptoms. Acute changes must be differentiated from mental status alterations occurring as a result of chronic conditions. This article focuses on the emergency evaluation, treatment, and differential diagnosis of this symptom complex.

Evaluation of abdominal pain in the elderly.

Evaluation of the older patient presents a unique challenge to the emergency physician. The increased age of the population, a high incidence of comorbidity, general poverty of history and clinical signs in acute abdominal conditions, poor reliability of diagnostic procedures, and the variable presentations of diseases with significant morbidity and mortality summarize the problems to be encountered with the complaint of abdominal pain in the elderly. The correct diagnosis is often difficult to establish and coexisting complicating diseases influence the patient's condition and the ED management. The emergency physician must maintain a wide differential and have a low threshold for admission and more extensive evaluation in this patient population.

An emergency medicine approach to violence throughout the life cycle. SAEM Public Health and Education Committee.

This document by the SAEM Public Health and Education Committee outlines the public health impact of interpersonal violence as it pertains to acute emergency care. This paper provides an overview of violence through the life cycle (i.e., child abuse, youth violence, intimate violence, and elderly abuse). It also makes specific recommendations regarding the role emergency physicians can play in reducing violence through medical education, research, surveillance, public education, advocacy, and clinical practice.

C-terminal mutations that alter the turnover number for 3-O-methylglucose transport by GLUT1 and GLUT4.

Turnover numbers for 3-O-methylglucose transport by the homologous glucose transporters GLUT1 and GLUT4 were compared to those for truncated and chimeric transporters expressed in Xenopus oocytes to assess potential regulatory properties of the C-terminal domain. The ability of high intracellular sugar concentrations to increase the turnover number for sugar entry ("accelerated exchange") by GLUT1 and not by GLUT4 was maintained in oocytes. Replacing the GLUT1 C terminus with that of GLUT4 stimulated turnover 1.6-fold, but abolished accelerated exchange. Thus, the GLUT1 C terminus permits accelerated exchange by GLUT1, but in doing so must interact with other GLUT1 specific sequences since the GLUT4ctrm1 chimera did not exhibit this kinetic property. Removal of 38 C-terminal amino acids from GLUT4 reduced its turnover number by 40%, whereas removing only 20 residues or replacing its C terminus with that of GLUT1 increased its turnover number 3.5-3.9 fold. Therefore, using mechanisms independent of those which alter transporter targeting to the plasma membrane, C-terminal mutations in either GLUT1 or GLUT4 can activate transport normally restricted by the native C-terminal domain. These results implicate the C termini as targets of physiological factors, which through covalent modification or direct binding might alter C-terminal interactions to regulate intrinsic GLUT1 and GLUT4 transporter activity.

A prospective study of the impact of helmet usage on motorcycle trauma.

STUDY OBJECTIVE: To determine the effect of the use of a motorcycle helmet on reducing the mortality, morbidity, and health care costs resulting from motorcycle crashes. DESIGN: A prospective, multicenter study of all eligible motorcycle crash victims. SETTING: The emergency departments of eight medical centers across the state of Illinois, including representatives from urban, rural, teaching, and community facilities. TYPE OF PARTICIPANTS: All motorcycle crash victims presenting less than 24 hours after injury for whom helmet information was known. Data were collected from April 1 through October 31, 1988. MEASUREMENTS AND MAIN RESULTS: Fifty-eight of 398 patients (14.6%) were helmeted, and 340 (85.4%) were not. The nonhelmeted patients had higher Injury Severity Scores (11.9 vs 7.02), sustained head/neck injuries more frequently (41.7 vs 24.1%), and had lower Glasgow Coma Scores (13.73 vs 14.51). Twenty-five of the 26 fatalities were nonhelmeted patients. By logistic regression, the lack of helmet use was found to be a major risk factor for increased severity of injury. A 23% increase in health care costs was demonstrated for nonhelmeted patients (average charges $7,208 vs $5,852). CONCLUSION: Helmet use may reduce the overall severity of injury and the incidence of head injuries resulting from motorcycle crashes. A trend toward higher health care costs was demonstrated in the nonhelmeted patients.

Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome.

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.

Management of diabetic ketoacidosis.

Diabetic ketoacidosis is an all too frequent and sometimes preventable complication of Type I diabetes mellitus, responsible for significant morbidity and mortality within the diabetic population. Precipitating diseases account for the majority of deaths occurring in patients admitted in diabetic ketoacidosis, but some deaths are still attributable to ketoacidosis alone, despite recent advances in therapy and management. Recognition of the ketoacidotic state is paramount to optimal therapy, and often hinges on the diagnostic acumen of the physician. Since 20 to 30% of patients presenting in diabetic ketoacidosis do so as the initial manifestation of their previously undiagnosed disease, physicians must maintain a high level of suspicion for this condition. Understanding the pathogenetic mechanisms leading to and prevailing in diabetic ketoacidosis will allow physicians to intervene in a rational manner, approaching therapy with specific end-points in mind: (a) restoration of optimal volume status; (b) reversal of acidosis; (c) reduction of serum glucose levels; (d) replacement of specific electrolytes in a timely manner; (c) institution of appropriate therapy for any precipitating cause; and, (f) careful monitoring of the patient's biochemical, physical and mental parameters to allow adjustment in therapy as necessary. The mainstay of treatment for diabetic ketoacidosis is appropriate fluid and insulin therapy. Low-dose intravenous infusion is now the accepted mode of insulin delivery for patients with this condition. Potassium replacement is almost always necessary, often requiring massive amounts of this ion due to the total body depletion seen with the development of ketoacidosis. Controversy still surrounds routine use of phosphate in diabetic ketoacidosis but replacement may be needed if serum levels fall toward the lower limits of normal values, to avoid the potential adverse effects of phosphate depletion. Administration of bicarbonate is also controversial and should be reserved for patients whose pH is less than 7.0 to 7.1 and then it should be added to intravenous fluids, not given as an intravenous bolus. Efforts toward preventing diabetic ketoacidosis should be of prime importance to physician and patient alike. Preventive measures should include patient education about diabetes mellitus, precipitating factors of diabetic ketoacidosis, signs and symptoms of early metabolic decompensation, rational insulin therapy during minor illness and appropriate timing of physician contact to help avoid this serious and sometimes fatal complication of diabetes mellitus.