for the lethargic state does not necessary complete the list of possible comorbid sources for the patient’s lethargic state. Coma Coma (derived from the same word in Greek meaning ‘‘deep sleep’’) is a ‘‘state of profound unconsciousne ss from which one cannot be roused [1].’’ Relevant etiologies for this state include disorders of: abnormal levels of sodium, calcium, magnesium, phosphate, and potassium, and porphyria, Wenicke’s diseas e, and myxedema coma from profound hypothyroidism. Further discussion of these endocrine and metabolic disorders is found elsewhere in this issue. Of note, while disease states such as Wernicke’s disease are not classified typically as a metabolic disorder, the correction of this thiamine deficiency only will reverse the resultant coma if the magnesium deficiency, a necessary cofactor in the metabolism of thiamine, is repleted. Coma can be a supratentorial manifestation of hypomagnesemia by itself [12]. Uncontrolled diabetes also can lead to hyperosmolar hyper- glycemia, resulting in coma. In fact, severe hyperosmolar hyperglycemia has been noted by at least one author to be the most frequent cause of an altered state of consciousness in patients with uncontrolled diabetes. Often, these patients are chronically ill and have depleted stores of potassium, phosphate, and magnesium [13,14]. Seizure Seizures, ‘‘convulsion; an epileptic fit’’ [1], are less typically related to metabolic or endocrine disorders, but they indicate a high level of severity. For purposes of this discussion, the term seizure is considered synonymous with the tonic–clonic (formerly known as grand mal) type of seizure. Relevant etiologies for this condition include hy pernatremia (or its rapid correction), hyponatremia, hypercalcemia, hypocalcemia, hypomagnesemia, thyrotoxicosis, pyridoxine deficiency, pellagra, and hypoglycemia. The emergency physician should be aware of not only the typical electrolyte abnormalities but also the secondary causes. For example, the teenage patient seizing in the resuscitation room with a pacifier around his neck may be refractory to lorazepam therapy, because he may have syndrome of inappropriate antidiuretic hormone (SIADH) from the use of 3,4 Methylenedioxymethamphetamine (ecstasy) with concomitant free water intake in his attempt to prevent hyperthermia while at a rave party earlier that evening [15]. The alcoholic seizing patient may be experiencing ethanol withdrawal, but hypoglycemia and pellagra may be prudent to consider also. Patients presenting to the ED after trauma can have altered mental status, focal neurological deficits, or seizures that can be attributed to a head trauma when hypoglycemia is actually the cause [16]. 904 BAZAKIS & KUNZLER The Endocrine Response to Critical Illness: Update and Implications for Emergency Medicine Scott C. Gibson, MD, FACEP * , David A. Hartman, MD, FACEP, Jason M. Schenck, MD MSU-KCMS EM, 1000 Oakland Drive, Kalamazoo, MI 49008, USA The effect of severe trauma, disease, infection, and surgery can result in remarkable metabolic stresses on the human body. Survival of such insults depends in great part upon a functioning neuroendocrine system. The initial response to stress results in energy conservation toward vital organs, modulation of the immune system, and a delay in anabolism. This acute response to critical illness is generally considered to be an appropriate and adaptive response that occurs in the first days after insult [1–4]. It is the phase most germane to the practice of emergency medicine. Because of its protective nature, it is also the phase that most authors suggest pr ovides little need for medical hormonal intervention. The body’s response to protracted critical illness (weeks to months) also results in marked neuroendocrine changes. Whereas many of the chronic endocrine responses are similar to the acute phase, research is revealing that the two entities do have distinct differences [1,5,6]. The endocrine response to this prolonged critical illness can even be maladaptive. Protein breakdown and fat deposition often proceed unchecked, resulting in what has been described as a ‘‘wasting syndrome’’ [7,8]. In addition, a persistent hyperglycemic response and insulin resistance can ensue, and this is increasingly seen as potentially deleterious in the long run [9–15]. Although this chronic endocrine response to crit ical illness is of less relevance to the emergency physician than the acute phase, a working understanding of such a continuum can prove useful in identifying potential * Corresponding author. E-mail address: gibsons@bronsonhg.org (S.C. Gibson). 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.03.015 emed.theclinics.com Emerg Med Clin N Am 23 (2005) 909–929 Index Note: Page numbers of article titles are in boldface type. A Acetazolamide, hyperchloremic anion gap acidoses and, 782 Addison’s disease, 692 Adolescents, abuse of steroids by, 821 Adrenal emergencies, recognition and management of, 687–702 Adrenal gland, incidentalomas of, 699 pathophysiology of, 692–694 physiology of, 691 Adrenal hyperplasia, congenital, 879–880 Adrenal insufficiency, clinical characteristics of, 692, 693 corticosteroid therapy and, 697–699 definition of, 692 etiologies of, 692–694 evaluation in, 696–697, 916–918, 919 features suggesting, 917 management of, 918–921 pathophysiology of, 914–916 presentation in, 694–696, 914 AIDS, steroids in, 822 Amenorrhea, osteopenia in, 793 Amiodarone, as cause of hypothyroidism, 653 Amiodarone-induced thyroiditis, 672 Anabolic steroids, 815–826 abuse of, by adolescents, 821 epidemiology of, 815–816 adverse effects of, 819–820 effects on organs, 816 efficacy of use of, 818 physiology of, 816 trade names of, 819 use in medical practice, 821–823 Androstenedione, 803–804 Anion gap acidoses, elevated, ethylene glycol poisoning and, 779–780 etiologies of, 772–781 in lactic acidosis, 777–779 in salicylate toxicity, 780–781 iron and, 776–777 isoniazid and, 776 ketoacidoses and, 774–775 methanol and, 773 paraldehyde and, 775 uremia and, 773–774 hyperchloremic, acetazolamide and, 782 etiologies of, 782–784 hyperalimentation and, 781–782 in diarrhea and diuretics use, 783–784 in pancreatic fistula, 784 in ureteroenterostomy, 784 renal tubular acidoses and renal insufficiency and, 782–783 Anorexia nervosa, 792–794 Anticonvulsants, as cause of hypothyroidism, 653–654 Antidiuretic hormone, inappropriate secretion of. See SIADH. Anxiety, in endocrine and metabolic disorders, 906–907 B Bariatric surgery, nutritional consequences of, 796–797 Beta-hydroxy-beta-methylbutyrate, 802–803 Bicarbonate, in diabetic ketoacidosis, 620–621, 622 in hyperkalemia, 743 Bone, anatomy of, 703–704 and mineral metabolism, 703–721 effects of steroids on, 817–818 metabolism of, abnormalities of, management in, 706–707 pathophysiology of, 705–706 presentation in, 705 normal, 704–705 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/S0733-8627(05)00051-9 emed.theclinics.com Emerg Med Clin N Am 23 (2005) 931–936 . 776–777 isoniazid and, 776 ketoacidoses and, 774–775 methanol and, 773 paraldehyde and, 775 uremia and, 773–774 hyperchloremic, acetazolamide and, 782 etiologies of, 782–784 hyperalimentation and, 781–782 in. calcium, magnesium, phosphate, and potassium, and porphyria, Wenicke’s diseas e, and myxedema coma from profound hypothyroidism. Further discussion of these endocrine and metabolic disorders is found elsewhere. inappropriate secretion of. See SIADH. Anxiety, in endocrine and metabolic disorders, 906–907 B Bariatric surgery, nutritional consequences of, 796–797 Beta-hydroxy-beta-methylbutyrate, 802–803 Bicarbonate,