Endocrine and Metabolic Emergencies - part 10 pdf

Coma Coma derived from the same word in Greek meaning ‘‘deep sleep’’ is a ‘‘state of profound unconsciousness from which one cannot be roused[1].’’ Relevant etiologies for this state inc

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 unconsciousness 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 disease, 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 hypernatremia (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]

The Endocrine Response to Critical Illness: Update and Implications

for Emergency Medicine

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 provides 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 critical 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 matterÓ 2005 Elsevier Inc All rights reserved.

doi:10.1016/j.emc.2005.03.015 emed.theclinics.com

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 matterÓ 2005 Elsevier Inc All rights reserved.

doi:10.1016/S0733-8627(05)00051-9 emed.theclinics.com