Endocrine and Metabolic Emergencies - part 10 pdf

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: (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