Endocrine Emergencies: Recognition and Treatment
Preface
The purpose of this book is to update the management of
endocrine, diabetic, and metabolic emergencies by consensus of experts in the fi eld.
We believe that this book will bring the topic areas up to date, set a standard for
diagnosis and treatment in each category, and comprehensively cover the area
Each chapter begins with a Precis that presents, in concentrated form, what
the physician needs to know to begin the evaluation and emergency treatment of the
known endocrine emergencies
. This is followed by an extended discussion of the
pathophysiology that can be read after initial treatment has begun.
1
. Silverstein SR, Frommer D. Emergency management of metabolic and endocrine
disorders
. Rockville, MD: Aspen Publishers, Inc; 1988.
2
. Ober KP. The medical clinics of North America, endocrine emergencies
.
Philadelphia: W.R. Saunders Company; 1995.
3. Wagner MJ, Cowling K
. Emergency clinics of North America endocrine and
metabolic emergencies. Philadelphia; 2005.
4
. Van den Berghe G, LeRoith D. Endocrinology and metabolism clinics of North
America, acute endocrinology
. Philadelphia: Saunders; 2006.
Acute Adrenal Insuf fi ciency
There are two forms of acute adrenal insuf fi ciency
. Primary acute adrenal
insuf fi ciency is associated with destruction of both adrenal glands
. Autoimmunity,
infection, in fi ltration, infarction, and hemorrhage are common etiologies
. Both cortisol and aldosterone are de fi cient. Secondary acute adrenal insuf fi ciency is associated with ACTH de fi ciency caused by hypothalamic or pituitary dysfunction
. Only
cortisol is de fi cient. Aldosterone secretion, regulated by the renin–angiotension system, is normal in secondary adrenal insuf fi ciency
.
The clinical syndrome of acute adrenal insuf fi ciency was fi rst described by
Lipsett and Pearson [ 2 , 3 ]
. “We have withdrawn cortisone from adrenalectomized
patients in the attempt to maintain them without any steroid hormone administration
. It soon became apparent that this was not possible
. When cortisone was withdrawn, clinical collapse developed promptly
. Within 24 h of cortisone withdrawal,
the patient complained of malaise, lethargy, anorexia, and weakness
. At 48 h, the
patient noted giddiness in the upright position and such profound weakness that he
was unwilling to leave the bed. At 72 h, the patient was usually unable to take food,
and nausea, vomiting, diarrhea, and stupor frequently ensued
. The blood pressure
fell but not to shock levels as long as the patient remained horizontal
. The patient
developed a gaunt and ashen appearance, the skin was cold and gray, the pulse
weak, and it appeared that death would soon follow
. Administration of cortisone at
this time brought about dramatic clinical improvement usually within 12 h, so that
the patient was ready to eat and to ambulate, and he felt well
.”
Lipsett and Pearson then differentiated the syndrome of isolated aldosterone
de fi ciency from that of isolated cortisol de fi ciency. Figure 1.1 shows the clinical
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