potentially life-threatening form of the disease, the clinical presentation is one of an ill patient with symptoms and signs of adrenal insufficiency: hypotension, tachycardia, hypoglycemia, extreme fatigue, and nausea and vomiting. Also seen are failure to regrow shaved pubic hair, apathy, and failure to lactate [30]. One should consider this diagnosis in obstetrical patients with severe hemorrhage not responsive to blood replacement and prolonged hypotension. This disease may be seen by emergency physicians because of shorter postpartum hospitalizations. In the chronic form, the clinical presentation may be seen from weeks to years after delivery. The degree of hormone deficiency determines the clinical presentation. The syndrome may be subclinical in some patients and manifest only if the patient is stressed. Signs and symptoms may be vague and nonspecific: lightheadedness, fatigue, failure to lactate, persistent amenorrhea, decreased body hair, dry skin, loss of libido, nausea and vomiting, and cold intolerance. DI has been reported in severa l cases of Sheehan’s syndrome [8,38]. Pathophysiology The pituitary gland lies in the sella turcica within the sphenoid bone [32]. The pituitary normally enlarges during pregnancy. The gland is comprised of an anterior and posterior lobe, which are anatomically distinct [33]. The blood supply to the anterior pituitary is through the internal carotid arteries and superior hypophyseal arteries. The inferior hypophyseal arteries supply the blood to the posterior pituitary. The anterior pituitary gland produces six major hormones: prolactin (PRL), growth hormone (GH), corticotropin (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH). The posterior pituitary gland produces ADH and oxytocin. The pathogenesis of Sheehan’s syndrome is not understood fully. During pregnancy, the normal pituitary enlarges, predominantly because of pro- gressive lactotroph hyperplasia. Based on extensive pathologic studies of patients, Sheehan proposed pituitary necrosis caused by occlusive spasm of the pituitary vessels. The size of the necrosis depends on the severity, duration, and distribution of the spasm. Massive or submassive ischem ic necrosis of the pituitary gland should result in acute pituitary failure; however, delayed presentation of pituitary failure is common, with patients presenting years later with symptomatology. This slow clinical progression has led some authors to suggest a relationship between postpartum hemorrhage, pituitary anti- bodies, and the development of Sheehan’s syndrome [34–36]. Differential diagnosis Sheehan’s syndrome should be considered in the patient with a recent obstetrical delivery with findings of shock. The differential diagnosi s 837EXTERNAL CAUSES OF METABOLIC DISORDERS The Emergency Department Approach to Newborn and Childhood Metabolic Crisis Ilene Claudius, MD, Colleen Fluharty, MD * , Richard Boles, MD Department of Emergency and Transport Medicine, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, MS113, Los Angeles, CA 90027, USA For most emergency medicine physicians, the phrases ‘‘newborn workup’’ and ‘‘metabolic disease’’ are, at best, uncomfortable. This article, however, provides a simple approach to the recognition, evaluation, and treatment of infants with all manners of metabolic issues, including hypoglycemia, inborn errors of metabolis m, jaundice, and electrolyte abnormalities. The disorders are grouped based on symptomatology, and have simple guidel ines for work-up and management, with an emergency department practitioner perspective in mind. The workup of a newborn with metabolic disease in the emergency department (ED) is a daunting endeavor for any physician. This article provides a simple approach to the recognition, evaluation, and treatment of infants with all manner of metabolic issues, including hypoglycemia, inborn errors of metab olism, jaundice, and electrolyte abnormalities. Hypoglycemia Definition For years, the definition of hypoglycemia in neonates has varied widely, with some authors accepting a blood glucose of 30 mg/dL, while other sources change thresholds as an infant progresses through the first few days of life. More recently, neonatologists have accepted plasma glucose levels !45 mg/dL as a clear indication of hypoglycemia in any symptomatic * Corresponding author. E-mail address: cfluharty@chla.usc.edu (C. Fluharty). 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.03.010 emed.theclinics.com Emerg Med Clin N Am 23 (2005) 843–883 . diagnosi s 83 7EXTERNAL CAUSES OF METABOLIC DISORDERS The Emergency Department Approach to Newborn and Childhood Metabolic Crisis Ilene Claudius, MD, Colleen Fluharty, MD * , Richard Boles, MD Department. skin, loss of libido, nausea and vomiting, and cold intolerance. DI has been reported in severa l cases of Sheehan’s syndrome [8, 38] . Pathophysiology The pituitary gland lies in the sella turcica. metabolis m, jaundice, and electrolyte abnormalities. The disorders are grouped based on symptomatology, and have simple guidel ines for work-up and management, with an emergency department practitioner