The Massachusetts General Hospital Handbook of Neurology

Authors: Flaherty, Alice W.; Rost, Natalia S.

Title: Massachusetts General Hospital Handbook of Neurology, The, 2nd Edition

Copyright 2007 Lippincott Williams & Wilkins

> Table of Contents > Medicine > Glands

Glands

A. Adrenal

• Adrenal insufficiency:

  • Neurological complications of adrenal insufficiency: Lethargy, abdominal pain, neurological signs of low sodium (tremor, aphasia, ataxia, seizures, corticospinal tract signs) and high potassium. All male pts. with Addison's dz should be tested for X-linked adrenoleukodystrophy (see p. 144).

  P.199

  • Adrenal crisis is an emergency: Besides the above sx, there is dehydration and high BUN. Look for triggers, e.g., infection, MI.

  • Tests:

    • Cortisol: May be a better screen for adrenal suppression after pro-longed steroid use. Best to do 8 AM cortisol (normal 6-18 g/dL), but in an emergency, draw a random level before giving steroids.

    • ACTH stimulation test: Can be done on dexamethasone. For pts. on prednisone, hold it until after cortisol drawn. Give ACTH (Cortrosyn) 0.25 mg IV; measure cortisol then and 60 min later. Nl >18 g/dL, or >7 g/dL rise.

  • Rx: Immediate hydrocortisone 100 mg IV q8h.

• Adrenal excess (Cushing's syndrome), or exogenous steroids:

  • H&P: See Drugs, p. 173, for signs of adrenal excess.

  • Baseline 8 AM cortisol test: Normal is 6-18 g/dL.

  • Low-dose suppression test: Give dexamethasone 1 mg PO at 11 PM, draw serum cortisol at 8 AM. Cortisol <5 g/dL is normal, 5-10 is indeterminate, and >10 is evidence for Cushing's syndrome.

  • High-dose suppression test: Helps tell pituitary adrenocorticotropic hormone (ACTH) hypersecretion from adrenal tumor or ectopic ACTH secretion. Give dexamethasone 8 mg PO at 11 PM, draw cortisol at 8 AM. In 95% of pituitary ACTH hypersecretion, but not other causes, cortisol will decrease to <50% of baseline. Phenytoin may interfere with this.

B. Diabetes insipidus (DI)

Low antidiuretic hormone (ADH) causes dilute urine, water craving, danger of severely high Na.

• Causes: Pituitary damage, e.g., from surgery, head trauma, transtentorial herniation, neurosarcoid, A-comm aneurysm.

• DDx: Psychosomatic polydipsia, osmotic diuresis, nephrogenic DI.

• Tests: If there is high clinical suspicion, the following four criteria are usually sufficient:

  • Urine osms: 50-150 mOsm/L or specific gravity <1.005.

  • Urine output: >250 cc/h (or >3 cc/kg/h).

  • Serum sodium: Normal or high.

  • Normal adrenal function: The kidney needs mineralocorticoids to make free water, so steroids may unmask DI by correcting adrenal insufficiency.

• Rx: Intranasal desmopressin 10-40 g bid (typically 20 g); titrate to urine output.

  • Post-op transsphenoidal surgery: First try to keep up with fluid loss by IV or PO fluids, as desmopressin sometimes overtreats. Then try desmopressin in above dose range, although you will need to give it SQ or IV until nasal packs are out.

C. Diabetes mellitus

• Neurological complications of DM: Glucose-related mental status changes, neuropathy (see p. 93), increased stroke risk.

  • Hypoglycemia:

    • H&P: Decreased POs or increased DM medications, with variable tremulousness, fatigue, dysarthria, confusion, seizures

      P.200

      (glucose usually <30 mg/dL), coma with pupillary dilatation and extensor posturing (glucose usually <10).

    • Tests: Low fingerstick glucose.

    • Rx: Emergent correction of glucose. Hypoglycemic coma can cause permanent neurological damage.

  • DM ketoacidosis:

    • H&P: Often type 1 DM with precipitating illness. See subacute polyuria followed by anorexia, confusion (glucose >425 mg/dL), coma (glucose >600).

    • Tests: Glucose, anion gap, ketones, osmolarity, ABG.

    • Rx: Correction of glucose, dehydration, potassium. Central pontine myelinolysis can occur when blood osmolarity is lowered more rapidly than brain osmolarity.

  • Nonketotic hyperglycemic coma:

    • H&P: Often type 2 DM with infection. Steroids or phenytoin can sometimes be precipitants. Slower onset than DKA. Cerebral dysfunction and seizures are common.

    • Tests: Glucose, osmolarity, ABG.

    • Rx: First priority is maintaining blood pressure and cardiac output with IV fluid; correct glucose as needed.

• Regular insulin (CZI) sliding scale: See Admission Orders, p. 13. All diabetics should be covered with an insulin sliding scale while in house, even if they take only oral hypoglycemics at home. It is best to stop oral agents while pt. is in hospital, as glucose levels will vary from home levels.

• To convert regular (CZI) to NPH insulin: (2/3)(CZI used qd); give 2/3 of that in AM, 1/3 in PM.

• Insulin preparations:

D. Thyroid

• Neurological complications of hyperthyroidism: Tremor, seizures, brisk reflexes, ophthalmopathy, proximal myopathy.

• Neurological complications of hypothyroidism: Apathy, hung-up reflexes, myopathy, and high CPK. The slow muscle relaxation differs from myotonia in being more painful and worse with exercise. Sometimes see seizures, obstructive sleep apnea, ataxia, hearing loss.

  P.201

  T₃ (triiodothyronine) is better than T₄ (thyroxine) for treating neurological complications.

• Tests: First test TSH. If low, also check T₃, T₄, free T₄, and maybe antithyroid antibodies. If high, check T₄.

E. Parathyroid

Psychiatric sx. Hyperparathyroidism can cause myopathy; hypoparathyroidism can cause seizures and other signs of low calcium and magnesium.