Common Endocrine Issues in the Hospitalized Patient

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Common Endocrine Issues in the Hospitalized
Patient

• Jordan L. Geller, M.D.
• Attending Physician Cedars-Sinai Medical Center
  Division of Endocrinology
• Clinical Instructor of Medicine UCLA Geffen
  School of Medicine  

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Evidence Based Questions

• Diabetes
• -What is the optimal blood sugar in a inpatient?
• Thyroid
• -How can I distinguish euthyroid sick syndrome
  from hypothyroidism?
• Adrenal
• -Who is at risk for adrenal failure and what is
  the proper way to distinguish
• primary from secondary causes?
• Calcium
• -How can I urgently treat hypercalcemia without
  obscuring the diagnosis?

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Learning Objectives

• Become aware of common endocrine issues in the
  hospitalized patient
• Review the evidence for treatment of
  four key endocrine topics
• Know what pertinent data to gather for the
  consultant to use later on

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Glycemic Control

• What is the optimal blood
• glucose in an inpatient?

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Rationale for Glycemic Control

• Effects of hyperglycemia
• Fluid balance
• Immune function
• Inflammation
• Thrombosis
• Vascular reactivity

Montori VM et al. JAMA. 2002172167-2169
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Hyperglycemia is associated with bad outcomes

• Increased mortality and CHF in patients with
  acute MI
• Increased mortality, length of stay, prolonged
• nursing home care, higher risk of infection in
  MICU/SICU
• Greater mortality, increased deep-wound
  infections, and
• more overall infection in post-CABG
• Increased mortality, worse recovery in CVA

American Association of Clinical
Endocrinologists, 2004
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insulin improves outcomes
Setting Intervention and Controls Outcome
MICU 80 to 110 mg/dL w/ IV insulin vs conventional (insulin if BGgt 215) Benefit in pts in ICU gt3 days. RR of death declined 18.1 Total cohort improved renal function and vent time (Van Den Berghe et al, 2006)
SICU IV insulin to goal 80-110 mg/dL vs. 180-200 in controls Mortality reduction 34, sepsis 46, ARF 41, transfusions 50, neuropathy 44 (Van Den Berghe et al, 2001)
CSICU IV insulin to goal lt200 mg/dL x 3 postop days vs. sliding scale 57 reduction in sternal infection 66 mortality reduction, lowest w/ glucose lt150 (Furnary AP et al. 1999)
Diabetics with AMI IV insulin for 24 hrs then daily MDI x 3 months (126-180 mg/dL) vs. conventional treatment Long-term survival improved 28 (Malmberg K et al. 1999)
Wards prospective observational studies Hyperglycemia associated with nosocomial infections and mortality (Umpierrez GE et al 2004)
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Hyperglycemia Key Points

• Diabetes is a Vascular Disease
• Regardless of a prior history of DM, keeping
  glucose 80-110 mg/dl leads to better outcomes
• Standardized protocols improve glycemic control
  and lower rates of hypoglycemia
• Follow-up is essential

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Thyroid

• How can I distinguish euthyroid sick syndrome
  from hypothyroidism?

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The euthyroid sick syndrome is an adaptive
response to illness

• Not a primary thyroid disorder
• Results from changes in peripheral thyroid
  hormone metabolism and transport
• Causes include infection, malignancy,
  inflammation, MI, surgery, trauma, starvation

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Thyroid Functions in Acute Illness

• TSH levels normal or slightly low
• Total T4 decreases, and T3 resin uptake increases
  from reduced protein binding
• Free T4 usually normal
• Low total free T3 from impaired conversion of
  T4 to T3 in liver
• Elevated rT3

De Groot LJ et al, 2006
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Distinction of Euthyroid Sick Syndrome from
Hypothyroidism
TSH TT4 FT4 T3 RT3 T3RU
Euthyroid Sick ? ? ? ?? ? ?
Hypothyroid ? ? ? ? ? ?
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Treat Euthyroid Sick Syndrome?

• No consistent or convincing data demonstrating a
  recovery or survival benefit from treating
  euthyroid sick syndrome patients with either
  levothyroxine (LT4) or liothyronine (LT3)

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THYROID KEY POINTS

• Only check TSH if high likelihood of thyroid
  disease
• Euthyroid sick syndrome is an adaptive response
  to illness
• Do not treat euthyroid sick syndrome

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Adrenal

• What is the proper way to distinguish primary
  from secondary adrenal failure?

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Hypothalamic-Pituitary Adrenal Axis

• Secondary disorders more common in the hospital
• Exogenous steroids
• Opiates
• Pituitary adenomas
• Panhypopituitarism
• Stalk disruption
• Subarachnoid hemorrhage

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Diagnosis of Adrenal Failure

• RANDOM TESTING
• Diagnose with a cortisol lt5 µg/dL during severe
  physiologic stress
• Rule-out with a random cortisol gt20 ug/dL
• Simultaneous measurement of ACTH is helpful
• DYNAMIC TESTING
• 250 mcg IV Cosyntropin
• Cortisol level gt20ug/dL after 30-60 minutes
  excludes diagnosis
• Does not rule out a subtle or recent ACTH
  deficiency
• Additional testing (insulin-induced hypoglycemia,
  low dose-ACTH) may be necessary to demonstrate
  appropriate response to stress

Wiebke A et al. Lancet 2003 361 1881-93
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Algorithm for Suspected AI
Levy NT et al. (Mayo Clin Proc 199772818-822)
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ADRENAL KEY POINTS

• Think about adrenal failure
• Empiric dexamethasone will not interfere with the
  measurement of cortisol but will suppress ACTH
• When in doubt, give empiric steroids and reassess
  later on

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Hypercalcemia

• How can I treat hypercalcemia without obscuring
  the diagnosis?

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PTH or non-PTH-Mediated?

• If PTH is upper-normal or high then its likely
  primary hyperparathyroidism
• If PTH is suppressed than its likely malignancy
  or extra-renal vitamin D production
• Ca, urine Ca/cr, 25 and 1,25 vitamin D
• Empirically treat once labs are drawn

Al Zahrani et al. Lancet 1997352306-311
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Volume Replacement

• Calcium gt12 mg/dL requires urgent treatment
• First administer normal saline to enhance
  delivery of calcium to loop of Henle
• Once euvolemic, give loop diuretic to enhance
  calciuresis
• If still hypercalcemic, give loading dose of
  vitamin D along with IV bisphosphonate

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Bisphosphonates for Hypercalcemia

• Zolendronic acid 4 mg or 8 mg IV are superior to
  Pamidronate in hypercalcemia of malignancy
• If given to patients with vitamin D insufficiency
  (50 of the population), profound hypocalcemia
  may occur
• Give loading dose of vitamin D 50,000 units PO

Major P et al., J Clin Onc 2001 19558-567
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CALCIUM KEY POINTS

• Primary hyperparathyroidism and malignancy
  account for gt90 of causes of hypercalcemia
• 10-20 pts with primary hyperparathyroidism have
  iPTH in upper normal range
• Most patients are volume depleted
• Indiscriminate use of bisphosphonates may lead to
  profound hypocalcemia

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Thank You