ENDOCRINE

DISEASES
BY

CYNTHIA L. DIETRICH, D.O.

November 23, 2004

DIABETES MELLITUS
Problem

in glucose metabolism,
accompanied by predictable longterm vascular and neurologic
complications
Chronic disease
Significant morbidity and mortality

COMPLICATIONS
Hyperglycemia

+/- ketoacidosis
Hypoglycemia: activation of the
sympathetic nervous system
(diaphoresis, tremulousness and
tachycardia) and insufficient delivery
of oxygen to the brain (confusion,
seizures and unconsciousness

Retinopathy- microaneurysms cluster at

macula->terminal vessels obstructed>ischemia->new vessel proliferation
Nephropathy-leads to hypertension. Assoc
with the highest mortality.
Cardiovascular disease- silent ischemia
Peripheral neuropathy- numbness and
tingling progressing to total insensitivity
Stiff joint syndrome- prayer sign and
atlanto-occipital joint involvement

 Autonomic

nervous system
dysfunction
-orthostatic hypotension, resting
tachycardia, absent beat-to-beat
variation
-hypogylcemic unawareness
-gastroparesis occurs in 20-30%

IDDM

Prevalence 0.4%
Onset most often prior to age 20
Environmental influences are superimposed
on a genetic component located on
chromosome 6
Absolute insulin deficiency
Pancreatic beta islet cells are destroyed and
anti-islet cell antibodies appear
Clinical symptoms when 90% of the beta cells
destroyed
Associated with other autoimmune diseases:
rhuematoid arthritis and thyroid disease

Clinical presentation is unmistakable:

hypergylcemia, polyuria, polydipsia, weight
loss, blurred vision and ketoacidosis
Long term management requires exogenous
insulin, self monitoring, lifestyle adaptations
including diet and exercise
Insulin formulations rapid (regular),
intermediate (Lente, NPH) or long-acting
(Ultralente)
Goal- HbA1c less than 7.5%

DKA

Insulin transfers glucose and amino acids

into the cells.
Hyperglycemia->osmotic diuresis>dehydration->acidosis. Also, a build up of
amino acids in the blood->lipolysis->free
fatty acids->converted to ketone bodies in
the liver
Results in a intravascular fluid volume
deficit of 5-8 liters, potassium deficit of 200400 mEq, and NaCl deficit of 350-600 mEq

Treatment of DKA

Intubate for CNS depression

Regular insulin 10 units IVP followed by 510 units/hr IV
Normal saline 5-10 ml/kg/hr IV
Add 5% glucose when serum blood
sugar<250 mg/dl
Potassium 0.3-0.5 mEq/kg/hr IV
Monitor blood sugar, potassium, arterial pH
and urine ketones hourly
Identify cause (sepsis, MI, compliance)

ANESTHETIC MANAGEMENT
Goal- blood sugar between 120-180
mg/dl
Surgery scheduled early in the day
to usual daily dose of intermediate
acting insulin on the morning of surgery
Frequent blood sugar analysis, q 1-2
hours intraop
Treat blood sugar values above 250
mg/dl

Tracheal intubation in patients with

autonomic nervous system neuropathy (pretreat with metoclopramide)
Choice of drugs for induction and
maintenance less important than monitoring
of serum blood sugar
+/- regional anesthesia due to peripheral
neuropathies
Risk of peripheral nerve injury with
positioning
Bradycardia and hypotension may require epi

NIDDM

Obese, sedentary lifestyle, and advancing

age
Prevalence 6.6%
Insulin resistance and a decrease in insulin
secretion
Usual onset after age 40
Insulin resistance is inherited
Ketosis-resistant

Insulin-mediated stimulation of tyrosine

kinase is impaired. This is necessary for
normal function of insulin receptors.
Effect is reversible with improved control of
serum blood sugar
When dietary management fails
hypoglcemic drugs stimulate
endogenenous insulin secretion, or inhibit
gluconeogenesis in the liver and kidneys,
and increase glucose uptake in skeletal
muscles
Duration can be up to 36 hours

HYPEROSMOLAR,
HYPERGLYCEMIC NONKETOTIC
COMA

-elderly, insulin deficiency, renal insufficiency, thirst

deficiency
-sepsis, hyperalimentation or drugs (corticosteriods)
-glucose >600 mg/dl
-osmotic diuresis->hypokalemia and dehydration
-serum osmolarity >350 mOsm/L
-pH >7.3
-hypovolemia (severe, up to 25% total body water)
-patients are insulin deficient but liver insulin levels
sufficient for metabolism of free fatty acids->no
ketosis
-coma due to shrinkage of brain cells

TREATMENT OF HHNC

Regular insulin 10 units IVP then recheck

Isotonic salt solution 2-3 liters over the
first 1-2 hours
Subsequent half-strength saline
When plasma glucose level approaches
normal start D5W
When urine output is resumed supplement
potassium
Remember: this can be reversed with
fluids alone, go slowly

ANESTHETIC MANAGEMENT
Same

as IDDM except omit oral

hypoglycemic the morning of surgery
Keep in mind long duration of action
of oral hypoglycemic drugs
Obesity considerations

GESTATIONAL DIABETES

Glucose intolerance first detected during

pregnancy
2-3% of all pregnancies
Detected in the last trimester
Resembles NIDDM (50% develop NIDDM
within 10 years)
Risk factor for fetal morbidity
Neonatal hypoglycemia
Increased Respiratory Distress Syndrome,
cardiomegaly and congenital abnormalities

THYROID GLAND DYSFUNCTION

Overproduction or underproduction of T3
and/or T4
Negative feedback regulated by the
anterior pituitary gland and the
hypothalmus
T3 and T4 act on cells through the
adenylate cyclase system, producing
changes in speed of biochemical reactions,
total body oxygen consumption, and heat
production

HYPERTHYROIDISM

Prevalence: 2% women, 0.2% men

Decreased TSH and increased T4
Causes: Graves Disease, iatrogenic, Toxic
nodular goiter and Thyroiditis
Signs and symptoms: goiter, tachycardia,
anxiety, tremor, heat intolerance, fatigue,
weight loss, eye signs, skeletal muscle
weakness and atrial fibrillation
Stimulation of the sympathetic nervous
system

TREATMENT OF
HYPERTHYROIDISM

Antithyroid drugs: (methimazole,

carbimazole, propylthiouracil) inhibit
oxidation/formation of iodothyromines
before treatment with radioiodine or
surgery
B-adrenergic antagonists (propranolol,
nadolol, atenolol) decrease some of the
tachycardia, anxiety and tremor
Inorganic iodine inhibits the release of T4
and T3 for a limited time to prepare pts for
surgery or treat thyrotoxic crisis

 Radioiodine

therapy destroys thyroid

tissue
Subtotal thyroidectomy when
radioiodine is refused or a large
goiter is present causing tracheal
compression or cosmetic concerns

ANESTHETIC MANAGEMENT OF
HYPERTHYROIDISM

Elective surgery should be deferred until the

patient is rendered euthyroid and hyperdynamic
state controlled with B-blockers
Preop: anxiolytics and evaluation of upper airway
(CT scan of the neck)
Induction: Thiopental has antithyroid activity (no
ketamine)
Maintenance: isoflurane or sevoflurane (no
halothane) and fentanyl or remi. Attention to body
temp, heart rate and eye protection (exothalmos)
Muscle relaxation: avoid pancuronium and use
glycopyrrolate with reversal agent
Treat hypotension with phenylephrine

COMPLICATIONS OF SUBTOTAL
THYROIDECTOMY

Damage to the recurrent laryngeal nerve when

unilateral->hoarseness, when bilateral->total
airway obstruction
Damage to superior laryngeal nerve can lead
to aspiration
Airway obstruction from tracheomalacia (after
extubation) or hematoma (early postop period)
Hypoparathyroidism-> hypocalcemia develops
24-72 hours postop (but sometimes 1-3 hours
postop)->laryngeal stridor->laryngospasm

THYROTOXIC CRISIS (THYROID

STORM)

Medical emergency
Typically presents 6-18 hours after surgery
Abrupt onset of tachycardia, hyperthermia,
agitation, skeletal muscle weakness,
congestive heart failure, dehydration and
shock due to abrupt release of T4 and T3
into the circulation
Precipitated by surgery, infection, trauma,
toxemia, DKA

TREATMENT OF THYROID
STORM
Intraveneous cooled crystalloid solutions,
acetominophen and cooling blankets
Esmolol infusion with goal heart rate
<100
Potassium iodide to block release of T4
and T3
Propylthiouracil 100 mg po to inhibit
conversion of T4 to T3
Cortisol 100-200 mg IV

HYPOTHYROIDISM

Prevalence 0.5-0.8%
Increased TSH and decreased T4 and T3
Cause is primarily treatment of
hyperthyroidism, medically or surgically or
Hashimotos Thyroiditis
Signs and symptoms: lethargy, hypotension,
bradycardia, CHF, gastroparesis,
hypothermia, hypoventilation, hyponatremia,
and poor mentation
Treatment with Synthroid

ANESTHETIC MANAGEMENT OF
HYPOTHYROISM

Preop meds titrate and consider

supplemental cortisol
Induction: ketamine
Maintenance: nitrous oxide plus short
acting opioids, benzos or ketamine
Low dose muscle relaxants
Controlled ventilation of the lungs
(vulnerable to excessive decrease in PaCO2)
Treat hypotension with ephedrine
Watch for CHF, consider arterial line and PA
catheter

ADRENAL GLAND
DYSFUNCTION
Hypercortisolism= Cushings
Syndrome
2. Hypocortisolism= Addisons
Disease
3. Pheochromocytoma
1.

CUSHINGS SYNDROME

Caused by excessive secretion of

corticotropin by anterior pituitary
corticotroph tumors (microadenomas)
Increased aldosterone, cortisol and
testosterone in the adrenal cortex
Signs and symptoms: hypertension,
hypokalemic alkalosis, hyperglycemia,
hypernatremia, osteoporosis, easy bruising,
polyuria, buffalo hump, moon facies,
excessive body hair, menstrual
abnormalities, weight gain, skeletal muscle
wasting/weakness, depression and insomnia

 Diagnosis

with 24 hour urinary

secretion of cortisol
Dexamethasone suppression test
distinguishes Cushings disease from
the ectopic corticotropin syndrome
Treatment of choice is transsphenoidal
microadenomectomy or 85-90%
resection of the anterior pituitary gland

ANESTHETIC MANAGEMENT

Preop evaluation of systemic blood pressure,

electrolyte balance and the blood glucose
No single anesthetic the best
Replacement therapy hydrocortisone 10 mg/
hr for 24 hours
Treat hypertension and hypervolemia with a
potassium sparing diuretic
Treat hyperglycemia with insulin
Care when positioning patient due to
osteoporosis

CORTISOL
THE

ONLY ESSENTIAL HORMONE FOR

LIFE
Maintains blood pressure by
facilitating the conversion of norepi
to epi
Converts amino acids to glucose
Suppresses inflammation

ADDISONS DISEASE

Absense of cortisol and aldosterone due to

destruction of the adrenal cortex
Causes: hemorrhage in anticoagulated
patients, sepsis, surgical or accidental
trauma
Diagnosis by measurement of plasma
cortisol before and 1 hour after
administration of corticotropin
Signs and symptoms: weight loss, skeletal
muscle weakness, hypotension, fluid
depletion, hyperkalemia, hyponatremia,
hypoglycemia, abdominal/back pain

MANAGEMENT OF A PATIENT
WITH ADDISONS DISEASE
You must give exogenous
corticosteriods!
Intraveneous infusion of sodium
containing fluids
Invasive monitoring with arterial line and
CVP or PA catheter
Frequent measurements of glucose and
electrolytes
Decrease initial dose of muscle relaxants

PHEOCHROMOCYTOMA

Catecholamine-secreting tumor that originates in

the adrenal medulla or in the chromaffin tissues
along the paravertebral sympathetic chain,
extending from the pelvis to the base of the skull
Age: 30-50 years
50% deaths occur during unrelated surgery or
pregnancy
Diagnosis by 24 hour urine for norepinepherine
and CT scan
Associated with Multiple endocrine neoplasia
(MEN)

 Signs

and symptoms: tachycardia,

diaphoresis, headache, hypertension,
hyperglycemia, hypovolemia,
tremulous, palpitations, weight loss
Treatment is surgical excision of the
tumor(s)

ANESTHETIC MANAGEMENT OF
PHEOCHROMOCYTOMA

Correct hypovolemia (serial hematocrits)

Alpha blockade before beta blockade
Alpha blockage: phenoxybenzamine 10-20
mg PO bid for 14 days pre-op
Beta blockade: propranolol 40 mg PO bid
pre-op
Pre-op: benzo with scopalamine
Avoid histamine releasing drugs
Arterial line pre-induction

Induction: etomidate, thiopental or propofol

Lidocaine 1-2 mg/kg prior to intubation
Consider PA catheter
Maintenance: sevoflurane due to rapid
changes in concentration and fentanyl or
remifentanyl
Treat hypertension with phentolamine 1-5 mg
IV or nitroprusside
Treat reflex tachycardia with an esmolol
infusion