Transcript endocrineDiseases

ENDOCRINE DISEASES
DIABETES MELLITUS
Problem in glucose metabolism,
accompanied by predictable long-term
vascular and neurologic complications
 Chronic disease
 Significant morbidity and mortality
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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
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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 atlantooccipital joint involvement
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Autonomic nervous system dysfunction
-orthostatic hypotension, resting
tachycardia, absent beat-to-beat variation
-hypogylcemic unawareness
-gastroparesis occurs in 20-30%
IDDM
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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%
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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 200-400 mEq, and
NaCl deficit of 350-600 mEq
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Treatment of DKA
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Intubate for CNS depression
Regular insulin 10 units IVP followed by 5-10
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
 ¼ to ½ 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
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Tracheal intubation in patients with autonomic
nervous system neuropathy (pre-treat 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
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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
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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
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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
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GESTATIONAL DIABETES
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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
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HYPERTHYROIDISM
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Prevalence: 2% women, 0.2% men
Decreased TSH and increased T4
Causes: Grave’s 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 pt’s for surgery
or treat thyrotoxic crisis
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Radioiodine therapy destroys thyroid
tissue
 Subtotal thyroidectomy when radioiodine
is refused or a large goiter is present
causing tracheal compression or cosmetic
concerns
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ANESTHETIC MANAGEMENT OF
HYPERTHYROIDISM
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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
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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
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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
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HYPOTHYROIDISM
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Prevalence 0.5-0.8%
Increased TSH and decreased T4 and T3
Cause is primarily treatment of hyperthyroidism,
medically or surgically or Hashimoto’s Thyroiditis
Signs and symptoms: lethargy, hypotension,
bradycardia, CHF, gastroparesis, hypothermia,
hypoventilation, hyponatremia, and poor
mentation
Treatment with Synthroid
ANESTHETIC MANAGEMENT OF
HYPOTHYROISM
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Preop meds titrate and consider supplemental
cortisol
Induction: ketamine
Maintenance: nitrous oxide plus short acting
opioids, benzo’s 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
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Hypercortisolism= Cushing’s Syndrome
Hypocortisolism= Addison’s Disease
Pheochromocytoma
CUSHING’S 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
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Diagnosis with 24 hour urinary secretion
of cortisol
 Dexamethasone suppression test
distinguishes Cushing’s disease from the
ectopic corticotropin syndrome
 Treatment of choice is transsphenoidal
microadenomectomy or 85-90% resection
of the anterior pituitary gland
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ANESTHETIC MANAGEMENT
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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
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ADDISON’S 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
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MANAGEMENT OF A PATIENT
WITH ADDISON’S 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
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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)
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Signs and symptoms: tachycardia,
diaphoresis, headache, hypertension,
hyperglycemia, hypovolemia, tremulous,
palpitations, weight loss
 Treatment is surgical excision of the
tumor(s)
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ANESTHETIC MANAGEMENT OF
PHEOCHROMOCYTOMA
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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 preop
Pre-op: benzo with scopalamine
Avoid histamine releasing drugs
Arterial line pre-induction
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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