ENDOCRINE DISEASES

BYCYNTHIA L. DIETRICH, D.O.November 23, 2004

DIABETES MELLITUSProblem in glucose metabolism, accompanied by predictable long-term vascular and neurologic complications Chronic diseaseSignificant morbidity and mortality

COMPLICATIONSHyperglycemia +/- ketoacidosisHypoglycemia: 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 proliferationNephropathy-leads to hypertension. Assoc with the highest mortality. Cardiovascular disease- silent ischemiaPeripheral neuropathy- numbness and tingling progressing to total insensitivityStiff 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%

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

Clinical presentation is unmistakable: hypergylcemia, polyuria, polydipsia, weight loss, blurred vision and ketoacidosisLong term management requires exogenous insulin, self monitoring, lifestyle adaptations including diet and exerciseInsulin formulations rapid (regular), intermediate (Lente, NPH) or long-acting (Ultralente)Goal- HbA1c less than 7.5%

DKAInsulin 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 liverResults in a intravascular fluid volume deficit of 5-8 liters, potassium deficit of 200-400 mEq, and NaCl deficit of 350-600 mEq

Treatment of DKAIntubate for CNS depressionRegular insulin 10 units IVP followed by 5-10 units/hr IVNormal saline 5-10 ml/kg/hr IVAdd 5% glucose when serum blood sugar

ANESTHETIC MANAGEMENTGoal- blood sugar between 120-180 mg/dlSurgery scheduled early in the day to usual daily dose of intermediate acting insulin on the morning of surgeryFrequent blood sugar analysis, q 1-2 hours intraopTreat blood sugar values above 250 mg/dl

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 neuropathiesRisk of peripheral nerve injury with positioningBradycardia and hypotension may require epi

NIDDM

Obese, sedentary lifestyle, and advancing agePrevalence 6.6%Insulin resistance and a decrease in insulin secretionUsual onset after age 40Insulin resistance is inheritedKetosis-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 sugarWhen dietary management fails hypoglcemic drugs stimulate endogenenous insulin secretion, or inhibit gluconeogenesis in the liver and kidneys, and increase glucose uptake in skeletal musclesDuration 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 HHNCRegular insulin 10 units IVP then recheckIsotonic salt solution 2-3 liters over the first 1-2 hoursSubsequent half-strength salineWhen plasma glucose level approaches normal start D5WWhen urine output is resumed supplement potassiumRemember: this can be reversed with fluids alone, go slowly

ANESTHETIC MANAGEMENTSame as IDDM except omit oral hypoglycemic the morning of surgeryKeep in mind long duration of action of oral hypoglycemic drugsObesity considerations

GESTATIONAL DIABETESGlucose intolerance first detected during pregnancy2-3% of all pregnanciesDetected in the last trimesterResembles NIDDM (50% develop NIDDM within 10 years)Risk factor for fetal morbidityNeonatal hypoglycemiaIncreased Respiratory Distress Syndrome, cardiomegaly and congenital abnormalities

THYROID GLAND DYSFUNCTIONOverproduction or underproduction of T3 and/or T4Negative feedback regulated by the anterior pituitary gland and the hypothalmusT3 and T4 act on cells through the adenylate cyclase system, producing changes in speed of biochemical reactions, total body oxygen consumption, and heat production

HYPERTHYROIDISMPrevalence: 2% women, 0.2% menDecreased TSH and increased T4Causes: Graves Disease, iatrogenic, Toxic nodular goiter and ThyroiditisSigns and symptoms: goiter, tachycardia, anxiety, tremor, heat intolerance, fatigue, weight loss, eye signs, skeletal muscle weakness and atrial fibrillationStimulation of the sympathetic nervous system

TREATMENT OF HYPERTHYROIDISMAntithyroid drugs: (methimazole, carbimazole, propylthiouracil) inhibit oxidation/formation of iodothyromines before treatment with radioiodine or surgeryB-adrenergic antagonists (propranolol, nadolol, atenolol) decrease some of the tachycardia, anxiety and tremorInorganic 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 tissueSubtotal thyroidectomy when radioiodine is refused or a large goiter is present causing tracheal compression or cosmetic concerns

ANESTHETIC MANAGEMENT OF HYPERTHYROIDISMElective surgery should be deferred until the patient is rendered euthyroid and hyperdynamic state controlled with B-blockersPreop: 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 agentTreat hypotension with phenylephrine

COMPLICATIONS OF SUBTOTAL THYROIDECTOMYDamage to the recurrent laryngeal nerve when unilateral->hoarseness, when bilateral->total airway obstructionDamage to superior laryngeal nerve can lead to aspirationAirway 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 emergencyTypically presents 6-18 hours after surgeryAbrupt onset of tachycardia, hyperthermia, agitation, skeletal muscle weakness, congestive heart failure, dehydration and shock due to abrupt release of T4 and T3 into the circulationPrecipitated by surgery, infection, trauma, toxemia, DKA

TREATMENT OF THYROID STORMIntraveneous cooled crystalloid solutions, acetominophen and cooling blanketsEsmolol infusion with goal heart rate

HYPOTHYROIDISMPrevalence 0.5-0.8% Increased TSH and decreased T4 and T3Cause is primarily treatment of hyperthyroidism, medically or surgically or Hashimotos ThyroiditisSigns and symptoms: lethargy, hypotension, bradycardia, CHF, gastroparesis, hypothermia, hypoventilation, hyponatremia, and poor mentationTreatment with Synthroid

ANESTHETIC MANAGEMENT OF HYPOTHYROISMPreop meds titrate and consider supplemental cortisolInduction: ketamine Maintenance: nitrous oxide plus short acting opioids, benzos or ketamineLow dose muscle relaxantsControlled ventilation of the lungs (vulnerable to excessive decrease in PaCO2)Treat hypotension with ephedrineWatch for CHF, consider arterial line and PA catheter

ADRENAL GLAND DYSFUNCTIONHypercortisolism= Cushings SyndromeHypocortisolism= Addisons DiseasePheochromocytoma

CUSHINGS SYNDROMECaused by excessive secretion of corticotropin by anterior pituitary corticotroph tumors (microadenomas)Increased aldosterone, cortisol and testosterone in the adrenal cortexSigns 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 cortisolDexamethasone 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 glucoseNo single anesthetic the bestReplacement therapy hydrocortisone 10 mg/ hr for 24 hoursTreat hypertension and hypervolemia with a potassium sparing diureticTreat hyperglycemia with insulinCare when positioning patient due to osteoporosis

CORTISOLTHE ONLY ESSENTIAL HORMONE FOR LIFEMaintains blood pressure by facilitating the conversion of norepi to epiConverts amino acids to glucoseSuppresses inflammation

ADDISONS DISEASEAbsense of cortisol and aldosterone due to destruction of the adrenal cortexCauses: hemorrhage in anticoagulated patients, sepsis, surgical or accidental traumaDiagnosis by measurement of plasma cortisol before and 1 hour after administration of corticotropinSigns and symptoms: weight loss, skeletal muscle weakness, hypotension, fluid depletion, hyperkalemia, hyponatremia, hypoglycemia, abdominal/back pain

MANAGEMENT OF A PATIENT WITH ADDISONS DISEASEYou must give exogenous corticosteriods!Intraveneous infusion of sodium containing fluidsInvasive monitoring with arterial line and CVP or PA catheterFrequent measurements of glucose and electrolytesDecrease initial dose of muscle relaxants

PHEOCHROMOCYTOMACatecholamine-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 skullAge: 30-50 years50% deaths occur during unrelated surgery or pregnancyDiagnosis by 24 hour urine for norepinepherine and CT scanAssociated with Multiple endocrine neoplasia (MEN)

Signs and symptoms: tachycardia, diaphoresis, headache, hypertension, hyperglycemia, hypovolemia, tremulous, palpitations, weight lossTreatment is surgical excision of the tumor(s)

ANESTHETIC MANAGEMENT OF PHEOCHROMOCYTOMACorrect hypovolemia (serial hematocrits) Alpha blockade before beta blockadeAlpha blockage: phenoxybenzamine 10-20 mg PO bid for 14 days pre-opBeta blockade: propranolol 40 mg PO bid pre-opPre-op: benzo with scopalamineAvoid histamine releasing drugsArterial line pre-induction

Induction: etomidate, thiopental or propofolLidocaine 1-2 mg/kg prior to intubationConsider PA catheterMaintenance: sevoflurane due to rapid changes in concentration and fentanyl or remifentanylTreat hypertension with phentolamine 1-5 mg IV or nitroprussideTreat reflex tachycardia with an esmolol infusion