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Anesthesia and En Doc Raine Diseases

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    ENDOCRINE DISEASESENDOCRINE DISEASES

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    Endocrine ConsiderationsEndocrine Considerations

    in Anesthesiain Anesthesia

    Thyroid

    Diabetes

    Adrenal Gland

    Pituitary Gland

    Liver

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    Thyroid Gland HormonesT

    hyroid Gland HormonesThyroid Hormones

    1. Thyroxine (T4)

    2. Triiodothyronine (T3)

    A. Major regulators of cellular metabolic processes

    B. Essential for neurological and cardiopulmonary

    function

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    Thyroid Gland HormonesT

    hyroid Gland Hormones Thyrotropin (TSH) produced in anterior

    Pituitary gland

    TSH secretion regulated by hypothalamus

    hormone thyrotropin-releasing hormone

    (TRH)

    (T4) & (T3) regulation by TRH & TSH

    balance

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    Thyroid Gland ConsiderationsThyroid Gland Considerations

    in Anesthesiain Anesthesia

    Cardiovascular manifestations

    Heat regulation

    Metabolism

    Oxygen consumption

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    Thyroid Gland ConsiderationsThyroid Gland Considerations

    in Anesthesiain Anesthesia Thyroid hormones directly affect tissue

    responses to sympathetic stimuli

    Beta-adrenergic oby thyroid hormone

    Alpha-adrenergic qby thyroid hormone

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    HyperthyroidismHyperthyroidism1. Graves disease 20-40 y/o

    Predominantly female

    Opthalmopathy

    Dermopathy

    Club fingers

    2. Thyroiditis

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    HyperthyroidismHyperthyroidism3. Hashimoto

    (usually hypo but sometimes hyper)

    4. Adenomas

    5. Carcinoma

    6. Amiodarone drug induced(rich in iodine pthyrotoxicosis)

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    Hyperthyroidism SymptomsHyperthyroidism Symptoms Heat intolerance

    Nervous

    Weight loss

    Tachycardia

    Diarrhea

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    Tests ofThyroid Gland FunctionTests ofThyroid Gland FunctionLaboratory DeterminationsLaboratory Determinations

    Total plasma thyroxine (T4)

    = Detects > 90% of hyperthyroid patients

    Resin triiodothyronine uptake (RT3U)

    Clarifies if T4 changes are due to thyroid

    dysfunction or alterations in T4 - binding

    globulin

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    Tests ofThyroid Gland FunctionTests ofThyroid Gland Function

    Laboratory DeterminationsLaboratory Determinations Total plasma triiodothyronine (T3)

    Confirms diagnosis of hyperthyroidism

    Thyroid stimulating hormone (TSH)

    Confirms diagnosis of primary hypothyroidism

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    Tests ofThyroid GlandTests ofThyroid Gland

    FunctionFunction Thyroid scan

    Demonstrates iodide-concentrating

    of the capacity of thyroid gland

    Ultrasonography

    Distinguishes between cystic and solid

    nodules Antibodies

    Distinguishes Hashimotos thyroiditis from

    cancer

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    Differential Diagnosis ofDifferential Diagnosis of

    Thyroid Gland DysfunctionThyroid Gland DysfunctionT4 RT3U T3 TSH

    Hyperthyroidism Incr. Incr. Incr. Decr

    Hypothyroidism (P) Decr. Decr. Decr. Incr.

    Hypothyroidism (S) Decr. Decr. Decr. Decr.

    Pregnancy Incr. Decr. Normal Normal

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    HyperthyroidismHyperthyroidism

    SymptomsSymptoms

    Anxiety

    Heat intolerance

    Fatigue

    Skeletal muscle weakness

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    HyperthyroidismHyperthyroidism

    Goiter

    Tachycardia

    Atrial fibrillation

    Tremor

    Eye signs (proptosis) Weight loss

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    HyperthyroidismHyperthyroidism

    TreatmentTreatment

    Antithyroid drugs

    (propylthiouracil, methimazole)

    Propranolol

    Radioactive iodine

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    Subtotal ThyroidectomySubtotal ThyroidectomyComplicationsComplications

    Airway obstruction

    Hypoparathyroidism

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    Subtotal ThyroidectomySubtotal ThyroidectomyIntraoperative HazardsIntraoperative Hazards

    Circulatory disturbances

    Thyroid stormCooled saline infusion

    Esmolol

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    Subtotal ThyroidectomySubtotal Thyroidectomy

    Preoperative MeasuresPreoperative Measures

    Normalize thyroid function

    Utilize beta sympathetic blockers

    Avoid anticholinergic drugs

    Evaluate upper airway

    (computed tomography)

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    HypothyroidismHypothyroidism

    Symptoms & SignsSymptoms & Signs

    Lethargy

    Intolerance to cold

    Bradycardia

    Peripheral vasoconstriction

    Adrenocortical atrophy Hyponatremia

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    HypothyroidismHypothyroidism

    Adverse ResponsesAdverse Responses

    Sensitivity to depressant drugs (opioids)

    Hypodynamic circulation

    Slowed metabolism (drugs)

    Impaired ventilatory responses

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    HypothyroidismHypothyroidism

    Anesthetic ManagementAnesthetic Management Preoperative = supplemental hydrocortisone

    Induction = ketamine

    Maintenance = ultrashort acting drugs

    Postoperative = never extubation until patient

    is responsive and normothermic

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    THYROTOXIC CRISISTHYROTOXIC CRISIS

    (THYROID STORM)(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 THYROIDTREATMENT OF THYROID

    STORMSTORM Intraveneous cooled crystalloid solutions,

    acetominophen and cooling blankets

    Esmolol infusion with goal heart rate

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    ParathyroidParathyroid

    parathyroid hormones:parathyroid hormones:parathormonparathormon(PTH)(PTH)

    calcitoninecalcitonine

    act on bon kidney and gutact on bon kidney and gutPTH stimulate bonPTH stimulate bon resorptionresorption and inhibit renaland inhibit renal

    excretion of calcium lead toexcretion of calcium lead to hypercalcemiahypercalcemia

    calcitoninecalcitonine can be considered an antagonist tocan be considered an antagonist to

    PTHPTH

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    Parathyroid Gland DysfunctionParathyroid Gland Dysfunction

    Disturbance of calcium levels

    Muscle weaknessPolyuria and polydipsia

    Abdominal pain, vomiting

    Somnolence, psychosisInsensitivity to pain

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    HypercalcemiaHypercalcemia SignsSigns

    Renal Decreased GFR, stone formation

    Cardiac Hypertension, prolonged P-R, short Q-T

    Gastrointestinal

    Peptic ulcer, pancreatitis

    Skeletal Bone demineralization

    Ocular Band keratopathy, conjunctivitis

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    HypocalcemiaHypocalcemia Acute symptoms and signs

    Perioral paresthesias

    Restlessness

    Neuromuscular irritability (positive Chvostek or

    Trousseau sign, inspiratory stridor)

    Chronic symptoms and signs (renal failure)

    Fatigue, muscle weakness

    Prolonged Q-T interval

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    DIABET

    ES MELLITU

    SDIABET

    ES MELLITU

    S Problem in glucose metabolism,

    accompanied by predictable long-term

    vascular and neurologic complications

    Chronic disease

    Significant morbidity and mortality

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    COMPLICAT

    IONSCOMPLICAT

    IONS 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 tinglingprogressing to total insensitivity

    Stiff joint syndrome- prayer sign and atlanto-occipital 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%

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    Diabetes and Heart Failure:Diabetes and Heart Failure:

    Current KnowledgeCurrent Knowledge

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    Relation of GlucoseRelation of Glucose

    Tolerance Status to LVMTolerance Status to LVM

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    IDDMIDDM Prevalence 0.4%

    Onset most often prior to age 20

    Environmental influences are superimposed on agenetic 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 cellsdestroyed

    Associated with other autoimmune diseases:rhuematoid arthritis and thyroid disease

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    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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    DKADKA 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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    ANESTHETICANESTHETIC

    MANAGEMENTMANAGEMENT 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

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    Tracheal intubation in patients with autonomicnervous system neuropathy (pre-treat withmetoclopramide)

    Choice of drugs for induction and maintenanceless important than monitoring of serum bloodsugar

    +/- regional anesthesia due to peripheralneuropathies

    Risk of peripheral nerve injury with positioning

    Bradycardia and hypotension may require epi

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    NIDDMNIDDM

    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

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    Insulin-mediated stimulation of tyrosine kinase isimpaired. This is necessary for normal function ofinsulin receptors.

    Effect is reversible with improved control ofserum blood sugar

    When dietary management fails hypoglcemicdrugs 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,HYPEROSMOLAR,

    HYPERGLYCEMICHYPERGLYCEMIC

    NONKETOTIC COMANONKETOTIC 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 sufficientfor metabolism of free fatty acids->no ketosis

    -coma due to shrinkage of brain cells

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    T

    REAT

    MENT

    OF HHNCT

    REAT

    MENT

    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 normalstart D5W

    When urine output is resumed supplementpotassium

    Remember: this can be reversed with fluids alone,go slowly

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    ANESTHETICANESTHETIC

    MANAGEMENTMANAGEMENT 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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    GEST

    AT

    IONAL DIABET

    ESGEST

    AT

    IONAL DIABET

    ES Glucose intolerance first detected during

    pregnancy

    2-3% of all pregnancies

    Detected in the last trimester

    Resembles NIDDM (50% develop NIDDM within10 years)

    Risk factor for fetal morbidity Neonatal hypoglycemia

    Increased Respiratory Distress Syndrome,cardiomegaly and congenital abnormalities

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    ADRENAL GLANDADRENAL GLAND

    DYSFUNCTIONDYSFUNCTION1. Hypercortisolism= Cushings Syndrome

    2. Hypocortisolism= Addisons Disease

    3. Pheochromocytoma

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    CUSHINGS SYNDROMECUSHINGS SYNDROME

    Caused by excessive secretion of corticotropin byanterior pituitary corticotroph tumors(microadenomas)

    Increased aldosterone, cortisol and testosterone inthe adrenal cortex

    Signs and symptoms: hypertension, hypokalemicalkalosis, hyperglycemia, hypernatremia,

    osteoporosis, easy bruising, polyuria, buffalohump, moon facies, excessive body hair,menstrual abnormalities, weight gain, skeletalmuscle wasting/weakness, depression andinsomnia

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    Diagnosis with 24 hour urinary secretion of

    cortisol

    Dexamethasone suppression test

    distinguishes Cushings disease from the

    ectopic corticotropin syndrome

    Treatment of choice is transsphenoidalmicroadenomectomy or 85-90% resection

    of the anterior pituitary gland

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    ANESTHETICANESTHETIC

    MANAGEMENTMANAGEMENT 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

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    CORTISOLCORTISOL

    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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    ADDISONS DISEASEADDISONS DISEASE

    Absense of cortisol and aldosterone due todestruction of the adrenal cortex

    Causes: hemorrhage in anticoagulated patients,sepsis, surgical or accidental trauma

    Diagnosis by measurement of plasma cortisolbefore and 1 hour after administration ofcorticotropin

    Signs and symptoms: weight loss, skeletal muscleweakness, hypotension, fluid depletion,hyperkalemia, hyponatremia, hypoglycemia,abdominal/back pain

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    MANAGEMENT OF A PATIENTMANAGEMENT OF A PATIENT

    WITH ADDISONS DISEASEWITH 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

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    PheochromocytomaPheochromocytoma

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    PheochromocytomaPheochromocytoma

    1. Catecholamine Physiology/Pathophysiology2. Clinical Presentation

    1. Epidemiology

    2. Signs & Symptoms

    3. Diagnosis1. Biochemical

    2. Localization

    4. Management1. Preoperative

    2. Operative

    3. Postoperative

    4. Pregnancy

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    Catecholamine Producing TumorsCatecholamine Producing Tumors

    Neural Crest

    Sympathoadrenal ProgenitorCell

    (Neuroblasts)

    Chromaffin Cell Sympathetic Ganglion Cell

    Intra-adrenal Extra-adrenal

    PheochromocytomaGanglioneuroma

    Neuroblastoma

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    Pheochromocytoma

    Paraganglioma (extra-adrenal pheo) Originate in extra-adrenal sympathetic chain/chromaffin tissue

    Ganglioneuroma Behave like paraganglioma biochemically

    Neuroblastoma Common malignancy in children, adrenal or sympathetic chain

    Catecholamine humoral effects usually minor

    Rapid growth & widespread metastasis

    Some differentiate and spontaneously regress

    Rx complex (surgery, XRT, chemotherapy)

    Catecholamine Producing TumorsCatecholamine Producing Tumors

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    Cheodectoma Carotid body, behave like paraganglioma biochemically

    Glomus jugulare tumor Intracranial branch ofCN IX and X

    Behave like paragangliomoa biochemically

    Catecholamine Producing TumorsCatecholamine Producing Tumors

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    Tyrosine L-Dopa Dopamine

    Norepinephrine

    Epinephrine

    Catecholamines

    Normetanephrine

    Metaneprine

    PNMT

    DBH

    COMT

    COMT

    Metabolites

    Homovanillic acid

    (HVA)

    MAO, COMT

    Vanillymandelic Acid

    (VMA)

    MAO

    MAOTumor Secretion: Large Pheo: more metabolites

    (metabolized within tumor before release)

    Small Pheo: more catecholamines

    Sporadic Pheo:Norepi > Epi

    Familial Pheo: Epi > Norepi

    Paraganglioma:Norepi

    Cheodectoma, glomus jugulare:Norepi

    Gangioneuroma:Norepi

    Malignant Pheo: Dopamine, HVA

    Neuroblastoma: Dopamine, HVA

    TH

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    Adrenergic ReceptorsAdrenergic Receptors

    Alpha-Adrenergic Receptors E1: vasoconstriction, intestinal relaxation, uterine

    contraction, pupillary dilation

    E2: qpresynaptic NE (clonidine), platelet aggregation,

    vasoconstriction, q insulin secretion

    Beta-Adrenergic Receptors F1: o HR/contractility, o lipolysis, o renin secretion

    F2: vasodilation, bronchodilation, o glycogenolysis

    F3: o lipolysis, obrown fat thermogenesis

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    PheochromocytomaPheochromocytoma

    0.01-0.1% of HTN population Found in 0.5% of those screened

    M = F

    3rd to 5th decades of life

    Rare, investigate only if clinically suspicion: Signs or Symptoms

    Severe HTN, HTN crisis

    Refractory HTN (> 3 drugs)

    HTN present @ age < 20 or > 50 ?

    Adrenal lesion found on imaging (ex. Incidentaloma)

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    Pheo: Paroxysms, SpellsPheo: Paroxysms, Spells

    10-60 min duration

    Frequency: daily to monthly

    Spontaneous Precipitated:

    Diagnostic procedures, I.A. Contrast (I.V. is OK)

    Drugs (opiods, unopposed F-blockade, anesthesia induction,histamine, ACTH, glucagon, metoclopramide)

    Strenuous exercise, movement that increases intra-abdopressure (lifting, straining)

    Micturition (bladder paraganlgioma)

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    Pheo: HypPheo: Hypootension!tension!

    Hypotension (orthostatic/paroxysmal)

    occurs in many patients

    Mechanisms: ECFv contraction

    Loss of postural reflexes due to prolonged

    catecholamine stimulation

    Tumor release of adrenomedullin (vasodilatory

    neuropeptide)

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    Pheo: Signs & SymptomsPheo: Signs & Symptoms

    N/V, abdo pain, severe constipation (megacolon)

    Chest-pains Anxiety

    Angina/MI with normal coronaries:

    Catecholamine induced: o myocardial oxygen consumption orcoronary vasospasm

    CHF HTN hypertrophic cardiomyopathy diastolic dysfn.

    Catechols induce dilated cardiomyopathy systolic dysfn.

    Cardiac dysrhythmia & conduction defects

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    Pheo: Signs (metabolic)Pheo: Signs (metabolic)

    Hypercalcemia

    Associated MEN2 HPT

    PTHrP secretion by pheo

    Mild glucose intolerance

    Lipolysis

    Weight-loss Ketosis > VLDL synthesis (TG)

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    Pheo: Rule of 10Pheo: Rule of 10

    10% extra-adrenal (closer to 15%)

    10% occur in children

    10% familial (closer to 20%)

    10% bilateral or multiple (more if familial)

    10% recur (more if extra-adrenal)

    10% malignant

    10% discovered incidentally

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    24h Urine Collection24h Urine Collection

    24h urine collection: Creatinine, catecholamines, metanephrines,

    vanillymandelic acid (VMA), +/-dopamine

    HPLC with electrochemical detection or mass spect

    Positive results (> 2-3 fold elevation): 24h Ucatechols > 2-fold elevation

    ULN for total catechols 591-890 nmol/d

    24h Utotal metanephrines > 1.2 ug/d (6.5 umol/d)

    24h UVMA > 3-fold elevation

    ULN 35 umol/d for most assays

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    24h Urine Collection24h Urine Collection

    Test Characteristics:

    24h Ucatechols Sen 83% Spec 88%

    24h Utotal metanephrines Sen 76% Spec 94% 24h Ucatechols + Utotal metanephrines Sen 90% Spec 98%

    24h UVMA Sen 63% Spec 94%

    Sensitivity increased if 24h urine collection

    begun at onset of a paroxysm

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    2424h Urine: False Positiveh Urine: False Positive

    Drugs: TCAs, MAO-i, levodopa, methyldopa,

    labetalol, propanolol, clonidine (withdrawal), ilicit

    drugs (opiods, amphetamines, cocaine), ethanol,sympathomimetics (cold remedies)

    Hold these medications for 2 weeks!

    Major physical stress (hypoglycemia, stroke,

    raised ICP, etc.)

    OSA

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    Plasma MetanephrinesPlasma Metanephrines

    Not postural dependent: can draw normally

    Secreted continuously by pheo

    SEN 99% SPEC 89%

    False Positive: acetaminophen

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    Biochemical Tests: SummaryBiochemical Tests: Summary

    SEN SPEC

    Ucatechols 83% 88%

    Utotal metanephrines 76% 94%Ucatechols+metaneph 90% 98%

    UVMA 63% 94%

    Plasma catecholamines 85% 80%

    Plasma metanephrines 99% 89%

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    Suppression/Stimulation TestingSuppression/Stimulation Testing

    Clonidine suppression

    May precipitate hypotensive shock!

    Unlike normals, pheo patients wont suppress theirplasma norepi with clonidine

    Glucagon stimulation

    May precipitate hypertensive crisis!

    Pheo patients, but not normals, will have a > 3x

    increase in plasma norepi with glucagon

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    Localization: ImagingLocalization: Imaging

    CT abdomen

    Adrenal pheo SEN 93-100%

    Extra-adrenal pheo SEN 90%

    MRI

    > SEN than CT for extra-adrenal pheo

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    Localization: ImagingLocalization: Imaging

    CT abdomen

    Adrenal pheo SEN 93-100%

    Extra-adrenal pheo SEN 90%

    MRI

    > SEN than CT for extra-adrenal pheo

    MIBG Scan SEN 77-90% SPEC 95-100%

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    MIBG ScanMIBG Scan

    123I or131I labelled metaiodobenzylguanidine

    MIBG catecholamine precurosr taken up by the

    tumor Inject MIBG, scan @ 24h, 48h, 72h

    Lugols 1 gtt tid x 9d (from 2d prior until 7d afterMIBG injection to protect thyroid)

    False negative scan: Drugs: Labetalol, reserpine, TCAs, phenothiazines

    Must hold these medications for 4-6 wk prior to scan

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    Localization: Nuclear medicineLocalization: Nuclear medicine

    MIBG

    111Indium-pentreotide

    Some pheo have somatostatin receptors

    PET

    18F-fluorodeoxyglucose (FDG)

    6-[18

    F]-fluorodopamine

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    Pheo ManagementPheo Management

    Prior to 1951, reported mortality for excision ofpheochromoyctoma 24 - 50 %

    HTN crisis, arrhythmia, MI, stroke

    Hypotensive shock

    Currently, mortality: 0 - 2.7 % Preoperative preperation, E-blockade? New anesthetic techniques?

    Anesthetic agents

    Intraoperative monitoring: arterial line, EKG monitor, CVPline, Swan-Ganz

    Experienced & Coordinated team: Endocrinologist, Anesthesiologist and Surgeon

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    Preop W/upPreop W/up

    CBC, lytes, creatinine, INR/PTT

    CXR

    EKG

    Echo (r/o dilated CMY 2 catechols)

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    Preop Preperation RegimensPreop Preperation Regimens

    Combined E + Fblockade Phenoxybenzamine

    Selective E1-blocker (ex. Prazosin)

    Propanolol

    Metyrosine

    CalciumChannel Blocker (CCB) Nicardipine

    No Randomized Clinical Trials to comparevarious regimens!

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    Preop:Preop: EE ++ FF blockadeblockade

    Start at least 10-14d preop Allow sufficient time for ECFv re-expansion

    Phenoxybenzamine Special pharmacy access only (no DIN)

    Drug of choice

    Covalently binds E-receptors (E1 > E2)

    Start 10 mg po bid increase q2d by 10-20 mg/d

    Increase until BP cntrl and no more paroxysms

    Maintenance 40-80 mg/d (some need > 200 mg/d)

    Salt load:NaCl 600 mg od-tid as tolerated

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    Preop:Preop: EE ++ FF blockadeblockade

    Phenoxybenzamine (contd) Side-effect: orthostasis with dosage required to normalized

    seated BP, reflex tachycardia

    Drawback: periop hypotension/shock unlikely to respond topressor agent.

    Selective E1-blockers Prazosin, Terazosin, Doxazosin

    Some experience with Prazosin for Pheo preop prep

    Not routinely used as incomplete E-blockade Less orthostasis & reflex tachycardia then phenoxybenzamine

    Used more for long-term Rx (inoperable or malignant pheo)

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    Preop:Preop: EE ++ FF blockadeblockade

    F-blockade Used to control reflex tachycardia and prophylaxis

    against arrhythmia during surgery Start only after effective E-blockade (may ppt HTN)

    If suspect CHF/dilated CMY start low dose

    Propanolol most studied in pheo prep

    Start 10 mg po bid

    increase to cntrl HR

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    Preop:Preop: EE ++ FF blockadeblockade

    If BP still not cntrl despite E +Fblockade Add Prazosin to Phenoxybenzamine

    Add CCB, ACE-I Avoid diuretics as already ECFv contracted

    Metyrosine

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    Preop:Preop: EE ++ FF blockadeblockade

    Meds given on AM of surgery

    Periop HTN:

    IV phentolamine Short acting non-selective E-blocker

    Test dose 1 mg, then 2-5 mg IV q1-2h PRN or as continuous

    infusion (100 mg in 500cc D5W, titrate to BP)

    IV Nitroprusside (NTP)

    Periop arrhythmia: IV esmolol Periop Hypothension: IV crystalloid +/- colloid

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    Pheo: Rx of HTN CrisisPheo: Rx of HTN Crisis

    IV phentolamine

    IV NTP

    IV esmolol

    IV labetalol combined E + Fblocker

    P M t iP M t i

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    Preop: MetyrosinePreop: Metyrosine

    Synthetic inhibitor of Tyrosine

    Hydroxylase (TH)

    Special pharm access, no DIN

    Start 250 mg qid max 1 gm qid

    Severe S/Es: sedation, extrapyramidal, diarrhea,nausea/vomit, anxiety, renal/chole stones, galactorrhea

    Alone may insufficiently cntrl BP and reported HTN crises

    during pheo operation Restrict use to inoperable/malignant pheo or as adjunct toE +Fblockade or other preop prep

    Tyrosine L-Dopa Dopamine

    Norepinephrine

    Epinephrine

    PNMT

    DBH

    TH

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    Preop: CCBPreop: CCB

    Cleveland Clinic Experience Only 6 cardiovascular complications

    All occurred in patients with preop E-blockade

    30% received no medications preop if no HTN

    Patients not receiving phenoxybenzamine required less fluids

    (956 cc intraop, 479 cc POD#1)

    CCB

    Block norepi mediated Ca transport into vascular smoothmuscle

    Nicardipine: most commonly used agent

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    Preop: CCBPreop: CCB

    Nicardipine (France Study) Started po 24h to few weeks preop to cntrl BP and allow ECFv

    restoration

    After intubation IV Nicardipine gtt (start 2.5 ug/kg/min)

    IV Nicardipine adjusted to SBP

    Stopped prior to ligation of tumor venous drainage

    Tachycardia Rx with concurrent IV esmolol

    Advantage:periop hypotension may still respondto pressor agents as opposed to those patients who

    are completely E-blocked

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    Preop: CCBPreop: CCB

    Cleveland Clinic: Only 10% received phenoxybenzamine

    CCB 1st line agents as preop po med

    Selective E1-blockers (Prazosin, Terazosin,Doxazosin) added to CCB if BP still high

    Periop arrythmia: IV esmolol

    Periop HTN: IV NTP

    Periop hypotension: IV crystalloid or colloid

    Dopamine, norepi, epi, phenylephrine

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    O.R.O.R.

    Admit night before for overnight IV saline

    Arterial line, EKG monitor, CVP line

    Known CHF: consider Swan-Ganz

    Regardless of preop medications: Have ready: IV phentolamine, IV NTP, IV esmolol

    Rx hypotension with crystalloid +/- colloid 1st

    Aim forC

    VP 12 or Wedge 15 Inotropes may not work!

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    O.R.O.R.

    Anesthetic choice:

    Enflurane or isoflurane: dont sensitized

    myocardium to catecholamines Halothane: may sensitize heart arrhythmia

    Laprascopic adrenalectomy if tumor < 8cm

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    PostopPostop

    Most cases can stop all BP meds postop

    Postop hypotension: IV crystalloid

    HTN free: 5 years 74% 10 years 45%

    24h urine collection 2 wk postop

    Surveillance:

    24h urine collections q1y for at least 10y Lifelong f/up

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    Pheo: Unresectable, MalignantPheo: Unresectable, Malignant

    E-blockade Selective E1-blockers (Prazosin, Terazosin, Doxazosin) 1st line

    as less side-effects

    Phenoxybenzamine: more complete E-blockade F-blocker CCB, ACE-I, etc.

    Nuclear Medicine Rx:

    Hi dose 131I-MIBG or111indium-octreotide depending onMIBG scan or octreoscan pick-up

    Sensitize tumor with Carboplatin + 5-FU

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    Pheo & PregnancyPheo & Pregnancy

    Diagnosis with 24h urine collections and MRI

    No stimulation tests, no MIBG if pregnant

    1st & 2nd trimester (< 24 weeks): Phenoxybenzamine + Fblocker prep

    Resect tumor ASAP laprascopically

    3rd trimester:

    Phenoxybenzamine + Fblocker prep When fetus large enough: cesarian section followed by tumor

    resection

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    ISSUES OF THEISSUES OF THE

    PITUITARY ANDPITUITARY ANDANESTHESIAANESTHESIA

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    PITUITARY ISSUESPITUITARY ISSUES

    Acromegaly

    SIADH

    DI

    Empty Sella Syndrome

    Pituitary Dwarfism

    Pituitary Infarction (apoplexy)

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    PITUITARY ISSUESPITUITARY ISSUES

    What hormones?

    =6

    ACTH

    GH

    TSH

    FSH LH

    PROLACTIN

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY

    Excess GH (somatotropin)

    Promotes growth by Inc. rate of protein synthesis and dec. rate of protein

    breakdown (occurs rapidly)

    Inc mobilization of fatty acids for energy; enhances

    conversion fatty acids to acetyl co-enzymeA(requires several hrs to occur)

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    PITUITARY ISSUESPITUITARY ISSUES

    Acromegaly

    May be insulin resistant b/o diabetogenic effect

    of GH Affects bone growth and density by

    Inc. deposit of pro by chondrocytes&osteogenic

    cells

    Inc rate of cell reprod

    result-=deposit new bone

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    PITUITARY ISSUESPITUITARY ISSUES

    Acromegaly

    Bone growth (lengthening) occurs b/o

    effects of somatomedins (=insulin-likegrowth factors)

    Formed by the liver

    insufficiency=some forms of dwarfism

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    PITUITARY ISSUESPITUITARY ISSUES

    GH t1/2 = 20 min

    Somatocedin t1/2 = 20 hrs

    GH normally diminishes by age after

    adolescence (to 25% in elderly)

    Inc first 2 hrs deep sleep

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY

    S&S

    Enlargement hands and feet (Bone enlarge.)

    Enlarge soft tissue

    Lips, tongue, epiglottis, vocal cords

    Enl membraneous bonesCranium, nose, supraorb ridges, lower jaw, kyphosis

    engorge liver and kidneys

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY contd

    Subglottic tracheal narrowing

    Peripheral nerve/artery entrapmentConnective tissue overgrowth=recurrent laryng.

    N. paralysis

    Increased incide: HTN, IHD, osteoporosis and

    osteoarthritis

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY

    Coarse facial hair

    R laryngeal n paralysis Stridor

    Cricoarytenoid involvement

    Inc lung volumes with V/Q mismatch

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY

    Special airway concerns

    Difficult mask fit b/o facial anatomy distortion Difficult mask ventilation

    May be difficult intub b/o size of airway

    May require awake FOB

    Prone to subglottic stenosis

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    PITUITARY ISSUESPITUITARY ISSUES

    ACROMEGALY AND ANESTHESIAMANAGEMENT

    In addition to airway issues, remember tomonitor glucose

    Titrate muscle relax if h/o skeletal muscleweakness

    C

    onsiderations re: HTN, IHD Regionals may be difficult b/o skeletal changes

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH

    Syndrome of inappropriate antidiuretic hormone

    Characterized by hyponatremia b/o H2O retention;inapprop for plasma osmolality/plasma sodium

    conc.

    HALLMARK: hyponatremia in presence ofurinary osmolality higher than plasma osmolality

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH

    Inappropriate secretion antidiuretic hormone

    Intracranial tumors Hypothyroidism

    Lung CA

    Common after surgery (transient)

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH

    Normally:

    Serum: low Na, low osmolality

    Urine: low osmolality (dilute)=rid serum of

    extra H2O

    SIADH Serum: low Na, low osmolality

    Urine: high osmolality (concentrated)

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH

    Suspect in

    HYPONATREMIA

    Excreting urine that is hypertonic rel to plasma

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH

    Diagnosed by

    Low serum BUN, Cr, uric acid, albumin

    Serum sodium

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    PITUITARY ISSUESPITUITARY ISSUES

    ISADH

    Diagnosis

    Inapprop inc in urinary Na concentration

    Dec plasma osmolarity

    Inc urine osmolarity

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    PITUITARY ISSUESPITUITARY ISSUES

    ISADH

    Treatment

    Fluid restriction

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    PITUITARY ISSUESPITUITARY ISSUES

    SIADH S&S

    Hypertension b/o fld overload

    Hypokalemia

    Hyperglycemia

    Skeletal muscle weakness

    Osteoporosis

    Truncal obesity

    Hirsutism

    Menstrual abnormalities Poor wound healing/suscept to infections

    Emotional changes

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    PITUITARY ISSUESPITUITARY ISSUES

    DIABETES INSIPIDUS (DI)

    Caused by impaired renal conservation of

    H2O/results from low blood levels of ADH andreflects deficient ADH release

    Posterior pituitary-Vasopressin def

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    PITUITARY ISSUESPITUITARY ISSUES

    DI-Etiology

    Neurogenic

    Intracranial trauma, hypophysectomy, neoplasticinvasion, sarcoidosis

    Nephrogenic

    Hypokalemia, hypercalcemia, sickle cell anemia,

    obstructive uropathy, chronic renal insufficiency,lithium toxicity

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    PITUITARY ISSUESPITUITARY ISSUES

    Presentation

    Polydipsia

    Polyuria Poorly concentrated urine despite inc. plasma

    osmolarity

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    PITUITARY ISSUESPITUITARY ISSUES

    DI

    Treatment:

    Careful monitoring urine, plasma vol & plasmaosmolarity

    Isotonic flds until osmolar >290

    Osmolar >290=hypotonic fldsNeurogenic=desmopressin

    Nephrogenic: chlorpropamide

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA TUMORS

    Functioning (secretory) vs nonfunctioning

    Nonfunctioning are dx b/o enlargement=creates

    symptoms assoc with pressure on surrounding tissue h/a

    Visual changes

    Cranial n. palsies

    Inc ICP

    Hypopituitarism

    Chromophobe adenomas, carniopharyngiomas, meningiomas

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIANonfunctioning tumors may produce

    symptoms that are global/selective.

    Pituitary function may be impaired b/opressure of tumor on normal pituitary tissue

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Microadenomas=no mass effects

    Prolactin secreting

    ACTH secreting (Cushings)

    GH secreting (acromeg)

    CT scan and MRI will eval ICP

    Perioperative short term steroids

    Visual exam to evaluate optic chiasm

    Otolaryngol eval with nasal cultures preop

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA FUNCTIONING TUMORS

    Early diag b/o excessive hormone prod.

    Most commonly adenomas. GH secreting=gigantism (prepuberty)

    = acromegaly (postpuberty)

    ACTH secreting=Cushings, bilateral adrenal

    hyperplasia Prolactinomas=amenorrhea/galactorrhea syndrome

    (fem); impotence, dec libido(male)

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Evaluate endocrine effects/comorbidites

    If pt presents with Cushings

    DM, insulin-resist hyperglycemia

    Hyperaldosterism with dec Kmetabolic alkalosis

    HTN

    mild CHF

    obesitymedical issues should be optimized

    cardiac consult for IHD

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Pt presents with acromegaly

    Markedly enl hands,feet,

    All major organs enl Eval for HTN, diabetes, IHD

    Cardiomyopathy, CHF

    LISTEN TO THE VOICE

    S&S of recurrent lar. N problems?

    Stridor?

    Consider neck xrays to eval airway size

    Prone to post extub airway edema

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Parasellar tumors may produce

    panhypopituitarism

    Replacement RX with appropriate hormones Euthyroid

    Steroids

    Vasopressin

    All hormones preop to optimize

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Two options for surgical approach

    Transcranial

    Transsphenoidal

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA Transcranial approach

    Recommended for tumors of uncertain diag., with

    extension affecting the optic n/hypothalamus

    Allow direct visualization of suprasellar struct (incl.

    vasc. Ring, optic chiasm, hypothalamus, pituitary stalk)

    Disadv: potential damage to olfactory n., frontal lobe

    vasculature, optic N & chiasm. The incid of permanent

    DI l& ant pituitary deficiency is inc.

    PITUITARY SURGERY ANDPITUITARY SURGERY AND

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    PITUITARY SURGERY ANDPITUITARY SURGERY AND

    ANESTHESIAANESTHESIA TRANSSPHENOIDAL

    Lower incid DI, eliminates frontal retraction and scars,

    magnified visualization=tissue sparing, dec. freq.

    transfusions, shorter hospitalization

    Disadv: poss CSF leak & meningitis, inabil to visualize

    structures next to large tumor, inaccess. Tumors

    extending into mid & ant fossae, possibility of bleeding

    into cavernous sinus/carotid a. (leads to intracranhemorr->brain stem compression->inc blood loss)

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    PITUITARY SURGERYPITUITARY SURGERY

    Review:

    Secreting or nonsecreting

    Status if secreting What hormones were involved

    What medical therapy was used to suppress

    Not everybody for pituitary surgery will have adifficult airway

    Did the pt have a pneumoencephelogram?

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    PITUITARY SURGERYPITUITARY SURGERY

    Transcranial

    Basic considerations of neuroanesthesia

    Control of ICP Possibility of large amt blood loss

    PITUITARY SURGERYPITUITARY SURGERY--

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    PITUITARY SURGERYPITUITARY SURGERY

    TRANSSPHENOIDALTRANSSPHENOIDAL Considerations

    Oral Rae or reinforced ETT

    HOB will be elevated VAE possibilities=monitor

    Doppler

    CVP

    Visual evoked potentials?

    Throat packs

    S GS G

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    PITUITARY SURGERYPITUITARY SURGERY

    More considerations!

    Tongs & HTN response

    Make room for the C-arm Be ready for table turn, away arm tucked

    ENT surgeon starts

    Vasoconstricting locals!

    Prepares the way for the neurosurgeon

    PITUITARY SURGERYPITUITARY SURGERY--

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    PITUITARY SURGERYPITUITARY SURGERY

    TRANSSPHENOIDALTRANSSPHENOIDAL The surgeon will be working under the

    microscope

    TRANSSPHENOIDALTRANSSPHENOIDAL

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    TRANSSPHENOIDALTRANSSPHENOIDAL

    APPROACHAPPROACH Again-what are we going to worry about?

    Airway in

    Acromegalics=size issues

    Cushings=obese,HTN,cardiomyopathy,sleep apnea, diabetes

    Dysrhythmias & severe HTN b/o epi in local

    Hemorrhage (cavernous sinus)

    Air embolism

    Sequestration blood in airway

    DI=postop concern

    PITUITARY SURGERYPITUITARY SURGERY

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    PITUITARY SURGERYPITUITARY SURGERY

    Smooth emergence

    Awake extubation

    EBL usually

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Also called Panhypopituitarism

    GH deficiency=short stature with normal

    proportions Congenital/acquired

    Genetic mutations, absence of pituitary (empty

    sella syndrome), severe brain injury (includingbirth injury)

    PITUITARY DWARFISMPITUITARY DWARFISM

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Childs growth curve = flat (no growth) or

    very shallow (min growth)

    Puberty onset will depend on ability ofpituitary to produce necessary hormones

    PITUITARY DWARFISMPITUITARY DWARFISM

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Associated with deficiencies in

    Thyrotopin

    Vasopressin Gonadotropin

    ACTH

    Facial development abnormalities (cleft

    palate/lip)

    PITUITARY DWARFISMPITUITARY DWARFISM

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Presentation:

    Slow growth before age 5

    Short stature (child

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Testing:

    Studies to determine bone age

    GH levels to determine presence of pituitarydysfunction

    Measurement of other hormone levels

    Head Xray (?empty sella syndrome)

    MRI

    PITUITARY DWARFISMPITUITARY DWARFISM

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Rx

    Followed by endocrinologist

    Synthetic GH (avoids possibility ofdevelopment of Jakob-Creutzfeld)

    May require other hormonal replacement

    PITUITARY DWARFISMPITUITARY DWARFISM

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    PITUITARY DWARFISMPITUITARY DWARFISM

    Anesthesia considerations

    Small airway

    No anatomic abnormalities Tracheal tree is similar to pediatric patient of

    similar size

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    PITUITARY APOPLEXYPITUITARY APOPLEXY

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    PITUITARY APOPLEXYPITUITARY APOPLEXY

    LIFE THREATENING

    Leads to

    Rapid development of acute neurologicaldeficits

    Rapid decline in pituitary function

    PITUITARY APOPLEXYPITUITARY APOPLEXY

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    PITUITARY APOPLEXYPITUITARY APOPLEXY

    RX

    Corticosteroids

    Emergency decompression

    THE PITUITARY ANDTHE PITUITARY AND

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    ANESTHESIAANESTHESIA We will look at the other endocrine glands

    and their issues. Some of their

    malfunctions will be due to the pituitarymalfunction. Others will be independent of

    this control.

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    Hepatic DiseaseHepatic Disease

    Liver Disease HistoryLiver Disease History

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    Liver Disease HistoryLiver Disease History

    Jaundice

    Gastrointestinal bleeding

    Untoward effects of prior anesthetics

    Decreased exercise tolerance

    Physical FindingsPhysical Findings

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    Physical FindingsPhysical Findings

    Hepatosplenomegaly

    Arteriovenous fistulas (spider nevi)

    Ascites

    Cardiomyopathy

    Encephalopathy

    Hepatic Laboratory FindingsHepatic Laboratory Findings

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    Hepatic Laboratory FindingsHepatic Laboratory Findings

    Abnormal liver function tests

    Coagulopathy (PT, PTT increased)

    Thrombocytopenia Renal dysfunction (hypernatremia)

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    Changes in Hepatic CirrhosisChanges in Hepatic Cirrhosis

    Increased pulmonary shunting Renal dysfunction (sodium retention)

    Ascites and edema

    Anemia, thrombocytopenia

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    Changes in Hepatic CirrhosisChanges in Hepatic Cirrhosis Decreased clotting factors

    (II, VII, IX, X)

    Hypoalbuminemia

    Hepatorenal syndrome

    Encephalopathy

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    Differential DiagnosisDifferential Diagnosis

    of Hepatic Dysfunctionof Hepatic Dysfunction

    Bilirubin OverloadBilirubin Overload (Hemolysis)(Hemolysis)

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    Bilirubin OverloadBilirubin Overload (Hemolysis)(Hemolysis)

    Bilirubin

    Aminotransferases

    Alkaline phosphatase

    Prothrombin time

    Serum proteins

    Unconjugated

    Normal

    Normal

    Normal

    Normal

    Hepatocellular DysfunctionHepatocellular Dysfunction

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    Hepatocellular DysfunctionHepatocellular Dysfunction

    Bilirubin

    Aminotransferases

    Alkaline phosphatase

    Prothrombin time

    Serum proteins

    Conjugated

    Increased

    Normal

    Prolonged

    Decreased

    Causes of PostoperativeCauses of Postoperative

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    Causes of PostoperativeCauses of Postoperative

    Hepatic NecrosisHepatic Necrosis

    Hypoxemia

    Ischemia Sepsis

    Viral Infection

    Pre-existing liver disease Drugs

    Cardiovascular ChangesCardiovascular Changes

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    Ca d o ascu a C a gesCa d o ascu a C a ges

    Hepatic CirrhosisHepatic Cirrhosis

    Hyperdynamic circulation

    Increased cardiac output Decreased peripheral resistance

    Increased blood volume

    Arteriovenous fistulas

    Cardiovascular ChangesCardiovascular Changes

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    Cardiovascular ChangesCardiovascular Changes

    Hepatic CirrhosisHepatic Cirrhosis

    Decreased hepatic blood flow Portal hypertension

    Decreased arterial flow

    Cardiomyopathy

    Liver Disease Risk FactorsLiver Disease Risk Factors

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    Liver Disease Risk FactorsLiver Disease Risk Factors

    Bilirubin > 3 mg/dl

    Albumin < 3 g/dl

    Prothrombin time (secondsprolonged) > 6

    Poor nutritional state

    Ascites

    Encephalopathy

    Preanesthetic TreatmentPreanesthetic Treatment

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    (Liver Disease)(Liver Disease) Correct coagulation defects

    (vitamin K)

    Correct hypoalbuminemia Reduce edema

    (furosemide, mannitol)

    Liver Disease JaundiceLiver Disease Jaundice

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    Liver Disease JaundiceLiver Disease Jaundice

    Bilirubin overload

    (hemolysis from blood, hematoma)

    Cholestasis Intrahepatic (infection, drug-induced)

    Extrahepatic (bile duct injury, gallstones)

    Liver Disease JaundiceLiver Disease Jaundice

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    Liver Disease JaundiceLiver Disease Jaundice

    Hepatocellular injury

    Hypoxia or ischemia

    Drug-induced Exacerbation of pre-existing disease (stress)

    Viral hepatitis

    Conditions that LowerConditions that Lower

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    Conditions that LowerConditions that Lower

    Esophageal SphincterToneEsophageal SphincterTone

    Obesity

    Pregnancy Hiatal hernia

    Reflux syndromes

    D th t DD th t D

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    Drugs that DecreaseDrugs that Decrease

    Esophageal SphincterToneEsophageal SphincterTone

    Anticholinergics

    Opioids

    Volatile anesthetics

    Intravenous anesthetics

    D th t ID th t I

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    Drugs that IncreaseDrugs that Increase

    Esophageal SphincterToneEsophageal SphincterTone

    Anticholinesterases

    Succinylcholine Metoclopramide

    Causes of Upper GI BleedingCauses of Upper GI Bleeding

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    Causes ofUpper GI BleedingCauses ofUpper GI Bleeding

    Duodenal ulcer

    GastritisVarices

    Esophagitis

    Incidence (%)

    27

    23

    14

    13

    Causes of Upper GI BleedingCauses of Upper GI Bleeding

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    Causes ofUpper GI BleedingCauses ofUpper GI Bleeding

    Gastric ulcer

    Mallory-Weiss tearBowel infarction

    Idiopathic

    Incidence (%)

    8

    7

    3

    5

    Reducing Risk of AspirationReducing Risk of Aspiration

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    Reducing Risk of AspirationReducing Risk of Aspiration

    Nasogastric suction

    Metoclopramide

    H2 antagonists

    Reducing Risk of AspirationReducing Risk of Aspiration

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    g pg p

    Nonparticulate antacids (Sucralfate)

    Awake intubation

    Rapid sequence induction-cricoid pressure

    Acute Pancreatitis:Acute Pancreatitis:

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    Acute Pancreatitis:Acute Pancreatitis:

    Predisposing ConditionsPredisposing Conditions Alcohol abuse

    Gallstones

    Blunt abdominal trauma Penetrating peptic ulcer

    Cardiopulmonary bypass

    CholestasisCholestasis

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    Bilirubin

    Aminotransferases

    Alkaline phosphatase

    Prothrombin time

    Serum proteins

    Conjugated

    May be increased

    Increased

    May be prolonged

    May be increased

    Laparoscopic CholecystectomyLaparoscopic Cholecystectomy

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    p p y yp p y y

    Risk Factors

    Impaired venous return

    C

    arbon dioxide embolism Underventilation

    Gastric reflux (decompression desirable)

    Loss of hemostasis, requiring laparotomy

    Open Cholecystectomy:Open Cholecystectomy:

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    Ope C o ecystecto yOpe C o ecystecto y

    Risk factors

    Biliary spasm (opioids-Morphine? ) Postoperative pain

    Carcinoid SyndromeCarcinoid Syndrome

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    Carcinoid SyndromeCarcinoid Syndrome

    Carcinoid SyndromeCarcinoid Syndrome

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    yy

    Cutaneous flushing

    Labile blood pressure

    Diarrhea Bronchospasm

    Cardiac failure (cardiomyopathy)

    Carcinoid TreatmentCarcinoid Treatment

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    Fluid resuscitation

    H1 and H2 antagonists

    Serontonin (5-HT) antagonists Bronchodilators

    Vasoactive drugs

    Octreotide

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