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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