Anesthesia and En Doc Raine Diseases

8/9/2019 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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Goiter

Tachycardia

Atrial fibrillation

Tremor

Eye signs (proptosis) Weight loss


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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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Adverse ResponsesAdverse Responses

Sensitivity to depressant drugs (opioids)

Hypodynamic circulation

Slowed metabolism (drugs)

Impaired ventilatory responses


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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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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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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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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)



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Cheodectoma Carotid body, behave like paraganglioma biochemically

Glomus jugulare tumor Intracranial branch ofCN IX and X

Behave like paragangliomoa biochemically



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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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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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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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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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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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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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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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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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What hormones?

=6

ACTH

GH

TSH

FSH LH

PROLACTIN


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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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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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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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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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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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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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ACROMEGALY

Coarse facial hair

R laryngeal n paralysis Stridor

Cricoarytenoid involvement

Inc lung volumes with V/Q mismatch


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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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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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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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SIADH

Inappropriate secretion antidiuretic hormone

Intracranial tumors Hypothyroidism

Lung CA

Common after surgery (transient)


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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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SIADH

Suspect in

HYPONATREMIA

Excreting urine that is hypertonic rel to plasma


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SIADH

Diagnosed by

Low serum BUN, Cr, uric acid, albumin

Serum sodium


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ISADH

Diagnosis

Inapprop inc in urinary Na concentration

Dec plasma osmolarity

Inc urine osmolarity


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ISADH

Treatment

Fluid restriction


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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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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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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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Presentation

Polydipsia

Polyuria Poorly concentrated urine despite inc. plasma

osmolarity


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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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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



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ANESTHESIAANESTHESIANonfunctioning tumors may produce

symptoms that are global/selective.

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



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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



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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)



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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



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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



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ANESTHESIAANESTHESIA Parasellar tumors may produce

panhypopituitarism

Replacement RX with appropriate hormones Euthyroid

Steroids

Vasopressin

All hormones preop to optimize



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ANESTHESIAANESTHESIA Two options for surgical approach

Transcranial

Transsphenoidal



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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.



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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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Transcranial

Basic considerations of neuroanesthesia

Control of ICP Possibility of large amt blood loss

PITUITARY SURGERYPITUITARY SURGERY--


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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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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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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



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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)



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Childs growth curve = flat (no growth) or

very shallow (min growth)

Puberty onset will depend on ability ofpituitary to produce necessary hormones



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Associated with deficiencies in

Thyrotopin

Vasopressin Gonadotropin

ACTH

Facial development abnormalities (cleft

palate/lip)



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Presentation:

Slow growth before age 5

Short stature (child


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Testing:

Studies to determine bone age

GH levels to determine presence of pituitarydysfunction

Measurement of other hormone levels

Head Xray (?empty sella syndrome)

MRI



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Rx

Followed by endocrinologist

Synthetic GH (avoids possibility ofdevelopment of Jakob-Creutzfeld)

May require other hormonal replacement



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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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LIFE THREATENING

Leads to

Rapid development of acute neurologicaldeficits

Rapid decline in pituitary function



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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


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



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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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Bilirubin overload

(hemolysis from blood, hematoma)

Cholestasis Intrahepatic (infection, drug-induced)

Extrahepatic (bile duct injury, gallstones)



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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


Anticholinergics

Opioids

Volatile anesthetics

Intravenous anesthetics

D th t ID th t I


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Drugs that IncreaseDrugs that Increase


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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Nasogastric suction

Metoclopramide

H2 antagonists



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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


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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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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Anesthesia and En Doc Raine Diseases

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