MEKELLE UNIVERSITY-CHS

DEPARTMENT OF ANESTHESIOLOGY

ANESTHESIA MANAGEMENT OF PATIENTS

WITH ENDOCRINE & CO-EXISTING DISEASES

By Nurhussien (BSc) in

Anesthsiology

Course objectives• At the end of this course students will be able to: -Describe the normal physiology of thyroid,

parathyroid, pancreas and adrenal glands. -Assess the sign and symptoms of thyroid,

parathyroid, pancreatic and adrenal glands malfunctioning

-Determine the surgical complications, treatment and anaesthesia considerations

-Describe the Pathophysiology of MH, MG,Parkinsonism, Phaeochromocytoma, and ARDS.

-Finally determine the anaesthesia consideration and peri opertive management of the above pathologies.

ANESTHESIA FOR PATIENTS WITH THYROID GLAND

DISORDERS

Brain storming

What are the hormones secreted from the anterior part of the pituitary gland?

• TSH: Controlls synthesis and secretion of thyroid hormones

• FSH: Sperm cell maturation and follicular dev’t & estrogens synthesis in ovaries

• LH: Stimulates testosterone synthesis in testis and stimulates ovulation

• Growth hormone: Stimulates protein synthesis and overall body growth

Cont.• Prolactin: Stimulates milk production and

secretion in breasts• ACTH: Stimulates synthesis and secretion of

cortisol, androgens and aldosterone.• MSH: Stimulates melanin synthesis

The thyroid gland• Anatomy: The thyroid gland is formed by two lateral lobes

connected by the thyroid isthmus at about the second tracheal ring.

It is situated anterior to the trachea.

Is the first endocrine gland to appear during embryonic dev’t.

Weight 15-25 gms in adults

It is supplied by the superior and inferior thyroid arteries.

Venous drainage is through superior, middle and inferior thyroid veins

cont’d…… It is a highly vascularised endocrine gland Attached to the trachea by a loose connective tissues Covered by: -Anteriorly by skin and paltysma muscle -Antero laterally by @ Sternocleidomastoid muscle @Sternothyroid muscle @Sternohyoid bone -Posteriorly parathyroid glands are located on both

sides

• Thyroid gland contains two separate hormone producing cells.

1.Follicular cells: they synthesize, store and release thyroid hormones(T4 and T3)

• They also trap iodide from the circulation

• The iodide is then oxidized to iodine which is catalysed by thyroid peroxidase (organification) takes place on the apical membrane of the follicular cells

Cont.• They synthesize and secrete thyroglobulin a

substance containing tyrosine.

• This tyrosine is then iodinated by the oxidized iodine to form monoiodotyrosine(MIT) and diiodotyrosine

Cont’d……..

• MIT+DIT=T3

• DIT+DIT=T4

• This iodinated thyroglobulin is the storage form of thyroid hormones which is kept inside the follicle

3,5,3´-triiodothyronine (T3)

Thyroxine (T4)3,5,3´,5´-tetraiodothyronine

Iodide transport-trap iodide moving it into the thyroid follicle and then oxidizes it

Organification- iodine is combined with tyrosine to form MIT & DIT

Coupling- two DIT combine to make thyroxin (T4) or one MIT combines with one DIT to form triiodotyronine (T3)

Storage- hormones migrate to the colloid space in the centre of the thyroid follicular cells

Secretion- release of hormones by reversing process of storage reversal of migration through cell membranes.

cont’d……• TSH- it is one of the hormones produced in the anterior

part of the pituitary gland• It controls the function of follicular cells and secretion of

thyroid hormones(T3 & T4).• it stimulates the thyroid to release T3 & T4• It also increases thyroglobulin synthesis & iodine uptake• It’s secretion is regulated by TRH produced from the

hypothalamus• Excess T3 & T4 suppress the release of TSH (-ve

feedback mechanism).

Brain(hypothalamus) TRH

Anterior pituitary TSH

Thyroid

Thyroid hormones

Body tissues

cont’d………

Negative feedback mechanism\

Low blood levels of hormones stimulate hypothalamus Hypothalamus stimulates pituitary to release TSH TSH stimulates the thyroid to raise the amount of

hormones in the blood

cont’d……

NB: the over all result of any type of negative feedback in the endocrine system is :

-inhibition when the level of the hormone in the periphery is high

-stimulation when there is low amount of hormones in the periphery

2. Para follicular cells: They secrete calcitonin which has a minor role

in maintaining calcium homeostasis. Two main effects of calcitonin are : 1. It enhances excretion of calcium into urine 2. Inhibition of bone resorption of calcium,

which would minimize fluxes of calcium from bone to blood.

SPECIFIC ACTIONS OF THYROID

HORMONE: METABOLIC• Regulation of Basal Metabolic Rate (BMR).• Increases oxygen consumption in most target

tissues.• Permissive actions: TH increases sensitivity of

target tissues to catecholamines, thereby elevating lipolysis, glycogenolysis, and gluconeogenesis.

• The high sensitivity of target tissues to cathecolamines also causes tachycardia, palpitations and high cardiac out put.

SPECIFIC ACTIONS OF THYROID

HORMONE: DEVELOPMENT• TH is critical for normal development of

the skeletal system and musculature.• TH is also essential for normal brain

development and regulates synaptogenesis, neuronal integration, myelination and cell migration.

• Cretinism is the term for the constellation of defects resulting from untreated neonatal hypothyroidism.

1O Q

DISEASES OF THE THYROID

GLAND

HYPERTHYROIDISM• It is a syndrome caused by excessive secretion of TH

when there is over active thyroid gland.• This can be due to over functioning of the entire gland

or due to the presence single or multiple adenomas of the gland.

• Its clinical manifestation is thyrotoxicosis a syndrome caused when the body tissues are stimulated by a high level of TH.

• Causes :• The most common cause is graves disease(w/c is a

diffuse enlargement of the gland)• Thyroid adenoma • Thyroid carcinoma• TSH pituitary adenomas• Iatrogenic

Pathophysiology :• B/c the action of thyroid hormones on the body is

stimulatory, hyperthyroidism results in sympathetic over activity.

• The excessive amount of TH stimulates the cardiac system and increases the number and sensitivity of beta adrenergic receptors

-tachycardia -increased CO and stroke volume -increased adrenergic responsiveness -increased peripheral blood flow

cont’d Increased metabolism leads to: Negative nitrogen balance Lipid depletion Stage of nutritional deficiency Increased oxygen consumption TH and catecholamine work together in metabolic

acceleration Increased oxygen consumption, BMR, and heat

production Positive inotropic and chromo tropic effect by

increasing calcium-ATPase & beta receptors.

cont’d…..

There is also increased GI motility. Increased bone and protein turn over, glycogenolysis,

hepatic gluconeogenesis, intestinal glucose absorption, cholesterol synthesis and degradation.

High BMR => high body temperature =>peripheral vessel dilatation=>increased CO=> high out put failure.

Prolonged period of hyperthyroidism leads to bone destruction, and hunger damage due to increased catabolism of cellular proteins and fat.

Symptoms and signs: Symptoms:

Nervousness Increased sweating ( warm and moist skin )Heat intolerancePalpitationFatigue and weaknessWeight loss Increased appetiteHyperdefication

Signs:Thyroid enlargement TachycardiaAtrial fibrillationSystolic hypertension ( wide pulse pressure)Eye signs (exophthalmus )

TESTS NORMAL VALUES

INCREASED DECREASED

T4 60-120 nmole/L

-Hyperthyroidism-Thyroditis-Early hepatitis-Pregnancy-Oestrogen therapy-Exogenous T4

-Hypothyroidism-Androgens-Salicylates-Sulphonamides

T3 0.92-3 nmole/L Hyperthyroidism

-Hypothyroidism -Cirrhosis-Uraemia-Malnutrition

TSH 0.25-8micIU/L Primary hypothyroidism

Hyperthyroidism

TREATMENT• Anti thyroid drugs:

o PTU, methimazole and carbimazole- these drug inhibits the synthesis of TH by blocking the action of peroxidise enzyme (an enzyme that converts I- to I+ )

o PTU also inhibits the peripheral conversion of T4 to T3.

CONT.

o Potassium or Sodium iodide prevent the release of TH to the tissues

o Dosage : PTU 100-150 mg PO TID, Methimazole 15-60 mg PO BID, Carbimazole 20-40 mg PO TID for at least 6-8 weeks and potassium or sodium iodide 100 mg PO QID for7-10 days prior to surgery.

Beta blockers:

o Propranolol 40-80 mg PO QID. This drug blocks the high responsiveness of beta adrenergic receptors to catecholamine there by reducing pulse rate.

o Beta blockers also have little effect on preventing peripheral conversion of T4 to T3

• Although blockage of hormone synthesis is rapid, clinical improvement occurs after months.

• This is b/c a large pool of stored TH continues to be released from the gland.

• Most patients become euthyroid 2-3 months after the beginning of anti-thyroid therapy.

• After clinical improvements, dosage should be tapered to the minimum to maintain an euthyroid state.

• The drug should continue up to one year.

• A free T4 level should be checked after one month of therapy and then every 2-3 months

• Indications for surgery

Large goitre not amendable to RAI Compressive symptoms Children and young patients Patients with cancer or suspicious nodule Allergy to anti-thyroid drugs Pregnant and those with a desire to conceive

soon Moderate to severe opthalmopathy Cosmetic desire of the patient

ANESTHESIA MANAGEMENT

Preoperative preparation:

– Careful assessment of upper airway & tracheal deviation

– Thoracic inlet X-ray, CT scan– Patient must be rendered EUTHYROID – Use anti-thyroid drugs and B - blockers– Resting pulse rate 85-90 bpm

– Lugol’s iodine 3-5 drops BID for 10 days to decrease vascularity of the gland

– Benzodiazepines premedication

– Continue the morning dose of anti thyroid and beta blocking drugs.

Intraoperatively- Anesthetic options:A- No difficulty anticipated: - usual iv induction & intubation (fentanyl, non-depolarizing

muscle relaxantB- possible difficulty in intubation: - iv induction, test ventilation when pt is unconscious,

intubation +- suxamethoniumC- definite intubation problem / evidence of airway obstruction

awake fibreoptic intubation inhalational inductionchoice of ETT- armoured ETT (< risk of kinking) The size of ETT to be used should be 0.5 mm ID smaller

than the normal calculated size

cont’d…….. Intra operatively:Allow safe induction and awakeningMaintain adequate level of anaesthesia (avoid

exaggerated sympathetic response to surgical stimulus)

Drugs of choice• Etomidate, propofol and barbiturates for

induction• Atracurium, vecuronium for muscle relaxation• Isofulrane choice of inhalational.

cont’d…………..

Avoid drugs like:oAtropineoPancuroniumoHalothaneoketamine

Positioning and skin preparation:o Put an iv bag between scapulaso Protect eyeso ETT is strapped firmly in positionoGentle traction the arms along the side bodyo Put patient in a head up position 15-20

degrees to facilitate venous drainage o Surgeon stands on the opposite to the lobe to

be removedo Skin prepared and drapedo IV line on opposite

• If a hyperthyroid patient with clinically apparent disease requires an emergency surgery:

Propranolol 0.5 mg/kg iv is givenOr esmolol infusion 50-150 micg/kg/minuteIf the site allows regional technique is

preferred but adrenalin containing LA should be avoided.

It is also important to avoid all the causes of sympathetic stimulations

C) POSTOPERATIVE

Possible problems 1.Thyroid storm /crisis

An acute exacerbation of hyperthyroidism with excessive release of thyroid hormone

Onset – intraoperative or 6-24 hours after surgery

Sign and symptom:- hyperpyrexia, tachycardia or atrial fibrillation, hypotension, vomiting, dehydration, tachypnoea, acute abdominal pain simulating an acute abdomen, agitation, psychosis

Dx: primarily clinicalDDx: MH,Pheochromocytoma or light

anesthesia

Management:A) Supportive and medical management. Investigate for precipitants – FBC, , blood

glucose, FT4, FT3If the cause is Hyperthyroidism mange as

follows:1) Inhibition of thyroid hormone formation

PTU 900-1200mg/day orally / NG in 3-4 divided doses

OR Carbimazole 60-120mg/day 3-4 divided

doses orally / NG

Precipitants

- infection, surgery, poorly prepared thyroid surgery, diabetic ketosis, radioiodine therapy in a poorly prepared pt, MI

2) Inhibition of thyroid hormone release:- sodium iodide IV 1gm/24hr – slow infusion or- oral potassium iodide 100mg 6hrly- Given 1hr after 1st dose PTU/carbimazole

3) Steroids - iv dexamethasone 2mg 6hrly- inhibits thyroid hormone release &

peripheral conversion

4) Receptor blockade ( in the absence of HF)- Iv propranolol 1-2mg slowly 4-6hrly / oral

propranolol 40-80mg 6hrly5) Cardiac failure- diuretics, digoxin, O2 +-propranolol if d/t

uncontrolled AF with good LV function5) Hyperpyrexia- fans, tepid sponge, PCM 6) Dehydration- IV fluid replacement

2) Airway obstructionPossible causes: - neck hematoma with tracheal compression - tracheomalacia - incomplete reversal of NDMR - CNS depression

3) Tetany- clinical manifestations: circumoral tingling,

paraesthesia, laryngeal spasm, (+) ve Chvostek & Trousseau signs

- May result from respiratory alkalosis - over-ventilation in immediate postoperative period - hypocalcemia from hypoparathyroidismMx- calcium replacement- Slow injection of 10% calcium gluconate 10 mls

IV

4) RLN injury

Manifestations:1) Unilateral Asymptomatic unless larygoscopic

examination is done Weak and horse voice chocking and coughing

during drinking and aspiration2) Bilateral Usually manifests immediately after

extubation Laryngeal stridor, acute respiratory distress,

phonation lost and desaturation

• ManagementUnilateral Re intubation & observe for 6-12 minutes If normal function of cords is not returned with

in 6- 12 minutes Teflon injection Speech therapy Medialization and re -innervation Other than the above measures there is no

definitive Rx until 6 months

Cont’d….

Bilateral temporarily: = re intubation muscle paralysis = hydrocortisone 100 mg TID = if extubation fails after 48 hrs

Tracheostomy is mandatory

ANESTHESIA MANAGEMENT OF HYPOTHYROIDISM

• Definitiono It is a condition when the body

tissues are exposed to decreased circulating concentration of thyroid hormones.

• Causes 1. Primary- b/c of destruction of thyroid

gland Thyroid gland can be destructed byChronic thyroiditis( Hash Moto's disease)Previous STTPrevious RAI therapy Irradiation of the neck

• Hashimoto’s thyroiditis is an autoimmune destruction of the thyroid gland in which antibodies may either frankly destroy the gland or block TH synthesis.

• And this remains the most common cause of primary hypothyroidism

Cont’d….

Thyroid hormone deficiency secondary to:Anti thyroid drugsExcessive iodine ( inhibits TH release)Dietary iodine deficiency

Cont’d….2. Secondary – b/c of CNS dysfunction

Hypothalamic dysfunction which causes TRH deficiency

Anterior pituitary dysfunction which causes TSH deficiency

• NB: Depending on the cause, the level of TSH

may be increased or decreased.

If the defect is in the thyroid gland (e.g. thyroiditis) TSH level will be increased by a negative feedback mechanism as the low circulating level of TH will stimulate the pituitary to secrete more TSH

If the defect is in the hypothalamus or in the pituitary the level of TSH will be decreased.

Cont’d……

• Diagnosis

Is based on clinical signs and symptoms plus TFT

Signs and symptoms

Generalized decrement in metabolic activity

Cold intolerance Lethargy Decreased COP ( up to 40% ) and BV Prolonged circulation time and narrow

pulse pressure PVR to decrease heat loss

Treatment• Slow initiation

• Patients with; -severe hypothyroidism -older patient and - patients CVS disease may have increased sensitivity to TH and are at risk of acute CVS and other complications if hypothyroidism is corrected quickly.

Cont’d…..

• Therefore , these patients should be given a very small dose of TH initially -25 micgm of levo thyroxine which will gradually be increased to a full maintenance dose every 2-4 weeks for about 6-12 weeks period

• Rapid initiation

• Younger patients, and patients with less severe hypothyroidism may be given a slightly higher dose of TH ( 50 micgm levo thyroxine) & can be advanced to a full replacement dose quickly

• For example the dose may be raised to 100 micgn in 2 weeks & 125-150 micgm in the next 2 weeks

• Maintenance

• Most patients need 75-100 micgm of levo thyroxine daily

Anesthetic management

• Elective surgeries should be differed in poorly controlled hypothyroidism due to the high risk of CVS complications

• But there are no controlled studies about sensitivity of such patients to IAA & opioids

Cont’d….• Myxedema

• It is a severe form of hypothyroidism characterized by

StuporComaHypoventilation HypotensionHypothermia and hypernatremiaIt is a medical emergency with a mortality

rate of 25-50%

Cont’d…• Management

• ETTI and ventilation is needed• Sodium levo thyroxine 200-300micgm iv

over 10 minutes initially and maintenance 200 micgm iv daily

• Hydrocortisone 100mg iv then 25 mg iv QID to prevent coexisting adrenal gland suppression.

• Fluid and electrolyte supplementation• Avoid hypothermia

Cont’d….• Preoperative

Patients with uncorrected severe hypothyroidism or with myxedema coma should not undergo elective surgery and should be treated with TH prior to emergency surgery.

• Although an euthyroid state is ideal, mild to moderate hypothyroidism are not absolute CI to surgery

• Hypothyroid patients usually do not require much more preoperative sedation and are very prone to respiratory depression

• They fail to respond to hypoxia by increasing minute ventilation

• Since patients have delayed gastric emptying time Premedicating with metoclopramide and H2 blockers is important

• The normal dose of TH should be continued in the morning of surgery

• It should however be known that half life of most TH drug preparations is long

• For example half life of T4 is about 8 days.

Due to their depressant effect avoid opioids

Cortisol supplementation is considered if there is coexisting adrenal gland suppression.

If possible give the premedication in OR

Cont’d…..• Induction of anesthesia

Ketamine is a preferable induction agent

If no severe CVS depression, thiopental can be used

When using relaxants keep in mind that there is a coexisted skeletal muscle weakness

Cont’d…• Maintenance of anesthesia

N2O, +- short acting opioids , BZD or

ketamine

is best

Volatiles CI in overtly hypothyroid situation

Reduce MAC if body temperature is <37degree Celsius

CIPPV is indicated

Pancuronium is best relaxant

Cont’d….• Regional anesthesia

Preferable than GA

Maintain IVFV adequately

PNB- drug dose should be reduced

Cont’d…..• No special consideration about the use of

reversals

• IV fluids should contain Na+

• Delay extubation until patient responds appropriately with an accepted body temperature

• Monitor variables repeatedly

Cont’d…• Recovery

Emergence is delayed from GA due to hypothermia, respiratory depression and slow drug biotransformation

Prolonged post operative somnolence(sleep)

Inability to wean earlier => need mechanical ventilation

Avoid post operative hypothermia Give adequate anti pain Opioids drugs have depressant effects we

should use non opioid analgesics like ketorolac.

100 Q

THE PARATHYROID GLANDS

THE PARATHYROID GLANDS• ANATOMYo Four bean shaped glands are located

behind the upper and lower poles of the thyroid gland.

o Inferior glands are located ventral(to the front) to RLN.

o Superior glands usually dorsal( to the back) to the RLN at level of cricoid cartilage

Cont’d…..

• They get most of their blood supply from branches of inferior thyroid artery, although branches from superior thyroid supply at least 20% of upper glands.

• They drain their venous blood through superior, middle, and inferior thyroid veins

• PHYSIOLOGY• The main physiologic role of the

parathyroid glands is production of a polypeptide hormone called parathyroid hormone.

• Maintenance of calcium, phosphate and magnesium homeostasis is under the influence of two polypeptide hormones; parathyroid hormone(PTH), and calcitonin

Cont’d..• These hormones regulate the flow of

minerals in and out of the extracellular fluid compartments through their actions on intestine, kidneys, and bones.

• The PTH acts directly on the bones and kidneys and indirectly on the intestine through its effect on the synthesis of 1,25 (OH)2D3. Its production is regulated by the concentration of serum ionized calcium.

Cont’d..• Lowering of the serum calcium levels will

induce an increased rate of parathyroid hormone secretion

• Calcitonin is released by the “C” cells (Para follicular cells in the thyroid gland) in response to small increases in plasma ionic calcium. It acts on the kidney and bones to restore the level of calcium to just below a normal set point which in turn inhibits secretion of the hormone

Cont’d…• Calcitonin is therefore the physiological

antagonist of PTH. The two hormones act in concert to maintain normal concentration of calcium ion in the extracellular fluid.

• The total calcium concentration in the blood is 10mg/dl

• Of this 40% is bound to plasma proteins mainly albumin

• The remaining 60% is found in two different forms

• The first is complexed with anions ( sulfate, phosphate and citrate) which accounts about 10%

• About 50% is found as free ionized calcium and this is the only form of calcium which is biologically active.

• This free Ca++ is important foro Skeletal muscle contractiono coagulation,o neurotransmitter release,o endocrine function, other intracellular

functions

Actions of major calcium regulating

hormonesHORMONE

BONE KIDNEY INTESTINE

PTHIncrease resorption of calcium and phosphate

Incr. reabsorption of calcium

Decr. reabsorption of phosphate

Incr. conversion of 25OHD3

to 1,25(OH) 2 D3

No direct effect

Calcitonin

Decr. Resorption of calcium & phosphate

Decr. Reabsorption of calcium & phosphate

No direct effect

VtDMaintains calcium transport system

Decr. Reabsorption of calcium

Incr. reabsorption of calcium & phosphate

DISORDERS OF THE PARATHYROID GLAND

PRIMARY HPT• Primary HPT is due to excessive production

of PTH by one or more of hyper functioning parathyroid glands.

• This leads to Hypercalcemia and hypo phosphatemia

• It affects patients older than 40 years

• Female to male ratio is 3:1

• 85% caused by isolated adenoma, 14% by diffuse hyperplasia, 1% by parathyroid CA

HPT CONT’D….• C/M

• Clinical manifestations are mostly due to Hypercalcemia.

• CVS: HTN, arrhythmias, short QT, prolonged PR

• Renal: impaired renal concentration, metabolic acidosis ,polyuria, dehydration, polydipsia, renal stones (nephrolithiasis), renal failure

• GI: ileus, nausea & vomiting, pancreatitis,

Cont’d…

• Musculoskeletal: weakness, osteoporosis(a fragile bone) & pathological fractures

• CNS: mental status changes(delirium, psychosis and coma)

• Eyes- calcification, conjunctivitis

SECONDARY HPT

• An increase in PTH secretion which is adaptive and unrelated to intrinsic disease of the parathyroid glands is called secondary hyperparathyroidism.

• This is due to chronic stimulation of the parathyroid glands by a chronic decrease in the ionic calcium level in the blood

SECONDARY HPT CONT’D..• Is a compensatory hyper functioning of the

parathyroid glands caused by hypocalcemia or peripheral resistance to PTH

• Treating the underlying cause can reverse secondary HPT

• It is commonly seen in a patient with an end organ failure e.g. in chronic renal insufficiency

TERITIARY HPT

• It occurs in previous secondary HPT

• In such conditions the glandular hyper functioning continues despite correction of the underlying problem.

• Most of the c/m of secondary & tertiary HPT are the same as that of primary HPT as they are caused by Hypercalcemia

• DIAGNOSIS

• The presence of established Hypercalcemia in more than one serum measurement accompanied by elevated immunoreactive PTH is characteristic feature of HPT

oMarked increase in Ca++ usually b/o cancer

o Serum Ca++>2.8mmol/L; (NR=2.13-2.55)o Ionized Ca++>1.25mmol/L (NR=1.1-1.25)

Cont’d…

• Less commonly caused by

calcium malabsorption

VtD. Deficiency or deranged VtD metabolism

MEDICAL MG’T & ANESTHESIA

CONSIDERATIONSoMedical mg’t

o Saline infusion & loop diuretics

oBiphosphonates(cause binding &inhibit bone resorption) that may be administered IV when levels are life threatening

oCalcitonin produces transient results

• In acute severe forms the main stay of therapy is adequate hydration with saline and forced diuresis by diuretics to increase the urinary excretion of calcium rapidly along with sodium and prevent its reabsorption by the renal tubules

Cont’d…

oHem dialysis

o SURGERY. Resection of the parathyroid lesion is curative with recurrences observed mainly in the multiple glandular disease.

CONT’D…..• Anesthesia mg’t

Pre operative evaluation should include ass’t of volume status to avoid hypotension during induction.

• Hydration with normal saline and diuresis with furosemide usually decreases serum calcium to acceptable levels.

• Check labs• Evaluate status of co morbidities• Any issues with bone fragility?

Cont’d….Intraoperatively• Routine monitors

• Titration of muscle relaxants(pre existing muscle weakness)

• Issues of positioning

• If preoperative LOC decrease dose of anesthetic agents

• Protect the eyes

cont’d….• Avoid hypoventilation as acidosis can

cause an increase in ionized calcium which in turn causes cardiac dysrhythmias.

• Tracheal manipulation during dissection

• Proper patient positioning is important b/c osteoporosis predisposes patients to vertebral compression during laryngoscopy and bone fractures during transfer

Cont’d….Post operatively• • Smooth emergence

• Evaluate for recurrent laryngeal n. damage

• Pain control

Cont’d…..• Postop complications

• Worry aboutoNeck hematomao Laryngeal swelling/ glottis edemaoRecurrent laryngeal n. damageoHypocalcemia= tetanyoAcute arthritisoMetabolic acidosis with deterioration of

renal function (transient)

• PARATHYROID CRISIS:

oCA++ >15 mg/dl

oRequires hydration (dilutes Ca++) followed by diuresis with loop diuretic (promote Ca++ & H2O excretion)

oMay also be given,glucocorticoids, calcitonin, dialysis

HYPOPARATHYROIDISM

• Most common cause: accidental excision of all glands during thyroidectomy

• Also due to: neck trauma, neoplasia

• CRF

• Hypomagnesaemia

• Vt D deficiency

Cont’d…..

• Clinical manifestations

• CVS: hypotension, CHF, prolonged QT interval

• Musculoskeletal system: muscle weakness & cramps

Cont’d….• Neurologic

Neuro muscular irritability(e.g. laryngeal spasm, inspiratory stridor, tetany and seizures)

+Chvosteks signo Tap facial n at angle of mandible = facial

muscle twitch+Trousseau sign

oCarpopedal spasm after applying a tourniquet for 3 min

Perioral parasthesia mental status changes (e.g. dementia, depression and psychosis)

• Dx:o Serum Ca++<4.0 mEq/L, ionized

fractions <2.0 mEq/L

Cont’d…• RX includes:

oCalcium IV in acute conditions until neuromuscular signs are controlled

oCorrection resp/metabolic alkalosisoHypoparathyroid without

hypocalcemia=oral Ca++ and Vit Do Thiazides tend to increase serum Ca++

concentration

Cont’d..

Treatment of acute episode

o Prevent laryngospasm & seizures

o Secure airway

o IV Calcium slowly

oAnticonvulsants

ANESTHESIA CONSIDERATIONS

• PREOP EVALUATION

oCheck Ca++ and Mg levels

o Evaluate EKG ; how is the QT?

oReplace Ca++ if necessary

Cont’d…• Intraoperatively

o Anesthetics that depress the myocardium should be avoided.

o Increased sensitivity to Sux

o Titrate muscle relaxants slowly and monitor response

o Positioning considerations

Cont’d…

o Keep them warm b/c hypothermia may impair drug elimination & metabolism

o Remember co morbidities

o Avoid hyperventilation ( or anything that will change Ca++ level) as alkalosis will further decrease ionized calcium level

• Post operatively

o Assess for changes of serum calcium level

o Pain control

o Close air way follow up

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THANK YOU

THE ADRENAL GLANDS

THE ADRENAL GLANDS

• ANATOMY

• Anatomy was first described in 1563.

• Consists of the adrenal cortex and adrenal medulla

Adrenal Histology

CONT’D….

• PHYSIOLOGY

Activities are regulation of fluid volume and stress response

• Adrenal Cortex: The cortex synthesizes & secretes 30+ different steroids. oGlucocorticoidsoMineralocorticoidsoAndrogens

cont’d…

oMineralocorticoids

Aldosterone Function: Regulates electrolyte & fluid homeostasis

Cont’d…

oGlucocorticoids

Cortisol Hydrocortisone

Function:Stim. gluconeogenesis & h blood

glucoseAnti-inflammatoryAnti-immunityAnti- allergy

Cont’d…

oAndrogen

• Sex hormones Function: Female= Stim. Sex drive

Men = Negligible

• Adrenal Medulla

o Epinephrine(Adrenaline)

o Function• Prolong & h SNS (sympathetic nervous

system) response to stress

• Norepinephrine(noradrenaline) and dopamine.

o Function= the same as that of epinephrine

Adrenal Medulla:

A Modified Sympathetic Ganglion

• Sympathetic stimulationoCatecholamine release to blood• Epinephrine• Norepinephrine

o Travel to:• Multiple targets• Distant targets

Review of Efferent Pathways: Motor

and Autonomic

Mechanism: Norepinephrine

Release and Recycling

Catechalomines: Activity

• Stimulate the “fight or flight” reaction

• Increase plasma glucose levels

• Increase cardiovascular function

• Increase metabolic function

• Decrease gastrointestinal and genitourinary function

DISORDERS OF THE ADRENAL

GLAND

1. Pheochromocytoma( catecholamine excess)

2. Addisons’s disease(adrenal cortex insufficiency)

3. Conn’s syndrome (mineralocorticoid excess)

4. Cushing’s syndrome (glucocorticoid excess)

PHEOCHROMOCYTOMA

• History

• First recognized by Von Frankel

• Pheochromocytoma= dusky colored tumor

• Name coined by Pick in 1912

• Successful surgery for excision of tumor- Roux & Mayo ( 1926-27)

Cont’d…• Neuroendocrine tumour of the medulla of

the adrenal glands

• Originates from the chromaffin cells along the paravertebral sympathetic chain extending from pelvis to base of skull

• >95% are abdominal

• >90% in adrenal medulla

• Secretes excessive amounts of adrenaline and noradrenaline

• 80% occur unilateral

Called “tumor of ten per cent”

• 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

Tumor Secretion:

• Large Pheo: more metabolites (metabolized within tumor before release)

• Small Pheo: more catecholamines

• Sporadic Pheo: Norepi > Epi

• Familial Pheo: Epi > Norepi

• Malignant Pheo: Dopamine

• Epidemiology

0.01-0.1% of population with HT

Found in 10% of those screened

M = F

Common between 3rd and 5th decades of life but can occur at any age.

Rare

• Clinical manifestations

• The five P’s:• Pressure (HTN)• Pain (Headache)• Perspiration(diaphoresis)• Palpitation• Pallor(there is a decrease in red cell

mass)

• The Classical Triad:

1. Pain (Headache)

2. Diaphoresis (excessive sweating)

3. Palpitations

• Cardiac manifestations

• Sinus tachy, ventricular ectopic, • Catecholemine induced increased

myocardial oxygen consumption, coronary vasospasmoAngina/MIoCardiomyopathy- hypertrophic

Cardiomyopathy- diastolic dysfn- norepi induced

oDilated cardiomyopathy- systolic dysfn- epi induced

• Neurologic manifestations

o Hypertensive encephalopathy (altered mental status, focal neurological s/s, seizures)

o Stroke – cerebral infarction/ embolus

o Intracranial bleeding

Diagnosis

1. Biochemical

2. Localization

1. Biochemical • 24h Urine CollectionPositive results show 2-3 fold elevation from

the normal valueNormal values:-Dopa=424-2612nmol/d-Epi=10-110nmol/d, -Norepi=12-85.5micg/d-Metanephrine=0-4.9mivmol/d-Normetanephrine=573-933nmol/d

• Test Characteristics:

• 24h urinary catechol Sen 83% Spec 88%

• 24h U total metanephrine Sen 76% Spec 94%• 24h Ucatechols + Utotal metanephrines Sen 90%

Spec 98%

• Sensitivity increased if 24h urine collection begun at onset of a paroxysm

• Plasma free metanephrines sensitivity = 99% specificity = 89%

• Plasma catecholamine sensitivity 84% and specificity = 81%

2. Localization: Imaging

• CT abdomen• Adrenal pheo sensitivity 93-100%• Extra-adrenal pheo sensitivity 90%

• MRI• > sensitive than CT for extra-adrenal

pheo

• Abdominal U/S and x-ray

ANESTHESIA MANAGEMENT

• Prior to 1951, reported mortality rate for excision of pheochromoyctoma was 24 - 50 % due to

• HTN crisis, arrhythmia, MI, stroke• Hypotensive shock

Cont’d….• Currently, mortality: 0 - 2.7 %• The reasons are:

• Preoperative preparation, --blockade• New anesthetic techniques

• Anesthetic agents• Intraoperative monitoring:

arterial line, EKG monitor, CVP line

• Presence of experienced & coordinated team:

• Endocrinologist, Anesthesiologist and Surgeon

• Preoperative preparation

• Preoperative work up - CBC, electrolytes, creatinine - CXR - EKG - Echo (r/o CMY 2º to catechols)

• Preoperative & β blockade

• Start at least 10-14d preoperatively• Allow sufficient time for ECF re-expansion

• There must also be dose increments with time until there is optimal control of paroxysms

• Adrenergic Receptors

• Alpha-Adrenergic Receptors• -1= vasoconstriction, intestinal relaxation,

uterine contraction, pupillary dilation• -2= - presynaptic NE (clonidine), platelet

aggregation, vasoconstriction, - insulin secretion

• Beta-Adrenergic Receptors• -1= - HR/contractility, - lipolysis, - renin

secretion • -2= vasodilation, bronchodilation, -

glycogenolysis• -3:=- lipolysis

Alpha blockade

• Phenoxybenzamine (Dibenzyline) a non selective blocker.

• Drug of choice• Covalently binds --receptors (-1 > -2)

• Start 10 mg PO BID increase by 10-20 mg/d PO BID• Maintenance 40-80 mg/d (some need

> 200 mg/d)

• Phenoxybenzamine (cont’d)• Side-effect: orthostasis with dosage

required to normalized seated BP, reflex tachycardia• Drawback: periop hypotension/shock

unlikely to respond to pressor agents.• Prevents 2 mediated inhibition of

catecholamine release • Thus beta blockers needed to be

given alongside

• --blockade• Used to control reflex tachycardia and

prophylaxis against arrhythmia during surgery• Start only after effective --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 control HR• Initial dose 80-120 mg/d• IV 1-10 mg

• Propranolol ( cont’d)

o Side effects- may induce cardiac failure, bronchospasm

oOral bioavailability 25% (extensive 1st pass metabolism)

• Atenolol- selective B1

oDose 50- 100 mg/d POoMax 300 mg/do IV 2.5 to 10 mg/d

• Esmolol – selective B1 for rapid intraop BP controloBolus IV 500 µ/kg/mino Infusion 50 to200 µ/kg/min

• Labetolol –mixed ɑ+βoDose- 50- 100 mg/d POo IV 0.25 mg/kgoNot used as a sole drug due to

unpredictable control of BP

• If BP is still not controlled despite - + - blockade

Add Prazosin to PhenoxybenzaminePrazosin – competitive, selective -1 blocker

o T1/2- 2-3 Hrs.oDose -1-5 mg PO BDo Side effects- postural hypotension reflex

tachycardiaoOther selective -1 blockers- terazosin,

doxazocin

• Other antihypertensives• CCB-

oDiltiazem 60- 120mg/d, max 360mg/doT1/2- 3 to 5 hrs oSide effects- bradycardia, exacerbates

cardiac failureoNifedipine – 30mg/d PO Max. 360mg/doT1/2-1 to 2 hrsoSide effects- hypotension, peripheral

edema• Avoid diuretics as already ECF contracted

• Nicardipine • Started PO 24 Hrs to few weeks preop to

control BP and allow ECFV restoration• After intubation IV Nicardipine (start 2.5

ug/kg/min)• IV Nicardipine adjusted to SBP• Stopped prior to ligation of vein • Tachycardia Rx with concurrent IV esmolol

• Advantage: periop hypotension may still respond to pressor agents as opposed to those patients who are completely ---blocked

• Evaluation of - adrenergic blockade

• Roizen’s criteriaoArterial BP < 160/95 mm Hg in the last

48 hrs prior to surgery. Recommended to measure in stressful environment

oMild orthostatic hypotension indicates optimal - adrenergic blockade but not < 80/45.

o ECG- free of ST changes for > 2 wks, oVentricular ectopic < 1 over 5 min

• Premedication

• If patient is anxious give appropriate dose of BDZ in the night prior to the day of surgery

• Monitoring

ECGCVPDirect arterial pressure measurementsCapnographTemperature Arterial blood gas analysisBlood glucose levels

• Anesthetic technique • General anesthesia• Regional anesthesia- mid to low thoracic • Combined regional and general anesthesia• Preferred- combined regional and general

anesthesia techniqueoHere although regional anesthesia protects

against stresses of surgery, it cannot prevent catecholamine surges due to tumor manipulation.

o In extensive sympathetic blockade, severe hypotension after tumor removal,

• INDUCTION

• Essentially important to give induction agents slowly along with close monitoring of HR and arterial pressure

• Thiopentone / propofol widely used

• Etomidate –causes pain/ involuntary mov’t

• Ketamine – should be avoided

• Multimodal – BZD+ opioid(avoid pethidine & morphine)+ induction agent

• Attenuate pressor response

Important for laryngoscopy and tracheal intubation

2% lignocaine(with out adrenaline) – 1-1.5mg/kg one minute before laryngoscopy

Esmolol – 50- 100 µg/kg/min

During laryngoscopy catecholamine levels ↑o Normally- 200- 2000 pg/mlo During laryngoscopy - 2000- 20,000 pg/ml

• Neuromuscular blockade

NDMR drugs= vecuroniumSuxamethonium- avoided causes

fasciculation and rise in intra abdominal pressure

Atracurium/ mivacurium- best avoided due to release of histamine

Cisatracurium/rocuronium- safe cardio stable and least histamine release

• Maintenance

• Inhalational agent- isoflurane used extensively b/c it does not sensitize the myocardium to catecholamines

• Halothane undesirable due to it’s arrhythmogenic properties

• Sevoflurane used successfully (fast onset …..fast offset)

• During surgery• Have ready: IV phentolamine, IV NTP,

IV esmolol• Very high uncontrolled BP- tell

surgeons to stop manipulation of the gland• Ligation of adrenal vein- care for

sudden hypotension• Rx hypotension with crystalloid +/-

colloid 1st

• may need dopamine/ noradrenaline/ phenylephrine

• Postoperative

• Post op ventilation / ICU stay- depends upon the hemodynamic status…. Preferably ICU stay for 24 Hrs

• Hypoglycemia post op due to disinhibition of B cell supression….. Increased insulin secretion

• Glucose supplementation at end of surgery

• Post op( cont’d)

• Most cases can stop all BP meds postop• Postop hypotension: IV crystalloid• HTN free: 5 years 74% 10 years 45%

• 24h urine collection 2 week postop• Surveillance:

• 24 h urine collections every year for at least 10years• Lifelong follow up

• 5 year survival- non malignant pheo- 95%• Malignant- < 50 %

Conclusion• Long term outlook very good• Managed by an experienced team of

anesthesiologist, surgeon, endocrinologist & cardiologist

• Principles of anesthetic managementoGood adrenergic blockade preopoVigilant intraop monitoring and

treatment of hyper/ hypotensiono Post op ICU care

• Antihypertensive for a prolonged period

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