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J.J.M MEDICAL COLLEGE, DAVANGEREDEPT OF ANAESTHESIA

CHAIR PERSON PRESENTED BY Dr. Ravishankar M.D, D.A Dr. Pritam Professor Postgraduate Date – 18/02/2011

SEMINAR ON ANAESTHETIC MANAGEMENT OF PATEINT WITH

HYPERTHYROIDISM

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INTRODUCTION

• Thyrotoxicosis is defined as the state of thyroid hormone excess.

• Hyperthyroidism is the result of excessive thyroid function.

• The most common cause of hyperthyroidism being – Grave`s Disease.

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CAUSES

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GRAVES' DISEASEEpidemiology

• Its an hyper-metabolic state

• Accounts for 60–80% of thyrotoxicosis.

• Occurs in up to 2% of women but is 1/10 as frequent in men.

• Typically occurs between 20-50 years of age, but it also occurs in the elderly.

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Clinical Manifestations

• The clinical presentation depends on-Severity of thyrotoxicosis, Duration of disease, Individual susceptibility to excess thyroid hormone

and Patient's age.

• In the elderly, features of thyrotoxicosis may be subtle or masked, and patients may present mainly with fatigue and weight loss, a condition known as apathetic thyrotoxicosis.

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Central nervous system manifestations

• Hyperactivity, nervousness & irritability easy fatigability

• Insomnia & impaired concentration.

• Fine tremor.

• Hyperreflexia, muscle wasting & proximal myopathy without fasciculation.

• Chorea rare feature.

• Hypokalemic periodic paralysis

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Cardiovascular Manifestation:

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• Sinus tachycardia/supraventricular tachycardia palpitations

• The high cardiac output bounding pulse

• Systolic hypertension widened pulse pressure.

• Aortic systolic murmur

• Worsening of angina or heart failure

• Atrial fibrillation is more common in patients >50 years.

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Skin & Nail Manifestations• Warm and moist • Sweating & • Heat intolerance

• Palmar erythema, onycholysis, pruritus, urticaria & diffuse hyperpigmentation

• Hair texture fine • Diffuse alopecia occurs in up to

40% of patients.

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• Thyroid dermopathy occurs in <5%.

• Most frequent over the anterior & lateral aspects of the lower leg (hence the term pretibial myxedema).

• Typical lesion noninflamed, indurated plaque with a deep pink or purple color and an "orange-skin" appearance.

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• Thyroid Acropachy a form of clubbing found in <1% of patients with Graves' disease.

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Gastrointestinal System

• Transit time is decreased increased stool frequency diarrhea/steatorrhea.

• Weight loss inspite of increased appetite

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Reproductive system

• Frequent oligomenorrhea or amenorrhea;

• Pregnancy low birth weight babies & pre-eclampsia.

• In men impaired sexual function & rarely gynecomastia.

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Skeletal System

• Osteopenia in long-standing cases.

• Mild hypercalcemia occurs in up to 20% of patients, but hypercalciuria is more common.

• Small increase in fracture rate.

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Thyroid• Usually diffusely enlarged

to >2–3 times its normal size.

• The consistency is firm.

• Thrill or bruit increased vascularity of the gland and the hyperdynamic circulation.

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Eye signs & symptoms

• Lid retraction staring appearance sympathetic overactivity.

• Associated with specific eye signs that comprise Graves' ophthalmopathy.

• This condition is also called thyroid-associated ophthalmopathy.

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• The earliest manifestations of ophthalmopathy are usually a sensation of grittiness, eye discomfort & excess tearing.

• About 1/3 pts have proptosis,

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• Periorbital edema, scleral injection, & chemosis are also frequent.

• In 5–10% of patients, the muscle swelling is so severe that diplopia results.

• Most serious manifestation compression of the optic nerve at the apex of the orbit, leading to papilledema, peripheral field defects, & if left untreated, permanent loss of vision.

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The "NO SPECS" scheme is an acronym derived from the following eye changes:

• 0 = No signs or symptoms • 1 = Only signs (lid retraction or lag), no symptoms • 2 = Soft tissue involvement (periorbital edema) • 3 = Proptosis (>22 mm) • 4 = Extraocular muscle involvement (diplopia) • 5 = Corneal involvement • 6 = Sight loss

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Toxic Multinodular GoiterEtiology and Pathogenesis

• MNG occurs in up to 12% of adults.

• More common in women than men and increases in prevalence with age.

• It is more common in iodine-deficient regions

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Hyperfunctioning Solitary Nodule• A solitary, autonomously functioning thyroid

nodule Toxic Adenoma.

• Thyrotoxicosis is usually mild.

• Suggested by the presence of the palpable thyroid nodule & by the absence of clinical features suggestive of Graves' disease or other causes of thyrotoxicosis.

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DifferencesPrimary Secondary

Goitre is diffuse, vascular. Nodular

Onset-abrupt Insidious.

Symptoms appear 1st then thyroid

swelling

Thyroid swelling appears 1st.

More severe Less severe

CVS – rare involvement Present with CCF or AF

CNS – commonly involved Rarely involved

Eye signs & exophthalmos are

common.

Eye signs rare

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Laboratory Evaluation

• Normal thyroid function tests

TESTS NORMAL VALUES

TSH >0.4-5.0 mU/L

TOTAL T4 5.0-12.0 μg/dl

TOTAL T3 70-195 ng/dl

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TSH Assay single best test of Thyroid Hormone action at cellular level.

• Normal level 0.4-5.0 mU/L.• Subclinical hyperthyroidism TSH level is 0.1-

0.4mU/L with normal FT3 & FT4.• Overt hyperthyroidism TSH level is <0.03mU/L

with increased T3 & T4.• Thyroid Storm TSH level is <0.01mU/L.

Free T4 (FT4) approx 0.02% of total T4.• Elevated in 90% of patients with hyperthyroidism.• Decreased in 85% of patients with hypothyroidism.

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T3 resin uptake test (RT3U) • Indirect measure of unbound fraction of T4.• It quantitates the degree of saturation of TBG sites by T3

& T4.• It is directly proportional to FT4 & inversely proportional

to TBG sites.

FT4 index = T4 x RT3U. Normal value- 1.4-4.9

In 2–5% of patients, only T3 is increased (T3 toxicosis).

The converse state of T4 toxicosis hyperthyroidism is induced by excess iodine.

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Radioactive iodine uptake I123, I131 & Tc99

• Varies directly with functional state of thyroid.• 24 hr thyroid uptake is measured.• Normal value range – 10-25%• Used to confirm Hyperthyroidism.

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• TRH stimulation test used to test pituitary function.

• Measurement of TPO antibodies is useful in differential diagnosis.

• Measurement of TBII or TSI will confirm the diagnosis but is not needed routinely.

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Other tests• Serum Antimicrosomal Antibodies.

• Antithyroglobulin antibodies.

• Long acting thyroid stimulators (LATS).

• Thyroglobulin

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• Ultrasonography to differentiate between cystic, mixed or solid lesion in gland.

• Thyroid scan using I123 or Tc99 evaluate nodules as Warm/ NormalHot/ Hyperfunctioning.Cold/ Hypofunctioning.

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In Toxic Multinodular Goiter • The TSH level is low.

• The T4 level may be normal

or minimally increased;

• T3 is often elevated to

a greater degree than T4.

• Thyroid scan shows heterogeneous uptake with multiple regions of increased and decreased uptake;

• 24-h uptake of radioiodine may not be increased

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In Toxic Adenoma

• A thyroid scan provides a definitive diagnostic test.

• Focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of the gland, as activity of the normal thyroid is suppressed.

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Diagnosis of Hyperthyroidism: Wayne’s diagnostic index

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Index :• < 11: Non toxic• Between 11 – 19: Equivocal • > 19 : Toxic

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TREATMENT OF THYROTOXICOSIS

• Includes :

1. Antithyroid drugs 2. -adrenergic blockers and

other antihypertensive drugs3. Radioactive iodine 4. Surgery

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Antithyroid drugsIndications :

• In children

• In young adults with mild thyrotoxicosis

• Conjugation with radioactive iodine to hasten recovery, while awaiting the effects of radiation.

• In pregnant women

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Surgical Treatment

Reserved for MNG with

1. Severe hyperthyroidism in children2. Pregnant women who can’t tolerate ATD 3. Large goiters with severe Ophthalmopathy4. Large MNGs with pressure symptoms5. Who require quick normalization of thyroid

function

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Radioiodine Therapy

• Indications

1. Primary Thyrotoxicosis after 45yrs of age2. In autonomous toxic nodule3. In recurrent thyrotoxicosis.

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Preoperative Evaluation

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History• History of onset, duration, rate of growth• History suggestive of primary or secondary thyroid

toxicity• History of pain• History of palpitation, precordial pain, exhaustion• History of pressure effects- like dyspnoea,

dysphagia, hoarseness of voice.• Past history/family history.• Personal history-diet, menstrual, mental attitude,

sleep

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General Physical Examination

• Built, nourishment• Fullness of thyroid region, pallor, icterus,

cyanosis, clubbing, oedema• Temperature, Sleeping pulse rate, blood

pressure• Skin- hot and moist palm• Tremors• Mental status-anxiety, nervousness.• Airway assessment

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Local examination

Inspection :

• Whether diffuse/ nodular swelling

• Pizzillo's method : in obese and short necked patient hands are placed behind head and patient is asked to push head backwards against her clasped hand. Ask the patient to swallow, thyroid slowly moves upwards on deglutition.

• Pemberton's sign : Patient is asked to raise both the arm over his head until they touch the ears. This is maintained for a while, congestion of face and distress becomes evident because of obstruction of great veins at thoracic inlet.

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Palpation :

• Patient should be sit on a stool and neck slightly flexed.

• Lahey's Method • Crile's method• Kocher's test• Berry's Sign

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• Percussion : Over manubrium sterni to exclude presence of a retrosternal goiter.

• Auscultation : A systolic bruit may be heard over goiter due to increased vascularity in primary toxic goiter.

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Examination for toxic manifestation

1. Exophthalmos :

In early stages, may be unilateral but later may become bilateral.

• Stellwag's sign : Infrequent blinking of eyes with widening of palpabral fissure.

• Von Graefe`s sign : Upper eye lid lags behind the eye ball as the patient is asked to look downwards.

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• Dalrymphe's sign : Upper sclera is visible due to retraction of upper eye lid.

• Joffroy's sign : Absence wrinkling in the forehead on looking upwards with the face inclined downwards.

• Moebius sign : Inability or failure to converge the eye balls

• Gifford's sign: Difficulty in eversion of the upper lid.

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2. Tachycardia:

• Resting pulse rate should be recorded at early morning 3am & 3pm.

• 80-90 bpm -mild thyrotoxicosis • 90-110 bpm-moderate thyrotoxicosis • > 110 bpm- severe thyrotoxicosis

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3. Tremors : Fine tremors in stretched hands protruded tongue and fingers are seen in primary thyrotoxicosis.

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Systemic examination

CVS : • Enlarged heart• Atrial fibrillation• Signs of CCF.• Systolic murmurs

CNS : • Myopathy and tremors• Reflexes- hyperreflexia

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Investigation• Complete hemogram, BT, CT to rule out anaemia,

thrombocytopenia and agranulocytosis.

• Urine Albumin, Sugar, Microscopy

• RBS, B. Urea, Serum creatinine

• Thyroid function tests.

• ECG- Sinus tachycardia, ST elevation, QT shortening, atrial fibrillation/flutter, ventricular ectopic

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Chest X-ray

• PA view- position of trachea, deviation, retrosternal goiter, calcification.

• Lateral view and barium swallow- pressure effects on trachea and oesophagus

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Flow volume loop- best indications of airway obstruction.

CT scan and MRI scan-for airway evaluation and extension of thyroid.

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Pre operative preparation

• Admission

• Absolute bed rest.

• Sedation Diazepam 2mg-5mg-10mg.

• Β blockers, e.g propranolol 40mg 1-1-1

• Specific drugs, e.g Carbimazole 5mg 1 qid & then slowly reduced to 1 bd. Given for 4-6wks.

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• Resting pulse chart.

• Thyroid function tests should be done every 4wks till thyronormalcy.

• Thyroid steal

• Patient must be made euthyroid or near euthyroid at operation.

• Euthyroid is clinically assessed by-

– Sleeping pulse rate < 90/min

– Progressive weight gain

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– Disappearance of toxic symptoms like tremors, nervousness, anxiety etc .

– No requirement of sedation for sleep.

– Normal pulse pressure, sinus rhythm, disappearance of cardiac murmurs

• ENT check-up for mobility of cords.

• The last dose of ATD may be given on the evening before surgery.

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Plan of Anaesthesia

• General anesthesia,

• Regional – Cervical Epidural Anesthesia.

• Local blocks- Cervical plexus block (b/l)

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Premedication :

• Aim is to suppress sympathetic activity.

• Psychological : Reassurance to the patient.

• Pharmacological :

• T diazepam l0mg PO HS and 5mg PO in the morning or

• T Lorazepam 2-3mg oral 30 mins before operation.

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• Inj.Morphine 0.1 to 0.15mg/kg i.m. 30min before operation.

• Inj. Promethazine 25-50mg iv 30 min before operation.

• Premedication is avoided if airway problem is anticipated.

• Anti aspiration prophylaxis

• Anticholinergic drugs are not recommended.

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Monitoring :

• Pulse oximetry• NIBP• ECG• Temperature monitoring• ETCO2• Neuromuscular monitoring• CVP line• Urine output

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General Anaesthesia • Wide bore IV line is secured preferably in lower

limb after application of EMLA cream.

1. Pre-oxygenation : With 100% 02 for 3-5 minutes.

2. Induction.• Inj. Thipentone sodium 5-7mg/kg i.v is the drug

of choice.• Inj. Glycopyrolate- 0.0l mg/kg i.v

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• Attenuation of sympathetic response to intubation by Inj. Lignocaine 1.5-2mg/kg i.v or Opioid/Esmolol infusion can be used.

3. Relaxation: • Inj Scoline 2mg/kg if difficult airway anticipated.

• Inj Vecuronium 0.08-0.12 mg/kg iv or Inj. Rocuronium 0.5mg/kg iv if easy airway anticipated

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When airway problem is anticipated

• Awake/fibreoptic intubation can be done with local anaesthesia.

• Intubation with gentle laryngoscopy is done with cuffed armored tube/ cuffed ETT/north pole oral tracheal tube or intubating LMA with fiber optic bronchoscopy guidance.

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• Patient is positioned with sand bag between the shoulder blades and the head resting on a padded horse shoe or whit lock head rest.

• Avoid hyperextension.

• 20°-25° head up tilt to aid venous drainage & to decrease BP.

• Arms should be secured by the side

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4. Maintenance of Anaesthesia :

• Controlled ventilation is used with N20 + 02 + NDMR + inhalation agents + incremental doses of opioids.

NDMR :• Inj. Vecuronium 0.05 mg/kg or • Ini. Atracurium 0.3 - 0.4 mg/kg or • Inj. Rocuronium 0.3 - 0.4 mg/kg.

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• Already existing myopathy may prolong N-M blockade.

• Associated myosthenia gravis emphasize the need to reduce initial dose of muscle relaxation.

• Use of a peripheral nerve stimulator to monitor N-M blockade.

• Isoflurane is preferred to halothane.

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Reversal and Extubation:

• With Inj. Neostigmine 0.05 mg/kg + Inj. Glycopyrrolate 0.01 mg/kg

• Inj. Xylocaine 1-1.5mg/kg IV 60-90 sec. Before extubation.

• A fibreoptic endoscope may be used to view the vocal cord.

• When adequate spontaneous respiration and laryngeal reflexes have returned the patient is extubated.

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Complications of Thyroid Surgery

1. Intraoperative:

• Carotid sinus stimulation - bradycardia + hypotension

• Tachycardia

• Thyroid crisis

• Haemorrhage

• Air embolism

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contd

• Tracheal injuries,

• Pneumothorax,

• Pneumomediastinum

• Damage to nerves.

• Atrial fibrillation

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2. Post operative

Immediate Late

Thyroid crisis Hypoparathyroidism

Haematoma Hypothyroidism

Tracheomalacia

Damage to nerves

Laryngeal oedema

Hypoparathyroidism

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Thyroid storm

• Is a life threatening emergency

• Characterized by sudden appearance of clinical signs of hyperthyroidism due to the abrupt release of T4 and T3 into circulation.

• Mortality is as high as 25% to 30%.

• Commonly associated with Grave's disease.

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Predisposing conditions:

• Medical factors :• Infection• Fever• Uncontrolled toxicity• Irregular drug intake• Pregnancy, toxemia of pregnancy• Radio iodine therapy• DKA.

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Surgical factors:

• Anxious and nervous patient before surgery,

• Too much handling of gland just before surgery.

This can occur both intraoperative or in the immediate post operative period, but the latter is more common between 6-18 hours post operatively.

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Clinical features :

• Hyperthermia: rise of 2°C/hr over normal temperature

• Tachycardia: arrhythmias commonly atrial fibrillation

• Initially flushing and sweating later leading to dehydration

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• CCF - initially high output failure, Later may go for Low output failure.

• Shock - cardiogenic/hypovolemic

• Electrolyte imbalance

• Hypo/hyperglycemia may also be present.

• Marked anxiety, agitation, psychosis.

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Differential Diagnosis

• Malignant hyperthermia

• Neuroleptic Malignant Syndrome.

• Pheochromocytoma

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Treatment General measures :

• Stop manipulation

• Increase the FiO2 to 100%.

• Cooling measures : surface cooling - sponging, ice packs, decrease OT temperatures. Cold IV fluid

• Establishment of an indwelling arterial line to follow metabolic derangements and also to aid in diagnosis.

• Treat the precipitating cause.

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Suppression of hormonal activity :

• Propylthiouracil - 600mg loading dose and 200-300mg every 6th hour given through NGT.

OR• Carbimazole ->50-100 mg through NGT followed by 20mg

6th hrly.

• Iodine as sodium iodide 1gm over 24 hours IV or enterally as potassium iodide 100-200mg every 8th hourly

• X-ray contrast agent sodium ipodate 1gm/day can also be used alternatively.

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Suppression of sympathetic activity :

1) Propranolol 1-2 mg IVAntagonizes the peripheral effects of thyrotoxicosis and also inhibits peripheral conversion of T4.

2) Esmolol-> 100-300 g/kg/min

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Treatment of shock and CCF :

• Digoxin Low out failure states.

• IV fluids should be given with reference to CVP line, otherwise overinfusion may further worsen CCF.

• IV fluids preferably to crystalloids containing glucose to supply enough energy for increased metabolism.

Supplementation of corticosteroids :

• Hydrocortisone 100- 200mg IV 8th hrly.

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Air embolism

• Occurrence of air embolism is influenced by Volume of air (> 0.5ml/kg/min), Speed of injection, Pressure in veins, Posture and general conditions

• Tip of a venous catheter advanced into the thorax the negative intrathoracic pressures generated during spontaneous breathing drawing of air into the venous circulation venous air embolism.

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Clinical Presentation

• Acute onset of dyspnea during procedure.

• Hypotension and cardiac arrest can develop rapidly.

• Air can pass across a patent foramen ovale obstruct cerebral circulation acute ischemic stroke.

• A characteristic “mill wheel” murmur can be heard over the right heart, but this murmur may be fleeting.

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Therapeutic Maneuvers• A syringe attached to the hub of the catheter (to

prevent any further air entry), & attempt should be made to aspirate air through the indwelling catheter.

• The patient, placed with the left side down

• In dire circumstances, a needle inserted through the anterior chest wall into the right ventricle to aspirate the air.

• Unfortunately, in severe cases mortality is high despite any of the suggested therapeutic maneuvers.

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Nerve palsy3 types of nerve injuries can occur – Neuropraxia– Axonotemesis– Neurotemesis

Unilateral Recurrent laryngeal nerve palsy

Pt may present with

• In INCOMPLETE palsy – only abductors are paralysed, – Vocal cord assumes median position. – Voice is unaffected & – Pt remains asymptomatic.

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• In COMPLETE palsy

– both abductors & adductors are paralysed, – vocal cord assumes paramedian position, – hoarseness of voice present, – possibility of voice returning to normal if other

cord compensates by crossing midline for closing glottis during phonation

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Treatment • Specific treatment for cause.• If Asymptomatic no treatment.• Hoarseness

• Speech therapy• Teflon paste• Implantation of cartilage• Arytenoidopexy• Thyroplasty

• These procedures are attempted if paralysis has persisted for more than 9-12 mts.

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Bilateral Recurrent Laryngeal Palsy

• Both vocal cords assume median/paramedian position.

• Severe inspiratory dyspnea with stridor may result if paralysis is sudden in onset

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Treatment

• Specific treatment for cause.• Intubation due to severe inspiratory stridor, replaced by tracheostomy within 2wks prevent laryngeal stenosis.

• Tracheostomy• Arytenoidectomy• Nerve –muscle transplantation.

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Hypoparathyroidism• Rare cause 0.5%

• Mainly due to vascular spasm of parathyroid glands & rarely due to accidental removal of parathyroids.

• Occurs in 2nd -5th postop day.

• Presentation – Weakness.– Chvostek`s sign +ve.– Carpopedal spasm– Convulsions

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Treatment

• Depends on blood calcium level,

• 10ml of 10% Calcium gluconate/citrate is given 8th hrly.

• Later supplemented by oral Calcium 500mg 8th hrly.

• Drug is stopped after 3-6 wks & serum calcium level is repeated.

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REFERENCES

1. Harrisons Principle Of Internal Medicine – 17th ed.2. Stoeltings anesthesia & co-existing disease – 5th ed.3. Barash Clinical Anaesthesia - 5th ed.4. Millers clinical Anaesthesia – 7th ed.5. Yao & Artusio`s Anesthesiology – 6th ed.

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THANK YOU