Thyroid diseases and

anaesthesia
Presented by Dr. Bindu L. Shah
M.D. II yr anaesthesia
Moderator: Prof B.D. Jha
064/11/2
 Anatomy
 15 -25 grams in weight;; 2 lateral lobes
connected by an isthmus, lie at the level C4-
C7
 Closely attached to thyroid cartilage & to
upper end of trachea – thus moves on
swallowing
 Close relationship with rec. laryngeal
nerve
 Blood flow very high at 5 ml/min/gm (2x
kidney!)
 Supply: from superior (1st branch of
External Carotid) and inferior thyroid
arteries ,thyroidea ima artery
 Drainage: Sup. mid. and inf. veins
 Physiology
 Functions of the thyroid gland:
1. Hormone secretions- T3, T4
2. Synthesis of thyroglobulin
Iodine: raw material
Daily requirement: 300-1000 ug/day
Euthyroidism: 150ug/day
For prevention of goitre:75 ug/day
Pregnany: 200ug/day.
Neonatal: 40 ug/day
 Biosynthesis and release of thyroid
hormones
1. Iodide uptake:
2. Oxidation: In thyroid, Iodide is converted to
iodine with the help of thyroid perooxidase
3. Iodination of tyrosine residue that are part of
thyroglobulin molecule & formation of
MIT,DIT
4. Coupling / condensation: DIT+DIT=T4,
DIT+MIT=T3
5. Release : endosytosis T3=4ug/day,
T4=80ug/day
 Contd.
 1/3 of T4 is converted to T3 peripheral
tissue
 T3 : 13% (thyroid), 87% (T4)

T4 - 99.95% bind to plasma protein

T3 – 99.50% bind to plasma protein, lower
affinity to plasma protein contributes to
greater biological activity.
 contd
 T3 acts rapidly ,3-5 times more potent
than T4 because T3 is loosly bound to
plasma protein & binds more avidly to
thyroid hormone receptors
 PHYSIOLOGY OF HYPOTHALAMIC-
PITUITARY-THYROID AXIS
1. hypothalamus : TRH released
2. pituitary :TRH stimulates pituitary for
TSH release
3. Thyroid :TSH stimulates ,TSH receptor in
the thyroid, to synthesis both T4, T3 
increased plasma levels of T4 & T3
 Mechanisms of action of thyroid
hormones
 Thyroid hormones enters cells & bind to
thyroid receptors in nuclei that binds to
DNA, & increase or decrease the
expression of genes that regulate cell
function
 Effects of thyroid hormones
1. Influence the growth and maturation of
tissues.
2. Calorigenic action: increase o2 consumption,
increase BMR
3. CVS: increase heat production, increase body
temp. cutaneous vasodilatation, decrease
peripheral resistance, leading Na. & water
retention ----increase blood vol. CO, rate &
pulse pressure increased.
 Contd.

Nervous system:
1) low-slow mentation; reflexes time
prolomged
2) high-rapid mentation, irritability, restless,

reflexes time shortened.

Skeletal muscle : weakness, myopathy.

 contd
 Relation to catecholamine : intimately
related, however plasma level of
catecholamine is normal in
hyperthyroidism symptoms are relieved
with B blockers.
 Carbohydrate metabolism-
1. physiological- glycogenesis
2. Pharmacological: hyperglycemia
Protein metabolism:
1. Physiological- Anabolic

2. Excess- catabolic

Fat metabolism: lipolytic

Vitamin metabolism: thyroid hormone
converts carotene to vit. A
 Normal function of thyroid gland –
directed to secretion of T3 & T4
 Insufficient hormone secretion –
hypothyroidism /myxedema
 Excessive secretion – hyperthyroidism
 HYPERTHYROIDISM
Causes:
1. Grave’s disease
2. toxic multinodular goitre,
3. thyroiditis,
4. pituitary tumour ( excess TSH secretion)
5. overdosage of thyroid replacement hormone
6. Carcinoma of thyroid
Pathogenesis of graves disease
 TSH receptor abs( thyroid stimulating
immunoglobulins) reacts with the TSH
receptor to stimulate both function &
growth of thyroid gland.
 Clinical manifestation
 CVS is the most important organ
involvement.
1. Sinus tachycardia,
2. AF,
3. precipitation of IHD,
4. cardiac failure
5. Increase CO & pulse pressure
 Thyroid: diffuse or nodular goitre
 GIT: wt. loss, increased appetite, diarrhoea
 Nervous system: nervousness, emotional liability,
psychosis, hyperreflexia
 Muscular : fine tremors, muscle weakness, myopathy.
 Dermatological: increase sweating,
 Reproductive: menstrual disturbances, infertility,
impotence
 Miscellaneous: heat intolerance,fatigue
 Eye: exophthalmos,lid lag ,lid rectraction
 1. Medical Therapy

 a) Beta-blockade:
 most rapid method of reversing symptoms
 effective within 12 - 24 hrs
 may inhibit peripheral conversion of T4 to
T3 as well as blocking beta catech-olamine
receptors
 usually only used to tide over while other
therapies take effect
 b) Methimazole/Carbimazole
 carbimazole is the prodrug of methimazole
 iodinated molecule blocks iodination of tyrosine
residues
 effects seen after 3 - 4 weeks
 can be used as the sole therapy for
hyperthyroidism: given for a period of 12 -18
mths but relapse rate >50%
 SFx - rash, arthralgia, N&V
 agranulocytosis
 c) Propylthiouracil
 mechanism of action: a) as for carbimazole and
b) blocks peripheral conversion of T4 to T3
 faster onset of action cf carbimazole (due to 'b'
above)
 SFx same as carbimazole; can convert from one
drug to the other if SFx a problem
 d) Ablative Therapy
 Radioactive Iodine (I131)
 I131 concentrates in the thyroid and destroys
functioning cells
 takes 6 -10 weeks for clinical effect
 repeat doses often necessary
 hypothyoidism can occur up to years after therapy
 aside from hypothyroidism, few side effects
 pregnancy an absolute contraindication
 no evidence for inherited genetic damage in babies if
mother has had therapy in the past
 2. Surgery
 Due to I131, surgery for hyperthyroidism is less
commonly required now than in the past.
Subtotal thyroidectomy attempts to preserve the
correct amount of tissue to allow euthyroid state
post-op. Complications include:
 hypo- (or occasionally hyper-) thyroidism
 hypoparathyroidism
 ANAESTHETIC IMPLICATIONS
Hyperthyroidism
 Except for absolute emergency surgery, all patients
should be clinically euthyroid prior to surgery.
 Pharmacological stabilisation of hyperthyroid patient
requires at least 6 -8 weeks. Beta-blockade combined
with iodide (or lithium) can achieve euthyroid state in 1
-2 weeks but cardiac effects take longer to resolve.
 risk of thyroid storm provoked intraop or, more
frequently, postop
 other risks of hyperthyroidism:
 cardiac failure
 increased sensitivity to catecholamine-induced
arrhythmias
 Emergency Surgery in hyperthyroid
patient
 commence anti-thyroid Rx as soon as
diagnosis made (in conjunction with
specialist endocrinologist)
 preop sedation, eg with benzodiazepine
 Intraoperatively:
 avoid sympathetic stimulation, eg ketamine, pancuronium,
adrenaline in LA
 continue beta-blockade titrated to heart rate
 consider regional technique to decreased symp. stimulation
 monitor HR, Temp, IBP, ETCO2, SpO2, ABGs
 may have increased inhalational anaesthetic requirement due to
increased cardiac output, increased temperature, ? CNS
excitation
 care with exopthalmic eyes
 Postoperatively:
 intensive monitoring
 Thyroid Surgery

 Preoperative Assessment:
 1. Gland Function - is the patient clinically euthyroid?
 most important indicator of adequacy of medical preparation is
resolution of symptoms, weight gain & normal heart rate
 assess cardiac status
 history & examination
 investigations: CXR, ECG,ischaemia as indicated
 review investigations, esp. recent TFTs
 keep in mind possible associated conditions; myaesthenia gravis &
rheumatoid arthritis with Graves's disease and phaechromocytoma
with medullary Ca of the thyroid
- Airway:
- Determine ease of intubation
- Compression Symtoms:- hoarseness of voice,
stridor, dysphagia
- Cervical x-ray – tracheal deviation /
compressionr
- Retrosternal spread (SVC obstruction)
 Preparation of the patient
Current medication:
continue medication & serve on morning of surgery
Indirect laryngoscopy
- ENT review on vocal cord function as a baseline
finding
Premedication
1. reassurance

2. no premedication in pt with airway obstruction

3. Pt adequately sedated to prevent anxiety &

apprehension ( BDZ / narcotic premedication )
 Monitoring:

 Detection of disconnection or cyanosis essential

and difficult as patient is completely covered in
drapes. Ventilator alarm, precordial
stethoscope, ETCO2, oximetry, etc should be
considered.
 NIBP, ECG essential. Consider arterial line if
poorly controlled.
 Temperature monitoring and provision for
cooling .
 Induction

A- No difficulty anticipated:
- usual iv induction & intubation (fentanyl, STP, non-depolarizing
muscle relaxant
B- possible difficulty in intubation:
- iv induction, test ventilation when pt is unconscious, intubation
+- suxamethonium
C- definite intubation problem / evidence of airway obstruction
- awake fibreoptic intubation
- inhalational induction
- choice of ETT- armoured ETT (< risk of kinking)
 Intraop.

Control over cardiovascular refexes at all

times - adequate depth of anaesthesia
required.
Airway : secure it
Posture:
Head-down slightly, protect eyes and
nerves, extend neck.
 Intra op.
Choice of anaesthetic agents:
- induction agent – thiopentone
- muscle relaxant – atracurium, vecuronium
- volatile agent – isoflurane
- narcotic analgesics – fentanyl, morphine
- anaesthetic technique – balanced
anaesthesia with N2O-O2-isoflurane-muscle
relaxant-narcotic analgesics --- IPPV
Extubation: uncomplicate reverse &
extubate as usual
Check vocal cord movements .
 precautions
- avoid ketamine, pancuronium, indirect-acting adrenergic
agonists & other drugs that stimulate the sympathetic nervous
system
- Prone to exaggerated hypotensive response on induction
- Achieve adequate anaesthetic depth before laryngoscopy / any
surgical stimulation
- Administer neuromuscular blocking agent cautiously
( thyrotoxicosis a/w incidence of MG & myopathies )
- Hyperthyroidism does not  anaesthetic requirements
 Post op. mg.
 Monitoring aggresively.
 Complication: post.op

1)Airway obstruction
Possible causes:
- neck haematoma with tracheal
compression
- recurrent laryngeal nerve palsy
- tracheomalacia
- incomplete reversal
 Complication, contd.

2)Thyroid crisis / storm

Life-threating
- Decompensated hyperthyroidism with
excessive release of thyroid hormone

- May mimic :malignant hyperthermia,

pheochromocytoma
 Complication,contd

Symptoms/sign
Onset – intraoperative / 6-24 hours after surgery.
hyperpyrexia,sweating,hyperventilation
CVS: tachycardia atrial fibrillation,CCF,shok
GIT: vomiting, acute abdominal pain
simulation.
CNS: coma, agitation, psychosis, restless,
 Precipitants
- Infection
- surgery
- poorly prepared thyroid surgery
- diabetic ketosis
- radioiodine therapy in a poorly prepared pt
- MI
Investigate for precipitants – FBC, blood glucose, FT4,
FT3
 Management

 medical emergency; cannot wait for laboratory confirmation

 02, active cooling (not aspirin as it displaces T4 from TBG)
 Beta-blockade: I.V. Propanolol 1-5 mg slowly 4-6hrly, promptly
treats fever, tachycardia, tremor; does not reduce O2 consumption
 Care with Beta-blockers if heart failure (could try esmolol)
 steroids Rx often recommended due to possible "adrenocortical
exhaustion" iv dexamethasone 2mg 6hrly inhibits thyroid hormone
release & peripheral conversion,
 Iodide IV (as KI 60mg bd or NaI 1.0 - 2.5 g) rapidly controls
thyrotoxicosis
 Can use lithium if allergic to iodide
 Oral antithyroid drugs commenced as soon as possible
 complication
3)Tetany
- Hypocalcemia develops 24-72 hrs postop.
- clinical manifestations: circumoral tingling, paraesthesia,
laryngeal spasm,
- (+)ve Chvostek & Trousseau signs
- May result from respiratory alkalosis
- over-ventilation in immediate
postoperative period
- hypocalcemia from
hypoparathyroidism
 Management.
- Calcium estimation
- Slow injection of 10% calcium gluconate
10 mls IV
 HYPOTHYROIDISM
Causes
- autoimmune disease, thyroidectomy, radioactive iodine,
antithyroid medications, iodine deficiency, failure of
hypothalamic-pituitary axis
Clinical manifestations:
- weight gain, cold intolerance, muscle fatigue, lethargy,
constipation, hypoactive reflexes, depression, dull facial
expression,
 HR, stroke volume, CO
- Pleural, abdominal, pericardial effusion

Dx: low free T4 level

 Myxedema Coma
- Results from extreme hypothyroidism
- Precipitated by – infection, surgery, trauma
- C/f: - most pts are female, elderly
- impaired mentation
- hypoventilation
- hypothermia
- hypotension
- bradycardia
- comatose
- hyporeflexia
- hyponatremia
 Management
I)T3, T4, TSH, FBC,
ii) Should start on clinical grounds
iii) Thyroid hormone replacement
- T4:- iv 200 mcg bolus, daily dose
100mcg till pt can take orally
- T3:- iv/oral 10-20mcg bd till T4
can be given orally
iv)steroids:- iv hydrocortisone 100mg stat, 50-
100mg
ventilation: assisted ventilation if RF
vi) hypothermia:
- do not warm rapidly (>1C/hr)– CVS collapse

- Blankets & close temperature monitoring

vii) Hypotension
viii) Hyponatremia
- caused by dilution & redistribution

- Fluid restriction
ix) Tx of precipitating factors
* Full recovery – replacement thyroxine
dose titrated once / 2-3 weeks to maintain
euthyroid state.
 PREOPERATIVE

Severe hypothyroidism ( T4 <1mg/dL):

 Elective case – to correct first

 Emergency case – to treat with thyroid

hormone prior to surgery

Mild – moderate:- no absolute C/I
Airway
ii- CVS
Iii- endocrine status
- coarse dry skin, slow mentation, cold
intolerance,
- CO, hyporeflexia, hypoglycaemia
 Increased sensitivity towards anaesthetic agents &
central depressants
 Hypotension & cardiac arrest following induction

 Delayed recovery from GA

 Premedication
 Do not require much, prone to drug-
induced respiratory depression
 Histamine H2 antagonists &
metoclopramide – slowed gastric
emptying times
 INTRAOPERATIVE

susceptible to hypotensive effect of anaesthetic agents

-  CO
- blunted baroreceptor reflexes
-  intravascular volume
- induction agent of choice – ketamine

- does not  MAC

- Potential problems

- hypoglycemia, anemia, hypoNa+

- difficult intubation d/t large tongue
- hypothermia d/t low BMR
 POSTOPERATIVE
- delayed recovery – hypothermia,
respiratory depression, slowed drug
biotransformation
- Should remain intubated till awake & close
to normothermic
- Postoperative pain relief – nonopiod
(ketorolac
Thank you