THYROID- ANATOMICAL, PHYSIOLOGICAL

CONSIDERATIONS AND THYROID DYSFUNCTION

MODERATOR: Dr. Y. ATCHYUTH,

ASSISTANT PROFESSOR, DEPARTMENT OF
ANAESTHESIOLOGY, RANGARAYA MEDICAL COLLEGE
PRESENTOR: SINDHURA, PG STUDENT
Word THYROID was coined by THOMAS
WHARTON
Gr THYREOS=shield; EDIDOS= from
 THYROID ANATOMY
LOCATION: Lower part
of the front and side of
the neck opposite to the
c5,c6,c7 and T1
vertebrae, clasping the
upper part of the trachea
WEIGHT : about 20-25
grams
DIMENSIONS:
lobes: 5*3*2 cms
isthmus: 1.25*1.25 cms
 CAPSULE
TRUE CAPSULE: peripheral condensation of fibrous
stroma of the gland
FALSE CAPSULE: splitting of pretracheal fascia, it
attaches to body of hyoid and cricoid cartilage
As laryngeal cartilages move up and
down with swallowing, thyroid also
moves.
Dense venous capsule lies deep to
true capsule, so gland is removed
along with true capsule
RELATIONS OF THE GLAND
 Superior Thyroid Artery: A branch
ARTERIAL SUPPLY of external carotid artery. Lies close
to external laryngeal nerve and must
be ligated as close to the gland as
possible
Inferior thyroid artery: a branch
of thyrocervical trunk. Intimately
related to recurrent laryngeal nerve
and ligated as far away from the
gland as possible
Thyroid ima artery(30% cases):
branch of brachiocephalic trunk or
arch of aorta
Accessory thyroid arteries: arises
from tracheal and esophageal
arteries
Blood flow to the gland is 4-
6ml/gm/min. sometimes may reach
1litre/min in large goitres
 LYMPHATIC
VENOUS DRAINAGE DRAINAGE
NERVE SUPPLY
Parasympathetic supply- Vagus; recurrent laryngeal
nerve
Sympathetic supply- Superior, middle and inferior
cervical sympathetic ganglia.
PHYSIOLOGY- THYROID HORMONE
SYNTHESIS
1. IODINE TRAP:
Dietary iodine is reduced to iodide in the Gastro
Intestinal tract
It is absorbed into the thyroid gland against the
concentration gradient of 1:5
In thyrotoxicosis, the concentration gradient can be
as high as 1:20
2. OXIDATION AND ORGANIFICATION:
Iodine is oxidized to iodine and is bound to tyrosine
to form monoiodo and di iodo tyrosines by thyroid
peroxidase
3. COUPLING:
Mono iodo tyrosine and di iodo tyrosine coupled
enzymatically by thyroid peroxidase to form either T3 or T4
4. STORAGE:
T3 and T4 are stored after attaching to thyroglobulin protein
as colloid in the gland
5. RELEASE AND RECYCLING:
The release of T3 and T4 through proteolysis from
thyroglobulin and diffusion into the circulation.
The remaining mono iodo and di iodo tyrosines are recycled
for formation of T3 and T4.
THYROID HORMONES
T4: Daily T4 released: 80 to 100mcg/kg
Half life: 7 days
Highly protein bound
T3: 20% secreted by thyroid gland and 80% by extra
thyroidal conversion from T4
biologically active
Half life: 24 to 30 hours
PHYSIOLOGICAL EFFECTS OF THYROID HORMONES
THYROID DYSFUNCTION
HYPERTHYROIDISM
Hyper functioning of the
thyroid gland with
excessive secretion of
active thyroid hormones
Thyrotoxicosis is its
clinical manifestation
when the body tissue is
excessively stimulated
by increased Thyroid
hormones
PATHOPHYSIOLOGY
 Increase GI motility, O2 consumption, BMR and heat
production.
 Increased metabolism leads to :-
- Negative nitrogen balance.
- Lipid depletion.
- Nutritional deficiency.
- Increased O2 consumption
 Increase bone and protein turnover, glycogenolysis,
hepatic gluconeogenesis, intestinal glucose absorption,
cholesterol synthesis and degradation
 Thyroid Hormones results in positive inotropic and
chromotropic effect by increasing calcium- ATPase and β-
adrenergic receptors amount and sensitivity. This results:-
- Tachycardia
- Increased Cardiac Output and stroke volume.
- Increased adrenergic responsiveness.
- Increased peripheral vasodilation and blood flow.
High BMR → raises body Temperature→ peripheral
vessel dilatation → forces the CO to increase → may lead
to high output failure.
CLINICAL FEATURES:
Symptoms: hyperactivity, weight loss and tremor,
palpitation, anxiety/nervousness, diarrhea, intolerance to
heat, large muscle group weakness, menstrual abnormalities.
Signs: tachycardia ( ↑ sleeping PR), warm moist skin,
irregularly irregular pulse, fine brittle hair, ↑ Cardiac Output,
Ischemic Heart Disease, Heart Failure .
Eye signs: 1. Eyelid retraction.
2. Lid lag sign.
3. Joffroy sign-absence of wrinkling.
4. Mobius sign-difficulty in convergence.
5. Stellwag’s sign-absence of blinking.
 TREATMENT
Antithyroid drugs: methimazole or proylthiouracil ( PTU)
interfere with thyroid hormone synthesis. PTU also inhibits the
peripheral conversion of T4 to T3.
Carbimazole: 15-40mg daily till euthyroid & then 5-15mg
PTU:200-400mg daily till euthyroid & then 50-150mg
Methimazole:15-60mg divided every 12hrs.
Although blockage of hormones synthesis is rapid, clinical
improvement occurs after few weeks or months ,because a large
pool of stored hormone continues to be released from thyroid.
S/E: agranulocytosis, hepatotoxicity, vasculitis, teratogenicity.
Iodide: Inhibit hormone release. Effects occur immediately but
short –lived.
Reserved for hyperthyroid patients for surgery, thyroid storm.
Potassium iodide- 3 drops PO every 8 hrly for 10-14 days.
beta adrenergic antagonists: relieve signs and symptoms of
increased adrenergic activity. Propanolol has the added
feature-inhibit conversion of T4 to T3.
Propranolol 40mg BID or nadolol 160mg once daily; higher dose
may be needed
Nadolol and atenolol have a longer duration than
propranolol.
In emergency, pts. can be prepared for surgery in less than 1
hour by IV administration of esmolol. resting heart rate
should be <85-90bpm.
radioactive iodine and subtotal thyroidectomy: other
alternative to medical therapy.
Anesthesia management
Preoperative Assessment
History (hyper/hypo/euthyroidism features, adverse respiratory and CVS
effect due to compression and hormone)
Examination(size, type, retrosternal extension of mass/positive
Pemberton's sign and systemic effect of thyroid hormone)
Investigations including:
Complete Blood Counts
Thyroid Function Tests
Antroposterior or lateral CXR to see retrosternal extension
lateral neck x-ray to see tracheal compression
CT scan
Respiratory function tests
2D ECHO
Preoperative preparation
If elective, patient needs to be rendered euthyroid with drugs
β-blocking drugs- to abolish the clinical manifestation of the
toxic state.
It has very rapid control , operation is possible within a week or
two weeks.
Glucocorticoids –reduce TH release and peripheral conversion of
T4→T3
Iodides started 10-14 days before surgery and proceed until the
day
Lugol’s iodine (for 10 days, 3-5 drops BID) to decrease the
vascularity of the gland.
Benzodiazepine the night before the day of surgery.
Continue antithyroid and B-blockers until the morning of surgery.
Intraoperative management
Allow safe induction and awakening with adequate pain management.
Maintain adequate levels of anaesthesia ( avoid exaggerated sympathetic
response to surgical stimulus).
Barbiturates have antithyroid activity at high doses and is best for
induction
For treatment of hypotension decreased doses of direct-acting
vasopressors such as phenylephrine may be a better choice than
ephedrine, which acts in part by provoking the release of catecholamine.
Avoid:
- Atropine
- Pancuronium
- Halothane
- Ketamine
If hyperthyroid patient with clinically apparent disease
requires emergency surgery :
- Propranolol 0.5mg IV is given ( may be increased ).
- Esmolol (alternative) as a continuous infusion 50-
500mic/kg/min.
- Maintain heart rate below 90bpm.
Use dexametasone 8mg/ hydrocortisone 100 mg to
reduce incidence of airway edema.
Regional anesthesia(SA,EA) may be technique of choice
in hyperthyroid case for non thyroid surgery without
presence of CHF.
Continuous epidural may be preferable to spinal because
of the slower onset of sympathetic nervous system
blockade
Epinephrine should not be added to local anesthetics, as
systemic absorption of this catecholamine could produce
exaggerated circulatory responses
Monitor ECG and patient’s body temperature (for
thyroid storm)
 Complications
1. Thyroid Storm :
Acute life threatening exacerbation of hyperthyroidism. Happens intaoperatively or
postoperatively with in 24hr
Manifestations:
Hyperthermia (>40oC)
Tachycardia
CHF
Agitation
Confusion
Dysrhythmias, AF or VT
Severe hypertension
Differential Diagnosis : -
Malignant hyperthermia
Pheochromcytoma
Light anesthesia
Treatment of thyroid storm
PTU 200-400mg PO or via NGT Q6hr.
paracetamal and cold blanket
IV fluids
B-blocker; propranolol 10-40mg PO Q4-6hr /esmolol
infusion until HR<100bpm.
Steroids- hydrocortisone =50-100mg IV -Q6hr
Digoxin for uncontrolled atrial fibrillation and heart failure
Iodide therapy-decrease iodine uptake and thyroid hormone
secretion 250mg PO Or IV Q6hr.
O2 and hemodynamic support
2. Recurrent Laryngeal Nerve (RLN) injury :
-Manifestations of RLN injury:
Unilateral
Asymptomatic unless laryngoscopy done
Bilateral
Usually manifests immediately after extubation.
Laryngeal stridor, acute respiratory distress, vocal cord palsy/adduction,
phonation lost.
Treatment:
Could be temporary or permanent
Re-intubation, paralyzed.
Hydrocortisone 100mg tid.
Wound re-exploration for reversible cause.
If Can not maintain airway do tracheostomy
3. airway obstruction
Vocal cords can collapse together, producing total airway
obstruction during inspiration due to RLN paralysis
If occurs soon after tracheal extubation, despite normal
vocal cord function, suggests tracheomalacia
This reflects a weakening of tracheal rings by chronic
pressure of a goiter
Airway obstruction postoperatively may be due to tracheal
compression by a hematoma
Treatment will be reintubation. If not possible maintain
AirWay with tracheostomy.
4. Hypothyroidism:
Management: TFT on regular bases.
-Thyroxine- 50-200μgm|d.
-10% Cagluconate PO| IV
5 .Hypoparathyroidism & hypocalcaemia:
May be due to:
Trauma to the parathyroid gland,
Devascularization of parathyroid or removal of the gland.
If damage to parathyroid does occur, hypocalcaemia typically
develops 24 to 72 hours postop, but may manifest as early as 1-
3 hours postop
Laryngeal muscles are sensitive to hypocalcaemia. may go
from inspiratory stridor progressing to laryngospasm. Prompt
IV calcium till laryngeal stridor ceases is treatment.
Diagnosis:
Initially asymptomatic
Carpopedal spasm (spasmodic contraction of the muscles of
the hands and feet)
Trousseau’s (carpopedal spasm precipitated by cuff inflation)
Chvostek’s sign (spasm of the facial muscles by tapping the facial
nerve just below the zygomatic bone)
Circumoral paresthesia
Mental status changes
Seizure
QT prolongation or cardiac arrest.
TX:- IV calcium
LARYNGEAL PARALYSIS
ANATOMY OF LARYNX
NERVE SUPPLY OF LARYNX
SENSORY SUPPLY:
Above vocal cords: Internal Laryngeal branch of
superior laryngeal nerve
Below vocal cords: Recurrent laryngeal nerve
MOTOR SUPPLY:
All intrinsic muscles of larynx except cricothyroid
muscle are supplied by recurrent laryngeal nerve
Cricothyroid is supplied by external laryngeal branch
of superior laryngeal nerve.
 VOCAL CORD POSITIONS

During respiration, cords are in adduction

During Phonation, cords are in median position
THEORIES ON POSITION OF VOCAL
CORD IN PARALYSIS
SEMON’S LAW: In all progressive organic lesions,
abductor fibres which are phylogenitically newer are
more susceptable and are first to be paralysed.
WAGNER & GROSSMAN HYPOTHESIS: Complete
paralysis of the recurrent laryngeal nerve results in the
vocal cord being in the paramedian position because of
intact cricothyroid muscle, which adducts vocal cord.
When superior laryngeal nerve is also paralysed, the
vocal cord will be in cadaveric position because of loss
of adductive force.
CLASSIFICATION OF LARYNGEAL
PARALYSIS
May be unilateral or bilateral and may involve
1. Recurrent laryngeal nerve
2. Superior laryngeal nerve
3. Both recurrent and superior laryngeal
nerve( combined or complete paralysis)
UNILATERAL RECURRENT
LARYNGEAL NERVE PARALYSIS
Ipsilateral paralysis of CLINICAL
all intrinsic muscles of FEATURES:
larynx except Asymptomatic
cricothyroid change in voice which
Vocol cord assumes a gradually improves by
median or paramedian compensation from the
position and does not other side cord
move laterally on deep TREATMENT:
inspiration
No treatment required
BILATERAL RECURRENT
LARYNGEAL NERVE PARALYSIS
All intrinsic muscles of TREATMENT:
larynx are paralysed In acute stridor,
Vocal cords lie in Tracheostomy is
median or paramedian required
position due to  Usually 6 months is an
unopposed action of adequate time to wait
cricothyroid muscles for any spontaneous
CLINICAL recovery
FEATURES: lateralization of vocal
Dysnoea cords can be done
Stridor Type 2 thyroplasty
UNILATERAL SUPERIOR
LARYNGEAL NERVE PARALYSIS
Paralysis of cricothyroid muscle and ipsilateral
anesthesia of larynx above vocal cord
Loss of tension of vocal cord and shortening of vocal
cord
CLINICAL FEATURES:
Weak voice with decreased pitch
Occassional aspiration
TREATMENT:
Medialization laryngoplasty
Modified typr 4 thyroplasty
BILATERAL SUPERIOR LARYNGEAL
NERVE PARALYSIS
Both the cricothyroid muscles are paralysed along with
anaesthesia of upper larynx
CLINICAL FEATURES:
cough
choking fits
weak and husky voice
TREATMENT:
Tracheostomy with a cuffed tube & an oesophageal feeding
tube
Epiglottopexy to close laryngeal inlet to protect lung from
repeated aspirations
COMPLETE UNILATERAL VOCAL
CORD PARALYSIS
Paralysis of all muscles of larynx on one side except
interarytenoid which also receives innervation from opposite
side. Cadaveric position of vocal cord.
CLINICAL FEATURES:
Vocal cord lies in cadaveric position
hoarseness of voice
Aspiration
TREATMENT:
Speech therapy
Medialisation of vocal cord: Thyroplasty type 1, injection of
teflon paste
BILATERAL COMPLETE VOCAL
CORD PARALYSIS
Both cords lie in cadaveric position
Total anesthesia of larynx
CLINICAL FEATURES:
Aphonia
Aspiration, Inability to cough and Bronchopneumonia
TREATMENT:
Tracheostomy
Epiglottopexy
Total laryngectomy
HYPOTHYROIDISM
Hypothyroidism is a condition when the body tissues
are exposed to decreased circulating concentration of
thyroid hormones .
 SYMPTOMS SIGNS
Dry coarse skin; cool peripheral
 Tiredness, weakness extremities
 Dry skin Puffy face, hands, and feet
 Cold intolerance (myxoedema)
Diffuse alopecia
 Hair loss
Bradycardia
 Difficulty concentrating, poor
Carpal tunnel syndrome
memory
Serious cavity effusions
Constipation
Myocardial ischemia or dysrhythmia
Weight gain with poor appetite
Decreased function of respiratory center.
Dyspnea and hoarse voice Decreased cortisol production,
Menorrhagia inappropriate production of ADH
Impaired hearing Hyponatrmeia and Peripheral edema
Elevated TSH/ less T3/ both
Treatment
Patients with severe hypothyroidism, older patients and
patients with CVS disease may have increased sensitivity to
thyroid hormones.
Therefore, they should be given a small dose of thyroid
hormone initially-25μgm of L thyroxin which is gradually
increased every 2 to 4 weeks ,to a full maintenance dose
during 6-12 wks period .
 Younger patients and patients with less severe
hypothyroidism maybe started on slightly higher dose
(50μgm of Lthyroxin) and advanced to a full replacement
dose more quickly
Most pts require 75-100μgm of L_thyroxin daily.
 Myxedema
Severe form of hypothyroidism characterized by:-
stupor,
coma,
hypoventilation,
hypothermia,
hypotension and hyponateremia.
Medical emergency with mortality rate of 25-50%.
Sepsis in elderly or exposure to cold may be an initiating event
Management
Intubation and ventilation as needed.
Sodium Levothyroxine: 200-300μgm IV over 10min initially and maintenance
200mg|day IV.
Hydrocortisone -100mg IV ,then 25mg IV Q6hr.
Fluid and electrolyte supplementation
Avoid hypothermia
Anesthesia management
Preoperative Medication:
In uncorrected severe hypothyroidism or myxedema coma
postpone elective surgeries and should be treated with IV
T3 supplementation for emergency surgery
Mild to moderate hypothyroidism may not be absolute
contraindication for urgent surgeries.
Due to its depressant effect- avoid opioids
Cortisol supplementation and aspiration prophylaxis may
be considered
Continue thyroid hormone therapy until morning of
surgery.
Induction of Anesthesia:
Ketamine is preferable drug
 If no excessive CVS depression etomidate or thiopental can be used.
During calculating dose of relaxants keep in mind that the coexisting
skeletal muscle weakness.
Maintenance of Anaesthesia:
N2O and supplemental short acting opioids, BZD or Ketamine is best.
Volatiles contraindicated in overtly hypothyroid situation.
Hypothyroidism does not appear to decrease MAC but decrease in CO
speeds rate of induction by inhalational because CMRO2 is
independent of thyroid function.
Reduce MAC if body temperature is <37oC.
Pancronium is best relaxant.
No special consideration about reversals.
IV fluids should contain sodium.
Delay extubation until patient respond appropriately with
accepted body temperature.
postoperatively:
Prolonged postoperative somnolence & inability to wean
earlier, so needs mechanical support.
Avoid postoperative hypothermia & give adequate analgesic.
If patient comes for other surgery having hypothyroidism
Regional Anesthesia is best than GA
THYROID SURGERY UNDER REGIONAL
ANAESTHESIA- CERVICAL PLEXUS BLOCK
DEEP CERVICAL PLEXUS
Patient in supine position, with the head
tilted slightly backward and turned
about 45 degrees to the opposite side
A line drawn from caudal tip of mastoid
to chassaignac’s tubercle(transverse
process of C6) along posterior border
of sternomastoid.
Transverse process of c2, 1.5 cm caudal
mastoid process and 1cm dorsal to line
drawn identified and marked
The transverse processes of
C3,C4,C5 are also palpated and
marked. Distance between each of
them is 1.5 cm
The aim is to block anterior branches
of cervical plexus in the groove of the
transverse process.
The needle is advanced perpendicular
to the skin, medially and slightly
caudally.
After clear bone contact, minimal
withdrawal of the needle, careful
aspiration is done before delivering
drug
SUPERFICIAL
CERVICAL PLEXUS:
 The subcutaneous
tissues were infiltrated
in a fan like fashion in
the line of the posterior
border of
sternocleidomastoid
muscle in and around
its midpoint
DOSAGE:
30 ml of 0.75% ropivacaine or 0.25%-0.5% bupivacaine
Of this 10ml for superficial cervical plexus block and
20ml for anesthesia of deep cervical plexus. About 3 to
3.5 ml at each insertion point
THANK YOU