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ANAESTHESIA MANAGEMENT
THYROID DISEASE
MODERATOR- DR. KAMIL
PRESENTOR- ANIMESH AMAN SINGH
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
Boundaries
Superiorly: thyroid cartilage
Inferiorly: 4th or 5th tracheal ring
Anteriorly: Inferior hyoid
Ligaments
Posteriorly: cricoid and tracheal
cartilage
BLOOD AND NERVOUS SUPPLY
Blood Supply: Superior and Inferior thyroid artery.
Sympathetic: Superior cervical ganglion and cervicothoracic
ganglion.
Parasympathetic: Superior and recurrent laryngeal nerve
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 iodide 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
• Control of T3 &T4Secretion
• Low blood levels ofhormones stimulate hypothalamus ->TRH
• It stimulates pituitary torelease TSH
• TSH stimulates gland toraise blood levels
• T3 and T4 regulatethemselves through a negative feedback loop
System Effects
Cardiovascular Increases heart rate
Increases the force of cardiac contractions
Increases cardiac output as a result of the previous two effects
Promotes peripheral vasodilation
Central nervous Essential for normal brain development,such as cerebellar growth and nerve myelination
Necessary for normal intellectual development in infants
Necessary for emotional stability in adults
Gastrointestinal Increases appetite
Increases secretion of 'digestive juices'
Increases gastric mouity
Hematopoietic Influences erythropoiesis
System Effects
Metabolic Profoundly affects oxidative metabolism
Increases oxygen consumption in all tissues except the brain,gonads,and spleen
Promotes heat production
Influences synthesis and degradation of carbohydrate,fat,and protein
Respiratory Influences lung development
Necessary for surfactant production
ncreases rate and depth of respirations
Skeletal Indirectly promotes growth formation by actions on the pituitary gland
Acts synergistically with growth hormone and other growth factors that promote bone
formation
Directly affects skeletal maturation
Necessary for progression of tooth development and eruption
Skin Necessary for growth and maturation of the epidermis and hair follicles
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
1. Intrinsic thyroid disease
·Hyperfunctioning thyroid adenoma
·Toxic multinodular goiter
2. Abnormal TSH stimulator
·Graves disease
·Trophoblastic tumor
3. Disorders of hormone storage or
release
·Thyroiditis
4. Excess production of thyroid-
stimulating hormone
·Pituitary thyrotropin (rare)
5. Extrathyroidal source of
hormone
· Struma ovarii
· Functioning follicular
carcinoma
6. Exogenous thyroid
·latrogenic
·lodine induced
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(staring).
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
• 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
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
HYPOTHYROIDISM
• Hypothyroidism is a condition when the body tissues are exposed to decreased
circulating concentration of thyroid hormones .
• Causes of Hypothyroidism
• Primary hypothyroidism
• Autoimmune
• Irradiation to the neck
• Previous131 I therapy
• Surgical removal
• Thyroiditis(Hashimoto disease)
• Severe iodine depletion
• Medications (iodines,propylthiouracil,methimazole)
• Hereditarydefects in biosynthesis
• Congenital defects in gland development
• Secondary or tertiary
hypothyroidism
• Pituitary
• Hypothalamic
SYMPTOMS
• Tiredness, weakness
• Dry skin
• Cold intolerance
• Hair loss
• Difficulty concentrating, poor memory
• Constipation
• Weight gain with poor appetite
• Dyspnea and hoarse voice
• Menorrhagia
• Impaired hearing
SIGNS
 Dry coarse skin; cool peripheral
extremities
 Puffy face, hands, and feet
(myxoedema)
 Diffuse alopecia
 Bradycardia
 Carpal tunnel syndrome
 Serious cavity effusions
 Myocardial ischemia or dysrhythmia
 Decreased function of respiratory
center.
 Decreased cortisol production,
inappropriate production of ADH
 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
 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 is
infiltrated in a fan like fashion in
the line of the posterior border
of sternocleidomastoid muscle
in and around its midpoint.
LARYNGEAL PARALYSIS
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
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
all intrinsic muscles of
larynx except
cricothyroid
 Vocol cord assumes a
median or paramedian
position and does not
move laterally on deep
inspiration
CLINICAL FEATURES:
Asymptomatic
change in voice which
gradually improves by
compensation from the other
side cord
TREATMENT:
No treatment require
BILATERAL RECURRENT
LARYNGEAL NERVE
PARALYSIS
• All intrinsic muscles of larynx
are paralysed
• Vocal cords lie in median or
paramedian position due to
unopposed action of
cricothyroid muscles
• CLINICAL FEATURES:
Dysnoea
Stridor
TREATMENT:
 In acute stridor, Tracheostomy
is required
 Usually 6 months is an
adequate time to wait for any
spontaneous recovery
 lateralization of vocal cords
can be done
 Type 2 thyroplasty
COMPLICATIONS
Extubation problems:
 Laryngospasm
 Desaturation
 Respiratory distress
Solution:
Deep extubation
Baileys manouver
IV drugs: lidocaine, opioid
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
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
TRACHEOMALACIA
Increased incidence in large longstanding Goitre
Diagnosis: Air leak around deflated cuff
Management:
Reintubation; Tracheostomy;Ceremic ring support
Anaesthesia Management Thyroid by Dr. Animesh

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Anaesthesia Management Thyroid by Dr. Animesh

  • 1. ANAESTHESIA MANAGEMENT THYROID DISEASE MODERATOR- DR. KAMIL PRESENTOR- ANIMESH AMAN SINGH
  • 2. 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 Boundaries Superiorly: thyroid cartilage Inferiorly: 4th or 5th tracheal ring Anteriorly: Inferior hyoid Ligaments Posteriorly: cricoid and tracheal cartilage
  • 3. BLOOD AND NERVOUS SUPPLY Blood Supply: Superior and Inferior thyroid artery. Sympathetic: Superior cervical ganglion and cervicothoracic ganglion. Parasympathetic: Superior and recurrent laryngeal nerve
  • 4. 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 iodide and is bound to tyrosine to form monoiodo and di iodo tyrosines by thyroid peroxidase
  • 5. 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.
  • 6.
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  • 8. 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 • Control of T3 &T4Secretion • Low blood levels ofhormones stimulate hypothalamus ->TRH • It stimulates pituitary torelease TSH • TSH stimulates gland toraise blood levels • T3 and T4 regulatethemselves through a negative feedback loop
  • 9. System Effects Cardiovascular Increases heart rate Increases the force of cardiac contractions Increases cardiac output as a result of the previous two effects Promotes peripheral vasodilation Central nervous Essential for normal brain development,such as cerebellar growth and nerve myelination Necessary for normal intellectual development in infants Necessary for emotional stability in adults Gastrointestinal Increases appetite Increases secretion of 'digestive juices' Increases gastric mouity Hematopoietic Influences erythropoiesis
  • 10. System Effects Metabolic Profoundly affects oxidative metabolism Increases oxygen consumption in all tissues except the brain,gonads,and spleen Promotes heat production Influences synthesis and degradation of carbohydrate,fat,and protein Respiratory Influences lung development Necessary for surfactant production ncreases rate and depth of respirations Skeletal Indirectly promotes growth formation by actions on the pituitary gland Acts synergistically with growth hormone and other growth factors that promote bone formation Directly affects skeletal maturation Necessary for progression of tooth development and eruption Skin Necessary for growth and maturation of the epidermis and hair follicles
  • 11.
  • 12. 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
  • 13. 1. Intrinsic thyroid disease ·Hyperfunctioning thyroid adenoma ·Toxic multinodular goiter 2. Abnormal TSH stimulator ·Graves disease ·Trophoblastic tumor 3. Disorders of hormone storage or release ·Thyroiditis 4. Excess production of thyroid- stimulating hormone ·Pituitary thyrotropin (rare) 5. Extrathyroidal source of hormone · Struma ovarii · Functioning follicular carcinoma 6. Exogenous thyroid ·latrogenic ·lodine induced
  • 14. 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
  • 15. • 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.
  • 16. 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(staring).
  • 17. 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.
  • 18. • 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.
  • 19. 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
  • 20. 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.
  • 21. 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
  • 22. • 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.
  • 23. • 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)
  • 24. 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
  • 25. 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
  • 26. 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
  • 27. 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.
  • 28. 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
  • 29. 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
  • 30. HYPOTHYROIDISM • Hypothyroidism is a condition when the body tissues are exposed to decreased circulating concentration of thyroid hormones . • Causes of Hypothyroidism • Primary hypothyroidism • Autoimmune • Irradiation to the neck • Previous131 I therapy • Surgical removal • Thyroiditis(Hashimoto disease) • Severe iodine depletion • Medications (iodines,propylthiouracil,methimazole) • Hereditarydefects in biosynthesis • Congenital defects in gland development • Secondary or tertiary hypothyroidism • Pituitary • Hypothalamic
  • 31. SYMPTOMS • Tiredness, weakness • Dry skin • Cold intolerance • Hair loss • Difficulty concentrating, poor memory • Constipation • Weight gain with poor appetite • Dyspnea and hoarse voice • Menorrhagia • Impaired hearing SIGNS  Dry coarse skin; cool peripheral extremities  Puffy face, hands, and feet (myxoedema)  Diffuse alopecia  Bradycardia  Carpal tunnel syndrome  Serious cavity effusions  Myocardial ischemia or dysrhythmia  Decreased function of respiratory center.  Decreased cortisol production, inappropriate production of ADH  Hyponatrmeia and Peripheral edema  Elevated TSH/ less T3/ both
  • 32. 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.
  • 33. 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
  • 34. 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
  • 35. 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.
  • 36. • 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
  • 37. 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
  • 38.  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
  • 39. SUPERFICIAL CERVICAL PLEXUS:  The subcutaneous tissues is infiltrated in a fan like fashion in the line of the posterior border of sternocleidomastoid muscle in and around its midpoint.
  • 41. 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.
  • 42.
  • 43. VOCAL CORD POSITIONS  During respiration, cords are in adduction  During Phonation, cords are in median position
  • 44. 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)
  • 45. UNILATERAL RECURRENT LARYNGEAL NERVE PARALYSIS  Ipsilateral paralysis of all intrinsic muscles of larynx except cricothyroid  Vocol cord assumes a median or paramedian position and does not move laterally on deep inspiration CLINICAL FEATURES: Asymptomatic change in voice which gradually improves by compensation from the other side cord TREATMENT: No treatment require
  • 46. BILATERAL RECURRENT LARYNGEAL NERVE PARALYSIS • All intrinsic muscles of larynx are paralysed • Vocal cords lie in median or paramedian position due to unopposed action of cricothyroid muscles • CLINICAL FEATURES: Dysnoea Stridor TREATMENT:  In acute stridor, Tracheostomy is required  Usually 6 months is an adequate time to wait for any spontaneous recovery  lateralization of vocal cords can be done  Type 2 thyroplasty
  • 47. COMPLICATIONS Extubation problems:  Laryngospasm  Desaturation  Respiratory distress Solution: Deep extubation Baileys manouver IV drugs: lidocaine, opioid
  • 48. 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
  • 49. 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 Epiglottopexy to close laryngeal inlet to protect lung from repeated aspirations
  • 50. 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
  • 51. 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
  • 52. TRACHEOMALACIA Increased incidence in large longstanding Goitre Diagnosis: Air leak around deflated cuff Management: Reintubation; Tracheostomy;Ceremic ring support