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Anesthesia management

for thyroid surgery


Prepared by: Metages Hunie

Advisor: Sr. Lemlem Getachew


OUT LINE OF THE PERSENTATION
Objective
Introduction
Anatomy of thyroid gland
Synthesis and secretion of thyroid hormones
Transport of thyroid hormones
Regulation of thyroid hormone secretion
Physiological function of thyroid hormones
 Disease of thyroid gland
Medical management &anesthesia consideration of thyroid diseases
Conclusion
References
objectives
Describe the basic anatomy and physiology of thyroid
gland
Describe synthesis and secretion of thyroid gland
Describe regulation of thyroid hormone
Describe function of the thyroid gland
Differentiate different types thyroid gland disorders
Explain the medical and anesthetic management of
thyroid disorders
INTRODUCTION
An intimate knowledge of the anatomy, physiology,
pathophysiology, pharmacology, and specific issues
related to anesthesia case management for thyroidectomy
is essential to provide high-quality care.
Airway management may be difficult despite a normal
airway examination due to impingement of a thyroid
mass on the laryngeal and tracheal structures.
Anesthetists must be prepared to use emergency airway
adjuncts in case a patient cannot be ventilated or
intubated
ANATOMY OF THYROID GLAND
Cont…
 located immediately below the larynx on each side of and anterior to
the trachea.
 It is one of the largest of the endocrine glands, normally weighing 15
to 20 grams in adults
 Four parathyroid glands are located posterior to each pole of the
thyroid.
 Recurrent laryngeal nerves traverse the lateral borders of the thyroid
gland

 Is highly vascular &soft in consistency.


 Blood flow=5x(weight of the gland) each minute.
Synthesis and secretion of thyroid hormones
There are two biologically active thyroid hormones:
- tetraiodothyronine (T4; usually called thyroxine)
- triiodothyronine (T3)

 Thyroid secretion is controlled primarily by TSH


secreted by the anterior pituitary gland.
About 93 % T4, and 7 % T3.
Thyroid Hormone Synthesis

Iodine ingested Iodides (in the jejunum) absorbed


from the GIT iodide trapping(pump)- transport of
iodides from the blood into the thyroid glandular cells

and follicles peroxidase(H2o2) Oxidation of the Iodide Ion


(Conversion of the iodide ions to an oxidized form of
iodine) Organification (the binding of iodine
with the Tg molecule Coupling -takes place within
the Tg molecule (MIT+DIT,DIT+DIT)
T3&T4
Transport of thyroid hormones

 T3& T4 are lipid-soluble.


• Thus, they are found in the circulation associated with
binding proteins:
- Thyroid Hormone-Binding Globulin (~70% of
hormone)
- Pre-albumin (transthyretin), (~15%)
- Albumin (~15%)
• <1% of thyroid hormone is found free in the circulation.
• Only free and albumin-bound thyroid hormone is
biologically available to tissues.
Regulation of thyroid hormone secretion
Cont…
Thyroid hormone synthesis and secretion is regulated by

two main mechanisms:

I. an “auto regulation” mechanism, which reflects the


available levels of iodine
- low iodide levels increase iodine transport into follicular cells
- high iodide levels decrease iodine transport into follicular cells

Thus, there is negative feedback regulation of iodide


transport by iodide
Cont…
II. Regulation by the hypothalamus and anterior pituitary
TRH cause ↑ed production and release of TSH
TSH acts on follicular cells of the thyroid.
- ↑ iodide transport into follicular cells
-↑ production and iodination of Tg
- ↑ endocytosis of colloid from lumen into follicular cells
• Thyroid hormones also inhibit TRH synthesis
Physiological function of Thyroid Hormones

On nutrients
o Stimulation of Carbohydrate Metabolism:
 Enhances glycolysis, enhanced gluconeogenesis,
 ↑ protein synthesis at low levels of T3&T4
 ↑ protein degradation at high levels
o Stimulation of Fat Metabolism
 ↓ the concentrations of cholesterol, phospholipids, &
triglycerides.
↑ numbers of low‐density lipoprotein receptors on the liver
cells,
Cont.….
↑the Transcription of Large Numbers of Genes.
↑Cellular Metabolic Activity.
↑the Number and Activity of Mitochondria.
↑Active Transport of Ions Through Cell Membranes.
 CNS
 Enhances wakefulness and alertness
Enhances memory and learning capacity
Required for normal emotional tone
↑ speed and amplitude of peripheral nerve reflexes
Respiratory system
 ↑ resting respiratory rate
 ↑Minuet Ventilation
 ↑ ventilatory response to hypercapnia and hypoxia
CVS
↑ HR
↑ CO
↑ SV
↑ force of cardiac contractions
Up-regulate catecholamine receptors
Renal
↑RBF
↑ GFR
Reproductive system and growth
Required for follicular development and ovulation

Required for the normal maintenance of pregnancy

 spermatogenesis

↑ growth and maturation of bone

↑ tooth development

↑growth and maturation of epidermis, hair follicles & nails

↑ rate and force of skeletal muscle contraction


Thyroid function testing
Thyroid Function Test Measurement Normal Range
Total T4 (TT4) bound and free T4 4.5 -11.5 ug/dL
Free T4 (FT4) free T4 0.8 -2.8 ng/dL
Free T4 Index (FT4I) estimate of free T4 1.0 -4.3 U
FT4I = TT4 x RT3U
Total T3 (TT3) bound and free T3 75 -200 ng/dL
Resin T3 Uptake (RT3U) binding capacity of TBG 25 -35%
TRH TRH 5 -25 mIu/mL
TSH TSH 0.3 - 5.0 U/mL
Thyroglobulin Thyroglobulin 5-25 ng/mL
Diseases of the Thyroid

Simple goiter
It is a greatly enlarged thyroid gland which doesn't result
from inflammatory or neoplastic process.
 It is characterized by
 normal thyroid hormones,

 no hypothyroidism,

 no inflammatory process in the gland,

 no carcinoid of thyroid gland.


Major forms of simple goiter

Endemic goiter : deficiency(lack) of iodine


Sporadic goiter : defective iodine use
 Goiter due to exposure to goiterogens: consuming
goiterogenous foods such as cabbage, soybean
Pathophysiology
Lack of iodine or defective iodine use→ prevents
production of T3 & T4 →no inhibition of production of
TSH → secretion of large amounts of TSH→ TSH then
stimulates the thyroid cells to secrete Tg into the follicles
→ But because of lack of iodine& faulty iodine utilization,
T3&T4 production does not occur in the Tg molecule and
does not cause the normal suppression of TSH →the gland
grows larger and larger
Signs and symptoms

 Large goiter (Thyromegaly)


Swelling and distention of the neck
Respiratory distress
Dysphagia
Venous engorgement particularly if retrosternal growth
of the goiter
Diagnosis

PE & Hx
Thyroid function tests: to rule out hypo or
hyperthyroidism.
• TSH - normal , high normal,
• T4 - Low/Normal
• T3 - Normal
 Urinary iodine – low
Medical treatment

 Aim: to reduce thyroid enlargement


 Exogenous thyroid hormone (Levothyroxine)
 Strong iodine solution such as Lugol's solution to
decrease size and vascularity
Surgical Treatment
The main indications are:

• If compression of the trachea or esophagus and venous


outflow obstruction.
• If non responsive for medical management

• If the goiter is very large

• Cosmetically
Anesthetic management

Suspect and consider difficult air way management and


be ready for difficult airway maneuver
Patient should be euthyroid 
Induction
- Thiopentone and succinylcholine
are desirable
- Glycopyrrolate is good choice
Post-operative complication
Recurrent laryngeal nerve injury
 Unilateral nerve injury is more common and is often transient. It is
characterized by hoarseness and a paralyzed vocal cord.
 Bilateral recurrent laryngeal nerve injury is an extremely rare injury and
causes aphonia which necessitates reintubation and ventilation with oxygen
Bleeding or hematoma
Unintentional pneumothorax is a possible complication of neck exploration
Hypoparathyroidism
 Secondary to the inadvertent surgical removal of parathyroid glands is most
frequently seen after total thyroidectomy
Tracheomalacia
Hyperthyroidism
It is a hyper metabolic state, resulting from excessive thyroid
hormone function.
Causes of Hyperthyroidism
Primary hyperthyroidism  
Graves disease

Toxic multinodular goiter

Toxic adenoma

Functioning thyroid carcinoma metastases

Drugs: iodine excess


 

Secondary hyperthyroidism
TSH-secreting pituitary adenoma

Thyroid hormone resistance syndrome: occasional patients

may have features of thyrotoxicosis


Chorionic gonadotropin-secreting tumors

Gestational thyrotoxicosis (hcg) stimulates T3&T4


Pathophysiology
 Thyroid gland ↑ to 2 to 3x →number of cells ↑→ each
cell ↑es its rate of secretion →Plasma TSH ↓
→substances having actions similar to TSH bind with the
same membrane receptors that bind TSH ( i.e. thyroid-
stimulating immunoglobulin (TSI )→ induce
activation of the cAMP → ↑ TH → hyper metabolism →
↑SNS → ↑ B receptor number (↑HR, ↑Co, Adrenergic
responsiveness, ↑ SV) →And hyper metabolism leads to
negative nitrogen balance, lipid depletion and state of
nutritional deficiency and weight loss.
Sign and Symptoms

 High state of excitability,


Intolerance to heat,
Sweating,
Weight loss (↑ basal metabolic rate, catabolism)
Diarrhea,
Muscle weakness
Nervousness
Extreme fatigue but inability to sleep
Tremor of the hands.
Exophthalmos
Cont…
Diagnoses

Clinical presentation
 Laboratory test
 ↓ TSH
 ↑T3 & T4
 The most accurate diagnostic test is direct measurement
of the concentration of “free”T4( sometimes T3) in the
plasma, using appropriate radioimmunoassay
procedures.
Medical management

 Antithyriod drugs(e.g. PTU, Methimazole):


 Inhibit the oxidation of iodine and coupling of iodotyrosines,
 ↓ the synthesis of T4 to T3
 ↓ conversion of T4 to T3 in peripheral tissues.
 Dose: Propylthiouracil: 100 to 150mg TID
 Methimazole: 15 to 60 mg Bid
 Radioactive I-destroys thyroid tissue (not recommended in
pregnant; destoys fetal thyroid)
 Inorganic iodine(e.g. KI, NaI): inhibits hormone synthesis and
release of T3 and T4 from the gland.
 Other symptomatic treatments:
• Propranolol: 80 to 200 mg QID
Surgical management

Total thyroidectomy
Indications
 thyroid cancer
 Subtotal thyroidectomy
Indications:
 failed medical therapy,

 Benign tumor of thyroid gland

 symptomatic goiter.
Anesthesia management

Preoperative 
 Patients should be euthyroid

 P/E, x-ray, CT or MRI-to predict difficult airway

 Evaluate recurrent laryngeal nerve function

 Control hyper dynamic CVS- resting HR <85beats/min is

recommended
 Thyroid function tests
Cont…
Premedication
 no premedication in pt with airway obstruction
 Pt adequately sedated to prevent anxiety &apprehension ( BDZ /
narcotic premedication )
 Bzds are a good choice for preoperative sedation
 Anticholinergic drugs (i.e., atropine) should be avoided
 Short acting anti thyroid medications ,and B-blocker should be
continued through the morning of surgery.
 In emergency cases, the use of β-blocker, cortisol, or dexamethasone and
PTU is usually necessary.
o Emergency surgery –IV esmolol 0.5 mg/kg bolus followed by
infusion (50-150ug/kg/min)
 The anesthetist should be prepared to manage thyroid storm, especially in
patients with uncontrolled or poorly controlled disease who present for
emergency surgery
Intraoperative
 Adequate anesthetic depth before laryngoscopy or surgical
stimulation to avoid SNS.
 CVS function and body temperature monitoring
 Eye protection (eye drops, lubricant, eye pads) is important, as
the exophthalmos of Graves’ disease ↓ the risk of corneal
abrasion or ulceration.
 Raise head of the operating table 15–20° to aid venous drainage
and ↓ blood loss
 Drugs that stimulate the SNS should be avoided (i.e., ketamine,
pancuronium, atropine, ephedrine, epinephrine ).
 Muscle relaxants should be chosen based on their interaction
with the SNS and their hemodynamic effects.
 Because patients with hyperthyroidism or thyrotoxicosis may
have co-existing muscle disease such as myopathies and
myasthenia gravis, NDMRs should be reduced
Cont…
Sux and the NDMRs with limited hemodynamic effects (e.g.,
vecuronium, rocuronium) can be used safely for intubation.
 Hyperthyroidism does not increase anesthetic requirements
i.e., there is no change in MAC
 Maintenance of anesthesia, any of the potent inhalation
agents may be used.
 Isoflurane is the best because it has no myocardial sensitization for
catecholamine and ↓ sympathetic responsiveness.
 N2o and opioids are safe and effective in hyperthyroid
patients.
 Organ toxicity secondary to ↑in drug metabolism
 Reversal glycopyrrolate instead of atropine in combination
with an acetyl cholinesterase inhibitor.
Cont…
 Treatment of intraoperative hypotension, a direct-acting
vasopressor (phenylephrine) is preferred
 Removal of the thyrotoxic gland does not mean immediate
resolution, therefore, β-blocker therapy may need to be
continued in the postoperative period.
 Antithyroid drug therapy can be discontinued.
 It is necessary to evaluate vocal cord function before and
after surgery by laryngoscopy.
 Postoperative extubation should be performed under
optimal conditions
Post-operative complications and
management
 Recurrent laryngeal nerve damage
 Bleeding
 Hematoma formation
 Hypo parathyroidism
 Unintentional pneumothorax
 Tracheomalacia
 Thyroid storm
Hypothyroidism
It is cxzed by ↓ed circulating levels of unbound T3 & T4.
Classification
  Primary : a thyroid hormone deficiency as a result of
thyroid gland disease.
 Secondary : results from TSH deficiency as a result of
malfunction of pituitary gland.
 Tertiary : results from TRH deficiency due to tumor or
other destructive lesion in the hypothalamus leads to
decreased production of TRH.
Causes of Hypothyroidism
Primary hypothyroidism
Autoimmune disease: Hashimoto's thyroiditis, atrophic
thyroiditis
Iatrogenic: Iodine treatment, subtotal or total
thyroidectomy, external irradiation of neck for lymphoma
or cancer
Drugs: iodine excess (including iodine-containing contrast
media and amiodarone),
Congenital defect: absent or ectopic thyroid gland
Iodine deficiency
 Secondary hypothyroidism
Hypopituitarism: tumors, pituitary surgery or irradiation,
Sheehan's syndrome, trauma
TSH deficiency or inactivity
Idiopathic

Tertiary hypothyroidism
Tumor or other destructive lesion in the hypothalamus
leads to decreased production of TRH
Signs and Symptoms

• Libido is decreased in men


• Menorrhagia (later oligomenorrhea or amenorrhea),
• Dry skin, Hair loss,  
• Constipation, Weight gain with poor appetite,
•  Dyspnea, Hoarse voicery
• Cool peripheral extremities    
• Pallor, often with a yellow tinge to the skin due to carotene accumulation.
• Bradycardia 
• Carpal tunnel syndrome as is impairment of muscle function with
stiffness, cramps, and pain.
• Pericardial effusions
• Puffy face, hands, and feet (myxedema)
DIAGNOSIS

↓T3 and T4 in all forms of hypotyroidism


TSH will be increased or decreased.
 primary hypothyroidism :TSH ↑.
 secondary and tertiary hypothyroidism: TSH ↓
Medical Treatment

 Daily replacement of levothyroxine 1.6 g/kg

 Maintain body temperature normal as well as give extra heat.

 Apply oily cream to prevent dryness of skin

 Vegetable and /or sometimes laxatives to prevent constipation.

 Steroid replacement
eg, hydrocortisone, 100 mg IV TID is routinely given in case of
coexisting adrenal gland suppression.
May have adrenal atrophy: dec cortisol production, dilutional
hyponatremia, diminished H2O excretion
Management of Anesthesia

 Preoperative
 Euthyroid state is ideal, mild to moderate hypothyroidism does
not appear to be an absolute contraindication to surgery.
 In severely hypothyroid patients postponed surgery if possible.
 Patients with uncorrected severe hypothyroidism (T4 < 1 mg/d
L) or myxedema coma should not undergo elective surgery
and should be treated with thyroid hormone prior to
emergency surgery
 Patients who have been rendered euthyroid may receive their
usual dose of thyroid medication on the morning of surgery
Cont…
 Premedication
• Preoperative sedation should be avoided and usually do not
require
• These patients can be extremely sensitive to narcotics and
sedatives
• Premedicate these Pt with H2 antagonists and
metoclopramide because of their ↓ed gastric-emptying
times.
• Supplemental cortisol may be considered.
Induction

 Hypothyroid patients are more susceptible to the


hypotensive effect of anesthetic agents because of
 blunted baroreceptor reflexes, and
 decreased intravascular volume.
 their decreased CO
 ketamine has been proposed as the ideal induction agent
 RSI or an awake intubation if a difficult airway is present.
 SUX or intermediate-acting NDMR can be used for
intubation
Intraoperative

 ↑sensitivity to anesthetic drugs.


 MAC not changed-remember the exaggerated cardiac
depressant response
 RA is a good choice b/c it provided the intravascular
volume is well maintained.
 Airway compromise secondary to a swollen oral cavity,
edematous vocal cords, or goitrous enlargement may be
present.
 ↓gastric emptying ↑the risk of regurgitation and
aspiration.
Cont…
 A hypo dynamic cardiovascular system characterized by ↓ CO,
SV, HR, baroreceptor reflexes, and intravascular volume may
be compromised by surgical stress and cardiac depressant
anesthetic agents.
 ↓ventilatory responsiveness to hypoxia and hypercarbia are
enhanced by anesthetic agents.
 Hypothermia occurs quickly and is difficult to prevent and
difficult to treat. Thus, attention should be paid to maintaining
normal body temperature.
 Anemia and platelet coagulation factor dysfunction,
hyponatremia, and hypoglycemia are common and require
close monitoring intraoperative.
 DNS is the recommended IV fluid to avoid hypoglycemia and
minimize hyponatremia secondary to impaired free water
clearance.
Cont…
 Maintaince with N2o+ short-acting opioids, Bzds,
or ketamine
 Volatile anesthetics may not be recommended for
fear of cardiac depression
 Intermediate and short-acting NDMRs are good
 Pancuronium may be selected for skeletal muscle
paralysis
 Intraoperative hypotension is treated with ephedrine,
dopamine, or epinephrine and not a pure α-
adrenergic agonist (phenylephrine).
 Unresponsive hypotension may require
supplemental steroid administration
Postoperative

 Recovery from general anesthesia may be delayed.


These patients often require prolonged mechanical
ventilation.
 Patients should remain intubated until awake and
normothermic.
 Because hypothyroidism increases vulnerability to
respiratory depression, a non opioid such as ketorolac a
good choice for relief of postoperative pain.
SUMMARY

Patients should be clinically and chemically euthyroid prior to


thyroid surgery
Perioperative airway complications are common and the expected or
unexpected difficult airway should be anticipated.
Postoperative complications of hematoma formation, recurrent
laryngeal nerve palsy, hypocalcaemia and tracheomalacia can all
cause airway compromise and must be acted upon quickly.
Thyroid storm although less common than it used to be, is a medical
emergency.
In emergency cases, the use of an intravenous β-blocker, cortisol, or
dexamethasone and PTU is usually necessary.
 
References

1. Textbook of medical physiology / Arthur C. Guyton, John E. Hall.—


11th ed.
2. Harrison’s principles of internal medicine text book 16th
3. Miller’s anesthesia, Ronald D.Miller, 7th edition.
4. Hines & Marshall: Steeling’s Anesthesia and Co-Existing Disease,
5th edition.
5. clinical anesthesia barash Cullen 6th ed
THANK YOU!!!

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