This document discusses endocrine diseases and their implications for anesthesia. It covers both hyperthyroidism and hypothyroidism in detail. For hyperthyroidism, it describes the signs and symptoms, causes, effects on the cardiovascular system, and treatment approaches including antithyroid medications, beta blockers, iodine, and surgery. It provides guidance on preoperative preparation and intraoperative management. For hypothyroidism, it discusses signs and symptoms, effects on the cardiovascular system, diagnosis, and treatment with levothyroxine. It notes risks for anesthesia and importance of rendering patients euthyroid prior to elective surgery.

1. Anaesthetic consideration for
endocrine diseases
Dr.Radhwan Hazem Alkhashab
Consultant anaesthesiologit & intensivist
2021

2. The underproduction or overproduction of hormones can have dramatic
physiological and pharmacological consequences. Therefore, it is not
surprising that endocrinopathies affect anesthetic management.
Introduction

3. Thyroid gland
The function of the thyroid gland is to secrete sufficient
quantities of thyroid hormones to regulate cellular metabolism
throughout the body.

4. The thyroid gland weighs approximately 20 g and is composed of two
lobes joined by an isthmus. The gland is closely affixed to the anterior
and lateral aspects of the trachea with the upper border of the
isthmus located just below the cricoid cartilage The recurrent
laryngeal nerve and external motor branch of the superior laryngeal
nerve are in intimate proximity to the gland
Anatomy and Physiology of the Thyroid Gland

5. The thyroid is composed of numerous follicles filled with
proteinaceous colloid. The major constituent of colloid is
thyroglobulin, an iodinated glycoprotein, that serves as the
substrate for thyroid hormone synthesis. Normal quantities of
thyroid hormones depend on exogenous iodine. The diet is the
primary source of iodine
Histologically

6. The thyroid contains approximately 90% (i.e., 8000 micg) of the total iodine
content in the body.Iodine is reduced to iodide in the gastrointestinal tract
and rapidly absorbed into the blood , Active transport of iodide from the
plasma into the thyroid follicular cell is known as iodide trapping. Within
the cell, iodide is converted to an oxidized form of iodine that is capable of
combining with tyrosine residues of thyroglobulin , Inactive
monoiodotyrosine (MIT) and diiodotyrosine (DIT) are formed
(MIT + DIT = T3 , DIT + DIT = T4 ), Active hormones are released into the
circulation

7. Regulation of thyroid function is controlled by the hypothalamus, pituitary,
and thyroid glands, participating in a classic feedback control system.
A decrease in TSH causes a reduction in synthesis and secretion of T4
and T3, An increase in TSH yields an increase in hormone production
and release.

8. Normal thyroid hormone levels do not exclude thyroid disease, and
abnormal levels are not always indicative of disease. The
laboratory tests most commonly used to evaluate thyroid
function are serum free T4 (F T4) and serum TSH
Diagnosis

9. Hyperthyroidism

10. Hyperthyroidism refers to hyperfunctioning of the thyroid gland with
excessive secretion of active thyroid hormones. The majority of
cases (i.e., 99%) of hyperthyroidism result from one of three
pathologic processes: Graves’ disease, toxic multinodular goiter,
or a toxic adenoma.
Signs and Symptoms

11. weight loss, heat intolerance, muscle weakness, diarrhea, hyperactive
reflexes, and nervousness. A fine tremor, exophthalmos, or goiter may be
noted, particularly when the cause is Graves’ disease. New onset of atrial
fibrillation is a classic presentation of hyperthyroidism, but cardiac signs
also include sinus tachycardia and congestive heart failure.
The diagnosis of hyperthyroidism is confirmed by abnormal thyroid
function tests, which may include an elevation in serum T4 and serum T3
and a reduced TSH level
Clinical manifestations

12. The cardiovascular system is most threatened with hypermetabolism of
peripheral tissues, increased cardiac work with tachycardia,
arrhythmias (commonly atrial) and palpitations, a hyperdynamic
circulation, increased myocardial contractility and cardiac output, and
cardiomegaly. Patients with subclinical hyperthyroidism are
potentially at future risk of cardiac (atrial fibrillation) and central
nervous system (emboli, cerebrovascular accident) complications.
CVS manifestation

13. Medical treatment of hyperthyroidism relies on drugs that inhibit thyroid
hormone synthesis (eg, propylthiouracil, methimazole), prevent hormone
release (e.g., potassium, sodium iodide), or mask the signs of adrenergic
over activity (e.g., propranolol). In addition, although β-adrenergic
antagonists do not affect thyroid gland function, they do decrease the
peripheral conversion of T4 toT3.
Treatment of hyperthyroidism

14. The first line of treatment for hyperthyroidism is the antithyroid drug
propylthiouracil (PTU) or methimazole. These agents interfere with
the synthesis of thyroid hormones by inhibiting organification and
coupling.
PTU has the added advantage of inhibiting the peripheral
conversion of T4 to T3. PTU is prescribed for adults as 200 to 300
mg orally every 8 to 12 hours and methimazole as 10 to 20 mg
orally every 12 hours. A euthyroid state can almost always be
achieved in 6 to 8 weeks with either drug if a sufficient dose is
given.
Treatment…cont.

15. Iodide in high concentration inhibits release of hormones from the
hyperfunctioning gland. Its effects occur immediately but last for
only several weeks. Therefore, iodide is usually reserved for
preparing hyperthyroid patients for surgery, managing patients
with actual or impending thyroid storm, or treating patients with
severe thyrocardiac disease. Antithyroid drug therapy should
precede the initiation of iodide because iodide alone will increase
thyroid hormone stores and exacerbate the thyrotoxic state.
Treatment…cont.

16. B-Adrenergic antagonists effect by relieve signs and symptoms of
increased adrenergic activity such as anxiety, sweating, heat
intolerance, tremors, and tachycardia. Propranolol 40 to 80 mg
orally every 6 to 8 hours, esmolol, metoprolol, and atenolol are
effective. Propranolol has added features of impairing the
peripheral conversion of T4 to T3 and reducing metabolic rate. For
emergency use, intravenous propranolol in 0.2- to 1.0-mg boluses
followed by an infusion or an intravenous esmolol 0.5 mg/kg to
restore a normal heart rate.
Beta Blocker uses

17. Surgery (i.e., subtotal thyroidectomy or possibly total thyroidectomy)
results in prompt control of disease and a lower incidence of
hypothyroidism

18. For elective surgery, all patients should be made euthyroid with a course
of an antithyroid drug (PTU or methimazole) for 6 to 8 weeks
preoperatively. In addition, potassium iodide (This medication contains
iodine and potassium iodide. It is used along with antithyroid medicines to prepare
the thyroid gland for surgical removal and to treat certain overactive thyroid conditions
(hyperthyroidism , thyroid storm). It works by shrinking the size of the thyroid gland and
by decreasing the amount of thyroid hormones the body makess) should be given
for 7 to 14 days prior to surgery.
Patient preparation for surgery

19. B-Adrenergic blockers may be added in the preoperative period to
control heart rate. Glucocorticoids (dexamethasone 2 mg IV every 6
hours) should be administered to decrease hormone release and
reduce the peripheral conversion of T4 to T3.

20. The treatment of hyperthyroidism during pregnancy includes low doses
of antithyroid drugs. However, these drugs do cross the placenta and
can cause fetal hypothyroidism. Radioactive iodine treatment is
contraindicated during pregnancy, and oral iodide therapy causes
fetal goiter and hypothyroidism and is therefore contraindicated. The
long term use of propranolol is controversial since intrauterine
growth retardation has been attributed to its use.
Hyperthyroid during pregnancy

21. Anesthetic Considerations

22. All elective surgical procedures, should be postponed until the patient is
rendered clinically and chemically euthyroid & this may last 6-8weeks. The
patient should have normal T 3 and T4 concentrations, and should not
have resting tachycardia. Antithyroid medications and β-adrenergic
antagonists are continued through the morning of surgery. If emergency
surgery must proceed despite clinical hyperthyroidism, the hyperdynamic
circulation can be controlled by titration of an esmolol infusion, cortisol, or
dexamethasone and PTU.
Preoperative preparation

23. The anesthesiologist should be prepared to manage thyroid storm, especially in
patients with uncontrolled or poorly controlled disease who present for
emergency surgery.
Premedication may include: the use of a barbiturate, benzodiazepine, and/or a
narcotic. Anticholinergic drugs (i.e., atropine) should be avoided since they
may precipitate tachycardia and alter heat-regulating mechanisms.

24. Cardiovascular function and body temperature should be closely
monitored in patients with a history of hyperthyroidism. Ketamine,
indirect-acting adrenergic agonists, and other drugs that stimulate the
sympathetic nervous system or are unpredictable muscarinic
antagonists are best avoided. Incompletely treated hyperthyroid
patients can be chronically hypovolemic and prone to an exaggerated
hypotensive response during induction of anesthesia
Intraoperative

25. Thiopental decreases the peripheral conversion of T4 to T3 and may have
a slight advantage over other induction agents. Succinylcholine and
the nondepolarizing muscle relaxants with limited hemodynamic
effects (e.g., vecuronium, rocuronium) have been used safely for
intubation. Nitrous oxide and opioids are safe and effective in
hyperthyroid patients. Muscle relaxants should be chosen based on
their interaction with the SNS and their hemodynamic effects.
Reversal of muscle relaxants should include glycopyrrolate instead of
atropine in combination with an acetylcholinesterase inhibitor

26. For the treatment of intraoperative hypotension, a direct-acting
vasopressor (phenylephrine) is preferred. Ephedrine, epinephrine,
norepinephrine, and dopamine are avoided or administered in
extremely low doses to prevent exaggerated hemodynamic
responses. Regional anesthesia can be safely performed
Treatment of hypotension

27. Thyroid storm is a life-threatening exacerbation of hyperthyroidism
precipitated by trauma, infection, medical illness, or surgery. It is a
clinical diagnosis. Thyroid function tests may not help in
differentiating thyroid storm from symptomatic hyperthyroidism. It
may be the acute, rapid increase in the plasma level that triggers the
event. It most often occurs in the postoperative period in untreated or
inadequately treated patients for emergency surgery. Patients
present with extreme anxiety, fever, tachycardia, cardiovascular
instability, and altered consciousness
The etiology is probably a shift from protein-bound thyroid hormone to
free hormone secondary to circulating inhibitors to binding..
Thyroid Storm

28. Includes rapid alleviation of thyrotoxicosis and general supportive care.
Dehydration is managed with intravenous glucose containing crystalloid
solutions, and cooling measures (e.g., cooling blanket, ice packs, cool
humidified oxygen) are used to counter the fever. Necessary
medications include propranolol, labetalol, or esmolol titrated to
decrease heart rate to less than 90 bpm, and dexamethasone 2 mg
every 6 hours or cortisol 100 to 200 mg every 8 hours .
Treatment of thyroid storm

29. Antithyroid drugs (PTU 200–400 mg every 8 hours) may be administered
through a nasogastric tube, orally, or rectally. If circulatory shock is
present, an intravenous direct vasopressor (phenylephrine) is
indicated. A b-adrenergic blocker or digitalis is recommended for atrial
fibrillation accompanied by a fast ventricular response. Serum thyroid
hormone levels generally return to normal within 24 to 48 hours and
recovery occurs within 1 week. Unfortunately, the mortality rate for
thyroid storm remains surprisingly high at approximately 20%.
Treatment of thyroid storm.. Cont.

30. Hypothyroidism

31. Hypothyroidism or myxedema is a relatively common disease affecting
0.5% to 0.8% of the adult population.
Primary hypothyroidism results in a decreased production of thyroid
hormones despite adequate or increased levels of TSH and accounts
for 95% of all cases of hypothyroidism
Signs and Symptoms

32. The second leading cause is idiopathic and probably autoimmune in origin,
with autoantibodies blocking TSH receptors in the thyroid. Unlike Graves’
disease, this immune response destroys receptors instead of stimulating
them. Hashimoto’s thyroiditis is autoimmune in origin and is characterized
by goitrous enlargement and hypothyroidism in middle-aged women.
Secondary hypothyroidism due to hypothalamic or pituitary disease
accounts for 5% of cases of hypothyroidism.

33. In mild cases, patients tired easily and experience weight gain. In moderate
to severe cases, patients develop fatigue, lethargy, apathy, and
listlessness. Their speech becomes slow and their intellect becomes
dull. With time, they experience cold intolerance, decreased sweating,
constipation, menorrhagia, and slowing of motor function secondary to
muscle stiffness and cramping. They gain weight despite a decrease in
appetite. Physically, they demonstrate dry thickened skin, coarse facial
features, dry brittle hair, a large tongue, a deep hoarse voice, and
periorbital and peripheral edema.
Signs & Symptoms

34. Physiologically, cardiac output is decreased secondary to reductions in
stroke volume and heart rate. Ventricular dysrhythmias may occur.
Peripheral vascular resistance is increased and blood volume is
reduced resulting in pale, cool skin. In advanced cases, myocardial
contractility becomes reduced secondary to systolic and diastolic
dysfunction, and the heart becomes enlarged and dilated (hypothyroid
cardiomyopathy). Pericardial effusions are common. Baroreceptor
function is also impaired. Hypothyroid patients usually have
hypercholesterolemia and hypertriglyceridemia and may have coronary
artery disease.

35. The electrocardiogram in patients with overt hypothyroidism shows
flattened or inverted T waves, low-amplitude P waves and QRS
complexes, and sinus bradycardia.
Maximum breathing capacity and diffusion capacity are decreased, and
ventilatory responsiveness to hypoxia and hypercarbia is depressed.
Pleural effusions may result in dyspnea.

36. Diagnosis of primary hypothyroidism is confirmed by reduced levels of
F T4, T4, T3, and an elevated TSH level.
Treatment:
L-Thyroxine (levothyroxine sodium) is usually administered for the
treatment of hypothyroidism. It has reliably restores levels of T4
and T3 to normal, and has a prolonged duration of action. L-
Thyroxine has a gradual onset (6–12 hours), a peak effect in 10 to
12 days
Diagnosis

37. L-Thyroxine 50 mg/day is the recommended starting dose with an increase to
100 mg/day within several weeks.A dose of 150 to 200 mg/day is
sufficient to maintain a clinically euthyroid state. Patients with hypothyroid
cardiomyopathy notice improvement in myocardial function in 2 to 4
months on 100 mg/day of L-thyroxine. A dose of 150 mg/day can reverse
myocardial impairment and pericardial effusions
Treatment…cont.

38. Hypothyroid patients may be at an increased risk when receiving either general
or regional anesthesia for a number of reasons. Airway compromise
secondary to a swollen oral cavity, edematous vocal cords, or goitrous
enlargement may be present. Decreased gastric emptying increases the
risk of regurgitation and aspiration. A hypodynamic cardiovascular system
characterized by decreased cardiac output, stroke volume, heart rate,
baroreceptor reflexes, and intravascular volume may be compromised by
surgical stress and cardiac depressant anesthetic agents. Decreased
ventilatory responsiveness to hypoxia and hypercarbia are enhanced by
anesthetic agents.

39. Elective surgery is contraindicated until these patients are euthyroid.
Decreased myocardial function and ventilatory drive return to normal
within 3 to 6 months on L-thyroxine 150 mg/day. If emergency surgery
is necessary, the potential for severe cardiovascular instability
intraoperatively and myxedema coma in the postoperative period is
high.
If emergency surgery can be delayed for 24 to 48 hours, intravenous
thyroid replacement therapy will be more effective.

40. L-Thyroxine 300 to 500 mg or L-triiodothyronine 25 to 50 mg
intravenously are acceptable initial doses. Steroid coverage with
hydrocortisone or dexamethasone is necessary since decreased
adrenal cortical function often accompanies hypothyroidism. When
managing hypothyroid patients for elective surgery, preoperative
sedation should be avoided. These patients can be extremely
sensitive to narcotics and sedatives and may even be lethargic
secondary to their disease.

41. Dextrose in normal saline is the recommended intravenous fluid to avoid
hypoglycemia and minimize hyponatremia secondary to impaired
free water clearance. General anesthesia should be administered
through an endotracheal tube following either a rapid sequence
induction or an awake intubation if a difficult airway is present.
Ketamine is the preferred induction agent since it will support blood
pressure and heart rate. Nitrous oxide may also be an effective
induction agent. Barbiturates or benzodiazepines may be used;

42. Succinylcholine or the intermediate-acting nondepolarizing muscle
relaxants can be used for intubation. For maintenance, nitrous oxide
70% with small doses of a short-acting opioid or benzodiazepine or
ketamine, and an intermediate-acting nondepolarizing muscle
relaxant (vecuronium, rocuronium) may offer an advantage.
Reversal of muscle relaxants is accomplished in the usual fashion
with an acetylcholinesterase inhibitor and an anticholinergic
agent

43. intraoperative hypotension is best treated with ephedrine, dopamine, or
epinephrine and not a pure a-adrenergic agonist (phenylephrine).
Unresponsive hypotension may require supplemental steroid
administration. Postoperative analgesia is best managed with regional
techniques or small doses of opioids and/or ketorolac

44. Myxedema coma is a rare severe form of hypothyroidism characterized by
delirium or unconsciousness, hypoventilation, hypothermia (80% of
patients), bradycardia, hypotension, and a severe dilutional hyponatremia.
It occurs most commonly in elderly women with a long history of
hypothyroidism.Most patients are not comatose. Hypothermia is a
cardinal feature and results from impaired thermoregulation from
defective hypothalamic function (a target tissue of thyroid hormone). It is
a medical emergency with a mortality rate greater than 50% and requires
immediate aggressive treatment
Myxedema Coma

45. Infection, trauma, cold, and central nervous system depressants predispose
hypothyroid patients to myxedema coma. This is the one indication
for intravenous thyroxine. L-Thyroxine in a 300- to 500-mg loading dose
followed by a maintenance dose of 50 to 200 mg/day or L-triiodothyronine in
a 25- to 50-mg loading dose followed by a maintenance infusion is
recommended.

46. Combinations of T4 and T3 can also be used. Intravenous hydration with
glucose-containing saline solutions, temperature regulation, correction of
electrolyte imbalances, and stabilizing the cardiac and pulmonary
systems are necessary. Mechanical ventilation is frequently necessary.
Heart rate, blood pressure, and temperature usually improve within 24
hours, and a relative euthyroid state is achieved in 3 to 5 days.
Intravenous hydrocortisone 100 to 300 mg/day is also prescribed to treat
possible adrenal insufficiency.

47. A goiter results from compensatory hypertrophy and hyperplasia of
follicular epithelium secondary to a reduction in thyroid hormone
output.
In most cases, a goiter is associated with a euthyroid state with
the increased mass and cellular activity eventually overcoming
the impairment in hormone synthesis. However, hypothyroidism or
hyperthyroidism occurs in some cases.
Goiter

48. Complications from surgery are a major disadvantage of this form of
therapy and include:
1) Hypothyroidism.
2) Hemorrhage
3) Tracheal compression.
4) Unilateral or bilateral damage to the recurrent laryngeal nerve(s),
5) Damage to the motor branch of the superior laryngeal nerve.
6) Damage to or inadvertent removal of the parathyroid glands.
7) Hypocalcemia.
8) Tracheomalacia.
Complications of surgery

49. Adequate anesthetic depth must be obtained, however, before
laryngoscopy or surgical stimulation to avoid tachycardia, hypertension,
and ventricular arrhythmias.
Thyrotoxicosis is associated with an increased incidence of myopathies
and myasthenia gravis; therefore, neuromuscular blocking agents (NMBs)
should be administered cautiously. Hyperthyroidism does not increase
anesthetic requirements; that is, there is no increase in minimum alveolar
concentration.

50. Hematoma formation may cause airway compromise from collapse of
the trachea, particularly in patients with tracheomalacia. Dissection of
the hematoma may distort the airway anatomy and may make
intubation difficult. Immediate treatment includes opening the neck
wound and evacuating the clot, then reassessing the need for
reintubation.
Hypoparathyroidism from unintentional removal of all four parathyroid
glands will cause acute hypocalcemia within 12 -72 h