[Yao's Anesthesiology] Thyrotoxicosis (1)

A 48-year-old man with thyrotoxicosis presented with diffuse neck enlargement
.

History of present illness: significant dyspnea, dysphagia, weight loss, paroxysmal palpitations and heat intolerance
.

Blood pressure 160/100 mmHg, heart rate 120 beats/min, hematocrit 29%
.

A.
Disease Status and Differential Diagnosis 1.
What is the diagnosis consistent with these symptoms? 2.
Describe the synthesis, release and peripheral transformation of tetraiodothyronine (T4) and triiodothyronine (T3)
.

3.
What is the role of the hypothalamic-pituitary axis in thyroid function? 4.
The role of thyroid hormones
.

5.
What is the cause of hyperthyroidism? 6.
What are the clinical symptoms and signs of thyrotoxicosis? 7.
How to differentiate thyroid storm and thyrotoxicosis? 8.
What are the causes of thyroid storm? 9.
What are the innervations of the larynx? B.
Preoperative Evaluation and Preparation 1.
Does an enlarged thyroid cause topographical changes? 2.
Describe the symptoms and signs of superior vena cava compression syndrome
.

3.
How is airway obstruction assessed? 4.
What are the laboratory tests for thyroid function? 5.
Treatment options to normalize thyroid function
.

6.
What are the benefits of adrenergic blockade? 7.
When can patients with hyperthyroidism undergo elective surgery? 8.
How to give preoperative medication to patients with hyperthyroidism? 9.
How to prepare for emergency surgery in patients with thyrotoxicosis? Partial breakdown A.
Condition and Differential Diagnosis A.
1.
What is the diagnosis consistent with these symptoms? These signs and symptoms are typical of hyperthyroidism
.

Differential diagnosis includes other hypermetabolic states such as pheochromocytoma, carcinoids, chronic infections, anxiety states, fatal catatonia, exercise-induced heatstroke and certain drugs such as inhalation anesthetics, sympathomimetics, serotonin antagonists , antipsychotics and other properties of drugs with anticholinergic effects
.

A2.
Describes the synthesis, release and peripheral transformation of tetraiodothyronine (T4) and triiodothyronine (T3)
.

The synthesis of thyroid hormones requires iodine
.

Sources of iodine are food intake or deiodination of pre-existing thyroid hormones
.

Iodine is actively transported to thyroid cells and accumulates in the form of iodide
.

Organization of iodine occurs when iodine binds to tyrosine residues on thyroglobulin (the receptor protein for iodine)
.

The iodinated tyrosine residues are present as T4 and T3 after conjugation
.

Under the regulation of thyrotropin, once thyroid hormone is cleaved from thyroglobulin, it is released into the circulation
.

90% of the hormones secreted by the thyroid gland are T4 and only 10% are T3.
T3 is biologically active but has a short half-life
.

In peripheral tissues, most of the T4 is converted to T3
.

T4 can also be converted to the inactive metabolite trans-T3
.

In the circulation, the majority of T4 and T3 are bound to plasma proteins (mainly thyroid hormone-binding globulin), a small portion is bound to albumin and prealbumin, and less than 1% of the hormones are present in free form in plasma
.

A3.
What is the role of the hypothalamic-pituitary axis in thyroid function? The hypothalamus secretes thyrotropin-releasing hormone (TRH), which in turn stimulates the anterior pituitary to synthesize and release thyrotropin (TSH)
.

TSH stimulates the thyroid to synthesize and secrete thyroxine
.

In pituitary cells, T4 is converted to T3, and the level of T3 in pituitary cells regulates the release of TSH from the pituitary
.

Low concentrations of T3 stimulate the release of TSH, while high concentrations of thyroid hormone inhibit TSH secretion
.

A4.
The role of thyroid hormones
.

Thyroid hormones act at the cellular, organ, and systemic levels
.

Effects on Organs • Thyroid hormones have a direct effect on the heart, increasing heart rate and myocardial contractility, thereby increasing cardiac output
.

• Thyroid hormones increase oxygen consumption and carbon dioxide production, thereby compensating for increased respiratory rate and tidal volume
.

• Thyroid hormones increase bone formation and catabolism, thereby altering parathyroid hormone levels
.

Systemic Effects • Thyroid hormones increase cellular metabolism and increase the production of metabolic end products, leading to vasodilation and increased tissue perfusion
.

A5.
What is the cause of hyperthyroidism? The etiology of hyperthyroidism (referred to as hyperthyroidism) is mainly Graves disease, accounting for 90% of the total cases
.

Thyroiditis is the second most common cause
.

Other less common causes, such as multinodular toxic goiter, single toxic thyroid nodules, excessive consumption of exogenous iodide, and side effects of certain medications can cause hyperthyroidism
.

Hyperthyroidism due to trophoblastic tumors such as moles and choriocarcinomas is rare
.

A6.
What are the clinical symptoms and signs of thyrotoxicosis? Factors such as the severity of thyrotoxicosis, the duration of the disease, the patient's susceptibility to excess thyroid hormone, and the patient's age determine the patient's clinical symptoms
.

Nonspecific symptoms such as hyperhidrosis, heat intolerance, weakness, and insomnia are common symptoms and signs of thyrotoxicosis
.

Because of the increase in metabolic rate, patients experience weight loss regardless of whether their appetite is normal or increased
.

Tremors and retraction of the eyelids often occur, resulting in decreased blinking, which are the result of sympathetic overexcitation
.

Thyrotoxicosis also significantly affects the cardiovascular system, leading to increased cardiovascular morbidity and mortality, mainly from heart failure and thromboembolism
.

Cardiovascular changes in thyrotoxicosis include tachycardia, increased stroke volume, increased cardiac output, increased oxygen consumption, and decreased systemic and pulmonary vascular resistance
.

In addition, the patient also showed increased myocardial contractility, autonomicity, and irritability
.

Pulse pressure increases as systolic blood pressure increases
.

Patients with coronary atherosclerosis may induce or exacerbate angina pectoris
.

Young adult patients usually tolerate hyperthyroidism without manifestations of cardiovascular decompensation
.

High-output congestive heart failure may occur in elderly patients and those whose hearts are already damaged
.

Patients with thyrotoxicosis may also present with sinus tachycardia, atrial fibrillation, complete heart block, and ventricular arrhythmias
.

Hypercapnia and increased oxygen consumption due to a hypermetabolic state compensatory increase minute ventilation, tachypnea, and tidal volume
.

Due to weakened muscle strength and reduced lung compliance, lung capacity is reduced, but lung diffusing capacity remains normal
.

During exercise, ventilation and oxygen uptake increase
.

Nervous system manifestations include anxiety, irritability, tremors, insomnia, muscle weakness, and cognitive dysfunction such as confusion and delirium
.

Severe cases may progress to stupor, dullness and even coma
.

Other manifestations include myopathy, periodic paralysis, seizures, chorea, and tremors at rest
.

EEG may be manifested as a rapid increase
.

Thyrotoxicosis shortens gastrointestinal emptying time and may lead to secretory diarrhea
.

Weight loss often occurs due to increased caloric requirements
.

Gastric acid secretion is sometimes reduced (30% of patients have parietal cell antibodies), which may interfere with drug absorption
.

Hematologic abnormalities include anemia, neutropenia, and thrombocytopenia
.

An increase in the number of red blood cells due to an increase in the need for oxygen
.

The effect on the kidneys increases tubular reabsorption and secretion, ultimately resulting in decreased potassium excretion and increased sodium excretion
.

A7.
How to identify thyroid storm and thyrotoxicosis? Thyrotoxicosis refers to the dysfunction of all organs of the body due to an increase in the concentration of thyroid hormones
.

Its clinical symptoms vary, and mild cases show asymptomatic biochemical abnormalities
.

In severe cases, multiple organ dysfunction may be life-threatening and the mortality rate is high
.

Thyroid storm often occurs when the patient's metabolism, thermoregulation, and cardiovascular system are decompensated
.

Thyroid storm has four main features: fever, tachycardia or supraventricular arrhythmias, central nervous system symptoms, and gastrointestinal symptoms
.

Early detection and aggressive treatment can reduce morbidity and mortality
.

There are no laboratory tests that can differentiate thyroid storm from thyrotoxicosis
.

Thyroid function tests are required
.

Therefore, once thyroid storm is suspected, active treatment should be started immediately, and treatment should not be delayed due to waiting for test results
.

The goals of treatment are to: reduce circulating thyroid hormone levels; inhibit the effect of circulating thyroid hormones on peripheral tissues; supportive care and removal of triggers
.

A8.
What are the causes of thyroid storm? Thyroid storm occurs suddenly, and the following conditions that cause a rapid rise in thyroid hormone levels are the causes of thyroid storm, such as thyroid surgery, discontinuation of antithyroid drug therapy, radioactive iodine therapy, lipiodol examination, and rough thyroid examination.
Check operation
.

Non-thyroid-related triggers include: non-thyroid surgery, infection, cerebrovascular accident, congestive heart failure, ileus, pulmonary embolism, pregnancy, childbirth, diabetic ketoacidosis, trauma, or certain iodine-containing drugs (amiodarone) ) application may also induce thyroid storm
.

The induction of thyroid storm is mainly related to drastic changes in thyroid hormone levels rather than absolute levels of thyroid hormones
.

A9.
What are the innervations of the larynx? The larynx is innervated by two branches of the vagus nerve: the superior laryngeal nerve and the recurrent laryngeal nerve
.

The superior laryngeal nerve is divided into two branches, the inner branch enters the larynx through the thyrohyoid periosteum (for the sensory and autonomic nerve branches), and the outer branch is outside the larynx (for the motor nerve branch)
.

The internal laryngeal nerve branches through the thyrohyoid membrane and are responsible for sensations in the larynx above the vocal cords
.

The external branch distributes on the surface of the thyrohyoid periosteum and innervates the cricothyroid muscle and part of the transverse arytenoid muscle
.

The recurrent laryngeal nerve innervates the movement of all intralarynx muscles and sensation in the larynx below the vocal cords
.

The cricothyroid muscle is the only tensor of the larynx
.

Bilateral recurrent laryngeal nerve injury will result in paralysis of all intralarynx muscles except the cricothyroid and part of the transverse arytenoid
.

The vocal cords are in a near-median position, causing airway obstruction
.

However, the vocal cords are not tense at this time, but are in a relaxed state
.

This is because the cricothyroid muscle requires confrontation with other muscles in the larynx to keep the vocal cords tight
.

In unilateral recurrent laryngeal nerve injury, the injured vocal fold is in a neutral position, while the other vocal fold remains normal
.

Among complications, hoarseness and aspiration were more common than airway obstruction
.

B.
Preoperative evaluation and preparation Bl.
Does enlarged thyroid cause topographical changes? The thyroid does not completely surround the trachea and esophagus
.

Enlarged glands can cause symptoms of tracheoesophageal compression, such as difficulty breathing and swallowing
.

The anatomical location of the glands on the suprasternal or substernal causes markedly different symptoms
.

Airway involvement includes: airway displacement, airway compression, and lumen stenosis
.

If the respiratory muscles are relieved by medication, the enlarged thyroid gland located under the sternum may cause unanticipated airway compression once the muscles relax
.

Airway invasion or intra-airway hemorrhage can be seen in patients with thyroid cancer
.

The superior vena cava in the thoracic cavity is prone to be compressed by mediastinal tumors due to its anatomical location
.

Patients with retrosternal goiter have also been reported to have bilateral vocal cord paralysis due to recurrent laryngeal nerve compression, secondary to acute respiratory insufficiency
.

B2.
Describe the symptoms and signs of superior vena cava compression syndrome
.

Superior vena cava compression syndrome is the result of chronic occult progressive compression/occlusion of the superior vena cava
.

The superior vena cava has low blood flow, low pressure, and thin wall, and is easily compressed by an enlarged mediastinal tumor
.

Low intraluminal pressures can easily lead to thrombosis, such as those caused by intravenous catheters
.

The obstruction of venous return leads to interstitial edema and the formation of collateral circulation, causing edema of the face, neck and upper extremities, collateral varicose veins in the neck and upper chest, headache and dizziness
.

Compression of the right innominate vein is more common because the right thyroid is relatively larger than the left
.

Compression of the superior vena cava will cause extensive collateral circulation such as the azygos plexus, internal mammary venous plexus, vertebral venous plexus, and lateral thoracic venous plexus
.

Venography is the "gold standard" for describing these anatomical changes
.

B3.
How to assess airway obstruction? Chest x-ray and neck CT can help assess the location of the trachea and the degree of airway obstruction
.

Pulmonary function testing is a non-invasive method used to assess the degree of airway obstruction in a patient
.

Flow-volume curve analysis can determine the degree and location of airway obstruction
.

The flow-volume curve is a circular curve obtained by inhaling forcefully to the total lung capacity, exhaling to the residual capacity, and then inhaling again to the total lung capacity
.

Different morphologies of the flow-volume curve can help distinguish between intrathoracic and extrathoracic airway obstruction (see Figure 1).
oFixed upper airway lesions, including airway tumors, subglottic strictures, and goiter, are inhaled in the flow-volume curve.
There are plateaus in both gas and expiratory phases (see Figure 1A).
Variable extrathoracic lesions are usually caused by vocal cord paralysis, vocal cord vegetation, and neck vegetation
.

A plateau appears in the inspiratory phase of the flow-volume curve
.

When inhaling, the negative pressure in the chest is created to close the airway outside the chest
.

During exhalation, the airflow keeps the airway open (see Figure 1B)
.

Variation of intrathoracic airway pathology, including endobronchial tumors, tracheal tumors, and tracheomalacia, caused only a plateau in the expiratory phase of the flow-volume curve
.

During inspiration, the negative pressure in the chest keeps the airway open, so the inspiratory phase is not affected
.

During exhalation, positive intrathoracic pressure narrows the airway and a plateau occurs in the expiratory phase of the flow-volume loop (see Figure 1C)
.

The forced vital capacity of these patients remained normal, but the forced expiratory volume in 1 second was significantly reduced
.

B4.
What are the laboratory tests to check thyroid function? B5.
Therapeutic regimen to restore normal thyroid function
.

There are three approaches to drug therapy: direct inhibition of thyroid hormone production, inhibition of thyroid hormone release, and control of the adrenergic effects of excess thyroid hormone
.

The initial treatment is mainly the use of antithyroid drugs to inhibit the synthesis of thyroid hormones, such as methimidine and propylthiouracil
.

These drugs are ineffective against synthesized thyroid hormones and cannot be fully effective until the synthesized hormones are consumed
.

Propylthiouracil also has the effect of inhibiting the conversion of T4 to T3 in peripheral tissues
.

Side effects of antithyroid drugs include: fever, urticaria, arthralgia, arthritis, leukopenia, agranulocytosis, and, more rarely, toxic hepatitis
.

Glucocorticoids inhibit the conversion of T4 to T3 in peripheral tissues, and have a synergistic effect when used together with propylthiouracil
.

After the use of antithyroid drugs, the addition of iodine (such as potassium iodide) can effectively inhibit the synthesis of thyroid hormones and inhibit the conversion of T4 to thereby reduce the level of thyroid hormones in the blood circulation
.

It begins to work within 24 hours of administration
.

Preoperative iodine treatment for 8-10 days reduces the vascular supply to the thyroid tissue
.

Iodine therapy needs to be continued for 2 weeks for maximum therapeutic effect
.

Before treatment with iodine, antithyroid drugs must be used to restore normal thyroid function, otherwise exogenous iodide can be used as a substrate to participate in the synthesis of new thyroid hormones
.

Exogenous iodine disrupts the function of thyroid cells and inhibits the binding of endogenous iodine
.

This Wolff-Chaikoff effect lasts only a few days
.

Thereafter, thyroid hormones begin to be resynthesized, although iodine continues to be ingested in high amounts
.

Therefore, iodine therapy is suitable for patients with hyperthyroidism and hyperthyroidism requiring emergency surgery
.

Iodine therapy is contraindicated in children, pregnant women, and lactating women, and it has been reported that it is safe to stop taking the drug for 4 months or more before pregnancy
.

Beta-blockers are used to block the peripheral adrenergic effects of hyperthyroidism
.

The patient's clinical symptoms can return to normal after medication, but if no other treatment is added, the patient's laboratory test results still show hyperthyroidism
.

Propranolol can also reduce the conversion of T4 to T3 in peripheral tissues, so it is the most commonly used β-adrenergic receptor antagonist in the treatment of hyperthyroidism
.

Patients with thyrotoxicosis may require higher doses of beta-blockers due to increased metabolism
.

Centrally acting adrenergic antagonists such as reserpine and calcium channel blockers such as diltiazem can be used in patients who cannot be treated with beta blockers
.

B6.
What are the benefits of adrenergic blockade? Catecholamines are associated with symptoms of thyrotoxicosis
.

Drugs that reduce catecholamine stores or block the effects of catecholamines
.

Can reduce heart rate, reduce cardiac output, reduce cardiac excitability
.

Medications used to treat symptoms of thyrotoxicity include beta-blockers, alpha-beta-blockers, and centrally acting adrenergic antagonists such as reserpine
.

The following related side effects may occur with the use of these drugs: hypotension, sedation, depression, myocardial depression, bronchospasm, and diarrhea
.

B7.
When can patients with hyperthyroidism undergo elective surgery? Treatment of patients should focus on relieving symptoms
.

The patient should return to a normal heart rate, pulse pressure, and sinus rhythm, with the resolution of a recent new heart murmur
.

Symptoms such as tremors, anxiety, palpitations, and heat intolerance should be relieved
.

B8.
How should patients with hyperthyroidism be given preoperative medication? The purpose of premedication in patients with thyrotoxicosis is to relieve anxiety and prevent excitation of the sympathetic nervous system
.

Benzodiazepines such as diazepam (5-20 mg orally) or central adrenergic inhibitors such as clonidine (3-5ug/kg orally) are often used before surgery
.

Antimuscarinic drugs such as atropine and scopolamine are not recommended because they can cause tachycardia and interfere with normal thermoregulation
.

B9.
How to prepare for emergency surgery in patients with thyrotoxicosis? When a patient needs emergency surgery, measures need to be taken to prevent hyperthyroidism
.

Propranolol can be tried to reduce the hyperadrenergic state and reduce the conversion of T4 to T3
.

Esmolol can also be used due to its β1 receptor specificity and short half-life
.

However, esmolol does not reduce the conversion of T4 to T3 in peripheral tissues
.

Antithyroid drugs should also be given to prevent further synthesis of thyroid hormones
.

Give propylthiouracil 200-400 mg orally every 6 hours or methimazole 20-40 mg orally every 6 hours as early as possible
.

Methimazole in aqueous solution can be used for rectal administration, propylthiouracil cannot
.

Both propylthiouracil and glucocorticoids can inhibit the conversion of T4 to T3 in peripheral tissues, and the combination of the two drugs can play a synergistic effect
.

Intravenous dexamethasone (2 mg every 6 hours) or hydrocortisone (40 mg every 6 hours) o potassium iodide saturated solution (5 drops orally every 6 hours) or Lugol's solution (30 drops every 6 to 8 hours) The release of T4 and T3 can be rapidly inhibited after administration
.

Anti-parasympathetic drugs such as atropine and pancuronium should be avoided because they relatively enhance the activity of the sympathetic nervous system
.

Treatment should also focus on correcting systemic decompensation
.

Fluids and electrolytes need to be adjusted to normal
.

Invasive monitoring is necessary to guide the use of inotropes and vasopressors when hypotension occurs that cannot be corrected by fluid infusion alone
.

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