Anesthesia and Hypothyroidism

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Anesthesia and Hypothyroidism:

Anesthesia and Hypothyroidism Dr. Mustafa khreshy

Anatomy and Physiology of the Thyroid Gland:

Anatomy and Physiology of the Thyroid Gland 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. A pair of parathyroid glands is located on the posterior aspect of each lobe. A rich capillary network permeates the entire gland. The gland is innervated by the adrenergic and cholinergic nervous systems. A network of adrenergic fibers is associated with each thyroid cell, and adrenergic receptors are located in the cell membranes. The recurrent laryngeal nerve and external motor branch of the superior laryngeal nerve are in intimate proximity to the gland. Histologically, 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. The wall of each follicle is composed of cuboidal cells that become columnar with glandular stimulation. Twenty to 40 follicles form a lobule, and lobules are separated by connective tissue. The thyroid gland also contains parafollicular C cells, which produce calcitonin Thyroid hormone increases myocardial contractility directly, decreases systemic vascular resistance via direct vasodilation, and increases intravascular volume

Cardiovascular Function and Thyroid Disease:

Cardiovascular Function and Thyroid Disease Normal Hyperthyroidism Hypothyroidism SVR (dyn-sec-cm -5 ) 1500–1700 700–1200 2100–2700 HR (bpm) 72–84 88–130 60–80 EF (%) 50–60 >60 < 60 CO (L/min) 4.0–6.0 >7.0 < 4.5 Blood volume (% of normal) 100 105.5 84.5

Introduction:

Introduction 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. The most common cause in the United States is ablation of the gland by radioactive iodine or surgery. 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.

Signs and Symptoms:

Signs and Symptoms In adults, hypothyroidism has a slow, insidious, progressive course. There is progressive slowing of mental and physical activity. In mild cases, patients tire 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. Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues is responsible for the immobile, nonpitting edema. 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 (see Table 16-8 ). 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. The electrocardiogram in patients with overt hypothyroidism shows flattened or inverted T waves, low-amplitude P waves and QRS complexes, and sinus bradycardia. Hyponatremia and impairment of free water excretion are also common. Maximum breathing capacity and diffusion capacity are decreased, and ventilatory responsiveness to hypoxia and hypercarbia is depressed. Pleural effusions may result in dyspnea. Gastrointestinal function is slow, and an adynamic ileus may occur. Deep tendon reflexes demonstrate a prolonged relaxation phase.

Diagnosis:

Diagnosis Diagnosis of primary hypothyroidism is confirmed by reduced levels of F T 4 , T 4 , T 3 , R T 3 U, and F T 4 index and an elevated TSH level. Subclinical hypothyroidism is more common than subclinical hyperthyroidism. Twenty percent of women older than 60 years of age have subclinical hypothyroidism. Like subclinical hyperthyroidism, it is associated with long-term cardiovascular consequences. Thyroid function tests demonstrate a normal T 4 and an elevated TSH from 5.0 to 10.0 mU/L (normal = 0.4–5.0 mU/L). Although most patients have few if any signs or symptoms, changes in myocardial structure and contractibility can occur secondary to systolic and diastolic dysfunction. Even though these changes are reversible with I -thyroxine, use of thyroid replacement remains controversial for subclinical disease. In mild hypothyroidism, patients have minor, nonspecific symptoms with a low or normal T 4 and a mean TSH of 18.0 mU/L. Overt hypothyroidism demonstrates obvious clinical signs and symptoms, a markedly low T 4 , and a mean TSH of 90.0 mU/L. Basal metabolic rate may be decreased by 30% to 50%. Secondary hypothyroidism is diagnosed by reduced levels of F T 4 , TSH, T 4 , T 3 , and R T 3 U. A TRH stimulation test can confirm pituitary pathology as the cause. This test measures the responsiveness of the pituitary gland to intravenously administered TRH, the hypothalamic stimulator of TSH. In primary hypothyroidism, basal levels of TSH are elevated, and following TRH administration, the elevation is exaggerated. With pituitary dysfunction, there is a blunted or absent response to TRH

Treatment:

Treatment I -Thyroxine (levothyroxine sodium) is usually administered for the treatment of hypothyroidism. It has consistent potency, reliably restores levels of T 4 and T 3 to normal, and has a prolonged duration of action. I -Thyroxine has a gradual onset (6–12 hours), a peak effect in 10 to 12 days, and a T 1/2 of 7.5 days. I -Thyroxine 50 μg/day is the recommended starting dose with an increase to 100 μg/day within several weeks. A dose of 150 to 200 μg/day is sufficient to maintain a clinically euthyroid state. For the elderly or patients with coronary artery disease, 25 μg/day increasing monthly by 25-μg increments is recommended until euthyroidism is achieved. Patients with hypothyroid cardiomyopathy notice improvement in myocardial function in 2 to 4 months on 100 μg/day of I -thyroxine. A dose of 150 μg/day can reverse myocardial impairment and pericardial effusions. The first evidence of a therapeutic response to thyroid hormone is sodium and water diuresis and a reduction in the TSH level. Other alternative preparations include thyroid extract USP, I -triiodothyronine (liothyronine sodium), and liotrix, a combination of T 4 and T 3 in a 4:1 ratio. Thyroid extract 60 mg is equivalent to 100 μg I -thyroxine, which is equivalent to 25 μg I -triiodothyronine. The optimal daily dose for each is based on clinical response and TSH or T 3 and T 4 levels. Although the combination of T 4 and T 3 has no advantages over T 4 alone in patients with primary hypothyroidism, a combination of T 4 and slow-release T 3 may yield better plasma levels and is recommended by some experts, although more studies are needed. This combination may more physiologically mimic normal thyroid gland secretion.

Management of Anesthesia:

Management of Anesthesia 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 . Hypothermia occurs quickly and is difficult to prevent and difficult to treat . Hematologic abnormalities such as anemia (25%–50% of patients) and platelet and coagulation factor (especially VIII) dysfunction , electrolyte imbalances (hyponatremia), and hypoglycemia are common and require close monitoring intraoperatively . Decreased neuromuscular excitability is enhanced by anesthetic drugs

Slide 9:

Despite these potential risks, patients with subclinical hypothyroidism usually present no anesthetic problems. Elective surgery can proceed without special preparation. Patients with mild to moderate disease should probably receive daily I -thyroxine (100–200 μg/day) in the preoperative period. If they do not receive preoperative thyroid supplementation, it is debatable as to whether they are at increased risk . Patients with overt disease are definitely at increased risk. Elective surgery is contraindicated until these patients are euthyroid. Decreased myocardial function and ventilatory drive return to normal within 3 to 6 months on I -thyroxine 150 μg/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. Although intravenous I -thyroxine takes 10 to 12 days to yield a peak basal metabolic rate , intravenous triiodothyronine is effective in 6 hours with a peak basal metabolic rate seen in 36 to 72 hours . I -Thyroxine 300 to 500 μg or I -triiodothyronine 25 to 50 μg intravenously are acceptable initial doses. Steroid coverage with hydrocortisone or dexamethasone is necessary since decreased adrenal cortical function often accompanies hypothyroidism. Phosphodiesterase inhibitors such as Milrinone may be effective in the treatment of reduced myocardial contractility since its mechanism of action does not depend on β-receptors, whose number and sensitivity may be reduced with hypothyroidism

Slide 10:

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 . Regional anesthesia is recommended if there are no contraindications (e.g., coagulation abnormalities) and the nature of the surgery permits it. Invasive monitoring is determined on an individual basis and depends on the type of surgery and the medical condition of the patient. Patients with a hypodynamic cardiovascular system frequently require intra-arterial blood pressure monitoring and a central venous pressure or pulmonary artery (Swan-Ganz) catheter or transesophageal echo to monitor intravascular volume and cardiac status. 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 if SNS activity is not impaired . Nitrous oxide may also be an effective induction agent. Barbiturates or benzodiazepines may be used; however, central nervous system and cardiovascular system depression is unpredictable and may be significant. 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.

Slide 11:

Hypothyroid patients are very sensitive to the myocardial depressant effects of the potent inhalation agents. Vasodilation in the presence of possible hypovolemia and impaired baroreceptor activity can produce significant hypotension. From a cardiovascular standpoint, pancuronium is a preferred muscle relaxant; however, reduced skeletal muscle activity in these patients coupled with a reduction in hepatic metabolism necessitates cautious dosing and close monitoring. Reversal of muscle relaxants is accomplished in the usual fashion with an acetylcholinesterase inhibitor and an anticholinergic agent. Controlled ventilation is recommended during all cases since these patients tend to hypoventilate if allowed to breathe spontaneously. Also, overventilation must be guarded against since metabolism is decreased and carbon dioxide production is reduced. Postoperative ventilatory support should be anticipated to manage possible delayed emergence. Pharmacologic support of intraoperative hypotension is best treated with ephedrine, dopamine, or epinephrine and not a pure α-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 .

Myxedema Coma:

Myxedema Coma 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. Ironically, most patients are not comatose. Hypothermia (as low as 80°F) 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. Infection, trauma, cold, and central nervous system depressants predispose hypothyroid patients to myxedema coma. This is the one indication for intravenous thyroxine. I -Thyroxine in a 300- to 500-μg loading dose followed by a maintenance dose of 50 to 200 μg/day or I -triiodothyronine in a 25- to 50-μg loading dose followed by a maintenance infusion is recommended. I -Triiodothyronine has a more rapid onset and may be preferred. Administration of at least 65 μg/day in the initial days of therapy is associated with lower mortality. Combinations of T 4 and T 3 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 (AI), a common sequela of hypothyroidism

Euthyroid sick syndrome:

Euthyroid sick syndrome occurs in critically ill patients with significant nonthyroidal illness who demonstrate abnormal thyroid function tests. These tests demonstrate low levels of T 3 and T 4 and a normal TSH. As illness increases in severity, the T 3 and T 4 levels decrease further. The etiology of this response is not understood. Euthyroid sick syndrome may be a physiologic response to stress, and it can be induced by surgery. No treatment for thyroid function is necessary. Differentiating hypothyroidism from euthyroid sick syndrome is necessary and can be extremely difficult. A serum TSH level is the best aid. Levels greater than 10 mU/L indicate hypothyroidism, while levels less than 5.0 mU/L indicate euthyroidism. Values between 5 to 10 mU/L may represent mild hypothyroidism. Hypothyroidism is diagnosed by clinical signs and symptoms (dry skin, depressed deep tendon reflexes, bradycardia, hypothermia), reduced T 3 and T 4 levels, and an elevated TSH. Once diagnosed, hypothyroid patients should receive I -thyroxine.

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