bubble_chart Overview

Hypothyroidism refers to a pathological state where there is insufficient or absent thyroid hormone action in tissues. Hypothyroidism is more common in women than in men, and its prevalence increases with age. The incidence of neonatal hypothyroidism is approximately 1/7000, decreases during adolescence, and rises again in adulthood. The most common cause of hypothyroidism is chronic lymphocytic thyroiditis.

bubble_chart Etiology

Clinically, it is practical to classify hypothyroidism based on the age of onset, which can be divided into the following three types:

1. Hypofunction beginning in the fetal period or shortly after birth is called cretinism;
2. Hypofunction beginning in the prepubertal childhood is called juvenile hypothyroidism, and in severe cases, juvenile myxedema;
3. Hypofunction beginning in adulthood is called hypothyroidism, and in severe cases, myxedema.

(1) Cretinism can be divided into endemic and sporadic types:

1. Endemic cretinism occurs in areas with endemic goiter, where maternal iodine deficiency leads to insufficient iodine supply to the fetus, resulting in thyroid hypoplasia and inadequate hormone synthesis. This type of hypothyroidism severely damages the rapidly developing nervous system, especially the brain, of the fetus, leading to irreversible neurological damage, which manifests as this condition. Some fetuses have a tendency to develop cretinism under conditions of iodine deficiency or insufficient thyroid hormones, and the disease mechanism may be related to genetic factors, which requires further research.
2. Sporadic cretinism occurs worldwide, and the disease cause is unknown. The mother has neither iodine deficiency nor goiter, and the speculated causes include:

   (1) Thyroid hypoplasia or absence: There are three possibilities:

   1. Defects in the growth and development of the child's thyroid itself;
   2. The mother has certain autoimmune thyroid diseases during pregnancy, with anti-thyroid antibodies in the serum that enter the fetus via the bloodstream through the placenta, destroying part or all of the fetal thyroid;
   3. The mother takes antithyroid drugs or other goitrogenic substances during pregnancy, hindering fetal thyroid development and hormone synthesis.
   (2) Impaired thyroid hormone synthesis: Often with a family history, the main types of hormone synthesis impairment are:
   1. Impaired thyroid iodine uptake: Affects iodine concentration, possibly due to dysfunction of the "iodine pump" involved in iodine entry into cells.
   2. Impaired iodine organification process:
      1. Peroxidase deficiency: In this type, the thyroid has strong iodine uptake, but iodide cannot be oxidized to active iodine, preventing tyrosine iodination.
      2. Iodotyrosine coupling defect: The generated monoiodotyrosine and diiodotyrosine in the thyroid fail to couple, leading to reduced synthesis of thyroxine (T4) and triiodothyronine (T3).
   3. Iodotyrosine deiodination defect: Due to deiodinase deficiency, free monoiodotyrosine and diiodotyrosine cannot be deiodinated, accumulating in the blood and excreted in urine, indirectly causing excessive iodine loss.
   4. Thyroglobulin synthesis and degradation abnormalities: Iodination of tyrosine residues and the formation of T4 and T3 from iodinated tyrosine residues occur within intact thyroglobulin molecules. Abnormal thyroglobulin can reduce T3 and T4 synthesis and produce butanol-insoluble globulin, affecting the biological efficacy of T4 and T3. Abnormal thyroglobulin degradation can increase inactive iodoprotein levels in peripheral blood.

(2) Juvenile hypothyroidism

The disease cause is the same as in adult patients.

(3) Adult hypothyroidism

The disease cause can be divided into three major categories: thyroid hormone deficiency (thyroprivic), thyrotropin deficiency (thyrotrophoprivic), and peripheral tissue resistance to thyroid hormones:

1. Thyroid hormone deficiency due to thyroid gland disorders can be classified into primary and secondary causes:
   (1) Primary: The disease cause is unknown, hence also termed "idiopathic," possibly related to thyroid autoimmunity. This group of cases often involves thyroid atrophy, accounting for 5% of hypothyroidism incidence. Occasionally, it may develop from Graves' disease or manifest as part of multiple endocrine deficiency syndrome (Schmidt syndrome).
   (2) Secondary: The following are relatively clear causes:
   1. Thyroid destruction: Surgical removal of the thyroid, or after radioactive iodine or radiation therapy.
   2. Thyroiditis: Mostly in the late stage [third stage] of chronic lymphocytic thyroiditis related to autoimmunity, rarely caused by subacute thyroiditis.
   3. Hypothyroidism with goiter or nodules: Commonly seen in chronic lymphocytic thyroiditis, occasionally in invasive fibrous (Reidel's) thyroiditis, may be accompanied by nodular endemic goiter and sporadic goiter due to iodine deficiency.
   4. Extensive intra-glandular lesions: Mostly seen in advanced stage stony goiter (thyroid carcinoma) and metastatic tumors, less commonly in thyroid subcutaneous nodes, amyloidosis, thyroid lymphoma, etc.
   5. Medications: Overdose of antithyroid drugs; excessive intake of iodides (organic or inorganic iodine); use of drugs that inhibit iodide uptake by the thyroid, such as potassium perchlorate, thiocyanate, resorcinol, sodium para-aminosalicylate (PAS), phenylbutazone, sulfonamides, cobalt nitrate, lithium carbonate, etc. Patients with hyperthyroidism who undergo surgical or ¹³¹iodine treatment are often more sensitive to the inhibitory effects of iodides on thyroid hormone synthesis and release, making them prone to hypothyroidism when taking iodine-containing medications again.
2. Due to insufficient thyrotropin (thyrotrophoprivic), it is further divided into pituitary and hypothalamic types:
   (1) Caused by insufficient secretion of thyroid-stimulating hormone (TSH) due to anterior pituitary hypofunction. Also known as pituitary (or secondary) hypothyroidism. The causes are varied; for details, see "Anterior (Adeno)hypophyseal Hypofunction." To avoid confusion with the aforementioned "secondary" thyroid destruction, it is more accurate to refer to it as pituitary hypothyroidism.
   (2) Caused by insufficient secretion of thyrotropin-releasing hormone (TRH) due to hypothalamic disorders. Also known as hypothalamic (or tertiary) hypothyroidism. The term "tertiary" is used in contrast to secondary pituitary hypothyroidism, so it is appropriate to refer to it as hypothalamic hypothyroidism.
3. Peripheral hypothyroidism: Refers to peripheral tissue resistance to thyroid hormone. There are two disease causes:
   (1) Due to the presence of thyroid hormone-binding antibodies in the blood, leading to the inability of thyroid hormone to exert its normal biological effects;
   (2) Due to a reduction in the number of thyroid hormone receptors in peripheral tissues and decreased receptor sensitivity to thyroid hormone, resulting in reduced responsiveness of peripheral tissues to thyroid hormone.

bubble_chart Clinical Manifestations

(1) Cretinism

The causes of the disease are numerous, and the clinical manifestations share common features as well as distinct characteristics of each type. At birth, there are usually no specific symptoms, but symptoms appear within a few weeks after birth. Common manifestations include: pale, thickened, and wrinkled skin with scaling; thick lips, a large tongue often protruding, an open mouth with excessive drooling, an unattractive appearance, pale or waxy complexion, a short and upturned nose with a flattened bridge, a forehead with many wrinkles, short stature, thick and short limbs, shovel-shaped hands, frequent umbilical hernias, slow heart rate, low body temperature, and growth and development below that of peers of the same age. In adulthood, affected individuals are often short.

Special manifestations of each type of cretinism:

1. Congenital thyroid dysplasia: The severity of symptoms and their timing depend on the degree of glandular abnormality. In cases of complete absence of the thyroid gland, the aforementioned symptoms may appear within 1–3 months after birth and are more severe, with no goiter. If there are remnants or ectopic thyroid tissue, typical symptoms often appear between 6 months and 2 years of age, possibly accompanied by compensatory thyroid enlargement.
2. Congenital thyroid hormone synthesis disorders: The severity varies depending on the degree of enzyme deficiency. Symptoms are usually not apparent in the neonatal period, but compensatory goiter gradually develops, often becoming significantly enlarged. Classic hypothyroidism may appear later and is referred to as goitrous cretinism, likely inherited as an autosomal recessive trait. In cases of iodine organification defects, besides goiter and hypothyroidism, congenital neural deafness and dumbness may occur, known as Pendred syndrome. These two types are more common in sporadic cretinism cases where the mother is not iodine-deficient and has normal thyroid function. Although the fetus cannot synthesize thyroid hormones, it can compensate by receiving them from the mother, thus avoiding severe neurological damage. However, after three months of age, when the maternal thyroid hormones are depleted, the lack of thyroid hormones due to the fetus's own thyroid dysplasia, absence, or synthesis defects leads to significant hypothyroidism, though intellectual impairment is relatively mild.
3. Congenital iodine deficiency: More common in endemic cretinism. Due to maternal endemic goiter, the fetus experiences iodine deficiency. When both fetal and maternal thyroid hormone synthesis are insufficient, the production or activity of enzymes essential for fetal nervous system development (such as uridine diphosphate (UDP)) is impaired, leading to severe and irreversible neurological damage in the fetus, as well as permanent intellectual deficits and hearing and speech impairments after birth. However, if iodine supply improves postnatally, the thyroid can enhance hormone synthesis, so hypothyroidism symptoms are not prominent. This type is also called "neurological" cretinism.
4. Maternal intake of goitrogenic agents or foods during pregnancy (e.g., cabbage, soybeans, p-aminosalicylic acid, thiourea, resorcinol, phenylbutazone, and iodine): These goitrogenic substances or drugs can cross the placenta and affect thyroid function, leading to transient goiter after birth, sometimes accompanied by hypothyroidism. This type is clinically mild and transient, often unnoticed. If large doses of iodine are taken orally for an extended period during pregnancy, iodine compounds can cross the placenta and cause neonatal goiter. Severe cases may lead to neonatal asphyxia and death, so pregnant women should avoid high-dose iodine. During lactation, iodine can also pass into breast milk, causing goiter and hypothyroidism in infants.

(2) Juvenile myxedema

Clinical manifestations vary depending on the age of onset. In young children, apart from less pronounced growth retardation and facial changes compared to cretinism, other symptoms are similar. In older children and adolescents, most cases resemble adult myxedema but are accompanied by varying degrees of growth retardation and delayed puberty.

(3) Adult hypothyroidism and myxedema

1. Clinical classification of hypothyroidism (including central hypothyroidism—hypothalamic and pituitary hypothyroidism, and thyroidal hypothyroidism):
   (1) Clinical hypothyroidism: Theoretically, it depends on thyroid hormones, but in practice, the severity and manifestation of clinical symptoms depend on the onset (acute or chronic), the speed and degree of hormone deficiency, and are also related to individual differences in response to reduced thyroid hormones. Therefore, severe thyroid hormone deficiency may sometimes present with mild clinical symptoms. Thus, the diagnostic criteria for clinical hypothyroidism should include varying degrees of clinical manifestations and decreased serum T3 and T4 levels, particularly serum T4 and FT4, which serve as objective laboratory indicators for clinical hypothyroidism. Clinical hypothyroidism can be divided into severe and mild types. The former exhibits obvious symptoms, affects multiple systems, and often presents with myxedema, while the latter has milder or atypical symptoms.
   (2) Subclinical hypothyroidism: No obvious clinical manifestations are present; serum T3 is normal, while T4 is normal or decreased. Diagnosis requires TSH testing and/or TRH stimulation test.
2. Adult myxedema is most common between the ages of 40 and 60, with a male-to-female ratio of 1:4.5. The onset is insidious, and the disease progresses slowly, sometimes lasting more than a decade before obvious symptoms of myxedema appear. In cases of unknown etiology, the lesions are often complete; in secondary cases, the lesions are mostly incomplete, and some patients may even recover (e.g., those caused by excessive medication for hyperthyroidism). For those whose condition arises from surgery or radiotherapy, the onset is not particularly insidious. Early symptoms begin around the 4th week, with typical symptoms commonly appearing after the 8th week. The earliest symptoms of myxedema include reduced sweating, cold intolerance, sluggish movements, mental lethargy, fatigue, drowsiness, intellectual decline, poor appetite, weight gain, and severe constipation. When typical symptoms emerge, the following manifestations are observed:
   1. **Low basal metabolic rate syndrome**: Fatigue, slow movement, drowsiness, significant memory impairment, and difficulty concentrating. Due to poor peripheral circulation and reduced energy production, patients exhibit extreme cold intolerance, absence of sweating, and subnormal body temperature.
   2. **Myxedema facies**: The facial expression can be described as "apathetic," "dull," "mask-like," "wooden," or even "idiotic." The cheeks and eyelids appear puffy, and in pituitary myxedema, the face may become round and full, resembling a moon face. The complexion is pale, anemic, or tinged with yellow or an old ivory hue. Sometimes, facial skin may show cyanosis. Due to reduced sympathetic tone weakening the effect on Müller's muscle, the eyelids often droop, or the palpebral fissure narrows. Some patients exhibit grade I exophthalmos, possibly related to retrobulbar tissue edema, though it poses no threat to vision. The nose and lips thicken, the tongue enlarges, leading to slurred speech, slow articulation, and a hoarse, low voice. Hair becomes dry, sparse, and brittle, with eyelashes and eyebrows falling out (especially the outer third of the eyebrows). In men, beard growth slows.
   3. The skin appears pale or, due to grade I anemia and thyroid hormone deficiency, exhibits impaired conversion of subcutaneous carotene to vitamin A and retinol, leading to elevated plasma carotene levels. Combined with anemic pallor, this often gives the skin a distinctive waxy yellow hue. The skin is rough, lacking luster, dry, thick, cold, and scaly, with pronounced scaling and keratinization, particularly on the hands, arms, and thighs. Hyperkeratotic skin manifestations may also occur. Non-pitting myxedema is present, though pitting edema may appear in the lower limbs. Subcutaneous fat thickens due to fluid retention, leading to weight gain in two-thirds of patients. Nail growth slows, becoming thick, brittle, and often cracked. Axillary and pubic hair may fall out.
   4. **Neurological and psychiatric manifestations**: Mental sluggishness, drowsiness, impaired comprehension, and memory loss. Vision, hearing, touch, and smell are dulled, accompanied by tinnitus and dizziness. Some patients may exhibit nervousness, delusions, hallucinations, depression, or paranoia. In severe cases, psychosis may occur, presenting as stupor, dementia, or coma. Untreated chronic patients and those newly undergoing treatment are particularly prone to psychiatric symptoms, generally attributed to reduced cerebral metabolism of oxygen and glucose. Occasionally, cerebellar syndrome may appear, with ataxia and other symptoms. Numbness in the hands and feet and abnormal pain sensation may occur. Changes in tendon reflexes are characteristic: the contraction phase is often brisk and lively, while the relaxation phase is delayed. Ankle reflex is diminished, with a latency exceeding 360 milliseconds aiding diagnosis. Knee reflexes are usually normal. EEG may show abnormalities. Cerebrospinal fluid protein may increase to 3g/L.
   5. **Musculoskeletal system**: Muscles become slack and weak, primarily affecting the shoulder and back muscles. Temporary stiffness, spasms, pain, or cogwheel-like movements may occur. The abdominal, back, and calf muscles may spasm and ache, and joint pain is common. Bone density may increase. A few cases exhibit muscle hypertrophy. During development, bone age is often delayed.
   6. The cardiovascular system: Slow pulse, bradycardia, weak heart sounds, and reduced cardiac output, often half of normal. Since tissue oxygen consumption decreases in parallel with cardiac output, myocardial oxygen demand is reduced, and cardiac colicky pain or heart failure rarely occurs. However, some patients may exhibit electrocardiographic signs of myocardial infarction, which can resolve after treatment. If heart failure does occur, the efficacy of treatment is often poor and toxicity is more likely due to the prolonged half-life of Rehmannia in the body and myocardial fiber elongation accompanied by mucinous edema. Generalized cardiac enlargement is relatively common, often accompanied by pericardial effusion, both of which can return to normal after treatment. Middle-aged and elderly women may experience elevated blood pressure. Circulation time is prolonged. Long-term illness can easily lead to complications such as atherosclerosis and coronary heart disease, resulting in cardiac colicky pain and arrhythmias.
   7. Digestive system: Poor appetite, anorexia, abdominal distension and fullness, constipation, tympanites, and even megacolon and paralytic ileus may occur. 50% of patients have achlorhydria or absence of gastric acid due to the presence of anti-gastrin antibodies. Liver function tests may show elevated SGOT, LDH, and CPK.
   8. Respiratory system: A combination of factors such as obesity, myxedema, pleural effusion, anemia, and poor circulatory system function can lead to tachypnea, reduced carbon dioxide diffusion capacity in the alveoli, resulting in respiratory symptoms or even carbon dioxide narcosis.
   9. Endocrine system: Adrenal cortical function is generally lower than normal, with decreased blood and urinary cortisol levels. ACTH secretion is normal or reduced, and the ACTH stimulation response is delayed, but there are no clinical manifestations of adrenal insufficiency. If the disease is accompanied by primary autoimmune adrenal insufficiency and diabetes, it is called polyendocrine deficiency syndrome (Schmidt syndrome). In patients with long-standing and severe disease, pituitary and adrenal function may decline, and these conditions may accelerate under stress or during rapid thyroid hormone replacement therapy.
      In long-term cases, the pituitary gland is often enlarged. In primary hypothyroidism, elevated TSH may concurrently increase prolactin levels, leading to milk regurgitation, though the mechanism of hyperprolactinemia in this disease remains unclear. Sympathetic nerve activity decreases in the absence of thyroid hormones, possibly related to reduced plasma cyclic AMP response to adrenaline. Adrenaline secretion rate and plasma concentration are normal, while norepinephrine-related functions increase. β-adrenergic receptors may decrease in hypothyroidism. Plasma serotonin concentration and urinary 5-hydroxyindoleacetic acid excretion are normal. Androsterone excretion is reduced. Insulin degradation rate decreases, and patients exhibit increased insulin sensitivity.
   10. Urinary system and water-electrolyte metabolism: Renal blood flow decreases, phenol red excretion is delayed, and thickening of the glomerular basement membrane may lead to mild proteinuria. Water diuresis tests are poor, and the diuretic effect cannot be corrected by cortisone but can be normalized by thyroid hormones. Impaired renal water excretion leads to tissue water retention. Na⁺ exchange increases, which may result in hyponatremia, but K⁺ exchange is usually normal. Serum Mg²⁺ may increase, while exchangeable Mg²⁺ and urinary Mg²⁺ excretion rates decrease.
   11. Hematologic system: Thyroid hormone deficiency suppresses hematopoietic function, reducing erythropoietin. Achlorhydria impairs iron and vitamin B12 absorption, and hypermenorrhea contributes to mild or grade II normochromic or hypochromic microcytic anemia in two-thirds of patients. A few (about 14%) have pernicious anemia (macrocytic type). ESR may increase. Deficiencies in factors VIII and IX weaken the coagulation mechanism, leading to a bleeding tendency.
   12. Unconsciousness: The most severe manifestation of myxedema, commonly seen in elderly, untreated patients. Most cases occur in cold winters, with exposure to cold and infection being the most common triggers. Other factors such as trauma, surgery, anesthesia, or sedative use may also precipitate it. A history of drowsiness often precedes unconsciousness. During unconsciousness, limbs are flaccid, reflexes are absent, body temperature is very low (may be below 33°C), breathing is shallow and slow, bradycardia, faint heart sounds, hypotension, and shock may occur, possibly accompanied by heart or kidney failure, often life-threatening.

bubble_chart Diagnosis

Early diagnosis of cretinism is extremely important. Conditions should be created to include serum thyroid hormone and TSH as routine neonatal screening tests. To avoid or minimize permanent intellectual developmental disabilities, treatment should begin as early as possible, making early diagnosis essential. Diagnosing this condition during infancy is challenging, requiring careful observation of growth, development, facial features, skin, diet, sleep, bowel movements, and other aspects. If necessary, relevant laboratory tests should be conducted. For suspected but unconfirmed cases, or where laboratory resources are limited, a trial treatment may be attempted. Due to the distinctive facial features of cretinism, it is important to differentiate it from congenital idiocy (Down syndrome, also known as trisomy 21).

The diagnosis of typical cases of myxedema is not difficult, but early mild or atypical cases are often confused with anemia, obesity, edema, nephrotic syndrome, low metabolic rate syndrome, menstrual disorders, and anterior pituitary hypofunction. Thyroid function tests are necessary for differentiation. Diagnosing peripheral hypothyroidism can sometimes be challenging. Patients exhibit clinical signs of hypothyroidism, but the main laboratory feature is elevated serum T4 levels. Thyroid ¹³¹I uptake may be increased, and treatment with T4 or T3 shows limited efficacy, suggesting receptor insensitivity. Some patients may also present with characteristic facial features, deafness and dumbness, and stippled epiphyses. No goiter is present.

bubble_chart Treatment Measures

(1) The earlier cretinism is treated, the better the efficacy. For neonatal cretinism, initially administer triiodothyronine (T3) orally at 5μg every 8 hours and L-thyroxine sodium (T4) at 25μg/d. After 3 days, increase T4 to 37.5μg/d. After 6 days, adjust T3 to 2.5μg every 8 hours. During the treatment process, gradually increase T4 to 50μg/d while tapering T3 until discontinuation. Alternatively, use T4 alone, starting at 25μg/d and increasing by 25μg/d weekly, reaching 100μg/d after 3–4 weeks, then slowing the increase to maintain serum T4 at 9–12μg/dl. If clinical efficacy is unsatisfactory, the dose may be slightly increased. Infants aged 9 months to 2 years require 50–150μg T4 daily. If skeletal growth and maturation do not accelerate, thyroid hormone should be increased. Although TSH values help assess treatment adequacy, clinical symptom improvement is more effective than serum T4 measurement for evaluating hypothyroidism treatment. Treatment should be lifelong.

(2) Juvenile myxedema

is treated similarly to older children with cretinism.

(3) Adult myxedema

shows significant improvement with thyroid hormone replacement therapy, which must be taken lifelong. Available preparations include synthetic thyroid hormones and thyroprotein derived from animal thyroid glands:

1. **Thyroid tablets** are widely used, starting at a low dose of 15–30mg daily, with a final dose of 120–240mg. If no effect is observed at 240mg, reconsider the diagnosis or evaluate for peripheral hypothyroidism. Once symptoms improve and pulse rate and basal metabolic rate normalize, reduce the dose to an appropriate maintenance level, typically 90–180mg daily. Discontinuation often leads to symptom recurrence within 1–3 months. If palpitations, arrhythmia, tachycardia, insomnia, dysphoria, or profuse sweating occur during treatment, reduce or temporarily suspend the dose.
2. **L-thyroxine sodium (T4) or triiodothyronine (T3)**: 100μg T4 or 20–25μg T3 is equivalent to 60mg of desiccated thyroid tablets. Start with a low dose, such as T4 at 25μg twice daily, then increase by 50μg every 1–2 weeks until reaching a final dose of 200–300μg. The usual maintenance dose is 100–150μg T4 daily. T3 is dosed at 60–100μg daily. T3 acts faster and more potently than T4 and desiccated thyroid but has a shorter duration, making T4 and desiccated thyroid preferable for replacement therapy. Due to unstable bioavailability of desiccated thyroid, T4 tablets are superior.
3. **T4 and T3 combination preparations**: A 4:1 ratio of T4 to T3 in a mixture or tablet mimics endogenous thyroid hormone action.
   For younger patients without heart disease, the initial dose may be slightly higher, and increments may be faster. For example, desiccated thyroid can start at 60mg daily, increasing by 60mg every 2 weeks until reaching the maintenance dose.
4. Thyroid extracts, USP, and purified porcine thyroglobulin have been used clinically.

**Elderly patients** should receive reduced doses. For those with coronary artery disease, other cardiac conditions, or psychiatric symptoms, thyroid hormone should start at a lower dose and increase more slowly. For example, begin desiccated thyroid at 15mg daily, increasing by 15mg every 2 weeks or longer until reaching the appropriate maintenance dose. If angina, arrhythmia, or psychiatric symptoms occur, promptly reduce the dose.

Since the normal range of serum T3 and T4 concentrations is broad and hypothyroidism severity varies, individualized treatment is necessary based on the patient’s needs and sensitivity to thyroid hormone.

In patients with anterior pituitary hypofunction and severe conditions, to prevent adrenal insufficiency, thyroid hormone therapy should be initiated after corticosteroid replacement therapy.

Peripheral hypothyroidism is more difficult to treat, and a higher dose of T3 may be attempted.

Patients with anemia should be given iron supplements, folic acid, vitamin B12, or liver preparations. When treating with iron supplements, attention should also be paid to gastric acid levels, and supplementation is required if levels are low.

For patients with cardiac symptoms, unless there is congestive heart failure, Rehmannia is generally unnecessary. After the application of thyroid preparations, cardiac signs and ECG changes can gradually disappear.

Patients with myxedema are highly sensitive to insulin, sedatives, and anesthetics, which may induce unconsciousness, so caution is advised when using them.

Treatment for myxedema unconsciousness:

1. Thyroid preparations: Since thyroid tablets and T4 act too slowly, the fast-acting triiodothyronine (T3) must be selected. In the initial stage, it is best to use intravenous preparations (D, L-triiodothyronine), with an initial dose of 40–120 μg, followed by 5–15 μg of T3 intravenously every 6 hours until the patient regains consciousness and can switch to oral administration. If this dosage form is unavailable, triiodothyronine tablets can be ground and administered via nasogastric tube with water, every 4–6 hours, 20–30 μg each time. If no fast-acting preparation is available, T4 can be used, with an initial dose of 200–500 μg intravenously, followed by 25 μg intravenously every 6 hours or 100 μg orally per day. Some also advocate an initial dose of 200 μg T4 and 50 μg T3 intravenously, followed by 100 μg T4 and 25 μg T3 intravenously daily. Alternatively, desiccated thyroid tablets can be used, 40–60 mg every 4–6 hours. The dose for newborns may be slightly higher, then gradually reduced as the condition improves. For patients with heart disease, the initial dose should be smaller, about 1/5–1/4 of the usual dose.
2. Administer oxygen, maintain airway patency, and perform tracheotomy or intubation if necessary to ensure adequate gas exchange.
3. Keep warm by adding blankets and raising room temperature. The room temperature should be increased gradually to avoid a sudden increase in oxygen consumption, which could be detrimental to the patient.
4. Adrenal corticosteroids: Hydrocortisone 50–100 mg can be given every 4–6 hours, then tapered or discontinued after the patient regains consciousness.
5. Actively control infections.
6. Vasopressors. If blood pressure does not rise after the above measures, small doses of vasopressors may be used, but combining vasopressors with thyroid hormones may easily cause arrhythmias.
7. Administer glucose solution and vitamin B complex, but avoid excessive fluid intake to prevent inducing heart failure.

If the condition improves within about 24 hours of the above treatment, recovery can be expected within a week. If there is no reversal after 24 hours, most cases cannot be saved.

bubble_chart Prognosis

It is extremely important to note that iodine deficiency during the embryonic stage of pregnant women is the key factor in the development of endemic cretinism. Therefore, in areas where endemic goiter is prevalent, pregnant women should be supplied with sufficient iodides. During the last 3–4 months of pregnancy, an additional 20–30 mg of potassium iodide can be administered daily. For pregnant women with Graves' disease treated with thiourea drugs, excessive doses should be avoided as much as possible, and small doses of thyroid preparations should be added concurrently. Radioactive ¹³¹I therapy is contraindicated in pregnant women with hyperthyroidism, and diagnostic tracers should be avoided orally, though in vitro tests are permissible.

Currently, in domestic endemic goiter areas, due to the vigorous implementation of preventive measures such as iodized salt and iodized oil, cretinism has become very rare.

In adults, hypothyroidism is often caused by surgical removal or the use of radioactive ¹³¹I for hyperthyroidism treatment. It is essential to carefully control the amount of thyroid tissue removed and the dose of radioactive ¹³¹I to avoid excessive resection or overly high doses, which may lead to this condition.