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Signs of postoperative hypothyroidism and clinical recommendations. Hypothyroidism according to ICD: main aspects of pathology Congenital hypothyroidism ICD code 10

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Atrophy of the thyroid gland (ACQUIRED), Congenital hypothyroidism without goiter (E03.1), Congenital hypothyroidism with diffuse goiter (E03.0), Unspecified hypothyroidism (E03.9), Other specified hypothyroidism (E03.8), Other chronic thyroiditis (E06 .5), Myxedema coma (E03.5), Post-infectious hypothyroidism (E03.3), Congenital iodine deficiency syndrome (E00), Unspecified thyroiditis (E06.9)

Endocrinology

general information

Short description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

Hypothyroidism- a clinical syndrome caused by persistent deficiency of thyroid hormones or a decrease in their biological effect at the tissue level.

INTRODUCTORY PART

ICD-10 code(s):

ICD-10 (children)
Code	Name
E00	Congenital iodine deficiency syndrome
E00.0	Congenital iodine deficiency syndrome, neurological form, endemic cretinism, neurological form
E00.1	Congenital iodine deficiency syndrome, myxedema form, endemic cretinism: hypothyroid. myxedema form
E00.2	Congenital iodine deficiency syndrome, mixed form, Endemic cretinism, mixed form
E00.9	Congenital iodine deficiency syndrome, unspecified, Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS.
E03	Other forms of hypothyroidism
E03.0	Congenital hypothyroidism with diffuse goiter, goiter (non-toxic) congenital: NOS parenchymal Excluded: transient congenital goiter with normal function (P72.0)
E03.1	Congenital hypothyroidism without goiter, aplasia of the thyroid gland (with myxedema) Congenital: atrophy of the thyroid gland. hypothyroidism NOS
E03.3	Post-infectious hypothyroidism
E03.4	Thyroid atrophy (acquired), Excludes: congenital thyroid atrophy (E03.1)
E03.5	Myxedema coma
E03.8	Other specified hypothyroidisms
E03.9	Hypothyroidism, unspecified, myxedema NOS
E06	Thyroiditis
E06.5	Thyroiditis: chronic: . NOS. fibrous. woody. Riedel
E06.9	Thyroiditis, unspecified

Date of protocol development/revision: 2013 (revised 2017).

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
VG	-	congenital hypothyroidism
Gastrointestinal tract	-	gastrointestinal tract
svT3	-	free triiodothyronine
SSS	-	the cardiovascular system
T4 general	-	total T3
T4 sv	-	free T4
TG	-	thyroglobulin
TPO	-	thyroid peroxidase
TSH	-	thyroid-stimulating hormone
thyroid gland	-	thyroid

Protocol users: general practitioners, therapists, pediatricians, endocrinologists, obstetricians-gynecologists, otorhinolaryngologists, neurologists, hematologists, cardiologists, psychiatrists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or high-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to the relevant population .
WITH	Cohort or case-control study or controlled trial without randomization with a low risk of bias (+), the results of which can be generalized to the relevant population or RCT with a very low or low risk of bias (++ or +), the results of which cannot be directly distributed to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice.

Classification

Clinical classification of hypothyroidism:
Primary:
Hashimoto's thyroiditis:
− with goiter;
− “Idiopathic” atrophy of the thyroid gland; presumably the final stage of autoimmune diseases - Hashimoto's thyroiditis or Graves' disease;
− neonatal hypothyroidism due to transplacental transfer of thyroid-blocking antibodies;
· Radioiodine therapy for Graves' disease.
· Subtotal thyroidectomy for Graves' disease, nodular goiter, or thyroid cancer.
· Consumption of excess amounts of iodide (algae, X-ray contrast agents).
· Subacute thyroiditis (usually transient).
· Iodide deficiency.
· Congenital defects in the synthesis of thyroid hormones.
· Medicinal substances (lithium, interferon-alpha, amiodarone).

Secondary:
· Hypopituitarism due to pituitary adenomas, removal or destruction of the pituitary gland.

Tertiary:
· Hypothalamic dysfunction (rare).

Peripheral resistance to thyroid hormones

Classification of primary hypothyroidism by severity:

Severity	Laboratory changes	Clinical picture
Subclinical	TSH - elevated, st. T4 - normal or reduced	Asymptomatic or only nonspecific symptoms
manifest	TSH - elevated, st. T4 - reduced	Characteristic symptoms of hypothyroidism are present
Complicated (severe)	TSH - elevated, st. T4 - reduced	Detailed clinical picture of hypothyroidism. There are heavy complications: “polyserositis”, heart failure, cretinism, myxedematous coma, etc.

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints:
· weakness;
· chilliness;
lethargy;
· drowsiness;
· “unreasonable” weight gain;
· paresthesia;
· constipation;
· hair loss;
· disturbances of the menstrual cycle (often menorrhagia) and reproductive function;
· convulsions.

Physical examination:
Excess weight, dense local or general edema up to anasarca (in severe cases - hydrothorax, hydropericardium, ascites), decreased timbre of voice, dry and cold skin, brittle hair, enlarged facial features, periorbital edema, narrowing of the palpebral fissures, tongue with teeth marks.

CNS:
Chronic fatigue, drowsiness, apathy, depression or “myxedematous psychosis”, lethargy, slowed movements and speech, dysarthria, inability to concentrate, decreased memory and hearing, hypo- or amymia.

The cardiovascular system:
expansion of the borders of the heart in diameter, decreased myocardial contractility, bradycardia, diastolic arterial hypertension, increased total peripheral resistance, decreased cardiac output.

Lungs:
Slow shallow breathing, impaired response of the respiratory center to hypoxia and hypercapnia. Respiratory failure is the main cause of death in patients with myxedema coma.

Gastrointestinal tract:
Slower peristalsis, constipation, possible fecal blockage and intestinal obstruction.

Kidneys:
Decreased GFR, fluid retention, possible water intoxication.

Neuromuscular disorders:
Painful muscle cramps, paresthesia and muscle weakness.

Reproductive system:
Impaired secretion of LH, FSH, anovulation and infertility in women, menorrhagia.

Laboratory research:
The thyroid hormonal profile is determined by the level of damage to the hypothalamus-pituitary-thyroid axis:

Increased levels of antibodies to TPO and/or TG in cases of hypothyroidism due to Hashimoto's thyroiditis.

Anemia due to impaired hemoglobin synthesis, deficiency of iron, vitamin B12 and folate (due to loss during menorrhagia and impaired absorption in the intestine), etc.
Hypercholesterolemia, increased LDL, lipoprotein A and homocysteine.

Instrumental studies:
· Ultrasound of the thyroid gland: often - a decrease in the volume of the organ, changes characteristic of AIT, nodular and cystic formations are possible;
· ECG: decreased voltage of QRS complexes, T and P waves, sinus bradycardia, impaired repolarization processes in the ventricular myocardium;
· Chest X-ray: increase in heart size due to interstitial edema of the myocardium, swelling of myofibrils, dilatation of the left ventricle and effusion in the myocardium, hydropericardium is possible;
· MRI or CT scan of the pituitary gland indicated for central hypothyroidism;
· EchoCG with severe heart failure.

Indications for consultation with specialists:
· consultation with a cardiologist - for CHF and suspected ischemic heart disease;
· consultation with an ophthalmologist, neurosurgeon, neurologist - for central hypothyroidism;
· consultation with a hematologist - for moderate and severe anemia.

Diagnostic algorithm:(scheme)

Differential diagnosis

Differential diagnosisand rationale for additional researchin adult patients with suspected hypothyroidism:

*Diagnosis*	*Rationale for differential diagnosis*	*Surveys*	*Diagnosis exclusion criteria*
Nephrotic syndrome	General: presence of edema	TSH, svT3, svT4 Determination of total protein, creatinine and urea levels in the blood, GFR, TAM, kidney ultrasound.	Absence of clinical and laboratory signs of kidney damage
Acromegaly	Enlargement of facial features	TSH, svT3, svT4 Determination of levels of growth hormone, IGF-1 in the blood, MRI of the pituitary gland with contrast enhancement.	Normal levels of growth hormone and IGF-1 in the blood, no changes on MRI of the pituitary gland. Presence of changes in the thyroid profile characteristic of hypothyroidism

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Treatment

Treatment (outpatient clinic)

TREATMENT TACTICS AT AN OUTPATIENT LEVEL: all patients with this diagnosis are treated at an outpatient level

Non-drug treatment: No

Drug treatment:
The main drug is levothyroxine sodium 25, 50, 75, 100, 125, 150 mcg in the table.
Starting daily dose for manifest hypothyroidism:
· in patients under 60 years of age - 1.6-1.8 mcg/kg;
· in patients with concomitant diseases of the cardiovascular system and over 60 years of age - 12.5-25 mcg, followed by an increase of 12.5-25 mcg every 6-8 weeks.
Take in the morning on an empty stomach no later than 30 minutes before meals. After taking thyroid hormones, avoid taking antacids, iron and calcium supplements for 4 hours.
The selection of a maintenance dose is carried out under the control of general condition, pulse rate and determination of the blood TSH level in case of primary hypothyroidism, st. T4 - with a central form.
The first determination is made no earlier than 6 weeks from the start of therapy, then once every 3 months until the effect is achieved.
After achieving a clinical and laboratory effect, to determine the adequacy of the dose of levothyroxine, a TSH or fT4 study is performed once every 6 months.

Replacement doses of T4 for adults are 50-200 mcg/day, on average 125 mcg/day.
After thyroidectomy for thyroid cancer, suppressive doses are used - 2.2 mcg/kg per day.

List of additional medicines - individually (according to indications).

Surgical intervention:No.

Further management:
Therapy with levothyroxine sodium drugs is lifelong replacement therapy under the supervision of a physician.

Indicators of treatment effectiveness:
An indicator of the effectiveness of treatment is the achievement of normal TSH levels in the blood. The target TSH level is determined individually, taking into account the patient’s age (adult - young, mature, elderly, senile) and concomitant pathology.

Treatment (inpatient)

TREATMENT TACTICS AT THE INPATIENT LEVEL: hospitalization is indicated only if complications occur: heart failure, adrenal insufficiency, liver failure, etc.

Patient observation card, patient routing ( schemes, algorithms): No.

Non-drug treatment: No.

Drug treatment: the main drug is levothyroxine sodium 25, 50, 75, 100, 125, 150 mcg in the table.
Take in the morning on an empty stomach no later than 30 minutes before meals.

List of essential medicines (having a 100% probability of use):

List of additional medications (less than 100% probability of use): the choice is determined by the accompanying syndrome.

Surgical intervention: No.

Further management:
· lifelong replacement therapy with thyroid drugs.

Indicators of treatment effectiveness:
The classic indicator of treatment effectiveness is the achievement of normal TSH levels in the blood.
In reality, the target TSH level should be determined individually, taking into account age and concomitant diseases. In elderly and senile patients, as well as in the presence of severe concomitant diseases, it may be higher than the normative values.

Hospitalization

INDICATIONS FOR HOSPITALIZATION, INDICATING THE TYPE OF HOSPITALIZATION

Indications for planned hospitalization:
· newly diagnosed hypothyroidism in elderly and senile people to initiate hormone replacement therapy;
· decompensated hypothyroidism in the absence of effect from outpatient treatment.

Indications for emergency hospitalization:
· gradual increase in drowsiness with transition to stupor (myxedema/hypothyroid coma), dynamic intestinal obstruction, pneumonia, myocardial infarction, thrombosis of cerebral arteries, gastrointestinal bleeding, convulsions with hyper- and hypocalcemia, hypothermia, hyponatremia (water intoxication).

Information

Sources and literature

Minutes of meetings of the Joint Commission on the Quality of Medical Services of the Ministry of Health of the Republic of Kazakhstan, 2017
1. 1) D. Gardner, D. Shobeck. Basic and clinical endocrinology, 2016. 2) Clinical protocol for the diagnosis and treatment of hypothyroidism in adults, Astana, 2014. 3) Sviridenko N.Yu., Abramova N.A. Endocrinology: national guide / ed. I.I. Dedova, G.A. Melnichenko- M.: GEOTAR-Media, 2016, - 1112 pp. 4) Zeltser M.E., Bazarbekova R.B. Directory of endocrinologist. 1st edition, Almaty, 2014, 368 pp. 5) TinsleyHarrison. Internal illnesses. Book six. – M, 2005, 415 pp. 6) Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) Jonklaas, Bianco, et al. Thyroid 24(12): 1670-1751, 2014.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of protocol developers with qualification information:
1) Dosanova Ainur Kasimbekovna - candidate of medical sciences, assistant of the department of endocrinology of JSC “Kazakh Medical University of Continuing Education”.
2) Rimma Bazarbekovna Bazarbekova - Doctor of Medical Sciences, Professor, Head of the Department of Endocrinology of JSC “Kazakh Medical University of Continuing Education”, Chairman of the RPO “Association of Endocrinologists of Kazakhstan”.
3) Smagulova Gaziza Azhmagievna - Candidate of Medical Sciences, Head of the Department of Propaedeutics of Internal Diseases and Clinical Pharmacology of the RSE at the West Kazakhstan State Medical University named after M. Ospanov.

Indication of absence conflict interests: No.

Reviewers: Nurbekova Akmaral Asylovna - Doctor of Medical Sciences, Professor of the Department of Internal Medicine No. 2 of the RSE at the Kazakh National Medical University named after S.D. Asfendiyarov."

Note conditions revision protocol: review of the protocol 5 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

Attached files

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Hypothyroidism is a condition of the body in which there is a lack of thyroid hormones, which causes a number of pathological symptoms.

There are several etiotropic factors of the disease, therefore ICD 10 hypothyroidism usually has the code E03.9, as unspecified.

Primary factors

Usually in this case there are congenital or acquired abnormalities of the thyroid gland. Pathological processes in the gland itself arise for the following reasons:

inflammation of organ tissue;
autoimmune nature of the development of pathology;
organ damage from radioactive iodine;
pronounced iodine deficiency in the body due to its absence in the environment;
postoperative hypothyroidism in ICD 10 with massive tissue removal (has code E89.0, which determines the plan of therapeutic measures, according to unified protocols for the treatment of patients with this pathology).

Very often, the development of hyperthyroidism has several causes or a generally unclear etiology, so in most cases, specialists deal with the idiopathic form of hyperthyroidism, which belongs to the large section of thyroid diseases E00-E07 in the International Classification of Diseases, 10th revision.

Secondary factors in the development of hypothyroidism

The secondary form of hypothyroidism is caused by damage to the system that controls the normal functioning of the thyroid gland. The hypothalamus and pituitary gland of the brain are usually involved, namely their interconnected effect on the functioning of the thyroid gland.

In both cases of impaired functioning of the thyroid gland, there is an insufficiency in the production of hormones and, as a consequence, a disruption of all metabolic processes.

Kinds

The primary form of this metabolic pathology is divided into several types, that is:

subclinical, which has virtually no pathological symptoms, but according to the results of specific tests, increased levels of thyroid-stimulating hormone of the pituitary gland (TSH) are noted against the background of normal levels of thyroid hormones (T4);
the manifest form is characterized by an increased level of TSH against a background of decreased T4, which has a very clear clinical picture.

The manifest form has a compensated or decompensated course. The code for hyperthyroidism in ICD 10 depends on the etiology, clinical course and pathological signs, which is usually provided by section codes E03.0-E03.9.

Symptoms

In medical practice, there is an opinion that the younger the person who has developed the manifest form of hypothyroidism, the more susceptible he is to the formation of disorders in the central parts of the nervous system and malfunctions of the musculoskeletal system. There are no specific symptoms for this pathology, but there are many signs, and they are very bright. The development of pathological changes in the body's metabolic processes can be suspected when the following symptoms appear:

increased body weight against the background of a modest diet;
hypothermia, a feeling of constant cold due to decreased metabolism;
yellowish color of the skin;
drowsiness, slow mental reaction, poor memory cause the code of hypothyroidism;
tendency to constipation, severe flatulence;
decrease in hemoglobin.

Early diagnosis of pathology involves the appointment of lifelong replacement therapy. The prognosis is unfavorable, especially in advanced cases.

I welcome one and all to my blog. Insufficient function of the endocrine organ in the form of a butterfly can arise not only due to an autoimmune disease, as many believe.
Hypothyroidism can occur after surgery to remove the thyroid gland, and in this case, hypothyroidism is called postoperative, which will be the subject of discussion (ICD code 10, treatment, prognosis).
When managing such patients, there are some nuances and difficulties in understanding, so we advise you to read carefully.

Hypofunction after thyroid surgery

It will probably be superfluous to explain that postoperative hypothyroidism is hypothyroidism (insufficient gland function) that developed as a result of partial or complete removal of an organ.
Although the question is clear, postoperative hypothyroidism is not always clear-cut. It turns out that it matters for what reason the operation on the thyroid gland was performed. Further tactics of management and compensation of hypothyroidism depend on this information. We'll talk about this later, but first let's mention some points...

ICD 10 code

This nosology belongs to the section “other forms of hypothyroidism”, which has the code E 03

Reasons why surgical interventions are performed

oncological diseases (total removal of the thyroid gland)
nodular goiter (subtotal resection of the thyroid gland or removal of the affected lobe)
substernal goiter (subtotal resection of the thyroid gland)
diffuse toxic goiter (subtotal resection of the thyroid gland)
functional autonomy (subtotal resection of the thyroid gland or removal of the affected lobe)

Why does hypothyroidism occur after thyroid removal?

Everything is very simple. As a result of a decrease in functional cells due to surgery, hormone production decreases. Hypothyroidism after surgery is a completely understandable thing.
Depending on the amount of tissue removed, the need for replacement therapy varies. For example, if only one lobe is removed, the second healthy lobe can take over the entire function of providing the body with hormones and there may be no hypothyroidism or it will not be very pronounced. If the remaining share is sick, then the dose will be higher.
If resection or total removal of gland tissue is performed, then replacement therapy with synthetic hormones - thyroxine and/or liothyronine - is always required. These drugs are prescribed immediately after surgery the next day.
The person will then have to maintain normal thyroid hormone levels with these medications for the rest of their life.

Symptoms of a hypofunction state

The symptoms and manifestations of insufficient thyroid function after its removal are no different from the manifestation of hypothyroidism for another reason. Below I have listed the main symptoms, and a more extensive list in the article. If after the operation a person is not prescribed replacement therapy, then very soon he will begin to feel the following symptoms:

severe weakness and loss of ability to work
weight gain
low mood and depression
dry skin and mucous membranes
swelling
hoarseness of voice
low blood pressure and pulse
constipation

All these unpleasant manifestations of thyroid hormone deficiency are easily eliminated by taking synthetic substitutes and natural thyroid hormones.

How to treat

As we said above, all treatment consists of lifelong replacement therapy. For these purposes, thyroxine - the T4 hormone - is taken, as well as synthetic combination drugs or natural “thyroid hormones”. Trade names of thyroxine that many people know:

L-thyroxine
Euthyrox
Bagotirox and others...

However, thyroxine alone is often not enough; it does not completely eliminate the negative symptoms of hypothyroidism. This may be due to the actual removal of gland tissue, or from the body due to concomitant pathology. In this case, additional T3 drugs or combination drugs are prescribed.
But triiodothyronine preparations are not sold in Russia, so you need to take care of purchasing the medicine through relatives living abroad or from intermediary distributors. There are communities on the Internet that help patients by bringing medicine from Europe or the USA.
Doses of drugs are selected individually and depend on the reason for the surgical intervention.
For example, after surgery for malignant cancer, the doses should be such as to cause mild hyperthyroidism, that is, almost completely suppress TSH, because it promotes the growth of thyroid cells, including malignant ones, which could well have been left and not completely removed . However, this is a topic for the next article, , so as not to miss.

Forecast

The prognosis is favorable. If the drugs are suitable and the dose is selected correctly, then the person’s quality of life does not suffer. An unfavorable prognosis may occur with cancer, but this risk is caused by the disease itself, and not by hypothyroidism after surgery.

With warmth and care, endocrinologist Lebedeva Dilyara Ilgizovna

Most often, primary hypothyroidism is the outcome of autoimmune thyroiditis, less often - the result of treatment of thyrotoxicosis syndrome, although a spontaneous outcome of diffuse toxic goiter into hypothyroidism is also possible. The most common causes of congenital hypothyroidism are aplasia and dysplasia of the thyroid gland, as well as congenital enzymopathies accompanied by impaired biosynthesis of thyroid hormones.

If iodine deficiency is extremely severe, iodine intake of less than 25 mcg/day for a long time) may develop iodine deficiency hypothyroidism. Many drugs and chemicals (propylthiouracil, thiocyanates, potassium perchlorate, lithium carbonate) can disrupt thyroid function. In this case, hypothyroidism caused by amiodarone is most often transient in nature. In rare cases, primary hypothyroidism is a consequence of replacement by a pathological process of thyroid tissue in sarcoidosis, cystinosis, amyloidosis, Riedel's thyroiditis). Congenital hypothyroidism can be transient. It develops under the influence of various causes, including prematurity, intrauterine infections, transplacental transfer of antibodies to thyroglobulin and thyroperoxidase, and maternal use of thyreostatics.

Pathogenesis of primary hypothyroidism

Hypothyroidism is characterized by a decrease in the rate of metabolic processes, which is manifested by a significant decrease in oxygen demand, a slowdown in redox reactions and a decrease in basal metabolic rates. The processes of synthesis and catabolism are inhibited. A universal sign of severe hypothyroidism is mucinous edema (myxedema), most pronounced in connective tissue structures. The accumulation of glycosaminoglycans, products of protein breakdown that have increased hydrophilicity, causes fluid and sodium retention in the extravascular space. In the pathogenesis of sodium retention, a certain role is assigned to excess vasopressin and deficiency of natriuretic hormone.

Deficiency of thyroid hormones in childhood inhibits physical and mental development and in severe cases can lead to hypothyroidism and cretinism.

Symptoms of primary hypothyroidism

Clinical manifestations of hypothyroidism include:

Hypothyroid or myxedema coma

This is a dangerous complication of hypothyroidism. Its causes are the absence or insufficient replacement therapy. The development of hippothyroid coma is provoked by cooling, infections, intoxication, blood loss, severe intercurrent illnesses and taking tranquilizers.

Manifestations of hypothyroid coma include hypothermia, bradycardia, arterial hypotension, hypercapnia, mucinous edema of the face and extremities, symptoms of central nervous system damage (confusion, lethargy, stupor, and possible urinary retention or intestinal obstruction. The immediate cause of death may be cardiac tamponade due to hydropericardium.

Classification of primary hypothyroidism

Primary hypothyroidism is classified according to etiology. Highlight

Diagnostics

Diagnosis of primary hypothyroidism includes establishing a diagnosis of hypothyroidism, determining the level of damage and clarifying the causes of primary hypothyroidism.

Diagnosis of hypothyroidism and determination of the level of damage: assessment of TSH and free T4 levels using highly sensitive methods.

Primary hypothyroidism is characterized by an increase in TSH levels and a decrease in free T4 levels. Determining the level of total T4 (i.e., both protein-bound and free biologically active hormone) has less diagnostic value, since the level of total T largely depends on the concentration of transporter proteins that bind it.

Determining the level of T 3 is also impractical, since in hypothyroidism, along with an increased level of TSH and a decrease in T 4, a normal or even slightly elevated T 3 level can be determined due to compensatory acceleration of the peripheral conversion of T 4 to the more active hormone T 3

Clarification of the causes of primary hypothyroidism:

Ultrasound of the thyroid gland;
thyroid scintigraphy;
puncture biopsy of the thyroid gland (according to indications);
determination of antibodies to thyroid peroxidase (if autoimmune thyroiditis is suspected).

Differential diagnosis

Primary hypothyroidism is first of all differentiated from secondary and tertiary. The leading role in differential diagnosis is played by determining the level of TSH and T4. In patients with normal or slightly elevated TSH levels, it is possible to conduct a TRH test, which makes it possible to differentiate primary hypothyroidism (increased TSH levels in response to TRH administration) with secondary and tertiary hypothyroidism (reduced or delayed response to TRH).

CT and MRI can detect changes in the pituitary gland and hypothalamus (usually tumors) in patients with secondary or tertiary hypothyroidism.

In patients with severe somatic diseases, primary hypothyroidism should be differentiated from euthyroid pathology syndromes, which are characterized by a decrease in the level of T3, and sometimes T4 and TSH. These changes are usually interpreted as adaptive, aimed at preserving energy and preventing protein catabolism in the body in severe general condition of the patient. Despite the reduced levels of TSH and thyroid hormones, thyroid hormone replacement therapy is not indicated for euthyroid pathology syndrome.

Treatment of primary hypothyroidism

The goal of treatment for hypothyroidism is complete normalization of the condition: disappearance of symptoms of the disease and maintenance of TSH levels within normal limits (0.4-4 mU/l). In most patients with primary hypothyroidism, this is achieved by prescribing T4 at a dose of 1.6-1.8 mcg/kg body weight. The need for thyroxine in newborns and children due to increased metabolism of thyroid hormones is noticeably greater.

Replacement therapy for primary hypothyroidism is usually carried out for life.

In patients under 55 years of age who do not have cardiovascular diseases, T 4 is prescribed at a dose of 1.6-1.8 mcg/kg body weight. For obesity, the dose of T4 is calculated based on the “ideal” weight for the patient. Treatment begins with a full dose of the drug.

Patients over 55 years of age and those with cardiovascular disease have an increased risk of T4 side effects. Therefore, they are prescribed T4 at a dose of 12.5-25 mcg/day and slowly increase the dose of the drug until the TSH level is normalized (on average, the required dose is 0.9 mcg/kg body weight). If it is not possible to ideally compensate for hypothyroidism in an elderly patient, the TSH level may remain within 10 mU/L.

Particular attention should be paid to compensation for hypothyroidism during pregnancy. During this period, the need for T4 increases on average by 45-50%, which requires adequate adjustment of the drug dose. Immediately after birth, the dose is reduced to the standard dose.

Taking into account the high sensitivity of the newborn’s brain to thyroid hormone deficiency, which subsequently leads to an irreversible decrease in intelligence, every possible effort must be made to begin treatment for congenital T4 hypothyroidism from the first days of life.

In the vast majority of cases, monotherapy with levothyroxine sodium is effective.

The synthetic levorotatory isomer of thyroxine Bagotirox stimulates tissue growth and development, increases tissue demand for oxygen, stimulates the metabolism of proteins, fats and carbohydrates, and increases the functional activity of the cardiovascular and central nervous systems. The therapeutic effect is observed after 7-12 days, during the same time the effect persists after discontinuation of the drug. Diffuse goiter decreases or disappears within 3-6 months. Bagotirox tablets 50, 100 and 150 mcg are produced using the proprietary Flexidose technology, which allows for “dosing steps” from 12.5 mcg.

Patients under 55 years of age who do not have cardiovascular diseases are prescribed:

Levothyroxine sodium orally 1.6-1.8 mg/kg 1 time per day in the morning on an empty stomach, long-term (in the vast majority of cases - for life).

In this case, the estimated initial dose for women is 75-100 mcg/day, for men - 100-150 mcg/day.

Patients over 55 years of age and/or with cardiovascular disease are prescribed.

Levothyroxane sodium orally 12.5-25 mcg 1 time per day in the morning on an empty stomach, long-term (every 2 months the dose should be increased by 25 mcg/day until the TSH level in the blood normalizes or the target dose of 0.9 mcg/kg/day is reached).

If symptoms of cardiovascular disease appear or worsen, it is necessary to adjust therapy together with a cardiologist.

If it is not possible to ideally compensate for hypothyroidism in an elderly patient, the TTT level can remain within 10 mU/L.

Newborns immediately after detection of primary hypothyroidism are prescribed:

Levothyroxine sodium orally 10-15 mcg/kg 1 time per day in the morning on an empty stomach for a long time.

Children are prescribed:

Levothyroxine sodium orally 2 mcg/kg (or more if necessary) 1 time per day in the morning on an empty stomach, for life.

With age, the dose of levothyroxine per kg of body weight decreases.

Hypothyroid coma

The success of treatment for hypothyroid coma depends primarily on its timeliness. The patient should be hospitalized immediately.

Complex treatment includes:

administration of an adequate dose of thyroid hormones,
use of glucocorticosteroids
combating hypoventilation and hypercapnia;
treatment of diseases that led to the development of coma

Treatment of coma begins with the administration of glucocorticosteroids; in a patient in a coma it is difficult to reject the presence of Schmidt's syndrome, as well as to carry out a differential diagnosis between primary and secondary hypothyroidism. When hypothyroidism is combined with adrenal insufficiency, the use of thyroid hormones alone can provoke the development of an adrenal insufficiency crisis.

Hydrocortisone intravenously 50-100 mg 1-3 times a day (up to a maximum dose of 200 mg/day), until stabilization.

Levothyroxine sodium 100-500 mcg (within 1 hour), then 100 mcg/day, until the condition improves and the patient can be transferred to long-term/lifelong oral medication in the usual dosage (in the absence of injectable drugs, levothyroxine sodium tablets can be administered in crushed form through gastric tube).

Dextrose, 5% solution, intravenous drip 1000 ml/day, until the condition stabilizes or
Sodium chloride. 0.9% solution intravenously, up to 1000 ml/day, until the condition stabilizes.

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Hypothyroidism according to ICD 10 - this name is used by medical workers in order not to use lengthy names for each type of disease, while each individual type is assigned an individual code.

This disease causes poor functioning of the thyroid gland due to an insufficient amount of hormones produced by the thyroid gland, as a result of which processes in the body slow down.

There are about ten similar diseases, all of them appear after a malfunction of the thyroid gland.

There is an opinion that hypothyroidism is not a disease at all, but a condition of the body in which a long-term lack of thyroid hormones produced by the thyroid gland is determined. It is associated with pathological processes that affect hormonal metabolism.

This disease is quite common, especially among women; men are less likely to suffer from this disease; for example, out of 20 identified patients, only one patient is male.

Sometimes the symptoms of the onset of the disease at the initial stage do not appear clearly and are very similar to signs of overwork, and sometimes to other diseases. Only an analysis of the level of thyroid-stimulating hormones can determine the exact signs of hypothyroidism at an early stage.

The following forms exist:

One of the reasons that can cause the disease is insufficient iodine intake or the influence of negative factors. This form is called acquired hypothyroidism. Infants suffer from it.
Only 1% of identified patients among infants are susceptible to the congenital form.
Chronic form or chronic autoimmune thyroiditis. Appears as a result of a malfunction of the immune system. In this situation, destructive processes of thyroid cells begin in the body. Clear manifestations of this occur several years after the onset of the pathological process.
A form of transient disease occurs, for example, together with postpartum thyroiditis. The disease can occur due to a viral infection of the thyroid gland or as a result of neoplasms of the thyroid gland.
The gestational form is observed in pregnant women and disappears after childbirth.
Subclinical – occurs due to iodine deficiency.
Compensated – does not always require specialized therapy.

Depending on the degree of infection of the body and the process of development of the disease, the following are distinguished:

Primary – development occurs when the thyroid gland is damaged and the level of TSH increases (90% of cases of hypothyroidism).
Secondary – damage to the pituitary gland, insufficient secretion of thyrotropin-releasing hormone and TSH.
Tertiary – disruption of the hypothalamus, development of thyrotropin-releasing hormone deficiency.

Hypothyroidism has many forms, that is, it manifests itself in different forms. The international classification of the disease assigns a specific code to each specific form. The qualification provides for possible territorial foci of iodine deficiency (endemic).

Why is classification according to ICD 10 needed? To keep clear records and compare disease clinics, to maintain statistics in different territories.

Classification according to the ICD has certain advantages:

Help in making an accurate diagnosis.
Choosing effective, correct treatment.

According to the classification of hypothyroidism according to ICD 10, each type of this disease is assigned a specific code. Example: subclinical, resulting from insufficient iodine intake, received a code according to ICD 10 - E 02.

Another example: a non-toxic single-node process received code E 04.1, which is characterized by one clear neoplasm. The progressive enlargement of the nodes causes discomfort and puts pressure on the organs located in the cervical region.

Treatment

Treatment for each type depends on the degree of development of the disease. For example, the primary phase of the disease can be cured by taking replacement hormones. The same cannot be said about the treatment of the peripheral form of hypothyroidism: sometimes it is very difficult, and sometimes, although difficult, it can be treated.

The compensated type of hypothyroidism sometimes does not require specialized therapy. If decompensation is observed, the patient is prescribed hormonal drugs, but the drug and dose are selected strictly individually, taking into account all the features.

Homeopathic medicines allow the patient to cope with the disease. But the patient must be prepared for a long treatment process and take them many times a day.

Modern medicine has several methods for treating hypothyroidism:

conservative;
operational;
iodine therapy and radiotherapy.

With late diagnosis and prolonged absence of treatment of the disease, a thyrotoxic crisis develops, which occurs due to the release of a large amount of hormones into the blood.

Complications can be avoided if you consult a doctor in a timely manner, who will choose the optimal treatment method and help you return to your normal rhythm of life.