Background
Thyroid crisis is a complication hypertiroidisme a rare but potentially fatal. Thyroid crisis must be recognized and addressed by the clinical manifestations because laboratory confirmation often can not be done in the timeframe that pretty quickly. Patients usually show hypermetabolik state characterized by high fever, tachycardi, nausea, vomiting, agitation, and psychosis. In the advanced stage, the patient may fall into a state of stupor or komatus accompanied by hypotensi.1
Thyroid crisis is a rare disease, which only happens about 1-2% of patients hypertiroidisme. While the overall incidence of hyperthyroidism itself only ranged from 0.05 to 1.3%, which most of them are subclinical. However, thyroid crisis unrecognized and untreated can have fatal consequences. Adult mortality in thyroid crisis reaches 10-20%. Even some of the research reports say as high as 75% of the patient population treated inap.1 With a controlled thyrotoxicosis and early treatment of thyroid crisis, the death rate can be reduced to less than 20% .2
Because the cause of hyperthyroidism is Graves' disease is an autoimmune disease most and that also affects other organ systems, conducting history is very important to enforce diagnosis.3 This is important because the diagnosis of thyroid crisis based on the clinical picture and not the picture laboratoris.2, 11.16 Another important note is that thyroid crisis is a crisis that requires fulminant intensive care and continuous supervision menerus.4 With early diagnosis and adequate treatment, the prognosis is usually going well.1 therefore need a proper understanding of thyroid crisis, especially regarding the diagnosis and penatalaksaannya.
Definition
some definitions:
Thyroid crisis is a condition where the symptoms of thyrotoxicosis with suddenly become great and accompanied by hyperpireksia, tachycardia and sometimes vomiting that continues menerus.11
Hypermetabolic thyroid crisis is a life-threatening condition and is characterized by high fever and dysfunction of the cardiovascular system, nervous system, and channel system cerna.5 Initially, arising hyperthyroidism which is a collection of symptoms caused by increased levels of circulating thyroid hormone with or without abnormal thyroid gland function. When the number was greatly exaggerated, there is a cluster of symptoms are more severe, the crisis tirotoksikosis.1 thyroid is a condition in which the body's happening decompensated thyrotoxicosis tersebut.6 Typically occurs in patients with untreated thyrotoxicosis or not completely heal triggered by surgery, infection , or trauma.1
Etiology
The etiology of thyroid crisis such as Graves' disease, toxic multinodular goiter, toxic nodules, Hashimoto's thyroiditis, tiroiditas deQuevain, metastatic follicular thyroid carcinoma, and TSH-producing tumor. The etiology of the most common cause of thyroid crisis is Graves' disease (diffuse toxic goiter) .7 Although not common, thyroid crisis can also be a complication of thyroid surgery. This condition is caused by the manipulation of the thyroid gland during surgery in patients with hyperthyroidism. Thyroid crisis can occur before, during, or after surgery. Surgery is generally only recommended when patients have Graves disease and other therapeutic strategies have failed or when the suspected presence of thyroid cancer. Thyroid crisis potential in such cases could lead to kematian.8
Thyroid crisis is also associated with severe hypocalcemia. A case of 30-year-old woman with thyroid crisis and impaired renal function showed hypocalcemia. Hypocalcaemia in the current case had serum creatinine is still normal. Normal serum levels of the amino acid fragment of parathyroid hormone end in a state of hypocalcemia in the case indicate a parathyroid dysfunction. Since normal serum magnesium and no history of thyroid surgery or radio-iodine therapy, are considered idiopathic hypoparathyroidism occurring. The seventh case was mentioned in the literature on Grave's disease are accompanied hypoparathyroidism idiopatik.9
Thyroid crisis is reported to occur in patients interstitial nephritis. The case of a 54-year-old man who had been treated with tiamazol (5 mg / day) showed that thyroid hormone levels rose sharply after eksodontia. Although the prescribed dose tiamazol raised after eksodontia on the fourth day, he underwent a thyroid crisis at day-52 post-eksodontia. Laboratory findings also indicate renal dysfunction (creatinine 1.8 mg / dL at day 37 post-eksodontia). Thyroid hormone levels back in the normal range after subtotal thyroidectomy. However, serum creatinine levels remained high. This man kemudia diagnosed with interstitial nephritis by renal biopsy and treated with prednisolone 30 mg / day. This case mewakilit thyroid crisis events that occurred despite increased dose tiamazol after eksodontia. It appears that as well as interstitial nephritis eksodontia is a factor that may increase thyroid function. After a poor response to anti-thyroid drugs, it is important to prevent thyroid crisis by determining these factors and treatment sesuai.10
Pathophysiology
In healthy people, the hypothalamus produces thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH) and the hormone that causes the thyroid gland releases thyroid hormones. Strictly speaking, these glands produce prohormone thyroxine (T4), which had deiodinasi mainly by the liver and kidneys to its active form, namely triiodothyronine (T3). T4 and T3 are in two forms: 1) free form and not bound active biological and 2) a form that is bound to thyroid-binding globulin (TBG). Levels of T4 and free T3 not bound strongly correlated with the clinical picture of the patient. This free form regulate thyroid hormone levels when they circulate in the blood circulation that supplies the pituitary gland anterior.1
From the standpoint of Graves' disease, thyrotoxicosis pathophysiology involves autoimmunity by B and T lymphocytes are directed at four antigens of the thyroid gland: TBG, thyroid peroxidase, sodium-iodide simporter, and TSH receptor. TSH receptor is what is the major autoantigen in the pathophysiology of this disease. The thyroid gland is stimulated constantly by autoantibodies against the TSH receptor and the subsequent secretion of TSH suppressed due to increased production of thyroid hormones. The most commonly found autoantibodies of subclasses of immunoglobulin (Ig)-G1. These antibodies cause the release of thyroid hormones and TBG mediated by 3, '5 '-cyclic adenosine monophosphate (cyclic AMP). In addition, this antibody also stimulates iodine uptake, protein synthesis, and the growth of the gland tiroid.3
Crises arise during decompensated thyroid cells in response to thyroid hormone causes severe hipermetabolisme involving multiple organ systems and is the most severe form of thyrotoxicosis. Clinical features associated with the effect of thyroid hormone intensified with increasing thyroid hormone release (with / without increased synthesis) or increased intake of thyroid hormones by the body's cells. In some degree, the cell's response to hormones is already too high for the survival of patients' lives and cause kematian.2 hypothesized that thyroid hormone can increase the density of beta receptors, cyclic adenosine monophosphate, and a decrease in the density of alpha receptors. Plasma levels and urinary excretion rate of epinephrine and norepinephrine normal in patients tirotoksikosis.7
Although the pathogenesis of thyroid crisis are not fully understood, these theories have been proposed to answer. Patients with thyroid crisis thyroid hormone levels were reported to have a higher rate than patients with thyrotoxicosis without complications although total thyroid hormone levels are not increased. adrenergic receptor activation is another hypothesis that appears. Menginervasi sympathetic nerves and catecholamines stimulate the thyroid gland thyroid hormone synthesis. Next, an increase in thyroid hormone increases beta-adrenergic receptor density so menamnah effects of catecholamines. Thyroid crisis dramatic response to beta-blockers and the emergence of thyroid crisis after swallowing adrenergic drugs, such as pseudoephedrine, supports this theory. This theory also explains the low or normal levels of plasma and urinary catecholamine excretion rate. However, this theory does not explain why beta-blockers failed to reduce levels of thyroid hormones on tirotoksikosis.2
Another theory suggests the rapid increase in hormone levels as a result of the pathogenic source. The sharp drop in levels of binding proteins that can occur after surgery may lead to a sudden increase in free thyroid hormone levels. In addition, hormone levels can rise quickly when the gland manipulation during surgery, during palpation during examination, or from the destruction of the follicle after radioactive iodine therapy (RAI). Other theories ever proposed, including changes in tissue tolerance to thyroid hormone, a substance similar to a unique catecholamines on the state thyrotoxicosis, and direct sympathetic effects of thyroid hormones due to similarity of structure with sebaai katekolamin.2
The clinical
History of the disease before patients include thyrotoxicosis or symptoms such as irritability, agitation, emotional lability, lack of appetite with weight loss is down, excessive sweating and temperature intolerance, and decreased school performance due to decreased attention span. History of disease is now a common complaint by patients is fever, sweating, decreased appetite and weight loss. Gastrointestinal complaints are often expressed by patients are nausea, vomiting, diarrhea, abdominal pain, and jaundice. While the complaint include neurological symptoms of anxiety (mostly on older teens), behavioral changes, seizures and koma.2
On physical examination, it was found fever with temperatures consistently exceed 38.5 oC. Patients can experience hyperpyrexia even exceed 41oC and excessive sweating. Cardiovascular signs were found between hypertension with a widened pulse pressure or hypotension in the next phase and accompanied by shock. Tachycardia occurred incompatible with fever. Signs of heart failure include arrhythmias (supraventricular most, such as atrial fibrillation, but ventricular tachycardia may also occur). While neurological signs include agitation and confusion, hiperrefleksia and transient pyramidal signs, tremors, seizures, and coma. Signs of thyrotoxicosis include orbital signs and goiter.2
In addition to typical cases described above, there is one case report of a patient with an atypical clinical picture (normotermi and normotensive) were accompanied by multiple organ dysfunction syndrome, such as lactic acidosis and liver dysfunction, both of which are very rare complication. This case shows that the two organ systems are involved in thyroid crisis and it is important to recognize this atypical picture in cases of thyroid crisis dihadapi.12
Overview laboratory
Diagnosis of thyroid crisis based on the clinical picture and not the picture laboratory. If the clinical picture is consistent with thyroid crisis, treatment should not be delayed because of waiting for laboratory confirmation of the thyrotoxicosis. On examination of the thyroid status, will usually be found to be consistent with the state of hyperthyroidism and useful only if the patient has not been previously diagnosed. Test results may not be obtained quickly and are usually not helpful for immediate handling. Findings typically include increased levels of T3, T4 and freely, increased resin uptake of T3, decreased TSH levels, and increased uptake of iodine 24 jam.2
TSH levels did not decline in the state of excessive TSH secretion but this rarely happens. Liver function tests generally show non-specific abnormalities, such as elevated serum for SGOT, SGPT, LDH, creatinine kinase, alkaline phosphatase, and bilirubin. In blood gas analysis, measurement of blood gases and electrolytes levels and urinalysis performed to assess and monitor the handling of long-pendek.2
Management
Management of thyroid crisis need to process in a few steps. Ideally, a given therapy should inhibit the synthesis, secretion, and peripheral thyroid hormone action. Handling an aggressive supportive done then to stabilize homeostasis and reverse multi-organ decompensation. Additional tests need to be conducted to identify and address the factors originators followed by definitive treatment to prevent recurrence. Thyroid crisis is a crisis that requires fulminant intensive care and continuous supervision menerus.4
Management: inhibits the synthesis of thyroid hormones
Anti-thyroid compounds such as propylthiouracil (PTU) and methimazole (MMI) is used to inhibit the synthesis of thyroid hormones. PTU also inhibits the conversion of T4 to T3 in the peripheral circulation and MMI preferable in cases of thyroid crisis. While MMI is farmakoogik agent commonly used in cases of hyperthyroidism. Both inhibit the incorporation of iodine into TBG within one hour after drinking. History of hepatotoxicity or agranulocytosis from previous tioamida therapy is contraindicated both drugs PTU tersebut.4 this gracious indicated hyperthyroidism caused by an illness Graves. Support research report showed an increased risk of liver toxicity compared with the use of PTU metimazol. Serious liver damage has been found in the use of metimazol in five cases (three of whom died). PTU is now considered as a second-line drug therapy except in patients who are allergic or intolerant to metimazol or for women with first trimester of pregnancy. Use metimazol during pregnancy reported to cause embriopati, including aplasia kutis, although a rare case ditemui.4
Supervise closely PTU therapy for possible onset of symptoms and signs of liver damage, especially during the first 6 months after starting therapy. For suspected liver damage, discontinue PTU therapy and gradual re-examined the results of liver damage and provide supportive care. PTU should not be used in pediatric patients unless the patient is allergic or intolerant to metimazol and there is no other available drug options. Provide education to the patient to contact the doctor if the following symptoms occur: fatigue, weakness, abdominal pain, loss of appetite, itching, or yellowing of the eyes or skin pasien.4
Management: inhibits secretion of thyroid hormone
After anti-thyroid therapy started, a hormone that has been released can be inhibited by a large number of lower doses of iodine iodine uptake in the thyroid gland. Lugol fluid or fluid saturated potassium iodide can be used for this purpose. Iodine therapy should be given after about one hour after administration of PTU or MMI. Please note that the iodine used singly will help increase thyroid hormone reserves and may increase thyrotoxic status. Teiodinasi contrast material for radiographic purposes, namely sodium ipodat, can be given for the purpose of iodine and to inhibit the conversion of T4 to T3 in the peripheral circulation. Potassium iodide can reduce blood flow to the thyroid gland and is only used before surgery in patients who are intolerant to tirotoksikosis.4 iodine can be treated with lithium were also interfere with thyroid hormone release. Patients who can not use PTU or MMI can also be treated with lithium for the use of a single iodine can be debated. Lithium inhibits the release of thyroid hormones through the administration. Plasmapheresis, plasma exchange, exchange transfusion with peritoneal dialysis, and charcoal plasma perfusion is another technique that is used to remove excess hormones in the blood circulation. However, these techniques are now used only in patients who do not respond to initial treatment line. Mixture of intravenous sodium iodide (1 g intravenously given slowly by 8-12 hours) has been withdrawn from pasaran.4
Management: inhibits the action of peripheral thyroid hormone
Propranolol is the drug of choice to fight peripheral thyroid hormone action. Propranolol inhibits beta-adrenergic receptor and prevents the conversion of T4 to T3. These drugs cause dramatic changes in the clinical manifestations and effective in reducing symptoms. However, propranolol produces the desired clinical response in thyroid crisis only in large doses. Intravenous administration requires continuous monitoring of the heart rhythm pasien.4
Now, esmolol is a beta-blocker agent ultra-fast action that successfully used in thyroid crisis. The agents Beta-blocker non-selective, such as propranolol and esmolol, can not be used in patients with congestive heart failure, bronchospasm, or a history of asthma. For these cases, medications may be used as guanetidin or reserpine. Treatment with reserpine successfully in cases of thyroid crisis that is resistant to large doses of propranolol. However, reserpine guanetidin and can not be used on the state of cardiovascular collapse or syok.4
Treatment: Supportive treatment
Therapy aggressive fluid and electrolyte necessary to treat dehydration and hypotension. Excessive hypermetabolic state with increased intestinal transit and takipnu will lead to a substantial loss of fluid. Fluid needs may increase to 3-5 L per day. Thus, invasive monitoring is recommended in patients with advanced age and with congestive heart failure. Agent that increases blood pressure can be used when hypotension persists after adequate fluid replacement. Give the conclusion of intravenous fluids containing glucose to support the nutritional needs. Multivitamins, especially vitamin B1, can be added to prevent Wernicke encephalopathy. Hyperthermia addressed through the central and peripheral actions. Acetaminophen is the drug of choice for this because aspirin can replace the thyroid hormone to bind to the receptor and instead increase the severity of thyroid crisis. Sponges are cold, ice, and alcohol can be used to absorb heat in the peripheral. Cool humidified oxygen is recommended for patients ini.4
The use of glucocorticoids on thyroid crisis was associated with increased life expectancy. Initially, glucocorticoids are used to treat a relative insufficiency due to the possibility of accelerating the production and degradation during hypermetabolic status lasts. However, patients may experience deficiency type 2 autoimmune Graves' disease which is accompanied by absolute adrenal insufficiency. Glucocorticoids can menurunkanuptake iodine and antibody titers were stimulated by thyroid hormone with woven vascular stabilization. In addition, dexamethasone and hydrocortisone may have the effect of inhibiting the conversion of T4 to T3. Thus, doses of glucocorticoids, such as dexamethasone and hydrocortisone, are now routinely diberikan.4
Although often appear in elderly patients, cardiac decompensation may also appear in younger patients and even in patients without previous heart disease. Provision of digitalis needed to control the ventricular rate in patients with atrial fibrillation. Nonsteroidal anti-coagulation may be needed for atrial fibrillation and can be given if there are no contraindications. Digoxin may be used at doses greater than the dose used in other situations. Monitor digoxin levels closely to prevent poisoning. With the improving state of the patient, the dose of digoxin can start down. Congestive heart failure emerged as a result of impaired myocardial contractility and may require supervision by catheter Swan-Ganz.4
Hiperadrenergik state has been reported in hyperthyroid patients. The loss of vagal tone during thyrotoxicosis can trigger transient myocardial ischemia and long-term monitoring electrocardiogram (ECG) can improve the detection of myocardial ischemia and the tachyarrhythmia. Calcium channel blockade therapy may be better suited to resist the effects of calcium agonist related to thyroid hormone imbalance in the myocardium and improve simpatovagal.13
Management: side effects
PTU side effects reported is bleeding or easy bleeding gums, liver damage (anorexia, pruritus, right upper abdominal pain, increased transaminase levels up to three times the normal value), infection (caused agranulocytosis), pruritus to exfoliative dermatitis, vasculitis and ulceration vaskulitik oral, and pyoderma gangrenosum. Although including a recommendation D, some expert opinion still recommend that these drugs should be taken into consideration as first-line therapy of Graves' disease during pregnancy. The risk of serious liver damage, such as liver failure and death, has been reported in adults and children, especially during the first six months terapi.3
Agranulocytosis is a rare side effect of the use of anti-thyroid drugs and is the etiology of community-acquired infections and life-threatening patients using these drugs. Frequent clinical manifestations are fever (92%) and sore throat (85%). The initial clinical diagnosis was acute pharyngitis is usually (46%), acute tonsillitis (38%), pneumonia (15%) and urinary tract infection (8%). Blood cultures were positive for Pseudomonas aeruginosa, Escherichia coli, Staphylococcus aureus, Capnocytophaga species. Deaths caused by uncontrolled infection, thyroid crisis and the multiple organ failure. Gram-negative bacilli, such as Klebsiella pneumoniae and P. aeruginosa, a pathogen most frequently encountered in clinical isolates. Broad spectrum antibiotics with anti-Pseudomonas activity should be administered to patients with agranulocytosis caused by anti-thyroid drugs that show clinical manifestations of infection berat.14
Complication
Complications can result from surgery, among others, hypoparathyroidism, laryngeal nerve damage rekurens, subtotal thyroidectomy or hypothyroidism in RAI therapy, visual disturbances atai diplopia due to heavy oftalmopati, localized pretibial myxoedema, heart failure with high cardiac output, reduced muscle mass and proksimal.1 muscle weakness Hypoglycemia and lactic acidosis is a rare complication of thyroid crisis occurs. A case of a 50-year-old Japanese woman who suffered cardiac arrest after an hour of hospital admission blood samples examined previously. Surprisingly, the levels of plasma glucose to 14 mg / dL, and lactic acid levels increased to 6.238 mM. Thus, if an atypical thyroid crisis shows normotermi hypoglycemic state and lactic acidosis, should be considered for diagnosis of thyroid crisis early because this condition requires emergency treatment. It is also important to apply the principles of standards in the handling of cases of thyroid crisis atipik.15
Prognosis
Thyroid crisis can be fatal if left untreated. Overall mortality rate of thyroid crisis is estimated to range between 10-20% but there are reports of research that says up to 75%, depending on the trigger factors or underlying disease thyroid crisis. With early diagnosis and adequate treatment, the prognosis is usually going well.1
Prevention
Prevention is by doing strict thyrotoxicosis therapy after diagnosis. Operations performed on patients only after blockade thyrotoxic thyroid hormone and / or beta-adrenergic receptors. Thyroid crisis after RAI therapy for hyperthyroidism caused by: 1) discontinuation of anti-thyroid drugs (usually stopped 5-7 days before RAI administration and detained until 5-7 days later), 2) the release of large amounts of thyroid hormone from the damaged follicles, and 3) the effects of RAI itself. Because the thyroid hormone levels are often higher before RAI therapy than after, many endocrinologists believe that the anti-thyroid drug withdrawal is a major cause of thyroid crisis. One option is to stop the anti-thyroid drugs (including metimazol) only 3 days prior to RAI therapy and drug re-start in 3 days later. The return of anti-thyroid drugs early after RAI therapy can decrease the efficacy of the therapy and require a second dose. It should also consider thyroid function tests prior to the operative procedure performed in patients at risk of hyperthyroidism (eg, patients with McCune-Albright syndrome) .2
Conclusion
Hypermetabolic thyroid crisis is a life-threatening condition and is characterized by high fever and dysfunction of the cardiovascular system, nervous system, and gastrointestinal system. The etiology of the most common cause of thyroid crisis is Graves' disease (diffuse toxic goiter). Crises arise during decompensated thyroid cells in response to thyroid hormone causes severe hipermetabolisme.
Diagnosis of thyroid crisis based on the clinical picture and not the picture laboratory. If the clinical picture is consistent with thyroid crisis, treatment should not be delayed because of waiting for laboratory confirmation of the thyrotoxicosis. Treatment of thyroid crisis should inhibit the synthesis, secretion, and peripheral thyroid hormone action. Handling an aggressive supportive done then to stabilize homeostasis and reverse multi-organ decompensation. Overall mortality rate of thyroid crisis is estimated to range between 10-75%. However, with early diagnosis and adequate treatment, the prognosis is usually good will.
Bibliography
Thyroid crisis is a complication hypertiroidisme a rare but potentially fatal. Thyroid crisis must be recognized and addressed by the clinical manifestations because laboratory confirmation often can not be done in the timeframe that pretty quickly. Patients usually show hypermetabolik state characterized by high fever, tachycardi, nausea, vomiting, agitation, and psychosis. In the advanced stage, the patient may fall into a state of stupor or komatus accompanied by hypotensi.1
Thyroid crisis is a rare disease, which only happens about 1-2% of patients hypertiroidisme. While the overall incidence of hyperthyroidism itself only ranged from 0.05 to 1.3%, which most of them are subclinical. However, thyroid crisis unrecognized and untreated can have fatal consequences. Adult mortality in thyroid crisis reaches 10-20%. Even some of the research reports say as high as 75% of the patient population treated inap.1 With a controlled thyrotoxicosis and early treatment of thyroid crisis, the death rate can be reduced to less than 20% .2
Because the cause of hyperthyroidism is Graves' disease is an autoimmune disease most and that also affects other organ systems, conducting history is very important to enforce diagnosis.3 This is important because the diagnosis of thyroid crisis based on the clinical picture and not the picture laboratoris.2, 11.16 Another important note is that thyroid crisis is a crisis that requires fulminant intensive care and continuous supervision menerus.4 With early diagnosis and adequate treatment, the prognosis is usually going well.1 therefore need a proper understanding of thyroid crisis, especially regarding the diagnosis and penatalaksaannya.
Definition
some definitions:
Thyroid crisis is a condition where the symptoms of thyrotoxicosis with suddenly become great and accompanied by hyperpireksia, tachycardia and sometimes vomiting that continues menerus.11
Hypermetabolic thyroid crisis is a life-threatening condition and is characterized by high fever and dysfunction of the cardiovascular system, nervous system, and channel system cerna.5 Initially, arising hyperthyroidism which is a collection of symptoms caused by increased levels of circulating thyroid hormone with or without abnormal thyroid gland function. When the number was greatly exaggerated, there is a cluster of symptoms are more severe, the crisis tirotoksikosis.1 thyroid is a condition in which the body's happening decompensated thyrotoxicosis tersebut.6 Typically occurs in patients with untreated thyrotoxicosis or not completely heal triggered by surgery, infection , or trauma.1
Etiology
The etiology of thyroid crisis such as Graves' disease, toxic multinodular goiter, toxic nodules, Hashimoto's thyroiditis, tiroiditas deQuevain, metastatic follicular thyroid carcinoma, and TSH-producing tumor. The etiology of the most common cause of thyroid crisis is Graves' disease (diffuse toxic goiter) .7 Although not common, thyroid crisis can also be a complication of thyroid surgery. This condition is caused by the manipulation of the thyroid gland during surgery in patients with hyperthyroidism. Thyroid crisis can occur before, during, or after surgery. Surgery is generally only recommended when patients have Graves disease and other therapeutic strategies have failed or when the suspected presence of thyroid cancer. Thyroid crisis potential in such cases could lead to kematian.8
Thyroid crisis is also associated with severe hypocalcemia. A case of 30-year-old woman with thyroid crisis and impaired renal function showed hypocalcemia. Hypocalcaemia in the current case had serum creatinine is still normal. Normal serum levels of the amino acid fragment of parathyroid hormone end in a state of hypocalcemia in the case indicate a parathyroid dysfunction. Since normal serum magnesium and no history of thyroid surgery or radio-iodine therapy, are considered idiopathic hypoparathyroidism occurring. The seventh case was mentioned in the literature on Grave's disease are accompanied hypoparathyroidism idiopatik.9
Thyroid crisis is reported to occur in patients interstitial nephritis. The case of a 54-year-old man who had been treated with tiamazol (5 mg / day) showed that thyroid hormone levels rose sharply after eksodontia. Although the prescribed dose tiamazol raised after eksodontia on the fourth day, he underwent a thyroid crisis at day-52 post-eksodontia. Laboratory findings also indicate renal dysfunction (creatinine 1.8 mg / dL at day 37 post-eksodontia). Thyroid hormone levels back in the normal range after subtotal thyroidectomy. However, serum creatinine levels remained high. This man kemudia diagnosed with interstitial nephritis by renal biopsy and treated with prednisolone 30 mg / day. This case mewakilit thyroid crisis events that occurred despite increased dose tiamazol after eksodontia. It appears that as well as interstitial nephritis eksodontia is a factor that may increase thyroid function. After a poor response to anti-thyroid drugs, it is important to prevent thyroid crisis by determining these factors and treatment sesuai.10
Pathophysiology
In healthy people, the hypothalamus produces thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH) and the hormone that causes the thyroid gland releases thyroid hormones. Strictly speaking, these glands produce prohormone thyroxine (T4), which had deiodinasi mainly by the liver and kidneys to its active form, namely triiodothyronine (T3). T4 and T3 are in two forms: 1) free form and not bound active biological and 2) a form that is bound to thyroid-binding globulin (TBG). Levels of T4 and free T3 not bound strongly correlated with the clinical picture of the patient. This free form regulate thyroid hormone levels when they circulate in the blood circulation that supplies the pituitary gland anterior.1
From the standpoint of Graves' disease, thyrotoxicosis pathophysiology involves autoimmunity by B and T lymphocytes are directed at four antigens of the thyroid gland: TBG, thyroid peroxidase, sodium-iodide simporter, and TSH receptor. TSH receptor is what is the major autoantigen in the pathophysiology of this disease. The thyroid gland is stimulated constantly by autoantibodies against the TSH receptor and the subsequent secretion of TSH suppressed due to increased production of thyroid hormones. The most commonly found autoantibodies of subclasses of immunoglobulin (Ig)-G1. These antibodies cause the release of thyroid hormones and TBG mediated by 3, '5 '-cyclic adenosine monophosphate (cyclic AMP). In addition, this antibody also stimulates iodine uptake, protein synthesis, and the growth of the gland tiroid.3
Crises arise during decompensated thyroid cells in response to thyroid hormone causes severe hipermetabolisme involving multiple organ systems and is the most severe form of thyrotoxicosis. Clinical features associated with the effect of thyroid hormone intensified with increasing thyroid hormone release (with / without increased synthesis) or increased intake of thyroid hormones by the body's cells. In some degree, the cell's response to hormones is already too high for the survival of patients' lives and cause kematian.2 hypothesized that thyroid hormone can increase the density of beta receptors, cyclic adenosine monophosphate, and a decrease in the density of alpha receptors. Plasma levels and urinary excretion rate of epinephrine and norepinephrine normal in patients tirotoksikosis.7
Although the pathogenesis of thyroid crisis are not fully understood, these theories have been proposed to answer. Patients with thyroid crisis thyroid hormone levels were reported to have a higher rate than patients with thyrotoxicosis without complications although total thyroid hormone levels are not increased. adrenergic receptor activation is another hypothesis that appears. Menginervasi sympathetic nerves and catecholamines stimulate the thyroid gland thyroid hormone synthesis. Next, an increase in thyroid hormone increases beta-adrenergic receptor density so menamnah effects of catecholamines. Thyroid crisis dramatic response to beta-blockers and the emergence of thyroid crisis after swallowing adrenergic drugs, such as pseudoephedrine, supports this theory. This theory also explains the low or normal levels of plasma and urinary catecholamine excretion rate. However, this theory does not explain why beta-blockers failed to reduce levels of thyroid hormones on tirotoksikosis.2
Another theory suggests the rapid increase in hormone levels as a result of the pathogenic source. The sharp drop in levels of binding proteins that can occur after surgery may lead to a sudden increase in free thyroid hormone levels. In addition, hormone levels can rise quickly when the gland manipulation during surgery, during palpation during examination, or from the destruction of the follicle after radioactive iodine therapy (RAI). Other theories ever proposed, including changes in tissue tolerance to thyroid hormone, a substance similar to a unique catecholamines on the state thyrotoxicosis, and direct sympathetic effects of thyroid hormones due to similarity of structure with sebaai katekolamin.2
The clinical
History of the disease before patients include thyrotoxicosis or symptoms such as irritability, agitation, emotional lability, lack of appetite with weight loss is down, excessive sweating and temperature intolerance, and decreased school performance due to decreased attention span. History of disease is now a common complaint by patients is fever, sweating, decreased appetite and weight loss. Gastrointestinal complaints are often expressed by patients are nausea, vomiting, diarrhea, abdominal pain, and jaundice. While the complaint include neurological symptoms of anxiety (mostly on older teens), behavioral changes, seizures and koma.2
On physical examination, it was found fever with temperatures consistently exceed 38.5 oC. Patients can experience hyperpyrexia even exceed 41oC and excessive sweating. Cardiovascular signs were found between hypertension with a widened pulse pressure or hypotension in the next phase and accompanied by shock. Tachycardia occurred incompatible with fever. Signs of heart failure include arrhythmias (supraventricular most, such as atrial fibrillation, but ventricular tachycardia may also occur). While neurological signs include agitation and confusion, hiperrefleksia and transient pyramidal signs, tremors, seizures, and coma. Signs of thyrotoxicosis include orbital signs and goiter.2
In addition to typical cases described above, there is one case report of a patient with an atypical clinical picture (normotermi and normotensive) were accompanied by multiple organ dysfunction syndrome, such as lactic acidosis and liver dysfunction, both of which are very rare complication. This case shows that the two organ systems are involved in thyroid crisis and it is important to recognize this atypical picture in cases of thyroid crisis dihadapi.12
Overview laboratory
Diagnosis of thyroid crisis based on the clinical picture and not the picture laboratory. If the clinical picture is consistent with thyroid crisis, treatment should not be delayed because of waiting for laboratory confirmation of the thyrotoxicosis. On examination of the thyroid status, will usually be found to be consistent with the state of hyperthyroidism and useful only if the patient has not been previously diagnosed. Test results may not be obtained quickly and are usually not helpful for immediate handling. Findings typically include increased levels of T3, T4 and freely, increased resin uptake of T3, decreased TSH levels, and increased uptake of iodine 24 jam.2
TSH levels did not decline in the state of excessive TSH secretion but this rarely happens. Liver function tests generally show non-specific abnormalities, such as elevated serum for SGOT, SGPT, LDH, creatinine kinase, alkaline phosphatase, and bilirubin. In blood gas analysis, measurement of blood gases and electrolytes levels and urinalysis performed to assess and monitor the handling of long-pendek.2
Management
Management of thyroid crisis need to process in a few steps. Ideally, a given therapy should inhibit the synthesis, secretion, and peripheral thyroid hormone action. Handling an aggressive supportive done then to stabilize homeostasis and reverse multi-organ decompensation. Additional tests need to be conducted to identify and address the factors originators followed by definitive treatment to prevent recurrence. Thyroid crisis is a crisis that requires fulminant intensive care and continuous supervision menerus.4
Management: inhibits the synthesis of thyroid hormones
Anti-thyroid compounds such as propylthiouracil (PTU) and methimazole (MMI) is used to inhibit the synthesis of thyroid hormones. PTU also inhibits the conversion of T4 to T3 in the peripheral circulation and MMI preferable in cases of thyroid crisis. While MMI is farmakoogik agent commonly used in cases of hyperthyroidism. Both inhibit the incorporation of iodine into TBG within one hour after drinking. History of hepatotoxicity or agranulocytosis from previous tioamida therapy is contraindicated both drugs PTU tersebut.4 this gracious indicated hyperthyroidism caused by an illness Graves. Support research report showed an increased risk of liver toxicity compared with the use of PTU metimazol. Serious liver damage has been found in the use of metimazol in five cases (three of whom died). PTU is now considered as a second-line drug therapy except in patients who are allergic or intolerant to metimazol or for women with first trimester of pregnancy. Use metimazol during pregnancy reported to cause embriopati, including aplasia kutis, although a rare case ditemui.4
Supervise closely PTU therapy for possible onset of symptoms and signs of liver damage, especially during the first 6 months after starting therapy. For suspected liver damage, discontinue PTU therapy and gradual re-examined the results of liver damage and provide supportive care. PTU should not be used in pediatric patients unless the patient is allergic or intolerant to metimazol and there is no other available drug options. Provide education to the patient to contact the doctor if the following symptoms occur: fatigue, weakness, abdominal pain, loss of appetite, itching, or yellowing of the eyes or skin pasien.4
Management: inhibits secretion of thyroid hormone
After anti-thyroid therapy started, a hormone that has been released can be inhibited by a large number of lower doses of iodine iodine uptake in the thyroid gland. Lugol fluid or fluid saturated potassium iodide can be used for this purpose. Iodine therapy should be given after about one hour after administration of PTU or MMI. Please note that the iodine used singly will help increase thyroid hormone reserves and may increase thyrotoxic status. Teiodinasi contrast material for radiographic purposes, namely sodium ipodat, can be given for the purpose of iodine and to inhibit the conversion of T4 to T3 in the peripheral circulation. Potassium iodide can reduce blood flow to the thyroid gland and is only used before surgery in patients who are intolerant to tirotoksikosis.4 iodine can be treated with lithium were also interfere with thyroid hormone release. Patients who can not use PTU or MMI can also be treated with lithium for the use of a single iodine can be debated. Lithium inhibits the release of thyroid hormones through the administration. Plasmapheresis, plasma exchange, exchange transfusion with peritoneal dialysis, and charcoal plasma perfusion is another technique that is used to remove excess hormones in the blood circulation. However, these techniques are now used only in patients who do not respond to initial treatment line. Mixture of intravenous sodium iodide (1 g intravenously given slowly by 8-12 hours) has been withdrawn from pasaran.4
Management: inhibits the action of peripheral thyroid hormone
Propranolol is the drug of choice to fight peripheral thyroid hormone action. Propranolol inhibits beta-adrenergic receptor and prevents the conversion of T4 to T3. These drugs cause dramatic changes in the clinical manifestations and effective in reducing symptoms. However, propranolol produces the desired clinical response in thyroid crisis only in large doses. Intravenous administration requires continuous monitoring of the heart rhythm pasien.4
Now, esmolol is a beta-blocker agent ultra-fast action that successfully used in thyroid crisis. The agents Beta-blocker non-selective, such as propranolol and esmolol, can not be used in patients with congestive heart failure, bronchospasm, or a history of asthma. For these cases, medications may be used as guanetidin or reserpine. Treatment with reserpine successfully in cases of thyroid crisis that is resistant to large doses of propranolol. However, reserpine guanetidin and can not be used on the state of cardiovascular collapse or syok.4
Treatment: Supportive treatment
Therapy aggressive fluid and electrolyte necessary to treat dehydration and hypotension. Excessive hypermetabolic state with increased intestinal transit and takipnu will lead to a substantial loss of fluid. Fluid needs may increase to 3-5 L per day. Thus, invasive monitoring is recommended in patients with advanced age and with congestive heart failure. Agent that increases blood pressure can be used when hypotension persists after adequate fluid replacement. Give the conclusion of intravenous fluids containing glucose to support the nutritional needs. Multivitamins, especially vitamin B1, can be added to prevent Wernicke encephalopathy. Hyperthermia addressed through the central and peripheral actions. Acetaminophen is the drug of choice for this because aspirin can replace the thyroid hormone to bind to the receptor and instead increase the severity of thyroid crisis. Sponges are cold, ice, and alcohol can be used to absorb heat in the peripheral. Cool humidified oxygen is recommended for patients ini.4
The use of glucocorticoids on thyroid crisis was associated with increased life expectancy. Initially, glucocorticoids are used to treat a relative insufficiency due to the possibility of accelerating the production and degradation during hypermetabolic status lasts. However, patients may experience deficiency type 2 autoimmune Graves' disease which is accompanied by absolute adrenal insufficiency. Glucocorticoids can menurunkanuptake iodine and antibody titers were stimulated by thyroid hormone with woven vascular stabilization. In addition, dexamethasone and hydrocortisone may have the effect of inhibiting the conversion of T4 to T3. Thus, doses of glucocorticoids, such as dexamethasone and hydrocortisone, are now routinely diberikan.4
Although often appear in elderly patients, cardiac decompensation may also appear in younger patients and even in patients without previous heart disease. Provision of digitalis needed to control the ventricular rate in patients with atrial fibrillation. Nonsteroidal anti-coagulation may be needed for atrial fibrillation and can be given if there are no contraindications. Digoxin may be used at doses greater than the dose used in other situations. Monitor digoxin levels closely to prevent poisoning. With the improving state of the patient, the dose of digoxin can start down. Congestive heart failure emerged as a result of impaired myocardial contractility and may require supervision by catheter Swan-Ganz.4
Hiperadrenergik state has been reported in hyperthyroid patients. The loss of vagal tone during thyrotoxicosis can trigger transient myocardial ischemia and long-term monitoring electrocardiogram (ECG) can improve the detection of myocardial ischemia and the tachyarrhythmia. Calcium channel blockade therapy may be better suited to resist the effects of calcium agonist related to thyroid hormone imbalance in the myocardium and improve simpatovagal.13
Management: side effects
PTU side effects reported is bleeding or easy bleeding gums, liver damage (anorexia, pruritus, right upper abdominal pain, increased transaminase levels up to three times the normal value), infection (caused agranulocytosis), pruritus to exfoliative dermatitis, vasculitis and ulceration vaskulitik oral, and pyoderma gangrenosum. Although including a recommendation D, some expert opinion still recommend that these drugs should be taken into consideration as first-line therapy of Graves' disease during pregnancy. The risk of serious liver damage, such as liver failure and death, has been reported in adults and children, especially during the first six months terapi.3
Agranulocytosis is a rare side effect of the use of anti-thyroid drugs and is the etiology of community-acquired infections and life-threatening patients using these drugs. Frequent clinical manifestations are fever (92%) and sore throat (85%). The initial clinical diagnosis was acute pharyngitis is usually (46%), acute tonsillitis (38%), pneumonia (15%) and urinary tract infection (8%). Blood cultures were positive for Pseudomonas aeruginosa, Escherichia coli, Staphylococcus aureus, Capnocytophaga species. Deaths caused by uncontrolled infection, thyroid crisis and the multiple organ failure. Gram-negative bacilli, such as Klebsiella pneumoniae and P. aeruginosa, a pathogen most frequently encountered in clinical isolates. Broad spectrum antibiotics with anti-Pseudomonas activity should be administered to patients with agranulocytosis caused by anti-thyroid drugs that show clinical manifestations of infection berat.14
Complication
Complications can result from surgery, among others, hypoparathyroidism, laryngeal nerve damage rekurens, subtotal thyroidectomy or hypothyroidism in RAI therapy, visual disturbances atai diplopia due to heavy oftalmopati, localized pretibial myxoedema, heart failure with high cardiac output, reduced muscle mass and proksimal.1 muscle weakness Hypoglycemia and lactic acidosis is a rare complication of thyroid crisis occurs. A case of a 50-year-old Japanese woman who suffered cardiac arrest after an hour of hospital admission blood samples examined previously. Surprisingly, the levels of plasma glucose to 14 mg / dL, and lactic acid levels increased to 6.238 mM. Thus, if an atypical thyroid crisis shows normotermi hypoglycemic state and lactic acidosis, should be considered for diagnosis of thyroid crisis early because this condition requires emergency treatment. It is also important to apply the principles of standards in the handling of cases of thyroid crisis atipik.15
Prognosis
Thyroid crisis can be fatal if left untreated. Overall mortality rate of thyroid crisis is estimated to range between 10-20% but there are reports of research that says up to 75%, depending on the trigger factors or underlying disease thyroid crisis. With early diagnosis and adequate treatment, the prognosis is usually going well.1
Prevention
Prevention is by doing strict thyrotoxicosis therapy after diagnosis. Operations performed on patients only after blockade thyrotoxic thyroid hormone and / or beta-adrenergic receptors. Thyroid crisis after RAI therapy for hyperthyroidism caused by: 1) discontinuation of anti-thyroid drugs (usually stopped 5-7 days before RAI administration and detained until 5-7 days later), 2) the release of large amounts of thyroid hormone from the damaged follicles, and 3) the effects of RAI itself. Because the thyroid hormone levels are often higher before RAI therapy than after, many endocrinologists believe that the anti-thyroid drug withdrawal is a major cause of thyroid crisis. One option is to stop the anti-thyroid drugs (including metimazol) only 3 days prior to RAI therapy and drug re-start in 3 days later. The return of anti-thyroid drugs early after RAI therapy can decrease the efficacy of the therapy and require a second dose. It should also consider thyroid function tests prior to the operative procedure performed in patients at risk of hyperthyroidism (eg, patients with McCune-Albright syndrome) .2
Conclusion
Hypermetabolic thyroid crisis is a life-threatening condition and is characterized by high fever and dysfunction of the cardiovascular system, nervous system, and gastrointestinal system. The etiology of the most common cause of thyroid crisis is Graves' disease (diffuse toxic goiter). Crises arise during decompensated thyroid cells in response to thyroid hormone causes severe hipermetabolisme.
Diagnosis of thyroid crisis based on the clinical picture and not the picture laboratory. If the clinical picture is consistent with thyroid crisis, treatment should not be delayed because of waiting for laboratory confirmation of the thyrotoxicosis. Treatment of thyroid crisis should inhibit the synthesis, secretion, and peripheral thyroid hormone action. Handling an aggressive supportive done then to stabilize homeostasis and reverse multi-organ decompensation. Overall mortality rate of thyroid crisis is estimated to range between 10-75%. However, with early diagnosis and adequate treatment, the prognosis is usually good will.
Bibliography
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