History

Fact Explanation
History of hyperthyroidism The thyroid crisis typically occurs in patients in whom preexisting hyperthyroidism has not been diagnosed or has been treated insufficiently.[1]Thyroid crisis has been reported to be precipitated by the discontinuation of antithyroid drugs.[2] It is the highest triggering factor for thyroid crisis.[3] This is a life-threatening condition requiring emergency treatment.[3]Graves Disease remains the most common cause of t thyroid crisis. However, toxic multinodular goitre and toxic adenoma may also progress to a thyroid crisis.[4]
Hyperpyrexia [5] Body temperature can rise up to 41° centigrade. [4] Occurs due to concomitant sympatho-adrenal hyperactivity.[1]
History of physical or emotional stress This includes: trauma, surgery, burn, myocardial infarction or childbirth.[5] The thyroid crisis has an abrupt onset, and is almost always evoked by a precipitating factor. [1]
History of infection Second commonest trigger for thyroid crisis is infection,particularly that of the upper respiratory tract.[1]
Radio-iodine therapy / Use of iodinated subtance Thyroid crisis may occur within days of radio-iodine therapy, as acute irradiation damage may lead to a transient rise in serum thyroid hormone levels. [6] The use of other iodinated substances can also act as triggers: disinfectants, antiseptics, and iodinated contrast agents. Amiodarone is the drug most often associated with thyroid stimulation. Under physiological conditions, increased serum levels of iodine results in inhibition of thyroid hormone synthesis and self regulatory inhibition of iodine transportation. Thus, the excess of iodine and absence of a regulatory system can lead to persistent increase in the production of thyroid hormone and thyroid crisis. [7]
Diarrhea Thyroid hormone Increases gut motility.[5] There is an increased frequency of bowel movements due to increased motor contraction in the small bowel leads to diarhea. [2]
Palpitation Thyroid hormone Increases heart rate and cardiac output. In addition it increases catecholamine sensitivity and β-adrenergic receptors in the myocardium this results in palpitations.[5]
Neuropsychiatric features Neuropsychiatric manifestations of thyrotoxicosis include emotional lability, restlessness, anxiety, agitation, confusion, psychosis and even coma[2]
Shortness of breath Shortness of breath may be due to decreased lung compliance, engorged pulmonary capillary bed or left ventricular failure.[2] Respiratory failure secondary to respiratory muscle paralysis can cause death in these patients. [4]
References
  1. MIGNECO, A., V. OJETTI, A.TESTA, A. DE LORENZO, N. GENTILONI silveri . Management of thyrotoxic crisis. European Review for Medical and Pharmacological Sciences[online]. Catholic University - Rome (Italy).2005, vol. 9(1),69-74. [viewed 25 April 2014] Available from : www.ncbi.nlm.nih.gov/pubmed/15850146
  2. NAYAK, B., K. BURMAN . Thyrotoxicosis and thyroid storm. Endocrinology Metabolic Clinics of North America[online]. Elsivier. September 2006, vol. 35(4). 663-86,[viewed 25 April 2014]. Available from: doi: 10.1016/j.ecl.2006.09.008
  3. AKAMIZU, T., T. SATOH , O. ISOZAKI , et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid.[online]. Mary Ann Liebert. Number 7, 2012. Vol . 22(7). 661-79.[viewed 28 April 2014]. Available from: doi: 10.1089/thy.2011.0334
  4. Bondugulapati, L.N.R., et al. Review-Thyroid Emergencies. SriLanka Journal of Critical Care.[online] Srilanka journals online.info. 2011, vol. 2(1). 1-12 [viwed 28 April 2014]. Available from: www.sljol.info/index.php/SLJCC/article/download/1782/3174‎
  5. KUMAR, P.J., M.L. CLARK. Kumar and Clark's Clinical Medicine. 8th ed. London: W.B. Saunders Company; 2012.
  6. COLLEDGE N.R., B.R. WALKER, S.H. RALSTON. Davidson's Principles and Practice of Medicine. 21st ed. London. Churchill Livingstone, 2010.
  7. DE ALMEIDA, C.E., E.F. CURI, C.R. De ALMEIDA, D.F. VIEIRA. Thyrotoxic crisis associated with gestational trophoblastic disease. Revista Brasileira de Anestesiologia.[online]. Elsevier. September 2011, vol. 61(5). 604-609 [viewed April 28, 2014]. Available from: www.ncbi.nlm.nih.gov/pubmed/21920210‎

Examination

Fact Explanation
Fever Thyroid hormones increase the basal metabolic rate (BMR). [1]This results in greater energy production leading to increased thermogenesis ;perspiration and heat intolerance.[2],[3] Temperature can rise up to 41° centigrade.[4]
Tachycardia Thyroid hormone increases heart rate and cardiac output. [1]
Signs of cardiac failure Thyroid crisis is often accompanied by varying degrees of congestive heart failure.[1] Congestive heart failure may be the initial clinical presentation in approximately 6% of patients with hyperthyroidism.[5] Dysrhythmias, cardiac failure and respiratory failure secondary to respiratory muscle paralysis are recognized causes of death in these patients.[4]
Atrial Fibrillation In thyroid crisis atrial tachydysrhythmias, occur due to increased catecholamine sensitivity and β-adrenergic receptor numbers in heart. [1], [4]
Wasting A common finding in thyroid crisis is weight loss, despite regardless of the calorie intake. Thermogenesis leads to increased perspiration and heat intolerance. [2] In addition thyroid hormones also stimulate lipolysis.[2]
Changes in thyroid gland With Graves’ disease, diffuse enlargement of the gland, and possibly a bruit, caused by increased vascularity and blood flow; can be appreciated. A toxic multi nodular goiter can have physical findings of one or more nodules. In subacute thyroiditis, a tender thyroid gland could be found, In older individuals, typical symptoms of thyroid crisis may not be apparent. Older patients may present with some atypical symptoms including weight loss, palpitations, weakness, dizziness, syncope, or memory loss, and physical findings of sinus tachycardia or atrial fibrillation.[2]
Jaundice Unexplained jaundice is suggestive of thyroid crisis, but is considered a poor prognostic sign[1] Occurs due to gastrointestinal-hepatic dysfunction in severe hyperthyroidism.[2]
References
  1. KUMAR, P.J., M.L. CLARK. Kumar and Clark's Clinical Medicine. 8th ed. London: W.B. Saunders Company; 2012
  2. NAYAK, B., K. BURMAN . Thyrotoxicosis and thyroid storm. Endocrinology Metabolic Clinics of North America[online]. Elsivier. September 2006, vol. 35(4). 663-86,[viewed 25 April 2014]. Available from: doi: 10.1016/j.ecl.2006.09.008
  3. MIGNECO, A., V. OJETTI, A.TESTA, A. DE LORENZO, N. GENTILONI silveri . Management of thyrotoxic crisis. European Review for Medical and Pharmacological Sciences[online]. Catholic University - Rome (Italy).2005, vol. 9(1),69-74. [viewed 25 April 2014] Available from : www.ncbi.nlm.nih.gov/pubmed/15850146
  4. Bondugulapati, L.N.R., et al. Review-Thyroid Emergencies. SriLanka Journal of Critical Care.[online] Srilanka journals online.info. 2011, vol. 2(1). 1-12 [viwed 28 April 2014]. Available from: www.sljol.info/index.php/SLJCC/article/download/1782/3174
  5. NOH, K.W., C.S. SEON, J.W. CHOI,Y.B. CHO, J.Y. PARK,H.J. KIM. Thyroid storm and reversible thyrotoxic cardiomyopathy after ingestion of seafood stew thought to contain marine neurotoxin. Thyroid[online] Mary Ann Liebert. November 2011. vol. 21(6), 679-82.[viewed 28 April 2014]. Available from: DOI: 10.1089/thy.2010.0276

Differential Diagnoses

Fact Explanation
Anxiety Disorder Patient will have a history of anxiety disorder. features that anxiety disorder share are palpitation,tachycardia, anxiety, and shortness of breath. But there is no hyper pyrexia, cardiac arrhythmia or jaundice.[1]
Congestive Cardiac Failure Thyroid storm it self can present with cardiac failure with ankle edema, shortness of breath, palpitation, and cardiac arrhythmias. But usually there is no jaundice and hyper pyrexia.[2]
Pheochromocytoma Phaeochromocytomas, tumors of the sympathetic nervous system, they will also gives rise to Anxiety or panic attacks ,Palpitations Tremor,Sweating,Weight loss, Constipation or diarrhoea Tachycardia/arrhythmias,Fever. But is usually present with episodic headache and hypertension.[1]
Supraventricular Tachycardia Supra ventricular tachycardias (SVTs) arise from the atrium or the atrioventricular junction.The leading symptom of most SVTs is rapid regular palpitations which isn't eliminated by Valsalva manoeuvres. Other features are anxiety, dizziness, dyspnoea, neck pulsation, central chest pain and weakness. There is no pyrexia, jaundice or signs of cardiac failure in this. [1]
References
  1. KUMAR, P.J., M.L. CLARK. Kumar and Clark's Clinical Medicine. 8th ed. London: W.B. Saunders Company; 2012.
  2. COLLEDGE N.R., B.R. WALKER, S.H. RALSTON. Davidson's Principles and Practice of Medicine. 21st ed. London. Churchill Livingstone, 2010.

Investigations - for Diagnosis

Fact Explanation
Triiodothyronine (T3) and L-thyroxine (T4) Since its pathophysiologic mechanisms have not been clarified, the diagnosis of TS is based on clinical manifestations[2], even if the symptoms and signs may not be specific[3].low levels of thyroid stimulating hormone (TSH) and high levels of free triiodothyronine (T3) and free L-thyroxine (T4) are characteristic, but as yet stated, not helpful in distinguishing uncomplicated thyrotoxicosis from thyroid crisis[1]
Thyroid stimulating hormone (TSH) Low levels of thyroid stimulating hormone (TSH) and high levels of free triiodothyronine (T3) and free L-thyroxine (T4) are characteristic of thyroid crisis,[1]
Random Blood sugar The hyperglycemia tends to occur because of a catecholamine-induced inhibition of insulin release, and increased glycogenolysis[4]
Serum Electrolytes This will show Hypercalcaemia, which is result of Haemoconcentration and bone resorption[5] as thyroid hormone increase bone turnover and resorption[6]
WBC/DC This will show leukocytosis with left shift as a result of stress response, with or without infection[5]
ECG Electrocardiogram manifestations of thyroid crisis most commonly include sinus tachycardia and atrial fibrillation[4]
Thyroid sonogram It is frequently helpful, and generally easier in the setting of an intensive care unit, to obtain a thyroid sonogram with Doppler flow to assess thyroid gland size, vascularity, and the presence of nodules that may require further attention. Typically, a thyroid gland secreting excessive hormones would be enlarged and have enhanced Doppler flow. On the other hand, in the setting of subacute, postpartum, or silent thyroiditis, or exogenous causes of hyperthyroidism, the thyroid gland would be expected to be small, with decreased Doppler flow.[4]
Nuclear medical imaging Although not always indicated for diagnosis, given the urgency and clinical context, nuclear medicine imaging with radioactive iodine uptake and scanning would reveal a greatly increased uptake of radioiodine as early as 1 or 2 hours after administration of the isotope, indicating rapid intraglandular turnover of iodine[4]
References
  1. MIGNECO, A., V. OJETTI, A.TESTA, A. DE LORENZO, N. GENTILONI silveri . Management of thyrotoxic crisis. European Review for Medical and Pharmacological Sciences[online]. Catholic University - Rome (Italy).2005, vol. 9(1),69-74. [viewed 25 April 2014] Available from : www.ncbi.nlm.nih.gov/pubmed/15850146
  2. AKAMIZU, T., T. SATOH , O. ISOZAKI , et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid.[online]. Mary Ann Liebert. Number 7, 2012. Vol . 22(7). 661-79.[viewed 28 April 2014]. Available from: doi: 10.1089/thy.2011.0334
  3. Liang, M., H. Wang, L.Tan, M. Feng, Y. Shen, Q. Wang. Successful treatment of thyrotoxic crisis after esophagectomy in an elderly woman with hyperthyroidism. The Annals of Thoracic Surgery[online]. Elsevier.January 2012. Vol. 93(6),141-142. [viewed 28 April 2014]. Available from: doi:10.1016/j.athoracsur.2011.12.042
  4. NAYAK, B., K. BURMAN . Thyrotoxicosis and thyroid storm. Endocrinology Metabolic Clinics of North America[online]. Elsivier. September 2006, vol. 35(4). 663-86,[viewed 25 April 2014]. Available from: doi: 10.1016/j.ecl.2006.09.008
  5. Bondugulapati, L.N.R., et al. Review-Thyroid Emergencies. SriLanka Journal of Critical Care.[online] Srilanka journals online.info. 2011, vol. 2(1). 1-12 [viwed 28 April 2014]. Available from: www.sljol.info/index.php/SLJCC/article/download/1782/3174‎
  6. KUMAR, P.J., M.L. CLARK. Kumar and Clark's Clinical Medicine. 8th ed. London: W.B. Saunders Company; 2012.

Management - General Measures

Fact Explanation
Paracitamol Because fever is very common with severe thyrotoxicosis, antipyretics should be used; Paracitamol 1g 8 horly is the preferable choice. Salicylates should be avoided in thyrotoxicosis because salicylates can decrease thyroid protein binding, causing an increase in free thyroid hormone levels. External cooling measures, such as alcohol sponging, ice packs, or a cooling blanket, can also be used[1]
Hydrocortisone The role of glucocorticoid therapy in thyrotoxic crisis has been contentious but is almost universally accepted. Glucocrticoids have a dual role in this situation. They inhibit peripheral conversion of T4 to T3 and will potentially reduce active homone levels. Furthermore, they will also correct possible adrenal insufficiency which may be present in patients who have a thyroid crisis on the basis of uncontrolled Graves’ disease. Hydrocortisone should be given at a dose of 100mg every 8 hours[2]
Anticoagulation There are conflicting views about the incidence of thromboembolic disease in atrial fibrillation (AF) complicating thyrotoxicosis. The standard risk factors for embolic events in AF, including increasing age and underlying heart disease, apply to these patients as well. The current recommendations are to apply these criteria in decisions about anticoagulation. Thyrotoxic patients may require a lower maintainance dose of warfarin because of the increased clearance of vitamin K dependant clotting factors[2]
Fluid and supportive therapy Fluid losses caused by reduced oral intake, increased sweating, fever, vomiting and diarrhoea should be vigorously treated, with central venous or arterial monitoring. Intravenous fluids containing isotonic saline with 5--]10% dextrose will better restore depleted hepatic glycogen[2]
References
  1. NAYAK, B., K. BURMAN . Thyrotoxicosis and thyroid storm. Endocrinology Metabolic Clinics of North America[online]. Elsivier. September 2006, vol. 35(4). 663-86,[viewed 25 April 2014]. Available from: doi: 10.1016/j.ecl.2006.09.008
  2. Bondugulapati, L.N.R., et al. Review-Thyroid Emergencies. SriLanka Journal of Critical Care.[online] Srilanka journals online.info. 2011, vol. 2(1). 1-12 [viwed 28 April 2014]. Available from: www.sljol.info/index.php/SLJCC/article/download/1782/3174‎

Management - Specific Treatments

Fact Explanation
Inhibition of new hormone production Large doses of propylthiouracil (600 mg loading dose and 200.300 mg every 6 h) should be given PO or by nasogastric tube or per rectum; the drugs inhibitory action on T4 to T3 conversion makes it the antithyroid drug of choice[3] or Methimazole 20–25 mg will po q 6 hourly will Inhibits new hormone synthesis[2] Both of these are used as First-line therapy.[1]All antithyroid drugs inhibit the function of thyroid peroxidase hormone , reducing oxidation and organification of iodide. These drugs also reduce thyroid antibody levels by mechanisms that remain unclear, and they appear to enhance rates of remission.[3]
Inhibition of thyroid hormone release One hour after the first dose of propylthiouracil, stable iodide is given to block thyroid hormone synthesis via the Wolff-Chaikoff effect (the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone). A saturated solution of potassium iodide (5 drops SSKI every 6 h), or ipodate or iopanoic acid (0.5 mg per 12 h),may be given PO. (Sodium iodide, 0.25 g IV every 6 h, is an alternative but is not generally available.)[3] Wolff-Chaikoff effect is is a reduction in thyroid hormone levels caused by ingestion of a large amount of iodine [4] It is an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream[5]
Beta-adrenergic blockade Propranolol 60–80 mg po q 4 h causes Beta-adrenergic blockade; causing reduction in adrenergic symptoms[3] and also decreases T4-to-T3 conversion,[1]or Atenolol 50–200 mg po qd used when cardioselective agents preferred.[1]Although other β-adrenergic blockers can be used, high doses of propranolol decrease T4 →T3 conversion, and the doses can be easily adjusted. Caution is needed to avoid acute negative inotropic effects, but controlling the heart rate is important, as some patients develop a form of high-output heart failure[3]
Alternative therapies 1. Lithium carbonate 300 mg po q 8 hd will blocks release of hormone from gland; inhibits new hormone synthesis Used when thionamide or iodide therapy is contraindicated; lithium levels should be checked regularly, 2. Potassium perchlorate 1 g po qds Inhibits iodide uptake by thyroid gland Used in combination with thionamide in treatment of Type II amiodaroneinduced thyrotoxicosis 3. Cholestyramine 4 g po qid Decreases reabsorption of thyroid hormone from enterohepatic circulation Used in combination with thionamide therapy.[1]
References
  1. NAYAK, B., K. BURMAN . Thyrotoxicosis and thyroid storm. Endocrinology Metabolic Clinics of North America[online]. Elsivier. September 2006, vol. 35(4). 663-86,[viewed 25 April 2014]. Available from: doi: 10.1016/j.ecl.2006.09.008
  2. Bondugulapati, L.N.R., et al. Review-Thyroid Emergencies. SriLanka Journal of Critical Care.[online] Srilanka journals online.info. 2011, vol. 2(1). 1-12 [viwed 28 April 2014]. Available from: www.sljol.info/index.php/SLJCC/article/download/1782/3174‎
  3. JAMESON J.L., Harrison's Endocrinology. 2nd ed. McGraw Hill Professional. New york. 2010.
  4. DORLAND W.A.N.Dorland's Illustrated Medical Dictionary.32 nd ed. Philadelphia, Saunders, 2012.
  5. GOODMAN L.S., GILMAN A.G., Goodman and Gilman's the pharmacological basis of therapeutics. 9th ed. New york. McGraw-Hill Companies, 1996.