Concurrent presentation of thyroid storm and diabetic ketoacidosis: a systematic review of previously reported cases.

BACKGROUND: Simultaneous development of thyroid storm and diabetic ketoacidosis (DKA) is a rare condition. The review aims to summarise its clinical presentation, investigation findings and treatment options. METHODS: Databases and reference lists of the selected articles were searched for case reports in English which describe concurrent presentation of thyroid storm and diabetic ketoacidosis. CARE guidelines were used for the quality assessment of the selected articles. RESULTS: Twenty-six cases from twenty-one articles were selected out of 198 search results. Western Pacific, and American regions contributed to 77% of the cases. Females were most affected (88%). Features of Graves' disease like hyperthermia and tachycardia, gastrointestinal and neuro-psychiatric disturbances were the common clinical presentations. In most of the cases, previous diagnosis of diabetes mellitus preceded that of Graves' disease (46%). Among patients having their drug compliance reported, all had poor compliance to their routine anti-thyroid (9/9) and anti-diabetic (2/2) agents. Moreover, in all cases where HbA1C (7/7) and T4 (16/16) were measured, the results were elevated and where TSH (17/17) was measured, the results were low. The recommended treatment for DKA and thyroid storm was used in most cases and methimazole was the thionamide of choice in the latest four cases reported. All cases survived except four (15%). CONCLUSIONS: Concurrent presentation of thyroid storm and diabetic ketoacidosis is rare but life-threatening. Therefore, efforts should be made to maximise patient compliance to anti-thyroid and anti-diabetic agents in treating such patients.

Thyroid storm: Is there a role for thyroid function test?

INTRODUCTION: Thyroid storm (TS) is an endocrine emergency. Early diagnosis for prompt treatment is essential as it has a high mortality rate. CASE REPORT: A 31-year-old lady with underlying hyperthyroidism, dilated cardiomyopathy with severe mitral regurgitation presented with shortness of breath. She was intubated and admitted due to decreasing Glasgow Coma Score. Her blood investigations revealed increased white cell count, raised free thyroxine with suppressed thyroid stimulating hormone, deranged liver, renal and coagulation profiles. As her condition did not improve with initial treatment, plasmapheresis was commenced on day 4. Biochemically, her thyroid function test (TFT) showed improvement; however, she succumbed due to multi-organ failure. DISCUSSION: Plasmapheresis is considered in TS if there is no clinical improvement within 24-48 hours of initial treatment. The improvement in patient's TFT post plasmapheresis signifies its role in treating TS. Unfortunately, there was a delay in commencing plasmapheresis due to haemodynamic instability in this patient.

Lethal thyroid storm after uncontrolled intake of liothyronine in order to lose weight.

Thyroid hormones are sometimes used for purposes for which they are not approved. Reasons for off-label use can be overweight, prevailing depressive mood, or various somatic symptoms. Information about the intake of thyroid hormones in order to lose weight can be easily obtained from inappropriate/nonmedical websites. The objective of this case report is to describe the first case of a lethal abuse of liothyronine. The case was a 29-year-old male (BMI 32) without relevant illnesses. An autopsy was performed and followed by histological, toxicological, and clinical chemistry examinations. The autopsy revealed no relevant pathology. Histology showed multiple areas of focal cell necrosis in the myocardium and signs of acute heart failure including severe edema of the lungs; the follicles of the thyroid gland were markedly plump. Postmortem laboratory results indicated lethal liothyronine intoxication. Despite prevailing opinion, uncontrolled intake of liothyronine can cause lethal thyroid storm in a euthyroid patient without manifested cardiac illnesses.

Candida tropicalis Thyroiditis Presenting With Thyroid Storm in a Pediatric Patient With Acute Lymphocytic Leukemia.

Suppurative thyroiditis is uncommon in the pediatric population and particularly rare to be caused by fungi. We present a case of Candida tropicalis thyroiditis in an adolescent male with acute lymphocytic leukemia that led to disseminated candidiasis, thyroid storm and eventual total thyroidectomy for source control.

Thyrotoxicosis and thyroid storm.

Thyroid storm represents the extreme manifestation of thyrotoxicosis as a true endocrine emergency. Although Grave's disease is the most common underlying disorder in thyroid storm, there is usually a precipitating event or condition that transform the patient into life-threatening thyrotoxicosis. Treatment of thyroid storm involves decreasing new hormone synthesis, inhibiting the release of thyroid hormone, and blocking the peripheral effects of thyroid hormone. This multidrug, therapeutic approach uses thionamides, iodine, beta-adrenergic receptor antagonists, corticosteroids in certain circumstances, and supportive therapy. Certain conditions may warrant the use of alternative therapy with cholestyramine, lithium carbonate, or potassium perchlorate. After the critical illness of thyroid storm subsides, definitive treatment of the underlying thyrotoxicosis can be planned.

Management of thyrotoxic crisis.

The thyrotoxic crisis is a medical emergency caused by an exacerbation of the hyperthyroid state characterized by decompensation of one or more organ systems. Early recognition and aggressive treatment are fundamental in limiting the morbidity and mortality associated with this condition. The crisis has an abrupt onset, and is evoked by a precipitating factor such as infectious diseases, ketoacidosis, acute trauma, thyroidal surgery, 131-I radio-metabolic treatment, administration of iodine-containing materials (amiodarone), parturition. The clinical picture is characterized by four main features: fever, tachycardia or supraventricular arrhythmias, central nervous system symptoms and finally gastrointestinal symptoms. The diagnosis of thyrotoxic crises is often made on the basis of clinical findings alone, since it is difficult in most emergency departments to obtain rapid confirmatory laboratory or nuclear medicine tests. The ultrasound thyroid scan, if available in the emergency room, may suggest an hyperthyroid state showing typical images of Basedow's disease or nodular goiter with their characteristic color-Doppler pattern of hyperactivity, easily distinguishable from a normal gland. The principles of thyroid storm treatments are: reduction of circulating TH's levels; inhibition of the peripheral effects of circulating thyroid hormones (TH); supportive care, in order to reverse systemic decompensation and treatment of the underlying precipitating event.

[An autopsy case of sudden death due to hyperthyroidism].

A rare autopsy case of death due to thyroid crisis is reported. A 45-year-old lean woman with pigmentation of the skin was found dead at the seaside. The autopsy findings were as follows: The enlarged thyroid gland (35.5 g) had a histological finding of diffuse hyperplastic goiter (hyperthyroidism). The thymus (28.5 g) was enlarged and parenchymatous. The lymphocytes in the thymus and spleen were conspicuously proliferated, probably due to secondary adrenal cortex insufficiency. The adrenal cortex was slightly atrophic. Hemosiderin-laden macrophages in the lung, and centrilobular necrosis, microscopic bleeding, fibrosis, and nodular regenerative hyperplasia of the liver indicated the persisted heart failure. A small pericardial scar was found at the right ventricle of the heart (280 g), and the histological finding of the heart was only congestion. Acetone was detected in a relatively high concentration in the blood (72 micrograms/ml), urine (139 micrograms/ml), bile (32 micrograms/ml) and gastric contents (38 micrograms/g), probably due to metabolic disorder from thyroid crisis. In conclusion, the cause of death was diagnosed as sudden death due to thyroid crisis from hyperthyroidism.

[Thyroid crisis diagnosed on the basis of anatomic-pathologic examination]. / Przelom tarczycowy rozpoznany na podstawie badania anatomopatologicznego.

Graves-Basedow disease is the most common cause of hyperthyroidism. Rhabdomyolysis is occasionally associated with metabolic coma or severe electrolyte disturbances. We describe rhabdomyolysis accompany ing thyroid crisis. A 48-years old man admitted with hypovolemic shock developed rhabdomyolysis, congestive heart failure, hepatic failure and renal failure and then died. It is interesting that correct diagnosis was done on the basis of microscopic examination of specimens of the thyroid gland.

[Experience of surgical treatment of diffuse thyrotoxic goiter in children and teenagers]. / Dosvid khirurhichnoho likuvannia dyfuznoho tyreotoksychnoho zobu u ditei ta pidlitkiv.

Results of surgical treatment of 137 children, operated on for thyrotoxic goiter (TG) in 1989-2002 yrs were analyzed. Thyrotoxic ophthalmopathy was revealed in 86 (62.7%) patients, papillary carcinoma on background of diffuse TG--in 3 (2.1%). Subtotal resection of thyroid gland according to O. V. Nikolayev was performed in 99 (72.2%) patients, almost thyroidectomy--in 30 (21.8%), thyroidectomy--in 8 (5.8%). All the patients are alive. Bilateral affection of nervus laryngeus recurrens was not observed. Unilateral injury of nervus laryngeus recurrens was revealed in 5 (3.6%) childs. Transient hypoparathyrosis was noted in 20 (14.5%) patients. The TG recurrence had occurred in 5 (3.6%) childs, postoperative hypothyrosis--in 100 (72.9%).

Development of thyroid storm after surgical resection of a thyrotropin-secreting pituitary adenoma.

OBJECTIVE: To describe a patient with a thyrotropin-secreting pituitary adenoma in whom postoperative thyroid storm developed. METHODS: We present a case report with details of the initial presentation, laboratory evaluation, surgical and pathologic findings, and subsequent course in a patient with a thyrotropin (thyroid-stimulating hormone or TSH)-secreting adenoma and postoperative thyroid storm. RESULTS: An 18-year-old male patient presented with severe headaches and was found to have a large suprasellar tumor and a mildly elevated level of TSH. Thyroid storm developed immediately after surgical resection of the pituitary mass. Results of laboratory evaluation undertaken preoperatively became available after the patient had undergone the surgical procedure and revealed thyroid hormone levels 2 to 3 times the upper limit of normal. Propylthiouracil and beta-adrenergic blocking agents controlled the postoperative thyrotoxicosis and were subsequently discontinued as his TSH and thyroid hormone levels normalized. CONCLUSION: This case demonstrates the rare case of a TSH-secreting adenoma in a young patient, which was complicated by the development of postoperative thyroid storm. In addition, this case emphasizes the importance of preoperative pituitary hormonal evaluation and treatment of hormonal abnormalities in all patients presenting with sellar or suprasellar tumors.

Thyroid crisis following interstitial nephritis.

A 54-year-old man with Graves' disease had been treated with thiamazole (5 mg/day). His thyroid hormone level was increased after exodontia in February 2006. Although his prescribed dose of thiamazole was increased after exodontia on the fourth day, he developed thyroid crisis on exodontia 52 nd day. Laboratory findings also showed renal dysfunction (from Cr 1.0 mg/dL in July 2005 to Cr 1.8 mg/dL on exodontia 37th day). His thyroid hormone level was normalized after subtotal thyroidectomy; however, serum Cr level was still high. He was diagnosed with interstitial nephritis as a result of renal biopsy, and he was treated with prednisolone 30 mg/day. This present case developed thyroid crisis even though the quantity of thiamazole was increased after exodontia. It seems that interstitial nephritis, as well as exodontia, is an aggravation factor of thyroid function. After a poor response to anti-thyroid drugs, it is necessary to prevent thyroid crisis by determining the aggravating factor and to then provide appropriate treatment.

[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis].

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.

[Hypokalemic thyrotoxic periodic paralysis: a case report]. / Paralysie périodique hypokaliémique thyrotoxique: à propos d'un cas.

A 25-year-old Caucasian man is admitted to hospital because of severe hyperthyroidism. Soon after his admission, he develops a lower limbs proximal muscles paresis with tendinous hyporeflexia. He has presented similar episodes in the previous months. Serum potassium level is 2.9 meq/l whereas it was 4.1 meq/l a few hours before. The patient receives intravenous potassium and propranolol. He will not develop a similar episode afterwards. Hypokalemic thyrotoxic periodic paralysis associated with Basedow's disease is diagnosed. Hypokalemic thyrotoxic periodic paralysis is a very rare cause of intermittent muscular weakness in the young Caucasian male. The frequency of this entity is at least ten times higher in Asiatic hyperthyroid people. Its physiopathology involves intracellular potassium shifts in which Na/K ATP-ases of cell membranes, the number and the activity of which increase in hyperthyroid people, seem to play a major role. Treatment consists of correction of hyperthyroidism and administration of potassium during the acute episode Propranolol is efficient in preventing recurrent episodes of paralysis. Points of comparison between hypokalemic thyrotoxic periodic paralysis and hypokalemic familial periodic paralysis are discussed.

[Iodine-induced hyperthyroidism in metastatic thyroid carcinoma]. / Jodinduzierte Hyperthyreose bei metastasiertem Schilddrüsenkarzinom.

A 75-year-old man with nodular goitre (for the preceding 2 years treated with 75 micrograms/dl L-thyroxine) complained of pain over the left hip: on auscultation an arterial flow murmur was audible over the hip. The radiograph demonstrated extensive osteolysis in the flat part of the ilium. Search for the primary tumour, including two pelvic angiographs, was unsuccessful. Examination of a biopsy from the right ilium revealed a metastasis from a highly differentiated follicular thyroid carcinoma, which could not be demonstrated scintigraphically because of a reduced 99mTc-pertechnetate and 123I-iodine uptake, the result of the L-thyroxine administration. A thyrotoxic crisis occurred 2 days after the second angiography (free thyroxine 3.17 ng/dl, triiodothyronine 219 ng/dl, thyroglobulin > 250 ng/ml). Treatment with thiamazole (40 mg/d) and perchlorate (1 g/d) reduced the concentration of peripheral thyroid hormone, but the patient's general condition improved only slowly. As a result, radioiodine treatment could not be started until 9 months later. He died a further 9 months later from septicaemia originating from the metastasis.