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Case Presentation Mohd Al Shamsi

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Jan 19th 2010 …

Jan 19th 2010
Case Presentation By Mohd Al Shamsi

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  • 1. Mohammed Al-Shamsi R4
  • 2. • 40 years old Pakistani man • Referred from Quriat hospital with 7 days h/o lt sided body weakness and slurred speech and 1 day h/o fever , confusion and irritability • 5 days prior to presentation he was seen in private clinic and he was prescribed aspirin • He had GTC convulsion the night before
  • 3. HX PRIMARY SURVEY SECONDARY SURVEY A VITAL SIGNS HEAD & NECK Lt sided Weakness, convulsion RR 16/min Confusion. B SPO2 97% RESP CVS C HR 150/min ABD BP 140/60 HPC D Temp 38.4 CNS MSKS More history E RBS 5.8 SKIN AMPLE MONITER, O2, IV LINES, labs, ECG 24/11/2009
  • 4. Detailed History • Past history: • Drug history: • Family history: • Occupational history • Travel history: • Social history
  • 5. Secondary Survey  Head & Neck:  RESP: clear, no added sounds  CVS: 140/mit, irregular pulse, s1s2, no murmur  ABD: soft, no mass palpable, no tenderness, BS+  CNS: uncooperative for detailed examination. He Looks drowsy. No neck stiffness Power: lt side 4/5, rt side : normal Planters: withdrawal.. Pupils: equal and reactive.  MSKS; nad, no dvt or pedal edema  Skin: warm to touch,
  • 6. HX PRIMARY SURVEY SECONDARY SURVEY Lt A VITAL SIGNS HEAD & NECK RR 16/min B SPO2 97% RESP CVS C HR 150/min ABD BP 140/60 MORE HX D Temp 38.4 CNS HPC MSKS AMPLE E RBS 5.8 SKIN MONITER,O2, IV LINES, ECG DDX 24/11/2009
  • 7. HX PRIMARY SURVEY SECONDARY SURVEY A VITAL SIGNS HEAD & NECK RR 16/min B SPO2 97% RESP CVS C HR 150/min ABD BP 140/60 MORE HX D Temp 38.4 CNS HPC MSKS AMPLE E RBS 5.8 SKIN MONITER,O2, IV LINES, ECG DDX LAB RADIOLOGY RX DISPOSTION 24/11/2009
  • 8. Labs • CBC: Hg=15.3 g/dl, WCC=13.5 neutrophils= 10.7 , lymph= 2 Plt=297 • RFT: na=1137, K=4.4 , hco3=21, cl=104, urea=2.3, creatinine=54 • Coagulation: normal • Trop T : 0.01 ug/L • LFT: bil=54 umol/L , ALT= 28 , ALP: 214 , total protein: 62, albumin= 34
  • 9. • Blood culture: no growth • Urinalysis : normal. • TSH < 0.003 ( 0.3- 4.3) • Free T4 > 77.2 ( 8.4-22.6)
  • 10. • Chest x-ray: looks normal • Ct head: normal • Echo: Mildly dilated LV with global hypokinesia with severe LV dysfunction ( EF=30%) , small soft thrombus in LA extending from LAA, Mild MR, no Pericardial effusion. Impression: cardiomyopathy with LA clot.
  • 11. Treatment in ED • In Quriat: Phenrgan 25 mg , Diazepam 10 mg, Adenosine , inderal. • In ED: IVF: NS 500 ml Paracetamol 1 gm Diltiazem 12.5 mg iv slowly Ceftrixone 2 gm IV
  • 12. • Inpatient: PTU and lugols iodine propranolol LMWH Warfarin Lisinopril Digoxin Frusemide Spironolactone
  • 13. Thyroid Storm • Definitions:  Rare live- threatening exacerbation of hyperthyroidism  life-threatening decompensation of poorly controlled, untreated, or unrecognized thyrotoxicosis • Common in female, 2 % of thyrotoxic patients , occurs predominately in Graves’ disease. • Mortality : 20 % ( if aggressively treated) • Clinical diagnosis. • Patients typically appear markedly hypermetabolic with high fevers, tachycardia, nausea and vomiting, tremulousness, agitation, and psychosis. • Late in the progression of disease patients may become stuporous or comatose with hypotension
  • 14. Pathophysiology • Increase in catecholamine-binding sites+ acute stress • In conjunction with high levels of free T4 and T3. • Hormone levels in thyroid storm are not generally distinguishable from poorly controlled thyrotoxicosis. • Generally the case except in hyperthyroid patient with sudden cessation of antithyroid drugs and blunt or penetrating trauma to the thyroid gland in which hormone leaks from injured acini, rapid rises in T4 and T3
  • 15. Clinical features • Often Dramatic • Many findings of thyrotoxicosis are evident on exam but certain features distinguish thyroid storm. • Distinguished from thyrotoxicosis by the presence : 1- fever up to 40- 41 degree 2-marked tachycardia ( up to 150/min) 3-central nervous system dysfunction 4- gastrointestinal symptoms(Severe nausea, vomiting, or diarrhea, and hepatic failure with jaundice) 5-Decompensation of one or more organ systems, such as shock or heart failure
  • 16. • Altered mental status is a hallmark of thyroid storm, ranging from restlessness and agitation to delirium, psychosis, seizures, and coma. • Gastrointestinal symptoms are often pronounced and can lead to dehydration and hypotention • Abdominal pain can mimic bowel obstruction. • An unusual complication of severe thyrotoxicosis is cholestatic jaundice, which carries a bad prognosis if hepatic failure ensues
  • 17. Diagnostic criteria of thyroid storm A score of 45 or more is highly suggestive of thyroid storm; a score of 25 to 44 supports the diagnosis; and a score below 25 makes thyroid storm unlikely
  • 18. PRECIPITANTS OF THYROID STORM Medical Drug-Related • Infection/sepsis • Iodine-131 therapy • Cerebral vascular accident • Premature withdrawal of antithyroid • Myocardial infarction therapy • Congestive heart failure • Ingestion of thyroid hormone • Pulmonary embolism • Iodinated contrast agents • Visceral infarction • Amiodarone therapy • Emotional stress • Iodine ingestion • Acute manic crisis • Anesthesia induction Trauma • Miscellaneous drugs (chemotherapy, • Thyroid surgery pseudoephedrine, organophosphates, aspirin) • Nonthyroid surgery Pregnancy-Related • Blunt and penetrating trauma to the • Toxemia of pregnancy thyroid gland • Vigorous palpation of the thyroid gland • Hyperemesis gravidarum • Burns • Parturition and the immediate postpartum period Endocrine • Hypoglycemia • Diabetic ketoacidosis • Hyperosmolar nonketotic coma
  • 19. Precipitating factors  Aspirin can increase serum free T4 and T3 concentrations by interfering with protein binding  Can occur without any obvious precipitating factors in pt with long-standing untreated hyperthyroidism
  • 20. Differential Considerations • Bacterial meningitis, and sepsis. • Drug overdose:  sympathomimetic (cocaine, amphetamine) .  anticholinergic intoxication. • Withdrawal syndrome (alcohol, narcotics, sedative-hypnotics) • Heatstroke • Neuroleptic malignant syndrome, • Serotonin syndrome.
  • 21. • In elders, the hyperadrenergic features of thyrotoxicosis may be masked, facial muscles may lack expression, and mental status may be depressed leading to the syndrome of apathetic hyperthyroidism. Patients with multinodular goiters and those older than 70 are most likely to present in this manner. New-onset atrial fibrillation and congestive heart failure exacerbations are often the presenting symptoms of apathetic hyperthyroidism. In addition, elders with thyrotoxicosis may have significant weight loss without increased appetite, suggestive of occult cancer
  • 22. Diagnosis • Free T4 and free T3 elevation with TSH suppression . • Hyperglycemia : common, 50 % of patients, ( related to glycogenolysis and catecholamine-mediated antagonism of insulin) • Bone: Mild hypercalcemia is seen in 10% of patients (hormone-mediated bone resorption, osteoporosis ) • LFT: mild increases in serum AST, ALT, bilirubin, and, most commonly ALP . • CBC: leukocytosis with a left shift, a mild normocytic normochromic anemia.
  • 23. Treatment 1-supportive care 2-Specific treatment 3-Treatment of underlying precipitating factors • The same principles of treatment are more often applied to patients with severe hyperthyroidism who do not fully meet the criteria for thyroid storm
  • 24. General Supportive Measures • critical to final outcome • Aggressive Volume resuscitation and replacement of glycogen stores(D5/0.9NS 125–1000 mL/hr depending on volume status and CHF) • Some pts may require diuresis because of congestive heart failure • Tylenol with caution( hepatic dysfunction) , avoid aspirin and NSAID. • Cooling blanket, fans, ice packs, ice lavage • Benzodiazepines for agitation and hypomania
  • 25. • Avoid interventions that may increase thyroid hormone levels or accentuate adrenergic stimuli .  iodinated contrast media or amiodarone, both of which present an iodine load that may enhance thyroid hormone production.  aspirin and NSAIDS( interfere with protein binding of thyroid hormone, leading to increases in free T4 and T3.)  Drugs such as pseudoephedrine, ketamine, and albuterol that increase sympathomimetic.
  • 26. Specific Treatment • Consists of multiple medications each of which has a different mechanism of action: 1-A beta-blocker to control the symptoms induced by increased adrenergic tone. 2-A thionamide, such as methimazole , to block new hormone synthesis. 3-An iodinated radiocontrast agent (if available) to inhibit the peripheral conversion of T4 to T3. 4-An iodine solution to block the release of thyroid hormone. 5- Glucocorticoids: to reduce T4-to-T3 conversion and possibly treat the autoimmune process in Graves' disease.
  • 27. Beta Blockers • Important aspect in treatment • Block the peripheral hyperadrenergic activity • Propranolol : drug of choice [ it also blocks conversion of T4 to T3] • Used with caution if the patient has congestive heart failure or other contraindications to beta-blockade. • However , that control of tachycardia may lead to improvement in cardiac function.
  • 28. • Propanolol PO: 60−80 mg PO every 6 hr or IV: 1.0 mg IV slow push test dose, then repeat q15 min to desired effect ( up to 5 mg) then 2– 3 mg every 3 hr • Metoprolol 50 mg PO every 6 to 12 hr • Esmolol :250–500 µg/kg bolus, then 50– 100 µg/kg/min infusion • Strict contraindication to beta-blocker: reserpine 0.5 mg PO every 6 hr
  • 29. Thionamide • Propylthiouracil, methimazole, carbimazole. • Block de novo thyroid hormone synthesis within 1-2 hours. • No effect on the release of preformed hormone. • Some consider PTU the drug of choice in thyroid storm, because PTU blocks T4-to-T3 conversion in the periphery. • However, we prefer methimazole as long as other drugs (such as iopanoic acid) are coadministered to block T4-to- T3 conversion. • Methimazole has a longer duration of action( 4h) than PTU(75 min) and is therefore more effective unless PTU is given at regular frequent intervals. • Since thionamide therapy may be interrupted, even in an ICU, we prefer to use the longer-acting drug
  • 30. • High dose. • Can be given PO , PR, IV • IV route should be considered only IF oral or rectal administration is not feasible or ineffective • Propylthiouracil: 600–1000 mg loading dose, then 200– 250 mg every 4 hr • Methimazole 20–25 mg initially, then 20–25 mg every 4 hr • No READY MADE IV preparation . • PTU can be prepared for IV administration by dissolving the tablets in isotonic saline made alkaline (pH 9.25) with sodium hydroxide, • Methimazole can be dissolved in pH-neutral isotonic saline and prepared for intravenous administration by filtering through a Millipore filter and and given 30 mg every 6 hr
  • 31. Iodinated radiocontrast agents • Iopanoic acid and other iodinated radiocontrast agents used for oral cholecystography have been used to treat hyperthyroidism • Little published data on their efficacy in thyroid storm. • Potent inhibitors of T4-to-T3 conversion. • extremely useful in treating severe hyperthyroidism or in preparing hyperthyroid patients for urgent surgery • In severe hyperthyroidism : 0.5 to 1 g given OD. • Given 1-2 h after thionamide
  • 32. Iodine • Blocks the release of T4 and T3 from the gland. • higher than usual dose. • Given 1-2 after thionamide • It has been suggested that 10 drops of Lugol's solution can be directly added to intravenous fluids since it is sterile .
  • 33. • Doses and routes: Saturated solution of potassium iodide (SSKI) 5 gtt by mouth, NG, or PR every 6 hr Lugol's solution 8 gtt by mouth, NG, or PR every 6 hr Sodium Iodide 500 mg in solution prepared by pharmacy IV every 12 hr
  • 34. Glucocorticoids • Importance: 1. Reduce T4-to-T3 conversion ( main action) 2. It also block the hormone release. 3. Relative adrenal insufficiency that can occur in thyroid storm 4. May have a direct effect on the underlying autoimmune process if the thyroid storm is due to Graves' disease. • It improves outcome . • Hydrocortisone 300 mg IV, followed by 100 mg every 6 hr Or • Dexamethasone 2–4 mg IV every 6 hr • Not routinely use in patients with severe, but not life-threatening, hyperthyroidism.
  • 35. Other Therapies • Lithium has also been given to acutely block the release of thyroid hormone. • its renal and neurologic toxicity limit its utility. • Used if the patient is allergic to iodine, • lithium carbonate 300 mg by mouth or NG every 6 hr • Cholestyramine, an anion exchange resin, binds thyroid hormone in the bowel lumen, thus interrupting enterohepatic recirculation • L-Carnitine has been described in thyroid storm, its suggested mechanism being the inhibition of thyroid hormone entry into cell nuclei • Plasmapheresis, plasma exchange, or dialysis has been tried when traditional therapy has not been successful
  • 36. Congestive Heart failure. If rate-related, high-output failure • Beta-blockade is first-line therapy • ACEI, digoxin, diuretics as needed If depressed EF • Avoid beta-blocker or 1/4 dose • ACEI if BP adequate • Digoxin and furosemide as needed
  • 37. AF • Beta-blocker preferred for rate control. • Calcium channel blockers: can cause hypotension; diltiazem 10-mg test dose. Avoid verapamil • Digoxin less effective but may be tried • Amiodarone should be avoided due to iodine load • Refractory to conversion to sinus unless euthyroid first
  • 38. Identifying and Treating the Precipitating Event • CXR, urinalysis, and blood cultures • ECG and troponin • antibiotics