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Adrenal and Thyroid Diseases ( seen in acutely ill patients)

Adrenal and Thyroid Diseases ( seen in acutely ill patients). January, 2010 Deepika Reddy, md. Case 1.

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Adrenal and Thyroid Diseases ( seen in acutely ill patients)

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  1. Adrenal and Thyroid Diseases( seen in acutely ill patients) January, 2010 Deepika Reddy, md

  2. Case 1 • The patient is a 22 year with no prior medical history. About 6 weeks prior to coming to the ER she started to have palpitations, tremors and diarrhea. She also reports 25 lb weight loss over the past 2 months. She presented to the emergency room with, nausea/vomiting and abdominal pain. • She also complained of an inability to catch her breath • She vomited 10 times in 24 hours

  3. Case 1 • On physical exam, her temp was 101.5 F. Her HR was 120. BP 130/90 • She was thin, skin was warm to touch. Mild bilateral proptosis • Thyroid was diffusely enlarged, soft, no nodules • Heart: tachycardic but regular, no murmurs. • Lungs CTA, no crackles, no wheezes • Abdomen: minimal discomfort on abdomen palpation, not localized • Ext: mild edema, tremors of hands

  4. Case 1 • Labs’: TSH was undetectable • FT4 : 7.72 (.76-1.46) • WBC 3.2, Hgb 11.4 • LFTs normal

  5. Signs and symptoms of Thyrotoxicosis • Neuropsychiatric/Neuromuscular Emotional lability • Anxiety • Confusion • Coma • Muscle wasting • Hyperreflexia • Fine tremor • Periodic paralysis • Gastrointestinal • Diarrhea • Reproductive Oligomenorrhea • Decreased libido • Gynecomastia • Spider angiomas • Thyroid gland Neck fullness • Tenderness • Diffuse enlargement • Bruit

  6. Signs and symptoms of Thyrotoxicosis • Cardiorespiratory Palpitations • Dyspnea • Chest pain • Atrial fibrillation • Sinus tachycardia • Hyperdynamicprecordium • Congestive heart failure • Dermatologic • Hair loss • Pretibialmyxedema • Warm, moist skin • Palmarerythema • Ophthalmologic Diplopia • Eye irritation • Exophthalmos • Ophthalmoplegia • Conjunctival injection • NOTE: Elderly patients may not have the classic symptoms: Apathetic hyperthyroidism

  7. Lab Findings in Thyrotoxicosis • Hyperglycemia (catecholamines reduce insulin secretion) • Hypercalcemia ( due to dehydration, increased bone resorption) • Increased LFTs • Increased alkaline phosphatase

  8. Diagnostic Criteria for Thyroid Storm • Thermoregulatory dysfunction • Temperature • 99–99.9 5 • 100–100.9 10 • 101–101.9 15 • 102–102.9 20 • 103–103.9 25 • R104.0 30 • Central nervous system effects • Absent 0 • Mild (agitation) 10 • Moderate (delirium, psychosis, extreme lethargy 20 • Severe (seizures, coma) 30 • Gastrointestinal-hepatic dysfunction • Absent 0 • Moderate (diarrhea, nausea/vomiting, abdominal pain) 10 • Severe (unexplained jaundice) 20

  9. Diagnostic Criteria for Thyroid Storm • Cardiovascular dysfunction • Tachycardia (beats/minute) • 90–109 5 • 110–119 10 • 120–129 15 • R140 25 • Congestive heart failure • Absent 0 • Mild (pedal edema) 5 • Moderate (bibasilar rales) 10 • Severe (pulmonary edema) 15 • Atrial fibrillation • Absent 0 • Present 10 • Precipitating event • Absent 0 • Present 10

  10. Diagnostic Criteria for Thyroid Storm • Scoring system: A score of 45 or greater is highly suggestive of thyroid storm; a score of 25–44 is suggestive of impending storm, and a score below 25 is unlikely to represent thyroid storm. • Endocrinol Metab Clin N Am 35 (2006) 663–686

  11. Management: General Plan • Stop synthesis of new hormone within the thyroid gland (anti thyroid drug ATD) • Halt the release of stored thyroid hormone from the thyroid gland ( iodide such as SSKI) • Prevent conversion of T4 to T3 (ATD, beta blocker, steroids) • Control the adrenergic symptoms associated with thyrotoxicosis (beta blocker) • Control systemic decompensation with supportive therapy (steroids, acetominophen)

  12. Decreased Synthesis of Thyroid hormone: Anti thyroid Medication • WHICH ONE IS BETTER? • PTU • It is a Thiouracil: reduces synthesis of hormone and reduces T4 to T3 conversion • Short half life • Associated with hepatitis and increased risk of hepatic failure compared to methimazole . Onset of hepatic dysfunction variable and unpredictable • Also associated with agranulocytosis (0.37%) It is idiosyncratic and not dose related. • Can dose PO or rectally • In storm, start at 200-300mg q6 hrs. • The drug of choice in pregnancy.

  13. Decreased Synthesis of Thyroid hormone: Anti thyroid Medication • Methimazole • Is an imidazole: decreases synthesis of thyroid hormone • Longer half life • Associated with hepatic dysfunction which is usually cholestatic. Onset is variable and unpredictable • Also see agranulocytosis (0.35%). It is dose dependent and rarely seen in doses less than 40 mg a day. • Can dose PO, rectally or IV • In storm can give 80 – 100 mg a day in divided doses.

  14. Halt Release of Stored Hormone from the Thyroid: IODIDE • Can be given in the form of Super Saturated Potassium Iodide (SSKI) or Lugols Solution • Lugols 4-8 drops q6-8 hrs • SSKI 5 drops q6 hrs • HAS TO BE GIVEN AFTER THE ATD • Wait at least 1 hour • Max effect 7-14 days, if no other Rx given patients will get toxic again in this time frame.

  15. Block Conversion from T4 to T3 • ATD (PTU) • Beta Blockers • Glucocorticoids • Glucocorticoids also treat relative adrenal insufficiency • Typically hydrocortisone 100 mg q8hrs • If patient is elderly and worried about fluid retension may try Decadron 2 mg IV q6 hrs

  16. Control Adrenergic Symptoms • Beta Blockers • Traditionally propranalol used. • Large doses may be required. Start at 40mg q8 hours titrate up to keep HR in 80’s • Can use Esmolol, atenolol, metoprolol as well

  17. Other agents • LITHIUM can be used if ATD allergy is encountered and surgery not an option • It reduces formation and release of thyroid hormone • Dose in thyroid storm 300 mg q8 hrs • Need to check Lithium levels and keep level between 0.6 – 1.0 • CHOLESTYRAMINE : Reduces Thyroid hormone absorption from gut. • It can affect absorption of other medications

  18. Supportive Care • Avoid salicylates: they cause decreased binding of thyroid hormones to proteins. • In atrial fibrillation, may need warfarin. If already on warfarin, may need to reduce dose due to increased clearance of Vit k dependent clotting factors.

  19. Case 1 continued • The patient was started on ATD, SSKI, beta blockers, steroids • On day 3, she was noted to have a significant drop in WBC count specifically a drop in granulocyte percentage. • Surgery was consulted since she was still symptomatic. She was taken to the OR and had a sub total thyroidectomy

  20. Surgical Option • When rapid control of thyrotoxicosis is required • When patients have allergies/side effects to ATD and need surgical intervention for thyrotoxicosis • Patients should be prepared with ATD ( if tolerated, iodide, steroids and beta blockers)

  21. Case 2 • The patient is a 33 year old African American patient with a past history of hypothyroidism presented with increasing lethargy and confusion reported by family. She had missed a clinic visit and did not get her thyroid medication refilled. She had been off levothyroxine for 4 months. She was seen about 5 months ago, at which point her TSH was 42, F T4 was .2 • Now her TSH is 55 and FT4 is .23 • She has had weight gain 37 lbs in six months, constipation, cold intolerance, amenorrhea for over a year. She recently had a URI. She has sleep apnea and was using her CPAP machine

  22. Case 2 • Physical • BP 112/70, HR 64, Temp 96.5 • Gen: Lethargic but arousable • HEENT: skin / hair dry, Periorbital edema, facial swelling. Significant swelling of the tongue, she did not completely close her mouth because of macroglossia • Lung: Good air movement in all lung fields • Heart: Slow normal in rate, regular • Abd: Obese, few BS, non tender • Ext: swelling of lower extremities • Neuro: drowsy but arousable, answering questions appropriately.

  23. Labs • ABG showed hypoxia and hypercapnea • Chemistry panel showed low glucose of 67 and • Sodium was 129

  24. Clinical Features of Myxedema • Lethargy and confusion • Hypothermia • Bradycardia • Reduced cardiac contractility • Hypotension • Hypoxia/ hypercapnia due to reduced respiratory drive • Nausea/abdominal pain/reduced gastric motility • Electrolyte abnormalities : hyponatremia, Hyperkalemia

  25. Management • Mortality rates high • Should be in ICU setting • Assess airway , May need mechanical ventilation. • Dextrose and fluid resuscitation since may be hypovolemic • Steroids should be considered especially if hypotensive • May need hypertonic saline and lasix if hyponatremia severe • Hypothermia should be corrected carefully since it may result in hypotension. • Also evaluate carefully for precipitating event such as infection/ischemia

  26. Management • Thyroid hormone replacement critical. • Some controversy over the way in which to replace the thyroid hormone • Some recommend large loading dose of T4 300-500 mcg IV followed by 50-100mcg daily IV • Use lower doses in the elderly with cardiovascular disease • Some suggest that the T4 to T3 conversion is impaired in the severely ill. They suggest T3 IV upto 20 mcg, the 2.5 -5 q6 hrs

  27. Management • Can switch to PO levothyroxine after the patient has a bowel movement. • Extubate only when patient has shown significant improvement. Wait till patient regains conciousness. • Monitor closely till vitals, cardio-respiratory status, neurologic and GI symptoms improve.

  28. Case 2 • Our patient was watched in the progressive care unit • On Bipap for her respiratory difficulties • Given ‘loading dose’ of 200 mcg of Levothyroxine IV. Then 100 mcg a day IV till she had a bowel movement then switched to a weight based dose ( 1.5 x weight in KG) Received dextrose, IVF. • Clinically improved over the next 3-4 days

  29. Case 3 • A 78 year old gentleman presented to the ER with N/V , loose stool, confusion over 24 hrs. In ER noted to have hypotension 70/50. • Relevant past history: Has had a GH secreting pituitary macroadenomaresected 30 years earlier. He was on Pred 5 mg a day. He had recent ( 2 weeks ago ) been to the dentist who noted he had an oral infection and given him and antibiotic. About 2 days prior to admission he started to have loose stool and over 24 hr had the rest of symptoms develop. He had not changed his does of steroid during this time • Labs: mild hypoglycemia, hyponatremia and elevated WBC count.

  30. Case 3 • PE: BP 78/60, HR 115 Temp 101.3 sats OK • Gen : Confused, not oriented. Unable to get any history. • HEENT: pupils were reactive to light • Lungs: good air movement and clear to ausculatation • Cardiac : tachycardic no murmurs • Abd : distended, tender, mostly lower quadrants • Skin: dry, no hyperpigmentation • Rest of exam unremarkable.

  31. Who presents in adrenal crisis? • Patients with undiagnosed chronic adrenal insufficiency who have a ‘stressful event’ such as an infection. Or recent event such as bilateral adrenal hemorrhage • Patients with known primary adrenal insuffieciency who did not received adequate glucocorticoid replacement. Like this patient. • There are instances where patients with secondary adrenal insufficiency present in crisis such and pituitary infarction.

  32. Presenting features of adrenal crisis • Shock • Abdominal tenderness, N/V • Psychiatric manifestations: confusion, delirium, stupor • Fever • Hyperpigmentation, vitiligo, • Evidence of androgen deficiency in women with primary Adrenal insufficiency • Hypoglycemia ( more common in secondary adrenal insufficiency) • Electrolyte abnormalities • Primary low NA and high K • Secondary may have low Na due to vasopressin excess but K is usually normal

  33. Evaluation of adrenal function in a patient with hypotension • Evaluation of adrenal function (which test to use) • Does the patient have primary or secondary adrenal insufficiency? • Evaluation of etiology if diagnosis has been confirmed • Are there other medical issues that need to be treated • Long term management of adrenal insufficiency • Interpretation of the test (does the test work as well in acutely ill patients?)

  34. Evaluation • Before Evaluation, ensure patient is stable • If a patient is in shock treat with steroid early • Use Decadron since it does not interfere with the testing • Hydrocortisone interacts with cortisol assay and therefore should be avoided prior to testing

  35. Evaluation: ACTH Stim Test( Make sure this is done right!!) • Draw baseline ACTH and cortisol. Note the ACTH should be in a EDTA tube and kept on ice! • Then give Cosyntropin 250 mcg IV over 1 min • Draw cortisol 30 min and 60 min later • Interpretation: cortisol level of at least 18-20 at either 30-60 min indicates normal study • Note if the patient has been given ANY steroid this will affect ACTH levels

  36. Assess level of defect/Etiology • The ACTH level ( if done before any steroids are given) can help separate primary from secondary adrenal insufficiency. • In adrenal crises, treat first if testing non – diagnostic or equivocal. Can figure out level of defect once patient is stable • Look for clues : • History of head trauma/radiation • post partum : severe headache, hypotension: think sheehans • On anicoagulation: ? Bilateral adrenal hemorrage • Infections: such as HIV may have primary adrenal insufficiency • Evidence of other pituitary hormone deficiency can be done when patient is stable. • In our patient: insufficient steroid when ill

  37. Management • 1)Treat with IV glucocorticoid Decadrone 2-4 mg IV before the study, Hydrocortisone after the study 100 mg IV q8hrs • 2) Continue with IVF • 3) Look for etiology and treat as needed

  38. Case 3 • Rapid improvement in mental status and cardiovascular complaints after steroids were given. • He was diagnosed with toxic megacolon due to clostriduim difficile. • Was advised on increasing steroid doses when ill • 2-3 times normal daily dose. Decaron emergency Kit if he has N/V. ER if unable to control any other way.

  39. Special considerations in acutely ill patients(patients in septic shock) • A systemic review (Annane et al JAMA 2009, 301 (22) 2362-2375) demonstrated that glucocorticoids do not affect 28 day mortality in patient with sepsis (including those in shock) • A sub group analysis showed that low dose, longer duration of glucocorticoids may have mortality benefit

  40. Special considerations in acutely ill patients • The ACTH stimulation test may not reflect adrenal function in acutely ill patients since hypoproteinemia can affect total cortisol levels. • Current recommendations suggest that low dose glucocortcoids may be considered in patients with hypotension, on fluids and vasopressors who do not respond to these measures

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