Presentation on theme: "Adrenal and Thyroid Diseases ( seen in acutely ill patients)"— Presentation transcript:
1Adrenal and Thyroid Diseases ( seen in acutely ill patients) January, 2010Deepika Reddy, md
2Case 1The 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 breathShe vomited 10 times in 24 hours
3Case 1On physical exam, her temp was F. Her HR was 120. BP 130/90She was thin, skin was warm to touch. Mild bilateral proptosisThyroid was diffusely enlarged, soft, no nodulesHeart: tachycardic but regular, no murmurs.Lungs CTA, no crackles, no wheezesAbdomen: minimal discomfort on abdomen palpation, not localizedExt: mild edema, tremors of hands
4Case 1 Labs’: TSH was undetectable FT4 : 7.72 (.76-1.46) WBC 3.2, Hgb 11.4LFTs normal
5Signs and symptoms of Thyrotoxicosis Neuropsychiatric/Neuromuscular Emotional labilityAnxietyConfusionComaMuscle wastingHyperreflexiaFine tremorPeriodic paralysisGastrointestinalDiarrheaReproductive OligomenorrheaDecreased libidoGynecomastiaSpider angiomasThyroid gland Neck fullnessTendernessDiffuse enlargementBruit
6Signs and symptoms of Thyrotoxicosis Cardiorespiratory PalpitationsDyspneaChest painAtrial fibrillationSinus tachycardiaHyperdynamic precordiumCongestive heart failureDermatologicHair lossPretibial myxedemaWarm, moist skinPalmar erythemaOphthalmologic DiplopiaEye irritationExophthalmosOphthalmoplegiaConjunctival injectionNOTE: Elderly patients may not have the classic symptoms: Apathetic hyperthyroidism
7Lab Findings in Thyrotoxicosis Hyperglycemia (catecholamines reduce insulin secretion)Hypercalcemia ( due to dehydration, increased bone resorption)Increased LFTsIncreased alkaline phosphatase
10Diagnostic 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
11Management: General Plan Stop synthesis of new hormone within the thyroidgland (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 withsupportive therapy (steroids, acetominophen)
12Decreased Synthesis of Thyroid hormone: Anti thyroid Medication WHICH ONE IS BETTER?PTUIt is a Thiouracil: reduces synthesis of hormone and reduces T4 to T3 conversionShort half lifeAssociated with hepatitis and increased risk of hepatic failure compared to methimazole . Onset of hepatic dysfunction variable and unpredictableAlso associated with agranulocytosis (0.37%) It is idiosyncratic and not dose related.Can dose PO or rectallyIn storm, start at mg q6 hrs.The drug of choice in pregnancy.
13Decreased Synthesis of Thyroid hormone: Anti thyroid Medication MethimazoleIs an imidazole: decreases synthesis of thyroid hormoneLonger half lifeAssociated with hepatic dysfunction which is usually cholestatic. Onset is variable and unpredictableAlso see agranulocytosis (0.35%). It is dose dependent and rarely seen in doses less than 40 mg a day.Can dose PO, rectally or IVIn storm can give 80 – 100 mg a day in divided doses.
14Halt Release of Stored Hormone from the Thyroid: IODIDE Can be given in the form of Super Saturated Potassium Iodide (SSKI) or Lugols SolutionLugols 4-8 drops q6-8 hrsSSKI 5 drops q6 hrsHAS TO BE GIVEN AFTER THE ATDWait at least 1 hourMax effect 7-14 days, if no other Rx given patients will get toxic again in this time frame.
15Block Conversion from T4 to T3 ATD (PTU)Beta BlockersGlucocorticoidsGlucocorticoids also treat relative adrenal insufficiencyTypically hydrocortisone 100 mg q8hrsIf patient is elderly and worried about fluid retension may try Decadron 2 mg IV q6 hrs
16Control Adrenergic Symptoms Beta BlockersTraditionally propranalol used.Large doses may be required. Start at 40mg q8 hours titrate up to keep HR in 80’sCan use Esmolol, atenolol, metoprolol as well
17Other agentsLITHIUM can be used if ATD allergy is encountered and surgery not an optionIt reduces formation and release of thyroid hormoneDose in thyroid storm 300 mg q8 hrsNeed to check Lithium levels and keep level between 0.6 – 1.0CHOLESTYRAMINE : Reduces Thyroid hormone absorption from gut.It can affect absorption of other medications
18Supportive CareAvoid 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.
19Case 1 continuedThe patient was started on ATD, SSKI, beta blockers, steroidsOn 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
20Surgical Option When rapid control of thyrotoxicosis is required When patients have allergies/side effects to ATD and need surgical intervention for thyrotoxicosisPatients should be prepared with ATD ( if tolerated, iodide, steroids and beta blockers)
21Case 2The 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 .2Now her TSH is 55 and FT4 is .23She 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
22Case 2 Physical BP 112/70, HR 64, Temp 96.5 Gen: Lethargic but arousableHEENT: skin / hair dry, Periorbital edema, facial swelling. Significant swelling of the tongue, she did not completely close her mouth because of macroglossiaLung: Good air movement in all lung fieldsHeart: Slow normal in rate, regularAbd: Obese, few BS, non tenderExt: swelling of lower extremitiesNeuro: drowsy but arousable, answering questions appropriately.
23Labs ABG showed hypoxia and hypercapnea Chemistry panel showed low glucose of 67 andSodium was 129
24Clinical Features of Myxedema Lethargy and confusionHypothermiaBradycardiaReduced cardiac contractilityHypotensionHypoxia/ hypercapnia due to reduced respiratory driveNausea/abdominal pain/reduced gastric motilityElectrolyte abnormalities : hyponatremia, Hyperkalemia
25Management Mortality rates high Should be in ICU setting Assess airway , May need mechanical ventilation.Dextrose and fluid resuscitation since may be hypovolemicSteroids should be considered especially if hypotensiveMay need hypertonic saline and lasix if hyponatremia severeHypothermia should be corrected carefully since it may result in hypotension.Also evaluate carefully for precipitating event such as infection/ischemia
26Management Thyroid hormone replacement critical. Some controversy over the way in which to replace the thyroid hormoneSome recommend large loading dose of T mcg IV followed by mcg daily IVUse lower doses in the elderly with cardiovascular diseaseSome suggest that the T4 to T3 conversion is impaired in the severely ill. They suggest T3 IV upto 20 mcg, the q6 hrs
27ManagementCan 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.
28Case 2 Our patient was watched in the progressive care unit On Bipap for her respiratory difficultiesGiven ‘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
29Case 3A 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 macroadenoma resected 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 timeLabs: mild hypoglycemia, hyponatremia and elevated WBC count.
30Case 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 lightLungs: good air movement and clear to ausculatationCardiac : tachycardic no murmursAbd : distended, tender, mostly lower quadrantsSkin: dry, no hyperpigmentationRest of exam unremarkable.
31Who 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 hemorrhagePatients 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.
32Presenting features of adrenal crisis ShockAbdominal tenderness, N/VPsychiatric manifestations: confusion, delirium, stuporFeverHyperpigmentation, vitiligo,Evidence of androgen deficiency in women with primary Adrenal insufficiencyHypoglycemia ( more common in secondary adrenal insufficiency)Electrolyte abnormalitiesPrimary low NA and high KSecondary may have low Na due to vasopressin excess but K is usually normal
33Evaluation 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 confirmedAre there other medical issues that need to be treatedLong term management of adrenal insufficiencyInterpretation of the test (does the test work as well in acutely ill patients?)
34Evaluation Before Evaluation, ensure patient is stable If a patient is in shock treat with steroid earlyUse Decadron since it does not interfere with the testingHydrocortisone interacts with cortisol assay and therefore should be avoided prior to testing
35Evaluation: 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 minDraw cortisol 30 min and 60 min laterInterpretation: cortisol level of at least at either min indicates normal studyNote if the patient has been given ANY steroid this will affect ACTH levels
36Assess 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 stableLook for clues :History of head trauma/radiationpost partum : severe headache, hypotension: think sheehansOn anicoagulation: ? Bilateral adrenal hemorrageInfections: such as HIV may have primary adrenal insufficiencyEvidence of other pituitary hormone deficiency can be done when patient is stable.In our patient: insufficient steroid when ill
37Management1)Treat with IV glucocorticoid Decadrone 2-4 mg IV before the study, Hydrocortisone after the study 100 mg IV q8hrs2) Continue with IVF3) Look for etiology and treat as needed
38Case 3Rapid 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 ill2-3 times normal daily dose. Decaron emergency Kit if he has N/V. ER if unable to control any other way.
39Special considerations in acutely ill patients (patients in septic shock) A systemic review (Annane et al JAMA 2009, 301 (22) ) 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
40Special 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