KRISIS TIROID.pptx

7/21/2019 KRISIS TIROID.pptx

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KRISIS TIROID



THYROID STORM

• the clinical picture characteristic of TS is notrelated to thyroid hormone levels

• patients presenting with TS have a larger

amount of catecholamine inding sitesui!uitously than hyperthyroid su"ects who donot develop it

• larger availaility of adrenergic receptors and a

reduction of thyroid hormone inding to T#$• lea% of catecholamine provo%ed y an acute

event &i'e'( triggering factor) *nally precipitates TS



T+R,-I



• fever proportion to an apparentinfection and dramatic diaphoresis

• Hyperthermia in thyroid crisis canrepresent defective thermoregulationy the hypothalamus and.orincreased asal metaolic rate(

increased o/idation of lipids eingresponsile for more than 012 of theresting energy e/penditure



3,4T54$ D,4 -,R56-,R5

• , high6output state is present( attriutaleto the increased preload secondary toactivation of the renin6angiotensin6

aldosterone a/is and to decreased afterloadsecondary to a direct rela/ing e7ect ofthyroid hormones on vascular muscle cells'

• most patients present with systolic

hypertension with widened pulse pressure'• dyspnea and tachypnea related to an

increased o/ygen demand'



-+48+R4,,4• diarrhea and vomiting can aggravate volume

depletion( postural hypotension( and shock withvascular collapse'

• The di7use adominal pain( possily caused y

impaired neurohormonal regulation of gastricmyoelectrical activity with delayed gastricemptying may even lead to a presentation suchas acute adomen or intestinal ostruction'

• The liver function anormalities and presence of "aundice warrant immediate and vigoroustherapy'

•



+9+KTRO9IT

• Increased serum calcium levels( caused y othhemoconcentration and %nown e7ects of thyroidhormone on one resorption &TSH may e a directnegative regulator of one turnover acting via the TSH

receptor on oth osteolasts and osteoclasts' Thus( TSH de*ciency could e partly responsile for thes%eletal loss seen in thyroto/icosis)

• The sodium( potassium( and chloride levels are usuallynormal'

• #ecause of the augmented lipolysis and %etogenesis(and the asal metaolic demands that e/ceed o/ygendelivery( %etoacidosis and lactic acidosis may occur'



$I43,9

• Hyperthyroidism is often associated with anaccelerated glomerular fltration rate(which may progress to glomerulosclerosis ande/cessive proteinuria'

• Renal failure may e caused y rhadomyolysis

• 5rinary retention associated with dyssynergy ofthe detrusor muscle and ladder dysfunction

and an autoimmune comple/:mediatednephritis concomitant with $raves disease'



H+M,TO9O$I

• , moderate leukocytosis with a mild shift to the leftis a common *nding( even in the asence of infection'

• Hyperthyroidism may e associated withhypercoagulaility caused y increased concentrations

of *rinogen( factors ;III and I<( tissue plasminogenactivator inhiitor =( von >illerand factor

• Increase in red lood cell mass secondary toerythropoietin upregulation( and a tendency toaugmented platelet plug formation'

• Ma"or thromoemolic complications are responsilefor =?2 of deaths caused y thyroto/icosis'



• serum total T@ levels may e even within normallimits( as these patients may have someunderlying precipitating illness that reduces TA to T@ conversion as is seen in the euthyroid sic%

syndrome'• Hepatic dysfunction in thyroid storm results in

elevated levels of serum lactate dehydrogenase(aspartate aminotransferase( and iliruin'

Increased levels of serum al%aline phosphatase arealso oserved( predominantly ecause ofincreased osteolastic one activity in response tothe augmentation of one resorption'



• >hen thyroto/icosis is prolonged( leading to thedepletion of glycogen deposits( hypoglycemiamay occur

• ,drenal reserve may e e/ceeded in thyroto/iccrisis ecause of the inaility of the adrenal glandto meet the metaolic demands and acceleratedturnover of glucocorticoids' Moreover( there is%nown coincidence of adrenal insuBciency with

$raves disease' This diagnosis should econsidered when there is hypotension andsuggestive electrolyte anormalities'



T+R,-I

• Cirst( speci*c antithyroid drugs must e used toreduce the increased thyroid production and releaseof TA and T@'

• The second approach comprises treatment intended

to loc% the e7ects of the remaining ut e/cessivecirculating concentrations of free TA and T@ in lood'

• The third arm involves treatment of any systemicdecompensation( for e/ample( congestive heart

failure'• The *nal component addresses any underlying

precipitating illness such as infection or %etoacidosis'



,4TITIROID

• Inhiition synthesis thionamide antithyroid drugs(such as carimaole( methimaole &Tapaole)( andpropylthiouracil &-T5)'

• $iven y nasogastric tue or per rectum as enemas or

suppositories• -T5 can e started with a loading dose of E11 to =111

mg followed y FE1 mg every A hours( and methimaoleshould e administered at daily dose of 01 to ?1 mg'

• -T5 will provide more rapid clinical improvement

ecause it has the additional advantage of inhiitingconversion of TA to T@( a property not shared ymethimaole



,4TITIROID

• Iodides may e given either orally as 9ugol solution or as asaturated solution of potassium iodide &@:E drops every 0 hours)'for intravenous use'

• It is important that iodine should e administered no sooner than =hour after prior thionamide dosage' Otherwise iodine will enhance

thyroid hormone synthesis( enrich hormone stores within the gland(and therey permit further e/aggeration of thyroto/icosis'

• >hen iodine is administered in con"unction with full doses ofantithyroid drugs( dramatic rapid decreases in serum TA are seen(with values approaching the normal range within A or E days

• ,lergi iodinG In patients who may e allergic to iodine( lithiumcaronate may e used as an alternative agent to inhiit hormonalrelease' 9ithium should e administered initially as @11 mg every 0hours( with suse!uent ad"ustment of dosage as necessary tomaintain serum lithium levels at aout 1'? to ='F m+!.9



R+HIDR,SI

• Cluid depletion caused y hyperpyre/ia and diaphoresis( aswell as y vomiting or diarrhea( must e vigorously replacedto avoid vascular collapse'

• ,ppropriate uid therapy will usually correct hypercalcemia(if present' 3udicious replacement of uids is necessary inelderly patients with congestive heart failure or other cardiaccompromise'

• Intravenous uids containing =12 de/trose in addition toelectrolytes will etter restore depleted hepatic glycogen'

• ;itamin supplements may e added to the intravenous uidsto replace proale coe/istent de*ciency'

• Hypotension not readily reversed y ade!uate hydration maytemporarily re!uire pressor and.or glucocorticoid therapy'



• -lasma or alumin solution givenduring therapeutic plasma e/changeprovides new inding sites to reduce

circulating levels of free thyroidhormones'

• +arly thyroidectomy has een

reported to reduce the mortality ratefrom F12 to A12 under standardtreatment to less than =12



• -ropranolol is the most commonly used agent' The oral dosage of01 to ?1 mg every A hours or intravenous doses of 1'E to = mgfollowed y suse!uent doses of F to @ mg given intravenouslyover =1 to =E min every several hours are recommended(alongside constant cardiac rhythm monitoring'

• -ropranolol also inhiit the conversion of TA to T@( ut asigni*cant e7ect is seen only with oral doses higher than =01mg.d'

• 5sage of loc%ers not only corrects the heart rate and diminishesthe o/ygen demand of the cardiac muscle( ut also improvesagitation( convulsions( psychotic ehavior( tremor( diarrhea( fever(and diaphoresis'

• ,sma G =6loc%ers or reserpine( guanethidine

• Short acting esmololinitial loading dose of 1'FE to 1'E mg.%g isfollowed y continuous infusion of 1'1E to 1'= mg.%g per minute'



• Hidro%ortison initial dose of @11 mghydrocortisone followed y =11 mgevery ? hours during the *rst FA to

@0 hours should e ade!uate menghamat %onversi TA men"adi T@



T+R,-I T+RH,D,- D+KOM-+4S,SI

SIST+MIK

• Cor fever( acetaminophen rather than salicylates is thepreferred antipyretic( ecause salicylates inhiit thyroidhormone inding and could increase free TA and T@(therey transiently worsening the thyroto/ic crisis'

•

Hyperthermia also responds well to e/ternal cooling withalcohol sponging( cooling lan%ets( and ice pac%s'

• Some investigators advocate the use of the s%eletalmuscle rela/ant dantrolene( ut signi*cant ris% associatedwith its use precludes routine recommendation'

• >hen present( congestive heart failure should e treatedroutinely' ,lthough less commonly used today( whendigo/in is used( larger than usual doses may e re!uiredecause of its increased turnover in the thyroto/ic state'



T+R,-I C,KTOR -+48+T5S

• #road6spectrum antiiotic coverageon an empiric asis may e re!uiredinitially while awaiting results of

cultures'

KRISIS TIROID.pptx

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