Treatment

Desired Outcomes

Therapeutic options for RICDs improve hemostasis via replacement of deficient blood coagulation factors while minimizing the development of immune tolerance.

Hemostatic levels should be maintained for the following conditions:

• Spontaneous bleeding—until bleeding stops.

• Major surgery—until incision site has healed.

Nonpharmacologic Therapy

Transfusional Therapies The primary treatment of RICDs is single-donor fi'esh-frozen plasma (FFP) that contains all coagulation factors. Disadvantages of FFP treatment include the risk of becoming volume overloaded, especially when repeated infusions are administered in order to improve and maintain hemostasis, risk of infections, and risk of inhibitor • development. PCCs licensed for the treatment of hemophilia B also contain significant levels of vitamin K-dependent factors and may be used off-label for treatment of RICD. Table 67-7 lists the recommended RICD treatment schedules in different clinical scenarios.

Pharmacologic Therapy

Less severe hemorrhages may be treated successfully with antifibrinolytic amino acids alone or in combination with factor replacement therapy. Tranexamic acid and amino-caproic acid may be administered IV or orally (for doses, see Pharmacologic Therapy for vWD).

Table 67-6 Clotting Factor Deficiency Characteristics

Factor

Inheritance

Estmiaied

DrfLciriH

pi|1«m

LibDulDry flbnDrmjïi Eïex

Scvcnl y and SIT» of Bltrciiiig

1

Aurinkvn.-ji domlrijni or recessive

Extremely lare

pnc4i>ng«t PT and tf'TT

M kl w mnrtmie umbilical iOifll iOond, and mucosal tract

v

Aurçivjmil ift^sfjç

lil.cw.w)

Plunged PT af-TT

mim ni modçraie mucttial h^i

vu

AuKKCfn.ll iCittiiut

ihjo.OOO

Prolonged i*T

MU m severe iinutoidi njti antr joint

x

Autosomal letcssiw

1:500jOOO

Prolonged PTdndrfT F

WilU to severe umbilical cord poind, and WuSilS

xi

Autosomal kttisM1

4*toi Askenaji Jews. tflticcwiii line

Prolonged aPTT

MW la mocJerjle poil traumatic blocking

XII

UnUnovm

unkjkwn

Prolonged jPTT

No Heeding

xiii

Autosomal recess«*?

Lew lhan iiJ-JOtKlt™

Noimal PT and al1! 1

Modoiate 1o severe urlxli.il cord, «VlracraniaLand joint blcodingt recurrent mfe ¡mpjiied vioimd hejiiny

i. iClivjwfl pi I rii I imomtwpli 5!in üme; PT. p<ipih(C*tiCifi (¡me.

i. iClivjwfl pi I rii I imomtwpli 5!in üme; PT. p<ipih(C*tiCifi (¡me.

Table 67-7 Treatment of Factor Deficiencies

F«ror Dflfldrnt

WjJcr iurjtry

iponinnfgui Bleeding

Htrng-mnk ltwlJ {unltj.'dL'i

î.frP: IS-JOmWtg

1. FfMi-ÄmUkfl

30-40

1. FIP ii-20 ml/hij

1, FFP: 15-JO m|_/1*j

li-iS

Vit

1. rfV*a: 15-30 mctf/kg CvLty 4-6 Iwuri

1 rF Via: 1S-30 incy/kg ever y IJ hours

10-20

X

I.PCC20-M units/kg Î.FTP; t5-30mukg

1. PC-C: 20-30 uniti/Vg J. fFP: 15-30 mL/kg

10-20

»

L FfP: 15-20 ml/kg

1 FFP; iS-20 mL/kg

10-20

kn

1. Pasbcvirlf«! plasm,i c oncentrate.

10-20 uriiivkü Î.Fffc IS-3ÛmL/kg XCryCCnxijDiwtell tnJ^pOf 10 kir)

1. Pasteufljed plasma concentrate.

10-20 urpitsflKj ¡. IÏP: 15-30 ml/kg i. cryc(*«N>uw-n twç ptr so kgû

3-5

'Thç liomoMalfc level repf««HI the lOweil iu"scefflr,ti<*h<ji(.utiyUtdrkifi ijtCor to juHain no"rnjl héttMsIâïK Pjlients undergoing major iimi^iyoi r-Kfu'M¡fr>'iiKI Mjnifir.Wii lUiH-tliivi ^htulcl achieve tmpliM f.iitm Invph than are minimally rrtjuiied (en mïm.il hemosiiiK

Number* iivlK-aie lny^iif therapy. ff f. fre^h-iitnen F1'*"™: FOC, pwttmomb&i «jqtptei cçjnceratalei-

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