the perioperative medicine consult handbook || postoperative thrombocytopenia
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175
X
Chapter 25
Postoperative Thrombocytopenia
Elizabeth Kaplan
BACKGROUND Common hematologic abnormality after major surgery, ■
although actual incidence not reported in literature [ 1 ] . De fi ned as platelet count <150,000. Generally, platelets >50,000 ■
are not associated with signi fi cant bleeding. Spontaneous bleeding usually does not occur with platelets >20,000.
EVALUATION ■ History : Review medications (e.g., heparin), transfusion his-tory, symptoms of infection, symptoms/history of liver disease. ■ Exam : Assess for infection, splenomegaly, signs of liver disease, evidence of thrombosis. ■ Differential diagnosis : Degree of thrombocytopenia is useful in helping to determine etiology, as shown in Table 25.1 . Other etiologies not speci fi c to the postoperative setting should also always be considered including ITP, sequestration, and malig-nancy-associated. ■ Labs : Consider the following studies; however send only those that are appropriate to the clinical situation: CBC, reticulocyte, haptoglobin, PT/PTT/INR, fi brinogen and peripheral smear, and heparin-induced thrombocytopenia (HIT) panel. ■ Consultation : Consider hematology consult if no obvious etiol-ogy is found or if levels are low enough that platelet transfusion is considered. ■ Treatment : Platelet transfusions are usually indicated only for platelets <10,000 or <50,000 with active bleeding—important to discuss with the surgical team. Intramuscular injections
C.J. Wong and N.P. Hamlin (eds.), The Perioperative Medicine Consult Handbook, DOI 10.1007/978-1-4614-3220-3_25, © Springer Science+Business Media New York 2013
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176 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK
TA
BL
E 2
5.1
POT
ENT
IAL
ETIO
LOG
IES
OF
POST
OPE
RAT
IVE
TH
ROM
BOC
YTO
PEN
IA
Pla
tele
t de
crea
se
Eti
olo
gy
Des
crip
tio
n
Mil
d–m
oder
ate
Con
sum
pti
on
See
n i
n la
rger
blo
od lo
ss s
urg
erie
s O
ccu
rs i
mm
edia
tely
aft
er s
urg
ery
Ret
urn
s to
war
d n
orm
al w
ith
in 2
–3 d
ays
Th
rom
boc
ytop
enia
du
e to
in
fect
ion
A
ssoc
iate
d w
ith
bot
h v
iral
an
d b
acte
rial
in
fect
ion
s In
sev
ere
case
s, p
art
of d
isse
min
ated
in
trav
ascu
lar
coag
ula
tion
(D
IC)
Oth
er m
ech
anis
ms
less
wel
l un
der
stoo
d [
1 ]
Pse
ud
o-th
rom
boc
ytop
enia
A
rtif
act
du
e to
ED
TA i
n C
BC
tu
be.
Clu
mp
ing
pre
sen
t on
sm
ear.
Red
raw
p
late
let
cou
nt
in t
ub
e co
nta
inin
g ci
trat
e in
stea
d o
f E
DTA
H
epar
in-i
nd
uce
d
thro
mb
ocyt
open
ia
HIT
—S
ee t
ext
Pos
ttra
nsf
usi
on
thro
mb
ocyt
open
ia
Occ
urs
soo
n a
fter
tra
nsf
usi
on (
may
be
soon
aft
er s
urg
ery
if t
ran
sfu
sion
s gi
ven
du
rin
g ca
se)
Sev
erit
y te
nd
s to
be
pro
por
tion
al t
o th
e vo
lum
e of
blo
od a
dm
inis
tere
d
Cli
nic
al c
ours
e u
sual
ly b
enig
n
Pla
tele
t co
un
t u
sual
ly r
etu
rns
to n
orm
al w
ith
in 3
–5 d
ays
afte
r b
lood
tr
ansf
usi
on [
1 ]
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177CHAPTER 25: POSTOPERATIVE THROMBOCYTOPENIA
X
Sev
ere
Dru
g-in
du
ced
im
mu
ne
thro
mb
ocyt
open
ia
Qu
inid
ine,
dig
oxin
, val
pro
ic a
cid
, alp
ha
met
hyl
dop
a, p
enic
illi
n c
lass
d
rugs
, th
iazi
des
, tri
met
hop
rim
/su
lfam
eth
oxaz
ole,
cim
etid
ine,
fam
otid
ine
Pla
tele
t co
un
t is
oft
en e
xtre
mel
y lo
w (
can
be
less
th
an 2
0,00
0)
Can
cau
se p
osto
per
ativ
e b
leed
ing
Pla
tele
t tr
ansf
usi
ons
use
ful
Ste
roid
s n
ot s
how
n t
o b
e u
sefu
l [ 1 ]
P
ostt
ran
sfu
sion
p
urp
ura
A
cute
th
rom
boc
ytop
enia
cau
sed
by
allo
imm
un
izat
ion
aga
inst
tra
nsf
use
d
pla
tele
ts o
ccu
rs ~
5–8
day
s af
ter
the
tran
sfu
sion
C
lin
ical
pre
sen
tati
on i
s si
mil
ar i
n i
ts s
ever
ity
to d
rug-
ind
uce
d i
mm
un
e th
rom
boc
ytop
enia
wit
h le
vels
dro
pp
ing
bel
ow 2
0,00
0 an
d s
ud
den
on
set
of
ble
edin
g [ 1
] D
IC
Can
occ
ur
in t
he
sett
ing
of s
ever
e in
fect
ion
as
men
tion
ed a
bov
e C
an a
lso
occu
r (s
epar
ate
from
in
fect
ion
) af
ter
sign
i fi ca
nt
surg
erie
s p
rese
nti
ng
wit
h a
n a
cute
th
rom
boc
ytop
enia
im
med
iate
ly a
fter
su
rger
y w
ith
a b
leed
ing
dia
thes
is t
hat
is
mor
e se
vere
an
d m
ore
exte
nsi
ve t
han
th
at
wh
ich
is
exp
ecte
d f
rom
th
e d
egre
e of
th
rom
boc
ytop
enia
(b
ecau
se i
t is
als
o as
soci
ated
wit
h a
coa
gulo
pat
hy)
D
IC, n
ot i
n t
he
sett
ing
of i
nfe
ctio
n, i
s h
ypot
hes
ized
to
be
init
iate
d b
y ex
ten
sive
su
rgic
al i
nju
ry t
o th
e en
dot
hel
ium
of
the
blo
od v
esse
ls a
nd
al
tera
tion
of
fun
ctio
n o
f th
e en
dot
hel
ial c
ell [
1 ]
TT
P
Rar
e. D
ecre
ased
pla
tele
ts, i
ncr
ease
d L
DH
, nor
mal
PT
/PT
T [
1 ]
Cla
ssic
pen
tad
is
feve
r, n
euro
logi
c sy
mp
tom
s/al
tere
d m
enta
l sta
tus,
ren
al
fail
ure
, mic
roan
giop
ath
ic h
emol
ytic
an
emia
, an
d t
hro
mb
ocyt
open
ia
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178 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK
should be avoided in patients who are thrombocytopenic. Other drugs that interfere with platelet function (NSAIDs, aspirin, beta-lactam antibiotics) should generally be avoided depending on the indication.
HEPARIN-INDUCED THROMBOCYTOPENIA HIT is an increasingly recognized cause of perioperative complica-tions, including skin necrosis, DVT, pulmonary embolism, venous sinus thrombosis, and stroke [ 2, 3 ] . HIT must be recognized in order to treat and prevent potentially catastrophic complications.
WHEN TO SUSPECT [ 2, 3 ] 1. Unexplained thrombocytopenia 2. Thrombosis associated with thrombocytopenia 3. Platelet count that has fallen 50% or more from a baseline value
(note that it may still be in the normal range) 4. Necrotic skin lesions at heparin injection sites
AND Prior exposure to heparin
Platelet counts do not usually fall below 20,000 as a consequence of ■
HIT, and other causes (drug-induced thrombocytopenia, DIC, ITP, etc.) should be suspected if the platelet count is in this range. Postoperative patients (particularly those with long spine surgeries) ■
often have depressed platelet counts for days postoperatively, but if the platelet count fails to rebound or falls 50% or more from a baseline value, a diagnosis of HIT should be entertained. Nonimmune-mediated decrease in platelet count is seen in many ■
patients within 2 days of starting heparin, but causes a lesser drop and will usually rebound despite continued heparin treatment.
TIME COURSE Development of HIT varies depending on patients’ prior exposure to heparin (and whether they already have antibodies). It is important to realize that a patient may present with HIT after stopping heparin (Table 25.2 ).
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179CHAPTER 25: POSTOPERATIVE THROMBOCYTOPENIA
X
DIAGNOSIS HIT is a clinical diagnosis, but certain lab tests are useful in support-ing the diagnosis. HIT is caused by antibodies against the heparin/platelet factor 4 complex, and multiple tests are available to assess for the presence of these antibodies. The ELISA immunoassay that is the most common test used is extremely sensitive but not speci fi c. A nega-tive test can be useful in ruling out the diagnosis, but a positive test does not con fi rm it without further supporting features. We recom-mend fi rst checking heparin antibody ELISA assay [ 4 ] . If the ELISA test is positive and there is a high clinical suspicion, then treat as HIT positive. If there is high clinical suspicion of false positive, a serotonin release assay (SRA) can be checked [ 4 ] .
TREATMENT Stop all heparin products (this includes heparin fl ushes). ■
Start a non-heparinoid anticoagulant (direct thrombin inhibi- ■
tors argatroban and lepirudin are approved for use in the USA).Pharmacy protocols exist for this treatment and will vary from hospital to hospital. Start warfarin (only AFTER non-heparinoid anticoagulant has ■
been started) with a plan to anticoagulate for at least 6 weeks, but NOT until the patient’s platelet count is greater than 100–150 K due to the risk of transient hypercoagulability. Therapy should be overlapped for at least 5 days prior to dis- ■
continuation of the direct thrombin inhibitor. Hematology consultation is indicated when treating hospital- ■
ized patients with HIT.
TABLE 25.2 TIMING OF PRESENTATIONS OF HIT
Early Within the fi rst 1–2 days of starting heparin
Seen in patients with prior exposure to heparin (usually in the preceding 3 months), and hence prior antibodies
Usual Within 5–10 days of starting heparin therapy
Presumed to be due to the formation of new antibodies
Late After discontinuation of heparin therapy. May be >2 weeks or more from last exposure to heparin
Can occur after the patient’s dis-charge from the hospital. Suspect in a patient returning to the hospital with a new thrombotic complication, particularly after an orthopedic or other surgery where heparin prophy-laxis was used
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180 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK
PREVENTION Low-molecular-weight heparins (enoxaparin, dalteparin, etc.) ■
appear to have a lower risk of HIT, and should be used when appropriate. Avoid unnecessary use of heparin. ■
CAN PATIENTS WITH A HISTORY OF HIT EVER BE RECHALLENGED WITH HEPARIN? While not recommended if other forms of anticoagulation are available, most patients with immune-mediated HIT lose their HIT antibodies within 3 months of ceasing therapy, and short-term hepa-rin use (such as for cardiac bypass surgery) has been shown to be safe [ 5 ] .
REFERENCES 1. Chang JC. Review: postoperative thrombocytopenia: with etiologic, diagnostic and therapeu-
tic consideration. Am J Med Sci. 1996;311(2):96–105. 2. Arepally G, Ortel T. Heparin-induced thrombocytopenia. N Engl J Med. 2006;355(8):809–17. 3. Coutre S. Heparin-induced thrombocytopenia. Topic update 10/17/2011. In: Basow DS, editor.
UpToDate. Waltham, MA; Wolters Kluwer 2012. http://www.uptodateonline.com . Accessed Jan 2012.
4. University of Washington Medical Center Anticoagulation Services suggestions for clinical management of suspected heparin-induced thrombocytopenia (HIT). http://uwmcacc.org/pdf/VTE_HIT.pdf . Accessed 1 Dec 2011.
5. Follis F, Schmidt CA. Cardiopulmonary bypass in patients with heparin-induced thrombocy-topenia and thrombosis. Ann Thorac Surg. 2000;70:2173–81.