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Management of Immunogenic Heparin-induced Thrombocytopenia

Immunogenic heparin-induced thrombocytopenia (HIT) is an immune response to heparin associated with significant morbidity and mortality in hospitalized patients if unidentified as soon as possible, due to thromboembolic complications involving both arterial and venous systems. Early diagnoses based on a comprehensive interpretation of clinical and laboratory information improve clinical outcomes. Management principles of strongly suspected HIT should not be delayed for laboratory result confirmation. Treatment strategies have been introduced including new, safe, and effective agents. This review summarizes the clinical therapeutic options for HIT addressing the use of parenteral direct thrombin inhibitors and indirect factor Xa inhibitors as well as the potential non-Vitamin K antagonist oral anticoagulants.

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Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 12
INTRODUCTION
U
nfractionated heparin (UFH) or related molecules
such as low-molecular-weight heparin (LMWH)
are widely used in both outpatient and inpatient
settings for many thromboembolic events. Paradoxically,
patients exposed to UFH or LMWH are at risk for thrombotic
complications that may include deep vein thrombosis,
pulmonary embolism, myocardial infarction, thrombotic
stroke, cerebral vein thrombosis, and disseminated
intravascular coagulation. These thrombotic complications
are due to a serious adverse reaction called immunogenic
heparin-induced thrombocytopenia (HIT).[1-5]
HIT is defined as a drop in platelet count during or after
heparin administration.[4-6]
The non-immune heparin-
associated thrombocytopenia, traditionally called type I
HIT, is mediated by direct interaction between heparin
and circulating platelets, causing platelet clumping or
sequestration. Heparin-associated thrombocytopenia is a
self-limiting thrombocytopenia that affects 
10% of patients
receiving heparin formulations, usually develops within the
first 72 h after heparin administration, and platelet counts do
not drop below 100,000/mm3
; it often normalizes once the
heparin is ceased.[7,8]
The immune-mediated HIT, known as
HIT Type II,[8-10]
is a prothrombotic and potentially lethal
disorder caused by platelet, endothelial, and monocyte-
activating antibodies that target multimolecular complexes of
platelet factor 4 (PF4) and heparin.[11]
The immune-mediated
HIT is reported count begins to fall between 5 and 10 days
after the initiation heparin formulation.[4,5,12-14]
The devastating clinical consequences of the immune-
mediated HIT, which may include amputation and death,
should alert clinicians to identify patients with HIT and those
with increased risk of the development of immune-mediated
HIT as soon as possible to initiate early management and
prevent serious complications. For the purpose of this review,
the term HIT refers to the immune-mediated Type II that
causes paradoxical thromboemboli.
REVIEW ARTICLE
Management of Immunogenic Heparin-induced
Thrombocytopenia
Fahad A. S. Aleidan1,2
, Laila A. K. Alzahrani2
1
Department of Medical Basic Sciences, College of Medicine, King Saud bin Abdulaziz University for
Health Sciences, Riyadh, Saudi Arabia, 2
Department of Primary Care, King Abdulaziz Medical City, Riyadh,
Saudi Arabia
ABSTRACT
Immunogenic heparin-induced thrombocytopenia (HIT) is an immune response to heparin associated with significant morbidity
and mortality in hospitalized patients if unidentified as soon as possible, due to thromboembolic complications involving both
arterial and venous systems. Early diagnoses based on a comprehensive interpretation of clinical and laboratory information
improve clinical outcomes. Management principles of strongly suspected HIT should not be delayed for laboratory result
confirmation. Treatment strategies have been introduced including new, safe, and effective agents. This review summarizes the
clinical therapeutic options for HIT addressing the use of parenteral direct thrombin inhibitors and indirect factor Xa inhibitors
as well as the potential non-Vitamin K antagonist oral anticoagulants.
Key words:  Heparin-induced thrombocytopenia, heparin, low molecular weight heparin
Address for correspondence:
Dr. Fahad A. S. Aleidan, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz
Medical City, Riyadh, Saudi Arabia. Tel.: +96-6118011111. E-mail: 
https://doi.org/10.33309/2639-8354.020103 www.asclepiusopen.com
© 2019 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
13 Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019
RISK FACTORS
Exposure to heparin is the main risk factor and a critical step
in the development of HIT [Table 1]. A heparin source such
as bovine lung is more immunogenic than those produced
from porcine intestine,[15]
and the risk of HIT rises with the
length and volume of exposure to heparin as well as the route
of administration[16]
and more likely with intravenous heparin
than subcutaneous administration.[17-19]
Nevertheless, HIT
can develop from any heparin exposure, including incidental
amounts from heparin flushes or heparin-coated devices.[20,21]
Although HIT is more common in patients receiving UFH
than in those treated with LMWH.
LABORATORY AND CLINICAL
ASSESSMENT
HIT may occur rapidly or with a delayed onset, depending
on the presence of heparin-PF4 antibodies from a previous
administration and sensitization of heparin and related
molecules may induce rapid-onset HIT.[22]
In patients exposed
toheparinforthe1st
time,theonsetofHITmayoccur5–10 days
after receiving heparin.[4,5,12,23]
The thrombocytopenia in HIT is
usuallymoderateinseverity,withamedianplateletcountbeing
between 50 and 80 109
/L, although the nadir platelet count
can remain at a level considered normal (i.e., 150 109
/L) but
having dropped by 50%. The immunoassays (enzyme-linked
immunosorbent assay) are very sensitive to detect the HIT
antibody that binds to the PF4/heparin complex. However,
not all antibodies detected (immunoglobulin [Ig] G, IgM, and
IgA) are capable to induce clinical HIT  Immunoassays are
both technically easier to perform and more sensitive than
functional assays. On the other hand, functional assays are
more specific and better in the diagnosis of clinical HIT.[1,24]
PLATELET MONITORING
Platelet count monitoring should be started as baseline
measurement before heparin administration, whereas routine
monitoring is recommended for most patients receiving
heparin formulation based on stratified incidence of HIT
according to patient’s population and type of heparin exposure
[Table 2].[3,4]
MANAGEMENT OF IMMUNOGENIC
HIT
Initially, a clinician should apply the 4Ts (thrombocytopenia,
timing of platelet count fall, thrombosis, and other cause of
thrombocytopenia) scoring system to identify patients who
are at high, intermediate, or low risk of developing HIT
[Table 3].
NON-HEPARIN ANTICOAGULANT
Direct thrombin inhibitors and indirect factor Xa inhibitors
are two anticoagulant classes that were used in the treatment
of HIT with or without thrombosis [Table 4]. The clinical
presentation of the patient, availability of the drugs, and
clinician experience should dictate the choice of therapy.
CONCLUSION AND RELEVANCE
The diagnosis of HIT requires clinical evaluation and
laboratory confirmation. Platelet count monitoring should
perform every 2 or 3 days in patient population with a risk
of HIT 1%. When HIT is strongly suspected, management
should include immediate discontinuation of all heparin
formulations and the start of alternative, non-heparin
anticoagulants. Vitamin K antagonist (VKA) should not
be given. Instead, if VKA was given, reverse elevated
international normalized ratio by administering Vitamin K
and avoid platelet transfusions. A serotonin release assay
may be performed for HIT antibody detection; however, if
such a test was not available, enzyme-linked immunosorbent
assay would be sufficient to confirm the diagnosis. Doppler
ultrasonography of the upper and lower limbs and computed
tomography of the chest should be performed when clinically
Table 1: Factors contributing to the development of heparin‑induced thrombocytopenia
Risk category Immunogenicity value (immunogenic effects)
Heparin source Bovine higher than porcine
Heparin type UFH more than LMWH
Volume of heparin dose Therapeutic dose  prophylactic  flush or heparin‑coated
devices
Heparin exposure
First exposure Platelet fall day 5–10 after heparin initiation
Previous exposure (within 90 days) Platelet fall within 1 day after heparin initiation
Patient population Post‑operative more than medical more than obstetric
Patient gender Female more than male
LMWH: Low‑molecular‑weight heparin, UFH: Unfractionated heparin
Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 14
Table 2: Platelet count monitoring guideline for HIT
Population Scenario Monitoring of platelet count
Recent heparin exposure Patient starting UFH and LMWH and who received
UFH within the previous 100 days; patients whose
heparin exposure history is unknown
Obtain baseline platelet count and repeat
platelet count within 24 h of starting
heparin
Acute, systematic
reactions after
intravenous UFH bolus
Patients with acute inflammatory,
cardiorespiratory, neurologic, or other unusual
symptoms and signs within 30 min after an
intravenous UFH bolus.
Obtain platelet count immediately to
compare with recent prior platelet counts
Risk* of HIT 1% Patients receiving UFH and LMWH at therapeutic
doses
Post‑operative patient receiving UFH/LMWH
antithrombotic prophylaxis
Obtain baseline then at least every 2 or
3 days until day 14 of treatment or until
heparin is stopped, whichever occurs first
Baseline then at least every 2 or 3 days
between post‑operative days 4 and 14 or
until heparin is stopped, whichever occurs
first
Risk of HIT 1% Medical/obstetric patients receiving prophylactic
dose UFH, or LMWH after receiving UFH,
post‑operative patients receiving prophylactic dose
LMWH, or intravascular catheter UFH flushes
As clinically indicated (no routine
monitoring)
LMWH: Low‑molecular ‑weight heparin, UFH: Unfractionated heparin, *Risk stratification is based on the overall incidence of HIT in different
patient population
Table 3: The pretest probability of HIT: 4Ts scoring system*
Clinical feature Score=2 Score=1 Score=0
Thrombocytopenia: Compare
the highest platelet count
within the sequence of
(declining platelet counts with
the lowest count to determine
the percentage of platelet fall
(select only one option)
50% platelet fall and
nadir of ≥20 and no
surgery within preceding
3 days
50% platelet fall but surgery
within preceding 3 days; any
combination of platelet fall and
nadir that does not fit criteria for
score of 2 or 0 (e.g., 30%–50%
platelet fall or nadir 10–19)
30% platelet fall; Any
platelet fall with nadir 10
Timing (of platelet count fall
or thrombosis*): Day 0=first
day of most recent heparin
exposure (select only one
option)
Platelet fall 5–10 days
after start of heparin
Platelet fall within 1 day
of start of heparin and
exposure of heparin with
the past 5–30 days
Consistent with platelet fall days
5–10 but not clear (e.g., missing
counts)
Platelet fall within 1 day of start
of heparin and exposure to
heparin in the past 31–100 days
platelet fall after day 10
Platelet fall ≥day 4 without
exposure to heparin in the
past 100 days
Thrombosis (or other clinical
sequelae; Select only one
option)
Confirmed new thrombosis
(venous or arterial)
Skin necrosis at
injection site
Anaphylactoid reaction to
IV heparin bolus
Adrenal hemorrhage
Recurrent venous
Thrombosis in a patient receiving
therapeutic anticoagulants
Suspected thrombosis (awaiting
confirmation with imaging)
Erythematous skin lesions at
heparin injection sites
Thrombosis suspected
Other causes of
thrombocytopenia (select
only one option)
No alternative explanation
for platelet fall is evident
Possible another cause is
evident:
Sepsis without proven microbial
source
Thrombocytopenia associated
with initiation of ventilator
Other
Probable another cause
present:
Within 72 h of surgery
Confirmed bacteremia/
fungemia
Chemotherapy or radiation
within the past 20 days
DIC due to non‑HIT cause
other
DIC: Disseminated intravascular coagulation, HIT: Heparin‑induced thrombocytopenia, IV: Intravenous, *Upon adding the score, the patient is
stratified into low (0–3 points), intermediate (4–5 points), or high (6–8 points) risk for having HIT. Table adapted with permission from Linkins et al.[4]
Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
15 Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019
indicated. At present, two parenteral therapeutic approaches
areavailabletotreatHITwithorwithoutthrombosis: (a) Direct
thrombin inhibitors or (b) indirect Xa inhibitors. The third
potential option for the treatment of HIT is using NOACs.
Unfortunately, all of the available anticoagulation agents
used to treat HIT are associated with hemorrhage and none
of these drugs has an antidote for rapid reversal. Adequate
hydration and early mobilization are supportive measures
may utilized in the prevention of thrombotic complication.
It is our recommendation and conviction that research should
continue to identify new therapeutic agents offering effective
and safe non-heparin alternatives for the management of
patients with HIT.
REFERENCES
1.	 Warketin TE. Heparin-Induced Thrombocytopenia:
Pathogenesis And Management. Br J Haematol 2003;121:
535-55.
2.	 Warketin TE. Heparin-induced thrombocytopenia. Diagnosis
and management. Circulation 2004;110:e454-8.
3.	 Cines DB, Bussel JB, McMillan RB, Zehnder JL. Congenital
and acquired thrombocytopenia. Hematol Am Soc Hematol
Educ Program 2004;2004:390-406.
4.	 Linkins LA, Dans AL, Moores LK, Bona R, Davidson BL,
Schulman S, et al. Treatment and prevention of heparin
induced thrombocytopenia: Antithrombotic therapy and
prevention of thrombosis, 9th
 ed: American college of chest
physicians evidence-based clinical practice guidelines. Chest
2012;141 Suppl 2:e495S-530.
5.	 Watson H, Davidson S, Keeling D, Haemostasis and
Thrombosis Task Force of the British Committee for Standards
in Haematology. Guidelines on the diagnosis and management
of heparin-induced thrombocytopenia: Second edition. Br J
Haematol 2012;159:528-40.
6.	 Warketin TE. An overview of the heparin-induced
thrombocytopenia syndrome. Semin Thromb Hemost 2004;30:
273-83.
7.	 Franchini M. Heparin induced thrombocytopenia: An update.
Thrombosis J 2005;3:14-20.
8.	 Rice L. Heparin-induced thrombocytopenia: Myths and
misconceptions. Arch Intern Med 2004;164:1961-4.
9.	 Kelton JG, Sheridan D, Santos A, Smith J, Steeves K, Smith C,
et al. Heparin induced thrombocytopenia: Laboratory studies.
Blood 1988;72:925-30.
10.	 Greinacher A, Potzch B, Amiral J, Dummel V, Eichner A,
Mueller-Eckhardt CM. Heparin-associated thrombocytopenia:
Isolation of the antibody and characterization as the major
antigen. Thromb Haemost 1994;71:247-51.
11.	 Amiral J, Bridey F, Dreyfus M, Vissoc AM, Fressinaud E,
Wolf M,et al.Plateletfactor4complexedtoheparinisthetarget
for antibodies generated in heparin-induced thrombocytopenia.
Thromb Haemost 1992;68:95-6.
12.	 Cuker A, Cines DB. How I treat heparin-induced
thrombocytopenia. Blood 2012;119:2209-18.
13.	 Lee GM,Arepally GM. Diagnosis and management of heparin-
induced thrombocytopenia. Hematol Oncol Clin North Am
2013;27:541-63.
Table 4:
Dosing
and
monitoring
guidelines
for
the
parenteral
treatment
options
of
HIT
Agent
Mode
of
action
Normal
dose
Dose
adjustment
Monitoring
FDA/ACCP
Approval/
Recommendation
for
HIF
Argatroban
Direct
thrombin
inhibition
2
µg/kg/min
IV
CKD:
No
change
HF:
0.5
µg/kg/min
aPTT
1.5–3×baseline (not
to
exceed
100
s)
DA:
Yes
ACCP:
2C
Desirudin
Direct
thrombin
inhibitor
15–30
mg
SC
every)
12
h
CKD:
CL
CR 
60
mL/min:
Adjustment
needed
HF:
No
change
None
needed
FDA:
No
ACCP:
2C
Bivalirudin
Direct
thrombin
inhibitor
0.15–0.20
mg/kg/h
IV
CKD:
CL
CR
10–29
mL/min:
0.06
mL/kg/h
IV:
CL
CR
10
Ml/min:
0.015
mg/kg/h
IV
aPTT
1.5−2.5×baseline
FDA:
Yes
ACCP:
C
Danaparoid
Indirect
factor
Xa
inhibitor
400 U/h
IV×h
then
300
U/h
IV×4
h
then
200
U/h
IV
Not
studied
in
patients
with
severe
renal
failure
Antifactor
Xa
level
0.5−0.8 U/mL
FDA:
Yes
ACCP:
2C
Fondaparinux
Indirect
factor
Xa
inhibitor
50
kg:
5mg
SQ:
50–100
kg:
7.5
mg
SQ:
100
kg:
10 mg
SQ
CKD:
CL
CR
30–50
mg/min:
Use
caution:
CL
CR
30
mL
min:
contraindicated
None
needed
FDA:
Yes
ACCP:
2C
ACCP:
American
college
of
chest
physician,
aPTT:
Activated
partial
thromboplastin
time,
CKD:
Chronic
kidney
disease,
CL
CR
:
Creatinine
clearance,
FDA:
Food
and
drug
administration,
HIT:
Heparin‑induced
thrombocytopenia,
HF:
Hepatic
failure
Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 16
14.	 Bhatt VR, Aryal MR, Armitage JO. Nonheparin anticoagulants
for heparin-induced thrombocytopenia. N Engl J Med
2013;368:2333-4.
15.	 Francis JL, Palmer GJ 3rd
, Moroose R, DrexlerA.A comparison
of bovine and porcine heparin in heparin antibody formation
after cardiac surgery. Ann Thorac Surg 2003;75:17-22.
16.	 Nand S, Wong W, Yuen B, Yetter A, Schmulbach E, Fisher SG,
et al. Heparin-induced thrombocytopenia with thrombosis:
Incidence, analysis of risk factors, and clinical outcomes in
108 consecutive patients treated as a single institution. Am J
Hematol 1997;56:12-6.
17.	 Lubenow N, Hinz P, Thomaschewski S, Lietz T, Vogler M,
Ladwig A. The severity of trauma determines the immune
response of PF4/heparin and the frequency of heparin-induced
thrombocytopenia. Blood 2010;115:1797-803.
18.	 Ban-Heofan M, Francis C. Heparin induced thrombocytopenia
and thrombosis in a tertiary care hospital. Thromb Res
2009;124:189-92.
19.	 Prechel M, Walenga JM. Heparin-induced thrombocytopenia:
An update. Semin Thromb Hemost 2012;38:483-96.
20.	 Kadidal VV, Mayo DJ, Horne MK. Heparin-induced
thrombocytopenia (HIT) due to heparin flushes: A report of
three cases. J Intern Med 1999;246:325-9.
21.	 Jang IK, Hursting MJ. When heparins promote thrombosis:
Review of heparin-induced thrombocytopenia. Circulation
2005;111:2671-83.
22.	 Warketin TE, Kelton JG. Temporal aspects of heparininduced
thrombocytopenia. N Engl J Med 2001;334:1286-92.
23.	 Warketin TE, Kelton JG. Delayed-onset heparin-induced
thrombocytopenia and thrombosis. Ann Intern Med 2001;
135:502-6.
24.	 Chong BH. Heparin-induced thrombocytopenia. J Thromb
Haemost 2003;1:1471-8.
How to cite this article: Aleidan FAS, Alzahrani LAK.
Management of Immunogenic Heparin-induced
Thrombocytopenia. Clin Res Hematol 2019;2(1):12-16.

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Management of Immunogenic Heparin-induced Thrombocytopenia

  • 1. Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 12 INTRODUCTION U nfractionated heparin (UFH) or related molecules such as low-molecular-weight heparin (LMWH) are widely used in both outpatient and inpatient settings for many thromboembolic events. Paradoxically, patients exposed to UFH or LMWH are at risk for thrombotic complications that may include deep vein thrombosis, pulmonary embolism, myocardial infarction, thrombotic stroke, cerebral vein thrombosis, and disseminated intravascular coagulation. These thrombotic complications are due to a serious adverse reaction called immunogenic heparin-induced thrombocytopenia (HIT).[1-5] HIT is defined as a drop in platelet count during or after heparin administration.[4-6] The non-immune heparin- associated thrombocytopenia, traditionally called type I HIT, is mediated by direct interaction between heparin and circulating platelets, causing platelet clumping or sequestration. Heparin-associated thrombocytopenia is a self-limiting thrombocytopenia that affects  10% of patients receiving heparin formulations, usually develops within the first 72 h after heparin administration, and platelet counts do not drop below 100,000/mm3 ; it often normalizes once the heparin is ceased.[7,8] The immune-mediated HIT, known as HIT Type II,[8-10] is a prothrombotic and potentially lethal disorder caused by platelet, endothelial, and monocyte- activating antibodies that target multimolecular complexes of platelet factor 4 (PF4) and heparin.[11] The immune-mediated HIT is reported count begins to fall between 5 and 10 days after the initiation heparin formulation.[4,5,12-14] The devastating clinical consequences of the immune- mediated HIT, which may include amputation and death, should alert clinicians to identify patients with HIT and those with increased risk of the development of immune-mediated HIT as soon as possible to initiate early management and prevent serious complications. For the purpose of this review, the term HIT refers to the immune-mediated Type II that causes paradoxical thromboemboli. REVIEW ARTICLE Management of Immunogenic Heparin-induced Thrombocytopenia Fahad A. S. Aleidan1,2 , Laila A. K. Alzahrani2 1 Department of Medical Basic Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia, 2 Department of Primary Care, King Abdulaziz Medical City, Riyadh, Saudi Arabia ABSTRACT Immunogenic heparin-induced thrombocytopenia (HIT) is an immune response to heparin associated with significant morbidity and mortality in hospitalized patients if unidentified as soon as possible, due to thromboembolic complications involving both arterial and venous systems. Early diagnoses based on a comprehensive interpretation of clinical and laboratory information improve clinical outcomes. Management principles of strongly suspected HIT should not be delayed for laboratory result confirmation. Treatment strategies have been introduced including new, safe, and effective agents. This review summarizes the clinical therapeutic options for HIT addressing the use of parenteral direct thrombin inhibitors and indirect factor Xa inhibitors as well as the potential non-Vitamin K antagonist oral anticoagulants. Key words:  Heparin-induced thrombocytopenia, heparin, low molecular weight heparin Address for correspondence: Dr. Fahad A. S. Aleidan, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Riyadh, Saudi Arabia. Tel.: +96-6118011111. E-mail:  https://doi.org/10.33309/2639-8354.020103 www.asclepiusopen.com © 2019 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
  • 2. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia 13 Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 RISK FACTORS Exposure to heparin is the main risk factor and a critical step in the development of HIT [Table 1]. A heparin source such as bovine lung is more immunogenic than those produced from porcine intestine,[15] and the risk of HIT rises with the length and volume of exposure to heparin as well as the route of administration[16] and more likely with intravenous heparin than subcutaneous administration.[17-19] Nevertheless, HIT can develop from any heparin exposure, including incidental amounts from heparin flushes or heparin-coated devices.[20,21] Although HIT is more common in patients receiving UFH than in those treated with LMWH. LABORATORY AND CLINICAL ASSESSMENT HIT may occur rapidly or with a delayed onset, depending on the presence of heparin-PF4 antibodies from a previous administration and sensitization of heparin and related molecules may induce rapid-onset HIT.[22] In patients exposed toheparinforthe1st time,theonsetofHITmayoccur5–10 days after receiving heparin.[4,5,12,23] The thrombocytopenia in HIT is usuallymoderateinseverity,withamedianplateletcountbeing between 50 and 80 109 /L, although the nadir platelet count can remain at a level considered normal (i.e., 150 109 /L) but having dropped by 50%. The immunoassays (enzyme-linked immunosorbent assay) are very sensitive to detect the HIT antibody that binds to the PF4/heparin complex. However, not all antibodies detected (immunoglobulin [Ig] G, IgM, and IgA) are capable to induce clinical HIT  Immunoassays are both technically easier to perform and more sensitive than functional assays. On the other hand, functional assays are more specific and better in the diagnosis of clinical HIT.[1,24] PLATELET MONITORING Platelet count monitoring should be started as baseline measurement before heparin administration, whereas routine monitoring is recommended for most patients receiving heparin formulation based on stratified incidence of HIT according to patient’s population and type of heparin exposure [Table 2].[3,4] MANAGEMENT OF IMMUNOGENIC HIT Initially, a clinician should apply the 4Ts (thrombocytopenia, timing of platelet count fall, thrombosis, and other cause of thrombocytopenia) scoring system to identify patients who are at high, intermediate, or low risk of developing HIT [Table 3]. NON-HEPARIN ANTICOAGULANT Direct thrombin inhibitors and indirect factor Xa inhibitors are two anticoagulant classes that were used in the treatment of HIT with or without thrombosis [Table 4]. The clinical presentation of the patient, availability of the drugs, and clinician experience should dictate the choice of therapy. CONCLUSION AND RELEVANCE The diagnosis of HIT requires clinical evaluation and laboratory confirmation. Platelet count monitoring should perform every 2 or 3 days in patient population with a risk of HIT 1%. When HIT is strongly suspected, management should include immediate discontinuation of all heparin formulations and the start of alternative, non-heparin anticoagulants. Vitamin K antagonist (VKA) should not be given. Instead, if VKA was given, reverse elevated international normalized ratio by administering Vitamin K and avoid platelet transfusions. A serotonin release assay may be performed for HIT antibody detection; however, if such a test was not available, enzyme-linked immunosorbent assay would be sufficient to confirm the diagnosis. Doppler ultrasonography of the upper and lower limbs and computed tomography of the chest should be performed when clinically Table 1: Factors contributing to the development of heparin‑induced thrombocytopenia Risk category Immunogenicity value (immunogenic effects) Heparin source Bovine higher than porcine Heparin type UFH more than LMWH Volume of heparin dose Therapeutic dose  prophylactic  flush or heparin‑coated devices Heparin exposure First exposure Platelet fall day 5–10 after heparin initiation Previous exposure (within 90 days) Platelet fall within 1 day after heparin initiation Patient population Post‑operative more than medical more than obstetric Patient gender Female more than male LMWH: Low‑molecular‑weight heparin, UFH: Unfractionated heparin
  • 3. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 14 Table 2: Platelet count monitoring guideline for HIT Population Scenario Monitoring of platelet count Recent heparin exposure Patient starting UFH and LMWH and who received UFH within the previous 100 days; patients whose heparin exposure history is unknown Obtain baseline platelet count and repeat platelet count within 24 h of starting heparin Acute, systematic reactions after intravenous UFH bolus Patients with acute inflammatory, cardiorespiratory, neurologic, or other unusual symptoms and signs within 30 min after an intravenous UFH bolus. Obtain platelet count immediately to compare with recent prior platelet counts Risk* of HIT 1% Patients receiving UFH and LMWH at therapeutic doses Post‑operative patient receiving UFH/LMWH antithrombotic prophylaxis Obtain baseline then at least every 2 or 3 days until day 14 of treatment or until heparin is stopped, whichever occurs first Baseline then at least every 2 or 3 days between post‑operative days 4 and 14 or until heparin is stopped, whichever occurs first Risk of HIT 1% Medical/obstetric patients receiving prophylactic dose UFH, or LMWH after receiving UFH, post‑operative patients receiving prophylactic dose LMWH, or intravascular catheter UFH flushes As clinically indicated (no routine monitoring) LMWH: Low‑molecular ‑weight heparin, UFH: Unfractionated heparin, *Risk stratification is based on the overall incidence of HIT in different patient population Table 3: The pretest probability of HIT: 4Ts scoring system* Clinical feature Score=2 Score=1 Score=0 Thrombocytopenia: Compare the highest platelet count within the sequence of (declining platelet counts with the lowest count to determine the percentage of platelet fall (select only one option) 50% platelet fall and nadir of ≥20 and no surgery within preceding 3 days 50% platelet fall but surgery within preceding 3 days; any combination of platelet fall and nadir that does not fit criteria for score of 2 or 0 (e.g., 30%–50% platelet fall or nadir 10–19) 30% platelet fall; Any platelet fall with nadir 10 Timing (of platelet count fall or thrombosis*): Day 0=first day of most recent heparin exposure (select only one option) Platelet fall 5–10 days after start of heparin Platelet fall within 1 day of start of heparin and exposure of heparin with the past 5–30 days Consistent with platelet fall days 5–10 but not clear (e.g., missing counts) Platelet fall within 1 day of start of heparin and exposure to heparin in the past 31–100 days platelet fall after day 10 Platelet fall ≥day 4 without exposure to heparin in the past 100 days Thrombosis (or other clinical sequelae; Select only one option) Confirmed new thrombosis (venous or arterial) Skin necrosis at injection site Anaphylactoid reaction to IV heparin bolus Adrenal hemorrhage Recurrent venous Thrombosis in a patient receiving therapeutic anticoagulants Suspected thrombosis (awaiting confirmation with imaging) Erythematous skin lesions at heparin injection sites Thrombosis suspected Other causes of thrombocytopenia (select only one option) No alternative explanation for platelet fall is evident Possible another cause is evident: Sepsis without proven microbial source Thrombocytopenia associated with initiation of ventilator Other Probable another cause present: Within 72 h of surgery Confirmed bacteremia/ fungemia Chemotherapy or radiation within the past 20 days DIC due to non‑HIT cause other DIC: Disseminated intravascular coagulation, HIT: Heparin‑induced thrombocytopenia, IV: Intravenous, *Upon adding the score, the patient is stratified into low (0–3 points), intermediate (4–5 points), or high (6–8 points) risk for having HIT. Table adapted with permission from Linkins et al.[4]
  • 4. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia 15 Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 indicated. At present, two parenteral therapeutic approaches areavailabletotreatHITwithorwithoutthrombosis: (a) Direct thrombin inhibitors or (b) indirect Xa inhibitors. The third potential option for the treatment of HIT is using NOACs. Unfortunately, all of the available anticoagulation agents used to treat HIT are associated with hemorrhage and none of these drugs has an antidote for rapid reversal. Adequate hydration and early mobilization are supportive measures may utilized in the prevention of thrombotic complication. It is our recommendation and conviction that research should continue to identify new therapeutic agents offering effective and safe non-heparin alternatives for the management of patients with HIT. REFERENCES 1. Warketin TE. Heparin-Induced Thrombocytopenia: Pathogenesis And Management. Br J Haematol 2003;121: 535-55. 2. Warketin TE. Heparin-induced thrombocytopenia. Diagnosis and management. Circulation 2004;110:e454-8. 3. Cines DB, Bussel JB, McMillan RB, Zehnder JL. Congenital and acquired thrombocytopenia. Hematol Am Soc Hematol Educ Program 2004;2004:390-406. 4. Linkins LA, Dans AL, Moores LK, Bona R, Davidson BL, Schulman S, et al. Treatment and prevention of heparin induced thrombocytopenia: Antithrombotic therapy and prevention of thrombosis, 9th  ed: American college of chest physicians evidence-based clinical practice guidelines. Chest 2012;141 Suppl 2:e495S-530. 5. Watson H, Davidson S, Keeling D, Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology. Guidelines on the diagnosis and management of heparin-induced thrombocytopenia: Second edition. Br J Haematol 2012;159:528-40. 6. Warketin TE. An overview of the heparin-induced thrombocytopenia syndrome. Semin Thromb Hemost 2004;30: 273-83. 7. Franchini M. Heparin induced thrombocytopenia: An update. Thrombosis J 2005;3:14-20. 8. Rice L. Heparin-induced thrombocytopenia: Myths and misconceptions. Arch Intern Med 2004;164:1961-4. 9. Kelton JG, Sheridan D, Santos A, Smith J, Steeves K, Smith C, et al. Heparin induced thrombocytopenia: Laboratory studies. Blood 1988;72:925-30. 10. Greinacher A, Potzch B, Amiral J, Dummel V, Eichner A, Mueller-Eckhardt CM. Heparin-associated thrombocytopenia: Isolation of the antibody and characterization as the major antigen. Thromb Haemost 1994;71:247-51. 11. Amiral J, Bridey F, Dreyfus M, Vissoc AM, Fressinaud E, Wolf M,et al.Plateletfactor4complexedtoheparinisthetarget for antibodies generated in heparin-induced thrombocytopenia. Thromb Haemost 1992;68:95-6. 12. Cuker A, Cines DB. How I treat heparin-induced thrombocytopenia. Blood 2012;119:2209-18. 13. Lee GM,Arepally GM. Diagnosis and management of heparin- induced thrombocytopenia. Hematol Oncol Clin North Am 2013;27:541-63. Table 4: Dosing and monitoring guidelines for the parenteral treatment options of HIT Agent Mode of action Normal dose Dose adjustment Monitoring FDA/ACCP Approval/ Recommendation for HIF Argatroban Direct thrombin inhibition 2 µg/kg/min IV CKD: No change HF: 0.5 µg/kg/min aPTT 1.5–3×baseline (not to exceed 100 s) DA: Yes ACCP: 2C Desirudin Direct thrombin inhibitor 15–30 mg SC every) 12 h CKD: CL CR  60 mL/min: Adjustment needed HF: No change None needed FDA: No ACCP: 2C Bivalirudin Direct thrombin inhibitor 0.15–0.20 mg/kg/h IV CKD: CL CR 10–29 mL/min: 0.06 mL/kg/h IV: CL CR 10 Ml/min: 0.015 mg/kg/h IV aPTT 1.5−2.5×baseline FDA: Yes ACCP: C Danaparoid Indirect factor Xa inhibitor 400 U/h IV×h then 300 U/h IV×4 h then 200 U/h IV Not studied in patients with severe renal failure Antifactor Xa level 0.5−0.8 U/mL FDA: Yes ACCP: 2C Fondaparinux Indirect factor Xa inhibitor 50 kg: 5mg SQ: 50–100 kg: 7.5 mg SQ: 100 kg: 10 mg SQ CKD: CL CR 30–50 mg/min: Use caution: CL CR 30 mL min: contraindicated None needed FDA: Yes ACCP: 2C ACCP: American college of chest physician, aPTT: Activated partial thromboplastin time, CKD: Chronic kidney disease, CL CR : Creatinine clearance, FDA: Food and drug administration, HIT: Heparin‑induced thrombocytopenia, HF: Hepatic failure
  • 5. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia Clinical Research in Hematology  •  Vol 2  •  Issue 1  •  2019 16 14. Bhatt VR, Aryal MR, Armitage JO. Nonheparin anticoagulants for heparin-induced thrombocytopenia. N Engl J Med 2013;368:2333-4. 15. Francis JL, Palmer GJ 3rd , Moroose R, DrexlerA.A comparison of bovine and porcine heparin in heparin antibody formation after cardiac surgery. Ann Thorac Surg 2003;75:17-22. 16. Nand S, Wong W, Yuen B, Yetter A, Schmulbach E, Fisher SG, et al. Heparin-induced thrombocytopenia with thrombosis: Incidence, analysis of risk factors, and clinical outcomes in 108 consecutive patients treated as a single institution. Am J Hematol 1997;56:12-6. 17. Lubenow N, Hinz P, Thomaschewski S, Lietz T, Vogler M, Ladwig A. The severity of trauma determines the immune response of PF4/heparin and the frequency of heparin-induced thrombocytopenia. Blood 2010;115:1797-803. 18. Ban-Heofan M, Francis C. Heparin induced thrombocytopenia and thrombosis in a tertiary care hospital. Thromb Res 2009;124:189-92. 19. Prechel M, Walenga JM. Heparin-induced thrombocytopenia: An update. Semin Thromb Hemost 2012;38:483-96. 20. Kadidal VV, Mayo DJ, Horne MK. Heparin-induced thrombocytopenia (HIT) due to heparin flushes: A report of three cases. J Intern Med 1999;246:325-9. 21. Jang IK, Hursting MJ. When heparins promote thrombosis: Review of heparin-induced thrombocytopenia. Circulation 2005;111:2671-83. 22. Warketin TE, Kelton JG. Temporal aspects of heparininduced thrombocytopenia. N Engl J Med 2001;334:1286-92. 23. Warketin TE, Kelton JG. Delayed-onset heparin-induced thrombocytopenia and thrombosis. Ann Intern Med 2001; 135:502-6. 24. Chong BH. Heparin-induced thrombocytopenia. J Thromb Haemost 2003;1:1471-8. How to cite this article: Aleidan FAS, Alzahrani LAK. Management of Immunogenic Heparin-induced Thrombocytopenia. Clin Res Hematol 2019;2(1):12-16.