Hematologic Emergencies:

DISSEMINATED INTRAVASCULAR COAGULATION &

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)

P R E S E N T E D B Y: S A B R I N A M . S H A L H O U T
COURSE: CRITICAL CARE 2
I N S T R U C TO R : D R B A S M A H S A L A M E H
Outline:
 Overview of Coagulation & Fibrinolysis
 DIC: Description
 Etiology
 Pathophysiology
 Assessment + Diagnosis
 Medical + Nursing Management
 HIT: Description + Etiology
 Pathophysiology
 Assessment + Diagnosis
 Medical + Nursing Management
Overview of Coagulation &
Fibrinolysis:
Hemostasis is the ability of the body to control bleeding and clotting, it is a balancing act
between the coagulation mechanism and fibrinolysis.

These four major actions are involved in achieving hemostasis:

1. local vasoconstriction to reduce blood flow,

2. platelet aggregation at the injury site and formation of a platelet plug,

3. formation of a fibrin mesh to strengthen the plug,

4. dissolution of the clot after tissue repair is complete.

Coagulation & Fibrinolysis:
The coagulation mechanism consists of 13 factors that
work together through a series of feedback loops to
achieve hemostasis
Depending on the initial triggering event, the
extrinsic or intrinsic coagulation pathway is
initiated. The extrinsic pathway begins when
vascular injury occurs, resulting in release of
tissue factor and activation of coagulation factor
VII (7). The intrinsic pathway is activated when
the damaged sub-endothelium comes into
direct contact with circulating blood. In this
contact phase, proteins activate additional
coagulation factors (XII (12), XI (11), IX,(9) and
VIII (8)). At this point, the two pathways
converge into a common pathway, and
prothrombin and fibrinogen are converted to
their active forms, resulting in clot formation
Fibrinolysis
The process of fibrinolysis promotes dissolution and remolding of the clot to
promote repair of the vessel wall and maintain flow through the vessel lumen.
Fibrinolysis begins as soon as the fibrin clot is formed. Circulating plasminogen, a
precursor to the powerful enzyme plasmin, binds to fibrin and is trapped within the
newly formed clot.
The injured epithelial wall releases tissue-type plasminogen activator, which
converts plasminogen to its active state, plasmin. The plasmin begins to digest the
fibrin, rapidly breaking down the clot. When fibrin is broken down, the fibrin
degradation products released act as anticoagulants.
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is a very rare but critical condition, Also known as

consumptive coagulopathy and defibrination syndrome, DIC is characterized by bleeding and

thrombosis, both of which result from depletion of clotting factors, platelets, and RBCs. If not

treated quickly, DIC will progress to multiple organ failure and death.
DIC Etiology:
There is a possibility that one may develop an infection of injury that affects the body’s normal blood clotting process. If not
treated quickly, DIC will progress to multiple organ failure and then death.

Several disease states may lead to the development, generally via one of the following two pathways:

• A systemic inflammatory response, leading to activation of the cytokine network and subsequent activation of

coagulation (eg, in sepsis or major trauma)

• Release or exposure of procoagulant material into the bloodstream (eg, in cancer, crush brain injury, or in obstetric cases)

According to Cleveland Clinic 2022, “DIC affects about 10% of all people who are very ill with sepsis, diseases such as cancer
or pancreatitis, as well as people recovering from traumatic injuries such as burns or serious complications from pregnancy
and delivery.
CAUSE OF DIC  EXAMPLE 
Infectious HIV .CMV. hepatitis virus .
Bacterial -Fungal -Parasitic (eg, malaria)

Hematologic (eg, acute myelocytic leukemia)

Malignancy  Or Metastatic 

Abruptio placentae
Acute peripartum hemorrhage
Obstetric Preeclampsia/eclampsia/hemolysis, elevated 
Retained stillbirth
Septic abortion 
Burns/Motor vehicle accidents/Snake bite 
Trauma

Transfusion Hemolytic reactions

Liver disease/acute hepatic failure*

Prosthetic devices
Others  Shunts (Denver or LeVeen)
Ventricular assist devices
Pathophysiology:
The common thread in the development of DIC is damage to the endothelium that results in activation of the
coagulation mechanism.

Direct damage to the endothelium results in the release of tissue factor and activation of this pathway.

The secondary surge of thrombin formation as a result of the intrinsic coagulation pathway leads to the massive
disruption of the delicate balance that is hemostasis.

Excessive thrombin formation results in rapid consumption of coagulation factors and depletion of regulatory
substances—protein C, protein S and anti-thrombin.

With no checks and balances, thrombi continue to form along damaged epithelial walls, resulting in occlusions of the
vessels
Classifications:
Acute DIC: it happens rapidly, the coagulopathy is dominant and major symptoms are bleeding
and shock, seen in severe infections, and amniotic fluid embolism.

Chronic DIC: it happens slowly, last several weeks, thrombosis and clotting are dominant, and
mostly seen in cancer.
Pathophysiology of Disseminated
Intravascular Coagulation:
Assessment & Diagnosis:
 Favorable outcomes for patients with DIC depend on accurate and timely diagnosis of the
condition. Realization of the role underlying pathology plays, recognition of clinical
manifestations and lab tests.
Clinical Manifestations
 There are 2 Primary pathophysiologic mechanisms of DIC
 Formation of Thrombi
 Bleeding

 In the beginning the formation of thrombi and bleeding. The Thrombi in peripheral capillaries can
lead to cyanosis, particularly in the fingers, toes, ears, and nose.
 As the condition progresses, ischemia worsens, and end organs are affected. The result of this is
more central ischemia, and can be seen with respiratory insufficiency and failure, acute kidney
injury, bowel infarction, and ischemic stroke.
As coagulation factors are depleted, bleeding from intravenous and other puncture sites is
observed. Ecchymoses may result from routine interventions such as the use of a manual blood
pressure cuff, bathing, or turning. Bloody drainage may also occur from surgical sites, drains, and
urinary catheters. With the progression of DIC, the patient is at risk for severe gastrointestinal or
subarachnoid hemorrhage.
Lab Tests
Continuous activation of the coagulation pathways results in the
consumption of coagulation factors. Because of this, prothrombin
time, activated partial thromboplastin time, and international
normalized ratio values are elevated. Although the platelet count
may be within normal ranges, serial examination reveals a
declining trend in values. An unexpected drop of at least 50% in
the platelet count, particularly in the presence of known
contributing factors and associated signs and symptoms, strongly
indicates DIC. Fibrinogen levels drop as more and more clots are
formed. Thrombus formation in small vessels narrows the vessel
lumen, forcing RBCs to squeeze through. The resulting damage and
fragmentation of these cells can be seen on microscopic
examination of blood samples. D-dimer is used to evaluate the
degree of clot dissolution and the severity of the coagulopathy
Medical Management:
The intervention in DIC is to prevent and to be wary of the conditions that commonly contribute to the development of DIC and

treating them vigorously and without any delays to ensure the best defense against this critical condition.

Once DIC has been identified, maintaining organ perfusion and slowing consumption of coagulation factors are the utmost

importance with achieving a favorable outcome.

It is essential to prevent end-organ ischemia and damage by supporting blood pressure and circulating volume. Administrating

intravenous fluids and inotropic agents and, if overt hemorrhaging is evident, infusion of packed RBCs are appropriate

interventions to replace blood volume

Another strategy that has been used to treat DIC is slowing consumption of coagulation factors but inhibiting the process

involved in the clot formation.

Nursing Management:
Patient management plan with patients that have DIC varies with the patients symptoms and issues.
The nurse plays a large and significant role in supporting the patient’s vital functions, initiating bleeding precautions,
providing comfort and emotional support, and maintaining observation for complications.
 Supporting the patient’s vital physiologic functions is critical to the outcome of the patient.
The patient should be closely monitored for any adverse reaction to blood products. Medications may include
heparin, antibiotics for infection (depending on the underlying cause), vasoactive agents for hemodynamic support,
and analgesics for pain.
 Close monitoring of vital signs, hemodynamic parameters, intake and output, and appropriate laboratory values
assists in the administration and titration of appropriate agents.
Frequent assessments of the patient’s neurologic status, kidney function, cardiopulmonary function, and
integumentary condition facilitate the early identification of impaired tissue or organ perfusion.
 Particular parameters to include are mental status and level of consciousness; BUN and creatinine levels;
prothrombin time, activated partial thromboplastin time, and international normalized ratio values; urine output; vital
signs and hemodynamic values including cardiac rhythm and oxygen saturation; and skin integrity.
Bleeding Precautions & Injury Prevention:
Heparin-Induced Thrombocytopenia:
(HIT Syndrome)
Thrombocytopenia overview:
Thrombocytopenia is defined as a platelet count less than 150,000/ mm3 or a decrease of
greater than 50% from the last measurement
 This disorder is described as mild when the platelet count is between 70,000/mm3 and
150,000/mm3 ,
 Moderate when the platelet count is between 20,000/mm3 and 70,000/mm3 ,
Severe when the platelet count is less 20,000/mm3 . 10 When the platelet count decreases to
less than 50,000/mm3 , at this count the patient is at severe risk for bleeding,
Thrombocytopenia occurs in 20% to 45% of critically ill patients.
Heparin-Induced Thrombocytopenia:
Description
Heparin-induced thrombocytopenia (HIT), is seen in critical care patients

Heparin-induced thrombocytopenia (HIT) is a complication of heparin therapy. 

There are two types of HIT. Type 1 HIT presents within the first 2 days after exposure to
heparin, and the platelet count normalizes with continued heparin therapy. Type 1 HIT is a
nonimmune disorder that results from the direct effect of heparin on platelet activation.  

Type 2 HIT is an immune-mediated disorder that typically occurs 4-10 days after exposure to
heparin and has life- and limb-threatening thrombotic complications.   
Heparin-Induced Thrombocytopenia:
Etiology:
Heparin-induced thrombocytopenia (HIT) is caused by antibodies that bind to complexes of
heparin and platelet factor 4 (PF4), activating the platelets and promoting a prothrombotic state.
HIT is more frequently encountered with unfractionated heparin (UFH) than with low molecular
weight heparin (LMWH). 

The risk of HIT is highest with prolonged use of heparin for postoperative thrombophylaxis.
Pathophysiology:
The thrombocytopenia that occurs with immune-meditated HIT is related to formation of heparin-
antibody complexes. These complexes release a substance known as platelet factor 4.
Platelet factor 4 attracts heparin molecules, forming immunogenic complexes that adhere to platelet
and endothelial surfaces. Activation of platelets stimulates the release of thrombin and the
subsequent formation of platelet clumps .
Patients with immune-meditated HIT are at greater risk for thrombosis than bleeding. Complications
develop in 20% to 50% of patients can occur in both the venous an d the arterial system.
Vessel occlusion can result in the need for limb amputation, stroke, acute myocardial infarction and
death.
Resultant formation of fibrin-and platelet-rich thrombi is the primary characteristic of HIT that
distinguishes it from other forms of thrombocytopenia and gives rise to its more descriptive name:
white clot syndrome.
Assessment & Diagnosis:
 HIT can be associated with severe consequences, Rapid
recognition of risk factors and subsequent development of
signs and symptoms is essential in treating this condition.
Clinical Manifestations:

Lab Test Findings:

Laboratory Findings The key indicator for identifying HIT is the
platelet count. General consensus in the literature considers a
platelet count of less than 100,000/mm3 or a sudden drop of
50% from the patient’s baseline after initiation of heparin
therapy to strongly indicate HIT
4T score for diagnosis of HIT
..
Medical Management:
 Early diagnosis is critical to managing the effects of immune-mediated HIT.

 Current guidelines suggest that platelet count monitoring be performed every 2

or 3 days from day 4 to day 14 for high risk patients. When a decrease in platelet
count is detected, heparin therapy is discontinued immediately, and the patient
is tested for presence of heparin anti-bodies.

 Drug of Choice for treatment:

 Direct thrombin inhibitors (DTIs): new class of anticoagulants that bind

directly to thrombin and block its interaction with its substrates.

 Examples of like: Argatroban, desirudin, bivalirudin

Nurse Management:
The patient care management plan for a patient with HIT
incorporates a variety of patient problems.
The nurse has a significant and important role with patient
care and decreasing the incidence of heparin exposure by
maintaining observation for complications, providing
comfort and support to the patient and educating the
patient and family during this process.
Preventing HIT is a major nursing focus, because most
critically ill patients receive heparin as part of their plan of
care and thus are at risk for this disorder.
Initial assessment is critical to identifying patients that are at
risk for HIT which includes taking medical history of previous
heparin therapy, deep vein thrombosis, or cardiovascular
surgery.
Research:
Superior outcomes with Argatroban for heparin‑induced thrombocytopenia: a Bayesian network
meta‑analysis
Abstract: Background Argatroban, lepirudin, desirudin, bivalirudin, and danaparoid are commonly used to manage heparin-
induced thrombocytopenia related complications. However, the most suitable drug for this condition still remains controversial.
Aim of the review This Bayesian network meta-analysis study compared the most common anticoagulant drugs used in the
management of heparin-induced thrombocytopenia.
Method: All clinical trials comparing two or more anticoagulant therapies for suspected or confirmed heparin-induced
thrombocytopenia were considered for inclusion. Studies concerning the use of heparins or oral anticoagulants were not
considered. Data concerning hospitalization length, thromboembolic, major, and minor hemorrhagic events, and mortality rate
were collected. The network analyses were made through the STATA routine for Bayesian hierarchical random-efects model
analysis with standardised mean diference (SMD) and log odd ratio (LOR) efect measures. Results Data from a total of 4338
patients were analysed. The overall mean age was 62.31±6.6 years old. Hospitalization length was considerably shorter in favour of
the argatroban group (SMD: −1.70). Argatroban evidenced the lowest rate of major (LOR: −1.51) and minor (LOR: −0.57)
haemorrhagic events. Argatroban demonstrated the lowest rate of thromboembolic events (LOR: 0.62), and mortality rate (LOR:
−1.16). Conclusion Argatroban performed better overall for selected patients with HIT. Argatroban demonstrated the shortest
hospitalization, and lowest rate of haemorrhages, thromboembolisms, and mortality compared to bivalirudin, lepirudin, desirudin,
and danaparoid.