Which occurrence may predispose a patient to developing chronic disseminated intravascular disorder

CONTENTS

• Rapid Reference 🚀
• Pathophysiology
• Symptoms
• Lab studies
• Causes
• Differential diagnosis
• Diagnostic criteria
• Sepsis-Induced Coagulopathy [SIC]
• Management
• Podcast
• Questions & discussion
• Pitfalls

sepsis induced coagulopathy [SIC]:

ISTH DIC score:

Normally, clots form locally at sites of vascular damage.  These clots are subsequently degraded after tissue damage is repaired.  The processes of clot formation and clot degradation [fibrinolysis] are localized and tightly regulated, based on a balance of counterregulatory proteins [procoagulants vs. anticoagulants regulate clot formation; fibrinolytics vs. antifibrinolytics regulate clot breakdown].

The fundamental pathophysiologic signature of DIC is widespread, uncontrolled clot formation.  Clotting may be initiated by a variety of factors [e.g., bacterial lipopolysaccharides, tissue factor released by monocytes or the placenta, or damage to the endothelial glycocalyx].  The fine balance of procoagulation vs. anticoagulation is broken, leading to widespread disseminated clot formation.  This clot burden places a massive strain on the fibrinolytic system, which is subsequently tasked with breaking down all of the clot.  The fine balance of fibrinolysis vs. antifibrinolysis may subsequently become disrupted, as numerous proteins are depleted.

DIC may cause a variety of life threats:

1. Disseminated microvascular thrombosis may cause tissue hypoperfusion and tissue damage.  This may be exacerbated by depletion of fibrinolytic proteins, which prevents clots from undergoing thrombolysis [“fibrinolytic shutdown”].
2. Depletion of anticoagulant proteins may predispose patients to form macrovascular thromboses [e.g., deep vein thrombosis and pulmonary emboli].
3. Depletion of procoagulant proteins may lead to hemorrhage.

Different causes of DIC tend to cause different problems.  Infection and septic shock tend to cause a more prothrombotic form of DIC, which predominantly causes excess clot formation.  Alternatively, DIC due to obstetric catastrophes or leukemia tends to cause depletion of fibrinogen leading to hemorrhage.  Consequently, DIC is not a monolithic construct – and appropriate treatment often depends on understanding the context.

• Acute DIC results from an acute trigger of coagulation [e.g., sepsis or trauma].  This leads to abrupt and exuberant depletion of coagulation factors, leading to hemostatic imbalances.
  • This chapter is predominantly about acute DIC – which is more immediately relevant to critical care medicine.
• Chronic DIC refers to chronic activation of coagulation, often due to disseminated adenocarcinomas.  This causes gradual consumption of coagulation factors, which can be compensated by the production of additional clotting factors.  Symptoms and laboratory abnormalities are consequently less notable [this is sometimes termed “chronic compensated DIC”].

DIC may be asymptomatic, or it may cause bleeding and clotting.  Symptoms may be dominated by either bleeding or clotting.  

• Microvascular thromboses may be an occult cause of organ failures.  With the exception of the skin, it is often difficult or impossible to tell that microvascular thrombosis is occurring.  The most common manifestations are: 
• [1] Renal failure is probably the most common.
• [2] Acute respiratory distress syndrome [ARDS].
• [3] Brain involvement may cause delirium, coma, seizure.
• [4] Adrenal failure [Waterhouse-Friedrichsen syndrome] may result from microvascular thromboses, followed by hemorrhagic transformation.  The net result is adrenal failure which can precipitate adrenal crisis.
• [5] Skin:  purpura fulminans [occlusion of microvasculature in the skin potentially causing gangrene].  This signifies an extreme form of DIC which requires aggressive management [more on this here]

• Primarily causes venous thrombosis [e.g., deep vein thrombosis, pulmonary embolism].

• Petechiae and purpura may occur on the skin.
• Oozing may originate from intravenous catheters or mucus membranes.
• Life-threatening hemorrhage can result from gastrointestinal or intracranial hemorrhage.  However, in most forms of DIC, severe bleeding is uncommon.

• Complete blood count [CBC]
• INR or PT, PTT
• Fibrinogen
• D-dimer

• D-dimer is invariably elevated in DIC, often dramatically so [e.g., >4,000 ng/mL].
• A normal D-dimer essentially excludes DIC.
• Advanced sepsis-induced DIC may impair fibrinolysis [“fibrinolytic shutdown”], which limits further increases in D-dimer.

• Moderate thrombocytopenia is usually seen in DIC.  Platelet counts of 20,000/uL]
• INR and fibrinogen levels are normal.