Question

what is the pathophysiology of DIC? Medical management and treatment?

Answer 1

Disseminated Intravascular Coagulation (DIC) is widespread inappropriate coagulation within the blood vessels (pathological disruption of the process of hemostasis).

A large primary event triggers the process of DIC:

1. Causes the body's self-preserving clotting mechanism to backfire on itself

2. the body will consume all its own clotting factors faster than it produces them

3. ineffective blood clotting creates further blood vessel & tissue damage

4. results in no available clotting factors & massive haemorrhage from multiple sites.

Pathophysiology :

The pathogenesis of DIC can occur by the simultaneous coexistence of four different mechanisms:

• increased thrombin generation
• suppression of the physiologic anticoagulant pathways
• impaired fibrinolysis
• activation of the inflammatory pathway

Typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin:
Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation $\rightarrow$  This process consumes exorbitant amounts of coagulation factors (especially platelets, factor V, prothrombin, fibrinogen, and factor VIII), causing thrombocytopenia, deficiencies in factors V and VIII, hypoprothrombinemia, and hypofibrinogenemia $\rightarrow$ Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrinogen degradation products (FDPs)  $\rightarrow$ The haemorrhage that occurs may be due largely to the anticoagulant activity of FDPs and depletion of plasma coagulation factors.

The systemic generation of thrombin has been shown to be mediated predominantly by the extrinsic (factor VIIa) pathway. In fact, while the abrogation of the tissue factor/factor VIIa pathway resulted in complete inhibition of thrombin generation in experimental animal models of endotoxemia, the inhibition of the contact system did not prevent systemic activation of coagulation.

Impaired function of physiological anticoagulant pathways may amplify thrombin generation and contribute to fibrin formation. Plasma levels of antithrombin are markedly reduced in septic patients as a result of a combination of increased consumption by the ongoing formation of thrombin, enzyme degradation by elastase released from activated neutrophils, impaired synthesis due to liver failure and vascular capillary leakage.

Treatment:

General :

• Treatment of the underlying condition
• Possibly supportive care alone if the patient isn't actively bleeding

Medications:

• Replacement therapy with administration of fresh frozen plasma, platelets, fibrinogen concentrates, or cryoprecipitate
• Anticoagulants, such as unfractionated heparin or low-molecular-weight heparin sodium
• Concentrates of coagulation inhibitors, such as recombinant activated protein C or antithrombin III
• Fluid replacement
• Oxygen administration

If the Patient is Actively Bleeding:

• Replacement therapy with administration of fresh frozen plasma, platelets, fibrinogen concentrates, or cryoprecipitate
• Anticoagulants, such as unfractionated heparin or low-molecular-weight heparin sodium
• Concentrates of coagulation inhibitors, such as recombinant activated protein C or antithrombin III
• Fluid replacement
• Oxygen administration

Other:

Broad-spectrum antibiotics for gram-negative sepsis

Nursing Management:

Nursing Interventions

• Focus on early recognition of signs of abnormal bleeding, prompt treatment of the underlying disorders, and prevention of further bleeding.
• Provide emotional support; allow the patient to verbalize concerns and fears.
• Provide adequate rest periods; cluster nursing activities to minimize energy expenditure and reduce oxygen demand.
• Give prescribed analgesics as necessary.
• Reposition the patient every 2 hours and provide meticulous skin care.
• Give prescribed oxygen therapy based on oxygen saturation levels from pulse oximetry or arterial blood gas results.