Disseminated intravascular coagulation (DIC) is defined as accelerated activation of the coagulation cascade disproportionate to normal feedback mechanisms, which results in thrombi formation throughout the microvasculature.
A. Clotting is normally triggered by tissue injury, vessel injury, or the presence of a foreign body in the blood. In DIC, normal mechanisms of abrogating an excessive clotting response are disabled, and the process of clotting is not balanced by normal fibrinolysis.
B. Because the primary pathophysiology is thrombotic, the major clinical consequence is systemic ischemia.
C. Hemorrhage results from the depletion of clotting factors and ongoing stimulation of fibrinolysis.
D. DIC may present as two distinct clinical syndromes with divergent prognostic implications—acute and chronic DIC.
1.Acute DIC is rapid in onset, and severe in clinical symptomatology. This is a more common presentation in acutely ill or septic patients and carries a mortality rate in excess of 50%.
2.Chronic DIC often manifests as a chronic low-level clotting stimulus that may only be recognizable by mild to moderate organ dysfunction and blood component consumption. This clinical presentation is not unusual in patients with large, solid tumors that cause chronic tissue damage and release of thromboplastin. These patients are plagued with persistent clinical symptoms but do not usually die of this syndrome.
E. The goal of treatment must be to remove or treat the trigger. If that is not possible, the goal of therapy becomes supportive.
II. Etiology
A. DIC is always secondary to an underlying predisposing condition.
B. Common etiologies of DIC are linked to strong clotting stimuli or triggering of clotting by way of multiple mechanisms (tissue injury, vessel injury, foreign body in bloodstream).
1. Severe illness with strong clotting stimulus: Cardiopulmonary arrest, shock, burns, traumatic injury.
2. Sepsis is the most common etiology of DIC. Gram-negative bacteria release endotoxins, enhancing the clotting stimulus and risk of DIC, although infection with any organisms may cause vascular endothelial or tissue damage resulting in DIC.
C. Cancer is a common etiologic mechanism for DIC.
1. Large tumors erode normal tissue, causing release of tissue thromboplastin and enhanced clotting.
2. Rapidly proliferating tumors (eg, acute leukemia, Burkitt’s lymphoma) cause autolysis of tumor cells, and the fragmented cells act as foreign bodies within the bloodstream that stimulate clotting.
3. Some cancers release procoagulants that enhance clotting.
b. Urologic tumors (prostate, renal) release urokinase, which can stimulate clotting.
c. Brain tissue contains high levels of tissue factor, and brain tumors or procedures (eg, surgery) cause its release with increased clotting.
4. Progranulocytic leukemia contains granules with procoagulant, and, when leukemic cells lyse, they result in abnormal coagulation.
D. Obstetric complications cause DIC by a variety of causes, but because DIC is often associated with toxemia, endothelial inflammation is thought to be the major triggering mechanism.
III. Management
A. Assessment: The clinical findings in DIC are associated with either the thrombotic pathology, or bleeding due to an inadequate reserve of coagulation factors. Thrombosis and bleeding pathology coexist simultaneously, and, consequently, clinical symptoms are mixed, even within the same organ system. A summary of the clinical findings of DIC are described in greater detail within Table 33-1.
B. Hallmarks of DIC
1. Thrombosis that involves both veins and arteries.
2. Demarcation cyanosis demonstrating the total occlusion of microvessels. This is evident by a line separating perfused and nonperfused tissue. It is more common in the digits (fingers and toes) but may also occur in other distal, poorly perfused areas such as earlobes.
3. Thromboses within the body organs may only present as subclinical organ dysfunction.
4. Bleeding is a manifestation of later disease where clotting factors have been depleted and are unavailable for simple hemostasis.
D. Diagnostic Tests. Serum laboratory tests are used for both presumptive and definitive diagnosis (Table 33-2). Some diagnostic tests are significant because they are early, but nonspecific, indicators of the presence of DIC.
1. Thrombocytopenia occurs first as the platelets are consumed with production of massive intravascular platelet plugs.
TABLE 33-1 Signs and Symptoms of Disseminated Intravascular Coagulation
Hemoptysis or bloody endotracheal aspirate when suctioned
Hypoxemia
Cardiovascular
Chest pain
Murmur followed by muffled heart sounds
Ischemia-ST depression, T wave inversion
ECG changes of pericarditis/effusion such as low voltage, precordial lead ST elevations
Injury/infarction—ST elevations, Q waves
Renal
Decreased urine output with pelvic or flank pain
Hematuria
Gastrointestinal
Ischemia—crampy abdominal pain, decreased bowel sounds, abdomen tender to palpation progressing to rebound tenderness
GI bleeding—heme positive, dark red-black, or frankly bloody nasogastric drainage or stool
Infarction—severe abdominal pain radiating to back or shoulder, rebound tenderness, absent bowel sounds, hypotension, fever, confusion
2. Hypofibrinogenemia usually follows the decrease in platelet count and is indicative of fibrinogen being used to create massive microvascular clotting.
3. Antithrombin III and protein C levels are reduced in patients with DIC, indicating a loss of normal fibrinolytic mechanisms.
4. Some diagnostic tests are significant because they are the definitive diagnostic indicator for the presence of disease.
a. Fibrin degradation products (FDP)/fibrin split products (FSP) become elevated with the breakdown of a large volume of clots and is the most reliable diagnostic indicator of DIC. These breakdown products have anticoagulant properties that may worsen the clinical bleeding symptoms associated with this disease.
b. Fibrinogen D-dimer levels are elevated as plasmin breaks down fibrin.
TABLE 33-2 Diagnostic Tests Used to Assess Patients With Disseminated Intravascular Coagulation
Diagnostic Test
Normal Values
Abnormality in DIC
Rationale for Abnormal Finding
Platelet count
150,000-400,000/mm3
↓
Early consumption to create microvascular platelet plugs
Fibrinogen level
200-400 mg/dL
↓
Moderately early consumption to create microvascular fibrin clots
Prothrombin time (PT)
11-15 s
↑
Expression of depleted extrinsic pathway factors (mostly vitamin K dependent factors)
Prothrombin time
1.0-1.2 × normal
↑
Expression of depleted extrinsic pathway factors (mostly vitamin K dependent factors)
Internationalized ratio (INR)
Partial thromboplastin time (PTT)
60-70 s
↑
Expression of depleted intrinsic pathway factors (VIII, XIII)
Indication of high levels of clot lysis relating to large clots, sudden onset of massive fibrinolysis, or excessive fibrinolytic disease
Fibrin D-dimer
<50 μg/dL
↑
Indication of excessive fibrinolysis
Antithrombin III level
80%-120%
↓
Depletion and reduced action in DIC
Protein C level
72%-142%
↓
Depletion and reduced action in DIC
Schistocytes of peripheral blood smear
Absent
↑
Fragmented cells are detected as schistocytes due to RBC destruction as they travel through clots or partially occluded vessels
Bilirubin level
0.1-1.2 mg/dL
↑
Intravascular red blood cell (RBC) hemolysis increases intravascular bilirubin that is cleared less efficiently by the liver
Blood urea nitrogen (BUN)
0.1-0.7 mg/dL
↑
Intravascular RBC hemolysis leads to elevated serum blood urea nitrogen until the kidneys can clear it
Bullock, B. A. & Henze, R. L. (2000). Unit 3, Appendix C: Normal blood coagulation values. In Bullock B. A., Henze R. L. (Eds.). Focus on pathophysiology. Philadelphia: Lippincott Williams & Wilkins, p. 398.
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