Description and Etiology
Disseminated intravascular coagulation (DIC) is a syndrome that arises as a complication of other serious or life-threatening conditions. Although DIC is not seen often, it can seriously hamper diagnostic and treatment efforts for the critically ill patient. An understanding of the etiologic and pathophysio- logic mechanisms of DIC can assist in anticipating the syn-drome’s occurrence, recognizing the signs and symptoms, and prompting intervention. Also known as consumptive coagulopathy, DIC is characterized by bleeding and thrombo-sis, 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.1
Many clinical events can prompt the development of DIC in the critically ill patient, but the exact underlying trigger may not be identifiable (Box 27-1). There are, however, some commonly known conditions associated with the develop-ment of DIC.
Sepsis, particularly that caused by gram-negative organ-isms, can be identified as the culprit in as many as 20%
of cases, making it the most common cause of DIC. In this instance, endotoxins serve as a trigger for activation of tissue factor and the extrinsic coagulation pathway. Meta- bolic acidosis and hypoperfusion associated with shock syn-dromes can result in increased formation of free radicals and damage to tissues. Tissue factor is activated, resulting in DIC. Massive trauma or burns are frequently associated with DIC. Direct tissue damage activates the extrinsic coagulation pathway, and damage to endothelial surfaces activates the intrinsic pathway.2 Obstetric emergencies, such as abruptio placenta, retained placenta, or incomplete abortion, are also associated with the development of DIC. Tissue factor is con-centrated in the placenta, and damage or disruption of this structure can activate coagulation pathways, resulting in coagulopathy.2
Pathophysiology
Regardless of the cause, the common thread in the develop-ment of DIC is damage to the endothelium that results in activation of the coagulation mechanism (Figure 27-1).3 The extrinsic coagulation pathway plays a major role in the devel-opment of DIC. 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 activa-tion of the intrinsic coagulation pathway leads to the massive disruption of the delicate balance that is hemostasis. Exces-sive thrombin formation results in rapid consumption of coagulation factors and depletion of regulatory substances—
protein C, protein S, and antithrombin.4 With no checks and balances, thrombi continue to form along damaged epithelial walls, resulting in occlusion of the vessels. As occlusion reaches a critical level, tissue ischemia ensues, leading to further tissue damage and perpetuating the process. Eventu-ally, end-organ function is affected by the ischemia, and failure is evident.3
In response to the formation of clots, the fibrinolytic system is activated. As plasmin breaks down the fibrin clots, fibrin split products are released, and they act as anticoagu-lants.2 Coupled with depletion of circulating clotting factors, activation of fibrinolysis results in excessive bleeding. The end result is shock and further tissue ischemia that aggravate end-organ dysfunction and failure. Death is imminent if this destructive cycle is not interrupted.5
Assessment and Diagnosis
Favorable outcomes for patients with DIC depend on accu-rate and timely diagnosis of the condition. Realization of the role underlying pathology plays, recognition of clinical mani-festations, and assessment of appropriate laboratory values are key steps in this process.
Clinical Manifestations
Clinical manifestations are related to the two primary patho-physiologic mechanisms of DIC: the formation of thrombi and bleeding. Thrombi in peripheral capillaries can lead to cyanosis, particularly in the fingers, toes, ears, and nose. In severe, untreated cases, this peripheral ischemia may progress to gangrene.1,2 As the condition progresses, ischemia worsens, and end organs are affected. The result of this more central ischemia can be respiratory insufficiency and failure, acute kidney injury, bowel infarction, and ischemic stroke. The tissue damage that results perpetuates the anomalies of DIC.2
As coagulation factors are depleted, bleeding from intra-venous and other puncture sites is observed. Ecchymosis may result from even routine interventions such as the use of a manual blood pressure cuff, bathing, or turning.1,2 Bloody drainage may also occur from surgical sites, drains, and Be sure to check out the bonus material, including review questions, on the Evolve website at
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FIG 27-1 Pathophysiology of Disseminated Intravascular Coagulation. (From Kumar V, et al.
Red blood cell and bleeding disorders. In: Kumar V, et al, eds. Robbins and Cotran Pathologic Basis of Disease. 8th ed. Philadelphia: Saunders; 2010.)
Massive tissue destruction
Activation of plasmin
Microangiopathic hemolytic anemia
Proteolysis of clotting factors
Fibrin split products
Inhibition of thrombin, platelet aggregation, and fibrin polymerization
Endothelial injury
Platelet aggregation
Consumption of clotting factors and platelets Sepsis
Fibrinolysis
Bleeding Ischemic tissue
damage Vascular occlusion Widespread microvascular
thrombosis Release of tissue
factor
Modified from Cotran RS, et al. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia: Saunders; 1999.
Obstetric Complications
• Abruptio placenta
• Placenta previa
• Retained dead fetus
• Septic abortion
• Amniotic fluid embolism
• Toxemia of pregnancy Infections
• Gram-negative sepsis
• Gram-positive sepsis
• Meningococcemia
• Rocky Mountain spotted fever
• Histoplasmosis
• Aspergillosis
• Malaria Neoplasms
• Carcinomas of pancreas, prostate, lung, and stomach
• Acute promyelocytic leukemia
• Tumor lysis syndrome
• Chemotherapy
Massive Tissue Injury
• Traumatic
• Crush injuries
• Burns
• Extensive surgery
• Heat stroke
• Acute transplant rejection Miscellaneous
• Acute intravascular hemolysis
• Snakebite
• Giant hemangioma
• Shock
• Heat stroke
• Vasculitis
• Aortic aneurysm
• Liver disease
• Cardiac arrest
BOX 27-1 Causes of Disseminated Intravascular Coagulation
urinary catheters. With progression of DIC, the patient is at risk for severe gastrointestinal or subarachnoid hemor-rhage.1,2 Table 27-1 lists many of the common signs and symptoms of DIC.
Laboratory Findings
Laboratory tests used to diagnose DIC essentially assess the four basic characteristics of this syndrome: 1) increased
coagulant activity, 2) increased fibrinolytic activity, 3) impaired regulatory function, and 4) end-organ failure.2
Continuous activation of the coagulation pathways results in consumption of coagulation factors. Because of this, the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the international normalized ratio (INR) values are elevated. Although the platelet count may fall within normal ranges, serial examination reveals a declining
SYSTEM SIGNS RELATED TO HEMORRHAGE
SIGNS RELATED TO THROMBI Integumentary Bleeding from
gums, venipunctures, and old surgical sites; epistaxis;
ecchymosis
Peripheral cyanosis, gangrene
Cardiopulmonary Hemoptysis Dysrhythmias, chest pain, acute myocardial infarction, pulmonary embolus, respiratory failure
Renal Hematuria Oliguria, acute
kidney injury, renal failure Gastrointestinal Abdominal
distention, hemorrhage
Diarrhea, constipation, bowel infarct Neurologic Subarachnoid
hemorrhage
Altered level of consciousness, ischemic stroke
TABLE 27-1 Common Signs and
Symptoms of Disseminated Intravascular Coagulation
TEST VALUE
Prothrombin time (PT) >12.5 sec
Platelets <50,000/mm3 or at least
50% drop from baseline Activated partial
thromboplastin time (aPTT)
>40 sec
D-dimer >250 ng/mL
Fibrin degradation
products (FDP) >40 mg/mL
Fibrinogen <100 mg/dL
TABLE 27-2 Key Laboratory Studies in Disseminated Intravascular Coagulation
trend in values. An unexpected drop of at least 50% in the platelet count, particularly in the presence of known contrib-uting factors and associated signs and symptoms, strongly indicates DIC.3 Fibrinogen levels drop as more and more clots are formed. Thrombus formation in small vessels narrow 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. Damaged, frag-mented RBCs are called schistocytes.1,2
In response to the excess clotting activity, the fibrinolytic process accelerates, and levels of byproducts increase. This is reflected in markedly elevated levels of fibrin degradation products. Another key laboratory test used to evaluate the degree of clot dissolution—and therefore the severity of the coagulopathy—is the D-dimer level.1 D-dimers exclusively indicate clot degradation because, unlike fibrin degradation products, which also result from the breakdown of free cir-culating fibrin, D-dimers result only from dissolution of clots.2 With progression of the coagulopathy, normal regulatory mechanisms are disrupted, as reflected in decreasing levels of inhibitory factors such as protein C, factor V, and anti-thrombin III.1,2,6
Unchecked DIC resulting in occlusion of vessels and tissue ischemia leads to end-organ dysfunction. Respiratory failure, indicated by abnormal arterial blood gas (ABG) levels;
liver failure, indicated by increasing liver enzymes, and renal impairment, indicated by rising blood urea nitrogen
(BUN) and creatinine levels, are common findings in advanced DIC.6
No single laboratory study can confirm the diagnosis of DIC, but several key results are strong indicators of the condi-tion (Table 27-2). The International Society of Thrombosis and Hemostasis emphasizes early detection of DIC through observation of abnormal trends in laboratory values.4
Medical Management
Without question, the primary intervention in DIC is preven-tion. Being aware of the conditions that commonly contribute to the development of DIC and treating them vigorously and without delay provide the best defense against this devastat-ing condition.1-3,6 After DIC is identified, maintaining organ perfusion and slowing consumption of coagulation factors are paramount to achieving a favorable outcome.1,2
Multiple organ dysfunction syndrome (MODS) frequently results from DIC and exacerbates the underlying pathology.5 It is essential to prevent end-organ ischemia and damage by supporting blood pressure and circulating volume. Adminis-tration of intravenous fluids and inotropic agents and, if overt hemorrhaging is evident, infusion of packed RBCs are appro-priate interventions to replace blood volume and essential, oxygen-carrying RBCs.
In the presence of severe platelet depletion (less than 50,000/mm3) and severe hemorrhage, platelet transfusions are often indicated.1,4 However, caution must be used when administering platelets because antiplatelet antibodies may be formed. These antibodies may become activated during future platelet transfusions and elicit DIC.7
Replacement of clotting factors in the patient with DIC is thought by some authorities to perpetuate the coagulopathy;
however, there is little scientific evidence to support this theory.3 Fibrinogen levels less than 100 mg/dL indicate the appropriateness of administering cryoprecipitate. A pro-longed PT indicates the need for fresh-frozen plasma.1,2,4
Slowing consumption of coagulation factors by inhibiting the processes involved in clot formation is another strategy used in treating DIC. The use of heparin, particularly low–
molecular-weight heparin (LMWH), to prevent formation of future clots is controversial.1 It is contraindicated in patients with DIC associated with recent surgery or with gastrointes-tinal or central nervous system (CNS) bleeding. However, heparin has been beneficial in obstetric emergencies such as
adequate hemodynamic support and tissue oxygenation is essential in preventing or combating end-organ damage.
Close monitoring of vital signs, hemodynamic parameters, intake and output, and appropriate laboratory values assists the critical care nurse in administering and titrating appro-priate agents.2
Initiating Bleeding Precautions
Awareness of the patient’s bleeding potential necessitates adjustments to normal nursing interventions. The nurse avoids unnecessary venipunctures that may result in bleed-ing, bruisavoids unnecessary venipunctures that may result in bleed-ing, or hematomas by drawing blood from and administering medications through existing arterial or venous lines. The use of manual or automatic blood pressure cuffs is avoided whenever possible. If tracheal or oral suction-ing is necessary, the use of low-level suction is recommended.6 Meticulous skin care is advised, keeping the skin moist and using specialty mattresses and beds as appropriate to prevent breakdown. Gentle care should be used when bathing or turning the patient to prevent bruising or hematoma formation.
Providing Comfort and Emotional Support
The development of DIC in the already critically ill patient can be stressful for the patient and his or her significant others. It is imperative to provide psychosocial support throughout this crisis. Calm reassurance and uncomplicated explanations of the care the patient is receiving can help to allay much of the anxiety experienced. The critical care nurse must answer all questions and provide information in terms best understood by all parties. The use of an interpreter when English is not the primary language can enhance understanding and help avoid misconceptions. Providing spiritual support as requested may also be of assistance. Col-laborative management of the patient with DIC is outlined in Box 27-3.