Disseminated Intravascular Coagulation (DIC)
Definition
Disseminated Intravascular Coagulation (DIC) is an acquired syndrome characterized by the intravascular activation of coagulation with a loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which, if sufficiently severe, can produce organ dysfunction (1). It is absolutely crucial to internalize that DIC is never a primary disease; it is always a secondary, downstream pathological process triggered by a separate, severe underlying illness (2). This core principle dictates the entire management approach: the definitive treatment is always the identification and aggressive management of the underlying trigger, not the DIC itself. The term "syndrome" highlights that DIC is a constellation of clinical and laboratory abnormalities, rather than a single disease entity with a uniform cause.
Epidemiology
The true incidence of DIC is challenging to pinpoint as it is a complication, not a primary diagnosis. However, it is estimated to affect approximately 1% of all hospitalized patients. This figure rises dramatically in high-acuity settings, complicating the course of 10-30% of patients in the Intensive Care Unit (ICU) (19). The development of DIC is a powerful and independent predictor of mortality. Its presence is strongly associated with the development of multiple organ failure, with overall mortality rates reported in the alarming range of 20% to 50% (9). For patients with sepsis, the most common trigger, the development of overt DIC nearly doubles the mortality risk compared to septic patients without this complication (10).
In the Malaysian and Southeast Asian context, the epidemiology is uniquely shaped by the high prevalence of specific infectious diseases, which must be at the forefront of a clinician's mind.
Sepsis: As with the rest of the world, sepsis remains the most common trigger for DIC in Malaysia. With sepsis being a leading cause of admission to local ICUs and carrying in-hospital mortality rates of over 50% in some Malaysian studies, the burden of sepsis-induced DIC is substantial (3, 23). The house officer must consider common local pathogens for bacterial sepsis, including E. coli, Staphylococcus aureus, Streptococcus pneumoniae, as well as regionally important pathogens.
Dengue Haemorrhagic Fever (DHF): Dengue virus infection is a major public health emergency in Malaysia, with frequent, large-scale outbreaks. While the hallmark of DHF is plasma leakage, a severe coagulopathy is a defining characteristic of its most severe form, Dengue Shock Syndrome (DSS). This coagulopathy often meets the full criteria for DIC and is a major contributor to bleeding and mortality (29). A landmark historical study conducted at Kuala Lumpur General Hospital directly linked DIC to fatalities in children with DHF, cementing its clinical importance in our local setting (36). The pathophysiology may have unique features, with some evidence suggesting a primary hyperfibrinolytic state driven by direct viral effects, which can lead to a more severe bleeding phenotype.
Other Endemic Infections: The differential diagnosis for the cause of DIC in a Malaysian patient must include other severe infections endemic to the region.
Melioidosis (caused by Burkholderia pseudomallei) and Leptospirosis are prevalent in Malaysia and are well-known causes of severe sepsis, septic shock, and consequently, fulminant DIC (37).
Severe falciparum malaria is a recognized cause of DIC, contributing to both bleeding and the critical thrombotic complications of cerebral malaria (10).
Etiology
Identifying and managing the underlying trigger is the absolute cornerstone of therapy. A systematic approach to the potential causes is essential.
Severe Infections and Sepsis (30-50% of cases): This is the most frequent cause. The systemic inflammatory response, driven by bacterial products (e.g., endotoxin) and host cytokines (TNF-α, IL-1, IL-6), triggers widespread expression of Tissue Factor on monocytes and endothelial cells, turning the vasculature into a procoagulant surface (3, 9).
Organisms: While classically associated with Gram-negative bacteria (E. coli, Neisseria meningitidis), it is critical to remember that Gram-positive organisms (S. aureus, S. pneumoniae), viruses (Dengue, Ebola, other haemorrhagic fevers), fungi (Candida), and parasites (Plasmodium falciparum) are also common culprits (3).
Major Trauma and Tissue Injury: This category accounts for another major proportion of acute DIC cases. The mechanism is the direct, massive release of procoagulant substances, including Tissue Factor and Damage-Associated Molecular Patterns (DAMPs), from extensively damaged tissues (4).
Examples: Polytrauma, severe crush injuries, major head trauma (brain tissue is rich in TF), extensive burns, heat stroke, and severe rhabdomyolysis are all potent triggers (3).
Malignancy: Cancer is a common cause of DIC, which can present acutely or, more commonly, as a chronic, compensated state (often called "Trousseau's syndrome").
Solid Tumours: Mucin-producing adenocarcinomas of the pancreas, stomach, lung, and prostate are notorious for causing a chronic, thrombosis-dominant DIC. The mucin produced by these tumours can directly activate Factor X, contributing to the prothrombotic state (8).
Haematological Malignancies: Acute Promyelocytic Leukaemia (APL) is the classic and most feared cause of severe, acute, bleeding-dominant DIC. The granules within the leukaemic promyelocytes are packed with Tissue Factor and fibrinolytic activators. Upon initiation of chemotherapy, these granules are released (differentiation syndrome), triggering a catastrophic, hyperfibrinolytic coagulopathy (9).
Obstetric Complications: Pregnancy-related disorders are well-established causes of acute, often severe, DIC. The primary trigger is the entry of thromboplastin-rich material from the placenta or amniotic fluid into the maternal circulation (4).
Examples: Placental abruption (premature separation of the placenta), Amniotic Fluid Embolism (AFE), severe pre-eclampsia, HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets), and retained intrauterine fetal demise are all major obstetric triggers (3).
Other Important Causes:
Severe Immunologic Reactions: An acute haemolytic transfusion reaction due to ABO incompatibility or severe acute transplant rejection can trigger DIC through widespread endothelial damage and complement activation (8).
Vascular Disorders: Conditions with extensive endothelial damage or abnormal blood flow can lead to localized coagulation that becomes systemic. Examples include large aortic aneurysms and giant haemangiomas (Kasabach-Merritt syndrome) (8).
Toxins: The venom of certain snakes, particularly vipers found in Southeast Asia, contains potent enzymes that can directly activate coagulation factors (e.g., prothrombin, Factor X) or convert fibrinogen to fibrin, leading to a rapid and severe consumptive coagulopathy (11).
Severe Organ Dysfunction: Acute pancreatitis involves the release of proteolytic enzymes that can damage the endothelium and activate coagulation. Severe acute liver failure impairs the synthesis of both clotting factors and anticoagulant proteins, creating a fragile haemostatic state that can easily tip over into DIC (3).
Pathophysiology
DIC is a state of haemostatic chaos, best understood as a "vicious cycle" where inflammation and coagulation fuel each other. The process unfolds in a series of catastrophic steps:
Initiation - The "Spark": A pathological trigger (e.g., bacterial endotoxin in sepsis, massive tissue injury in trauma) causes a massive, systemic exposure of blood to Tissue Factor (TF). TF is the primary initiator of coagulation and is normally hidden from the bloodstream. In DIC, it becomes widely expressed on circulating monocytes and damaged endothelial cells (4).
Amplification - The "Wildfire": The initial TF exposure ignites a wildfire of systemic thrombin generation. Thrombin is the central enzyme of coagulation, converting fibrinogen to fibrin. This process becomes self-sustaining through powerful positive feedback loops, where thrombin itself activates other clotting factors (V, VIII, XI), generating even more thrombin. Simultaneously, the body's crucial natural anticoagulant systems are overwhelmed and consumed:
Antithrombin (AT), the main inhibitor of thrombin and Factor Xa, is rapidly depleted.
The Protein C pathway, which normally inactivates cofactors Va and VIIIa, is impaired by inflammatory downregulation of its receptors (thrombomodulin) and consumption of Protein C and its cofactor, Protein S (1, 4).
Consequences - Clot and Bleeding: This uncontrolled cascade has two devastating and simultaneous effects:
Microvascular Thrombosis and Organ Failure: The massive generation of thrombin leads to the deposition of fibrin strands and platelet-rich microthrombi throughout the small and medium-sized vessels of the body. This widespread thrombosis obstructs blood flow, leading to tissue hypoxia, ischaemic injury, and ultimately, Multiple Organ Dysfunction Syndrome (MODS). The kidneys, lungs, liver, and brain are particularly vulnerable. It is critical to remember that this microvascular thrombosis, not the bleeding, is the principal cause of the high mortality associated with DIC (5).
Consumptive Coagulopathy and Bleeding: The rampant, unchecked clotting process consumes platelets and coagulation factors (especially Fibrinogen, Factor V, and VIII) faster than the liver and bone marrow can produce them. This severe depletion of haemostatic components creates a systemic bleeding diathesis (8).
Secondary Hyperfibrinolysis: The presence of widespread fibrin triggers a compensatory, but dysregulated, fibrinolytic response. Plasminogen is converted to plasmin, which breaks down the fibrin clots. This generates large quantities of Fibrin Degradation Products (FDPs) and, more specifically, D-dimer. The bleeding in DIC is therefore a "perfect storm": it is caused by the profound thrombocytopenia and lack of clotting factors, which is then exacerbated because the FDPs themselves interfere with normal fibrin polymerization and platelet function, further impairing the body's ability to form a stable clot at sites of injury (2, 9).
Clinical Presentation
The clinical picture of DIC is a dramatic and often confusing paradox of simultaneous bleeding and thrombosis. A high index of suspicion in any critically ill patient with a plausible trigger is essential. While bleeding manifestations are often more clinically obvious, it is the insidious, widespread microvascular thrombosis that is typically responsible for the progressive organ failure (5).
Diagnostic Clues
The most classic and highly suggestive sign of DIC is spontaneous bleeding or oozing from three or more unrelated sites. This finding is a powerful indicator of a systemic, rather than a local, haemostatic defect (3).
Pay meticulous attention to the patient's lines and wounds. Oozing from venipuncture sites, arterial line insertion points, or around intravascular catheters is often the first and most subtle sign. Bleeding from a surgical wound that was previously dry is also a major red flag.
Common Symptoms
Dermatological: The skin is often a window to the systemic process. Look for petechiae (small, pinpoint, non-blanching red/purple spots, often on dependent areas), ecchymoses (larger bruises that appear spontaneously or with minimal trauma), and purpura (widespread purple discolouration of the skin) (3, 8).
Mucosal Bleeding: Epistaxis (nosebleeds) and gingival (gum) bleeding are common and can be persistent (3).
Gastrointestinal (GI) Bleeding: This can range from occult blood in the stool to frank haematemesis (vomiting bright red blood) or melena (black, tarry stools from digested blood) (8).
Genitourinary (GU) Bleeding: Haematuria is a common finding, which may be macroscopic (visible to the naked eye) or microscopic (8).
Signs of Organ Dysfunction (from thrombosis): The development or worsening of organ dysfunction in a patient at risk for DIC should raise immediate suspicion.
Renal: Oliguria (urine output <0.5 mL/kg/hr), anuria, and a rapidly rising serum creatinine are classic signs of acute kidney injury (AKI) due to glomerular microthrombi (4).
Pulmonary: Dyspnoea, tachypnoea, worsening hypoxia, and the need for escalating respiratory support are signs of developing Acute Respiratory Distress Syndrome (ARDS), caused by damage to the pulmonary microvasculature (8).
CNS: Altered mental status, ranging from subtle confusion and delirium to obtundation and coma, can result from cerebral microthrombi or intracranial bleeding (3).
⚠️ Red Flag Signs & Symptoms
Purpura Fulminans: This is a true dermatological and haematological emergency. It is a severe form of acute DIC characterized by the rapid onset of extensive, symmetrical, and often painful areas of cutaneous haemorrhage and necrosis, typically affecting the extremities. Haemorrhagic bullae may also form. It represents widespread thrombotic occlusion of the dermal vasculature and often precedes limb loss (3).
Acral Cyanosis and Gangrene: Ischaemic necrosis of the distal parts of the body, such as the fingers, toes, nose, and genitalia, due to extensive microvascular thrombosis. This is a sign of severe, uncontrolled thrombosis (3).
Major Vessel Thrombosis: While microvascular thrombosis is the hallmark, DIC can also lead to thrombosis of larger vessels, presenting as deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, or myocardial infarction (4).
Life-Threatening Haemorrhage: Catastrophic bleeding can occur, most dangerously into the intracranial, intra-abdominal, or retroperitoneal spaces, leading to rapid haemodynamic collapse (2).
Complications
Complications are primarily driven by the dual insults of widespread microvascular thrombosis leading to ischaemic organ failure and bleeding into critical organs.
Neurological: Ischaemic stroke from microthrombi is common. Patients may also suffer from intracerebral or subarachnoid haemorrhage. The more common presentation is a diffuse encephalopathy or delirium due to widespread micro-ischaemia.
Cardiovascular: Myocardial ischaemia or infarction can occur from coronary microthrombi. Profound shock is often multifactorial, driven by the underlying condition (e.g., sepsis), hypovolemia from bleeding, and direct cardiac dysfunction.
Respiratory: Acute Respiratory Distress Syndrome (ARDS) is a frequent and severe complication, resulting from inflammatory damage and thrombosis in the pulmonary microcirculation. Pulmonary embolism from larger clots can also occur.
Renal: Acute Kidney Injury (AKI) is one of the most common organ failures in DIC, caused by fibrin deposition in the glomerular capillaries. This can rapidly progress to anuria requiring renal replacement therapy.
Gastrointestinal: Ischaemia of the gut can lead to ileus, ulceration, and life-threatening bowel necrosis. Ischaemic hepatitis can present with sharply rising liver transaminases.
Dermatological: In severe cases, widespread thrombosis can lead to gangrene of the extremities, requiring amputation. Purpura fulminans represents the most extreme form of this complication.
Prognosis
The development of DIC is a critical prognostic event that significantly worsens the outcome of the underlying disease. Overall mortality is high, ranging from 20% to 50% (9). In patients with sepsis, the presence of overt DIC nearly doubles the risk of death (10). Key factors that influence the prognosis include the nature and reversibility of the underlying cause, the severity of the coagulopathy as measured by the ISTH score, and, most importantly, the degree of established organ failure at the time of diagnosis.
Differential Diagnosis
Severe Liver Disease: In advanced liver failure, the synthesis of most clotting factors (II, V, VII, IX, X) and anticoagulant proteins (Protein C, S, Antithrombin) is impaired, leading to a prolonged PT/INR and aPTT that can mimic DIC. However, the synthesis of Factor VIII is largely extrahepatic. Therefore, in liver disease, Factor VIII levels are typically normal or even elevated (as it is also an acute-phase reactant), whereas in DIC, Factor VIII is consumed, and its level is low. This can be a key distinguishing test (11).
Thrombotic Thrombocytopenic Purpura (TTP): This is another form of microangiopathic haemolytic anaemia (MAHA) that presents with thrombocytopenia and organ dysfunction (especially neurological and renal). However, TTP is a medical emergency requiring urgent plasma exchange. The coagulation profile (PT, aPTT, Fibrinogen) is typically normal in TTP, which is a major point of differentiation from DIC. The definitive diagnosis of TTP is confirmed by finding severely deficient ADAMTS13 activity (<10%) (17).
Investigations
No single test is diagnostic in isolation. The diagnosis is made by recognizing a characteristic pattern of abnormalities that reflect the underlying pathophysiology of consumption and fibrinolysis, in a patient with a known trigger.
Immediate & Bedside Tests (The "DIC Screen")
Full Blood Count (FBC) and Peripheral Blood Film (PBF): An urgent FBC is essential to identify thrombocytopenia, a hallmark of platelet consumption in widespread microthrombi. A platelet count <100 x 10⁹/L is common. Crucially, a rapidly falling trend in the platelet count is often the most sensitive and earliest laboratory sign of developing DIC, even if the absolute count is still within the "normal" range (3). The PBF is vital to look for schistocytes (fragmented red cells), which are the morphological evidence of mechanical red cell damage from fibrin strands and strongly support a diagnosis of microangiopathic haemolytic anaemia (MAHA) (4).
Coagulation Profile (PT/INR, aPTT): The Prothrombin Time (PT) and Activated Partial Thromboplastin Time (aPTT) measure the extrinsic and intrinsic pathways, respectively. They are typically prolonged, reflecting the consumption of multiple coagulation factors (3). A clinical pitfall to be aware of is that in early, hyperacute DIC, circulating activated clotting factors can paradoxically lead to a normal or even shortened PT/aPTT, which can be dangerously misleading.
Fibrinogen: This is the primary substrate for fibrin clot formation and is consumed during DIC. However, as a potent acute-phase reactant, its synthesis by the liver is dramatically upregulated in inflammatory states like sepsis. This can mask the ongoing consumption, resulting in a fibrinogen level that is initially normal or even elevated. Therefore, a falling trend on serial measurements is a much more reliable indicator of consumptive coagulopathy than a single low value (3, 47). A level <1.5 g/L in a critically ill patient is highly concerning.
D-dimer: This is arguably the best single laboratory test for supporting a diagnosis of DIC. D-dimer is a specific degradation product formed only when cross-linked fibrin is broken down by plasmin. Its presence confirms that both thrombin (to form the clot) and plasmin (to lyse the clot) have been activated systemically. The test is highly sensitive; a normal D-dimer level has a very high negative predictive value and essentially excludes a diagnosis of overt DIC. However, it is not specific and can be elevated in many other conditions (e.g., VTE, surgery, trauma, malignancy). In DIC, the level of elevation is often dramatically high (e.g., >4,000 ng/mL or >10-20 times the upper limit of normal) (3, 47).
Gold Standard
The definitive diagnosis is established with the International Society on Thrombosis and Haemostasis (ISTH) Overt DIC Score. This objective and validated scoring system should be applied to any patient who has an underlying disorder known to be associated with DIC. It is a diagnostic tool, not a screening tool for the general hospital population (47).
A score of ≥ 5 is compatible with overt DIC. The patient should be managed as having DIC, and the score should be repeated daily.
If the score is < 5 but clinical suspicion remains high, this may represent an early, "non-overt" stage. The score should be recalculated every 1-2 days to monitor for progression.
ISTH Overt DIC Scoring System
Platelet count (x10⁹/L)
>100: 0 points
50 to <100: 1 point
<50: 2 points
Elevated Fibrin Marker (e.g., D-dimer)
No increase: 0 points
Moderate increase: 2 points
Strong increase: 3 points
Prolonged Prothrombin Time (PT) (seconds above normal)
<3 seconds: 0 points
3 to <6 seconds: 1 point
>6 seconds: 2 points
Fibrinogen level (g/L)
≥1.0 g/L: 0 points
<1.0 g/L: 1 point
(Source: Adapted from ISTH guidelines (47). Note: "Moderate" and "Strong" increases in D-dimer are based on local laboratory assays.)
Monitoring & Staging
Serial testing is crucial. DIC is a highly dynamic process. A single set of laboratory tests provides only a snapshot. It is essential to repeat the DIC screen (platelets, PT/INR, aPTT, fibrinogen) at regular intervals, typically every 12 to 24 hours, or more frequently if the patient is clinically unstable. This allows the clinician to monitor the trajectory of the coagulopathy, assess the response to treatment of the underlying cause, and guide supportive therapy (47).
Management
Management Principles
The management of DIC focuses on two synergistic pillars: (1) aggressive treatment of the underlying cause and (2) supportive management of the haemostatic failure to control bleeding and support organ function (1). The first principle is paramount; all supportive measures will ultimately fail if the primary trigger is not controlled.
Acute Stabilisation (The First Hour)
Supportive therapy with blood products is aimed at controlling active bleeding and preventing haemorrhage in high-risk situations (e.g., before an invasive procedure). It is critical to understand that transfusions are guided by the patient's clinical status (i.e., active bleeding), not by laboratory values alone. Prophylactic transfusion in a non-bleeding patient with abnormal lab values is generally not indicated, does not improve outcomes, and may carry risks (50). All decisions must be guided by the Malaysian Ministry of Health's "Handbook on Clinical Use of Blood" (56).
Platelet Concentrate:
Indication: For a patient with active bleeding and a platelet count < 50 x 10⁹/L. Also consider for non-bleeding patients with a count <10-20 x 10⁹/L due to the high risk of spontaneous haemorrhage, or if an invasive procedure is required.
Rationale: The goal is to provide sufficient platelets to form a primary haemostatic plug and control microvascular bleeding (56).
Dose: 1 unit of random donor platelet concentrate per 10-15 kg body weight, or one unit of apheresis (single donor) platelets.
Fresh Frozen Plasma (FFP):
Indication: For a patient with active bleeding and evidence of a significant coagulation factor deficiency, typically a PT and/or aPTT ratio > 1.5 times the mean normal control.
Rationale: FFP contains all coagulation factors and is essential to replace the multiple factors consumed during DIC, allowing for stable fibrin clot formation (56).
Dose: 15 - 20 mL/kg body weight.
Cryoprecipitate:
Indication: This is the primary and most concentrated source of fibrinogen. It is indicated for a patient with active bleeding and evidence of significant hypofibrinogenaemia, typically a fibrinogen level < 1.5 g/L.
Rationale: Fibrinogen is the final substrate for clot formation. Providing adequate levels is critical for achieving haemostatic stability. Cryoprecipitate is superior to FFP for this purpose as it provides a higher concentration of fibrinogen in a smaller volume (56).
Dose: 1 unit of cryoprecipitate per 5-10 kg body weight (typically a pool of 5-10 units for an adult).
Definitive Therapy
Treat the underlying cause: This is the single most effective intervention and must be pursued with urgency and aggression.
Sepsis: Rapid administration of appropriate broad-spectrum antibiotics (within the first hour), aggressive fluid resuscitation, vasopressor support for shock, and urgent source control (e.g., drainage of an abscess, removal of an infected line, debridement of necrotic tissue).
Trauma: Surgical or interventional radiological control of bleeding, stabilization of fractures, and management of massive tissue injury.
Obstetric Emergency: Prompt delivery of the fetus and placenta is often life-saving for the mother in cases of abruption, AFE, or HELLP syndrome.
APL: This is a haematological emergency. Specific therapy with All-Trans Retinoic Acid (ATRA) and often arsenic trioxide must be started immediately on suspicion, even before genetic confirmation, as it can rapidly reverse the coagulopathy.
Supportive & Symptomatic Care
Maintain organ perfusion with judicious fluid resuscitation and vasopressor support to target a mean arterial pressure (MAP) of ≥65 mmHg.
Ensure adequate oxygenation and consider mechanical ventilation for ARDS or respiratory failure.
Provide nutritional support, preferably via the enteral route, once the patient is stabilized.
Implement VTE prophylaxis with low-molecular-weight heparin (LMWH) or unfractionated heparin in most patients once bleeding is controlled, as they remain at very high risk for thrombosis.
Stress ulcer prophylaxis with a proton pump inhibitor may be considered in high-risk ICU patients.
Key Nursing & Monitoring Instructions
Strict hourly input/output chart monitoring to assess for AKI.
Hourly vital signs (HR, BP, RR, SpO2, Temperature) and neurological observations (GCS).
Meticulously and regularly inspect all line sites, wounds, drains, and skin for any new or worsening bleeding or signs of ischaemia (e.g., dusky digits).
Test stool and any nasogastric tube aspirate for occult blood.
Inform the medical team immediately of any signs of new bleeding, haemodynamic instability (e.g., systolic BP <90 mmHg, rising tachycardia), or worsening organ dysfunction (e.g., drop in urine output, change in mental status).
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient has signs of life-threatening bleeding (e.g., suspected intracranial haemorrhage, massive GI bleed with haemodynamic instability).
The patient develops worsening or new organ failure (e.g., requiring mechanical ventilation, new requirement for vasopressors, anuria).
There is clinical evidence of major vessel thrombosis (e.g., a cold, pulseless limb) or the development of purpura fulminans.
The diagnosis is uncertain, or the patient is not responding to initial management of the suspected underlying cause.
Referral Criteria
Refer to the Haematology team early for complex cases. Their expertise is invaluable for interpreting complex coagulation results, guiding nuanced transfusion strategies, and advising on the use of controversial therapies like heparin (for thrombosis-dominant DIC) or antifibrinolytics (for rare, hyperfibrinolytic bleeding-dominant DIC) (11, 50).
Refer to the relevant specialty for source control (e.g., General Surgery for an abdominal abscess, Interventional Radiology for embolization).
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