Disseminated Intravascular Coagulation (DIC)

Disseminated intravascular coagulation, commonly known as DIC, is a life-threatening syndrome in which the body's normal blood clotting mechanisms become dysregulated, causing simultaneous widespread clot formation and uncontrolled bleeding throughout the body. This seemingly paradoxical combination occurs because massive activation of the coagulation cascade leads to consumption of clotting factors and platelets faster than they can be replaced, leaving the horse unable to form clots when and where they are actually needed. DIC is not a primary disease but rather a catastrophic complication that develops secondary to severe underlying conditions including sepsis, severe colic, retained placenta, snake envenomation, massive tissue trauma, and other critical illnesses.

Disseminated intravascular coagulation can affect horses of any breed, age, or sex, with incidence determined entirely by the underlying conditions that trigger this secondary syndrome. Septic foals face high DIC risk when infections become overwhelming. Adult horses with severe gastrointestinal disease, particularly strangulating lesions causing tissue death, commonly develop DIC as a complication. Broodmares with retained placenta, dystocia, or postpartum complications are at significant risk. Horses experiencing heat stroke, severe trauma, hemolytic episodes, or cancer may develop DIC as part of their disease progression. Any condition causing systemic inflammation, tissue destruction, or bloodstream infection can potentially trigger this devastating cascade.

The impact of disseminated intravascular coagulation on equine health is severe and often fatal. The combination of microvascular clotting and hemorrhage damages multiple organ systems simultaneously. Microthrombi occlude small blood vessels, causing tissue ischemia and organ dysfunction affecting kidneys, lungs, liver, and other vital structures. Simultaneously, depleted clotting factors and platelets lead to spontaneous hemorrhage at puncture sites, from mucous membranes, and into body cavities and tissues. The underlying disease process continues while DIC adds its own devastating layer of pathology. Mortality rates for horses with clinical DIC are high despite intensive treatment.

Treatability of disseminated intravascular coagulation depends heavily on identifying and addressing the underlying cause while providing supportive care for the coagulation disorder itself. Horses in which the triggering condition can be resolved, such as through surgery for colic or uterine lavage for retained placenta, have better prognoses than those with uncontrollable underlying diseases. Early recognition of impending DIC, before full-blown clinical syndrome develops, allows intervention that may prevent progression. However, once established DIC is present with significant organ dysfunction and hemorrhage, prognosis is guarded to poor even with aggressive intensive care in hospital settings.

The primary cause of disseminated intravascular coagulation is not a single agent but rather the body's abnormal systemic response to various severe underlying conditions. The common thread among these triggering conditions is their ability to cause widespread activation of the coagulation cascade through release of tissue factor, endothelial damage, or direct activation of clotting proteins. Sepsis and systemic inflammatory response syndrome are among the most common triggers, as bacterial products and inflammatory mediators activate coagulation throughout the vasculature. Endotoxemia, where gram-negative bacterial cell wall components enter the bloodstream, is particularly potent at initiating DIC. Severe tissue injury from trauma, burns, or surgical complications releases tissue factor that triggers clotting.

Disseminated intravascular coagulation is not a hereditary condition, as it represents an acquired response to overwhelming illness rather than an inherited predisposition. However, individual variation in inflammatory and coagulation responses may influence susceptibility to DIC development when exposed to triggering conditions. Some horses may develop DIC in response to illness severity that other horses survive without coagulopathy, suggesting biological variation in thresholds for this response. No genetic testing is available or applicable since DIC is entirely an acquired syndrome.

Environmental and management factors contributing to DIC relate to conditions that predispose horses to the underlying diseases that trigger coagulopathy. Situations increasing sepsis risk, such as contaminated wounds, postoperative infections, or neonatal illness, indirectly increase DIC risk. Management failures leading to retained placenta, such as inadequate monitoring of mares post-foaling, create DIC risk. Delayed treatment of colic allowing intestinal compromise increases the likelihood of endotoxemia and secondary DIC. Heat exposure causing heat stroke, snake habitats where envenomation may occur, and any circumstances leading to severe tissue trauma or hemorrhage represent environmental risk factors for conditions that may trigger DIC.

Risk factors for developing disseminated intravascular coagulation in horses include any severe illness or injury, with specific high-risk scenarios well recognized in veterinary medicine. Septic foals, particularly those with failure of passive transfer, face substantial DIC risk as overwhelming infections progress. Horses requiring gastrointestinal surgery, especially for strangulating lesions, have elevated perioperative DIC risk. Broodmares experiencing dystocia, retained placenta beyond several hours, or metritis are at risk. Horses with severe hemolytic anemia from any cause may develop DIC. Cancer patients, particularly those with highly aggressive or widespread malignancies, may develop DIC. Prolonged shock from any cause depletes coagulation factors and may trigger consumptive coagulopathy.

The pathophysiology of disseminated intravascular coagulation involves a vicious cycle of clot formation and hemorrhage. Triggering events activate the coagulation cascade systemically rather than locally at sites of injury. Thrombin, the central enzyme in clot formation, is generated throughout the vasculature, converting fibrinogen to fibrin and activating platelets. Microthrombi form in small blood vessels throughout the body, causing end-organ ischemia. Simultaneously, coagulation factors and platelets are consumed faster than production can replace them, leaving the blood unable to clot effectively when needed. Fibrinolysis is also activated, breaking down clots and releasing fibrin degradation products that further interfere with hemostasis. The result is paradoxical simultaneous thrombosis and hemorrhage.

Early warning signs of disseminated intravascular coagulation may be subtle and easily attributed to the underlying disease process rather than recognized as an evolving coagulopathy. Clinicians should maintain high suspicion for DIC in any severely ill horse, as early recognition improves outcomes. Initial signs may include mild oozing from venipuncture sites or IV catheter insertion points that seems excessive for the procedure. Bruising may appear more readily than expected from normal handling. The horse may show signs of worsening systemic illness despite treatment, with declining cardiovascular parameters and progressive organ dysfunction. Laboratory abnormalities often precede clinical hemorrhage.

As disseminated intravascular coagulation progresses, common symptoms become increasingly apparent and alarming. Hemorrhage from multiple sites is the hallmark clinical finding, with blood oozing from venipuncture sites, injection sites, and around catheters. Petechiae and ecchymoses appear on mucous membranes, sclera, and skin, indicating spontaneous hemorrhage into tissues. Blood may appear in urine, feces, or respiratory secretions. Bleeding from the nose without trauma is common. Wounds, even minor ones, fail to stop bleeding normally. Simultaneously, signs of impaired tissue perfusion from microvascular thrombosis develop, including cool extremities, prolonged capillary refill, and organ dysfunction.

Behavioral changes in horses with DIC reflect the severity of systemic illness and blood loss. Affected horses are typically profoundly depressed, with minimal response to environmental stimuli. They may stand with head lowered or become recumbent and reluctant to rise. Appetite is absent in most cases. The horse may shift weight frequently or show signs of abdominal discomfort if gastrointestinal disease is the underlying cause. Weakness progresses as blood loss continues and organ function declines. Some horses become anxious or restless if blood loss is acute and rapid. Overall demeanor reflects a critically ill animal in systemic crisis.

Physical signs on examination of a horse with DIC demonstrate both hemorrhage and underlying illness severity. Mucous membranes may be pale from blood loss, yellow from liver dysfunction, muddy from poor perfusion, or show combinations of these abnormalities. Petechiae and ecchymoses are visible on gums, vulvar or prepuce mucosa, and sclera. Heart rate is elevated, often markedly so, reflecting hypovolemia and stress. Pulse quality may be weak. Respiratory rate is elevated, and lung sounds may be abnormal if pulmonary hemorrhage or edema is present. Temperature may be elevated from underlying infection or low from shock. Extremities may be cool with prolonged capillary refill time.

Symptom progression in disseminated intravascular coagulation is typically rapid once clinical hemorrhage begins. Initial mild oozing progresses to frank hemorrhage from multiple sites. Blood pools under skin as bruising expands. Internal hemorrhage may cause abdominal distension, respiratory compromise from hemothorax, or neurological signs from central nervous system bleeding. Signs of organ failure develop, including decreased or absent urine production from kidney damage, respiratory distress from lung dysfunction, and altered mentation from cerebral hypoxia or hemorrhage. Without intervention, shock progresses to cardiovascular collapse and death, often within hours to days of clinical DIC onset.

Emergency symptoms requiring immediate intensive intervention include any evidence of spontaneous hemorrhage in a critically ill horse, as this indicates probable DIC requiring urgent management. Rapid decline in perfusion parameters, including weakening pulses, cooling extremities, and deteriorating mentation, signals decompensation. Respiratory distress may indicate pulmonary hemorrhage or edema requiring immediate support. Frank blood from body openings, rapidly expanding bruising, or failure of wounds to clot demands immediate coagulation assessment and treatment. Any horse with underlying conditions predisposing to DIC that develops unexplained hemorrhage or rapid deterioration should be evaluated emergently for this syndrome.

Physical examination of a horse suspected of having disseminated intravascular coagulation reveals findings consistent with both the underlying triggering condition and the coagulopathy itself. The veterinarian notes hemorrhagic manifestations including petechiae, ecchymoses, and bleeding from venipuncture sites or wounds. Assessment of perfusion through mucous membrane color, capillary refill time, pulse quality, and extremity temperature helps characterize hemodynamic status. Vital signs typically show tachycardia, tachypnea, and variable temperature. The examination also focuses on identifying the underlying cause, whether gastrointestinal disease, sepsis, reproductive complications, or other triggering conditions. The clinical context of hemorrhage developing in a critically ill horse immediately raises suspicion for DIC.

Diagnostic tests essential for confirming disseminated intravascular coagulation include a coagulation panel revealing characteristic abnormalities. Prothrombin time and activated partial thromboplastin time are prolonged, reflecting depletion of coagulation factors. Platelet count is decreased, often dramatically, as platelets are consumed in microthrombus formation. Fibrinogen levels fall as this clotting protein is converted to fibrin and depleted. Fibrin degradation products, including D-dimers, are elevated as fibrinolysis breaks down the widespread clots being formed. Antithrombin III levels decrease as this natural anticoagulant is consumed. The complete blood count may show anemia from hemorrhage and fragmented red blood cells from passage through fibrin meshworks.

Advanced diagnostics help characterize DIC severity and monitor response to treatment. Serial coagulation testing tracks changes over time, with improving parameters indicating treatment effectiveness. Thromboelastography provides a global assessment of clot formation and breakdown dynamics, potentially offering earlier detection and more nuanced monitoring than traditional tests. Blood gas analysis reveals acid-base disturbances from poor tissue perfusion. Serum chemistry assesses organ function, with elevated kidney values, liver enzymes, and lactate indicating multi-organ involvement. Diagnostics targeting the underlying cause, such as abdominal imaging for colic or cultures for sepsis, guide treatment of the triggering condition essential for DIC resolution.

Differential diagnosis for the hemorrhagic manifestations of DIC includes other bleeding disorders and causes of multi-organ dysfunction. Thrombocytopenia from immune-mediated platelet destruction causes bleeding without the coagulation factor depletion seen in DIC. Inherited coagulopathies such as hemophilia are rare in horses and typically present earlier in life. Liver failure causes coagulation factor deficiency but through reduced production rather than consumption. Anticoagulant toxicity from rodenticide ingestion causes bleeding but has specific history and treatment. Severe sepsis and shock can cause multi-organ dysfunction without fulfilling DIC criteria. Laboratory assessment differentiates these conditions, with DIC showing the characteristic pattern of factor consumption, thrombocytopenia, and elevated degradation products.

Emergency treatment for disseminated intravascular coagulation focuses on aggressive resuscitation while addressing the underlying cause. Intravenous fluid therapy supports circulation and perfusion, though care must be taken not to exacerbate bleeding through excessive dilution of remaining clotting factors. Blood transfusion may be necessary if hemorrhage has caused significant anemia, providing both oxygen-carrying capacity and, with whole blood, some coagulation factors. Plasma transfusion delivers concentrated coagulation factors, antithrombin III, and other hemostatic proteins to replace consumed components. Platelet transfusion is challenging in horses but may be attempted in severe thrombocytopenia. Oxygen supplementation supports tissue oxygen delivery. The most critical intervention is treating the underlying cause triggering DIC.

Medical management of the underlying condition is essential since DIC will not resolve while the triggering process continues. Sepsis requires aggressive antimicrobial therapy with broad-spectrum coverage pending culture results, source control if possible, and intensive supportive care. Endotoxemia is addressed with anti-endotoxin therapies where available and supportive measures. Retained placenta requires uterine lavage and potentially oxytocin to encourage passage. Heat stroke demands cooling measures. Snake envenomation may require antivenin where available. Each underlying condition has specific treatment requirements, and successful DIC management depends on controlling the inciting cause.

Specific therapies targeting the coagulation dysregulation of DIC remain somewhat controversial and require case-by-case assessment. Heparin has been used in some DIC cases to prevent ongoing thrombus formation, but its use is debated as it may worsen bleeding in some situations. Low-molecular-weight heparin may offer advantages. Fresh frozen plasma provides coagulation factors, antithrombin III, and protein C that help restore normal hemostasis. Antithrombin III concentrates are available for human use and have been used in horses. Tranexamic acid and other antifibrinolytics might help reduce hemorrhage but could theoretically worsen thrombosis. Treatment decisions require weighing individual case characteristics and current evidence.

Supportive care for horses with DIC includes intensive monitoring and nursing in hospital settings. Continuous or frequent vital sign monitoring tracks response to therapy. Serial laboratory testing guides transfusion decisions and assesses treatment effectiveness. Careful fluid management maintains perfusion without exacerbating bleeding. Nutritional support provides energy and building blocks for clotting factor production. Pain management maintains comfort. Prevention of secondary problems including laminitis, decubital ulcers in recumbent horses, and nosocomial infections requires vigilant nursing care. The complexity and intensity of care required means DIC cases are best managed in hospital settings with experienced staff and laboratory support.

Surgical intervention may be necessary to address certain underlying causes of DIC. Colic surgery removes strangulated intestine and eliminates the source of endotoxemia and tissue factor release. Retained placenta unresponsive to medical management may require manual removal under appropriate conditions. Wound debridement eliminates devitalized tissue. Abscess drainage removes sources of ongoing sepsis. Surgical decisions in DIC cases must consider the bleeding risks inherent in operating on coagulopathic patients, balanced against the necessity of controlling the underlying cause. Some cases stabilize sufficiently with medical management to reduce surgical bleeding risk before proceeding.

Treatment decisions in DIC cases involve weighing prognosis, cost, and the horse's current condition. DIC indicates severe underlying disease, and mortality rates remain high despite intensive therapy. Cases where the underlying cause can be identified and effectively treated carry better prognoses than those with uncontrollable disease processes. Early-stage DIC detected through laboratory monitoring before clinical hemorrhage may be more amenable to treatment than established clinical coagulopathy. Intensive care for DIC is expensive, requiring hospitalization, transfusions, and constant monitoring over days. Honest prognostic discussions help owners make informed decisions about pursuing aggressive treatment versus humane euthanasia when prognosis is poor.

Recovery timeline for disseminated intravascular coagulation depends on successful treatment of the underlying cause and the extent of organ damage incurred before coagulopathy was controlled. Horses in which the triggering condition is eliminated and DIC is recognized early may show coagulation parameter improvement within twenty-four to forty-eight hours. Complete normalization of clotting function typically requires several days to a week as the liver produces new coagulation factors and platelet production catches up with losses. Clinical recovery from hemorrhage and organ dysfunction may take longer, with kidney injury or other organ damage potentially requiring extended recovery periods. Some horses recover fully, while others retain permanent organ compromise.

Post-treatment care and monitoring for horses recovering from DIC extends well beyond resolution of the coagulopathy itself. Serial coagulation testing confirms sustained normalization of clotting function and detects any relapse. Organ function monitoring through chemistry panels tracks kidney recovery, liver function, and other parameters. The underlying condition requires ongoing management specific to its nature, whether antimicrobials for resolved sepsis, wound care following surgery, or reproductive management after obstetric complications. Nutritional support aids recovery. Gradual return to activity follows clinical recovery assessment. Close monitoring continues until veterinarians are confident that both the underlying condition and its DIC complication have fully resolved.

Prognostic factors influencing recovery from DIC include the nature and severity of the underlying cause, the stage at which DIC was recognized, and the extent of organ damage. Cases where the triggering condition can be completely eliminated, such as through surgery for colic or resolution of infection, have better prognoses. Early recognition and intervention before clinical hemorrhage develops improves outcomes compared to established clinical DIC. Multi-organ dysfunction, particularly acute kidney injury or severe liver compromise, worsens prognosis. Horses that stabilize quickly with initial resuscitation fare better than those requiring prolonged support. Neonatal foals with DIC secondary to sepsis carry particularly guarded prognoses.

Long-term outlook for horses surviving DIC depends largely on any residual organ damage and the status of the underlying condition. Horses that recover without significant organ compromise may return to previous levels of function and activity. Those with persistent kidney disease, liver damage, or other organ impairment face ongoing management requirements and potential limitations. If the underlying triggering condition was fully resolved, recurrence risk is primarily related to exposure to future triggering conditions rather than persistence of the original problem. Prevention of future DIC centers on preventing severe illness through good management, prompt treatment of infections and other diseases, and appropriate perioperative care for horses requiring surgery.

Management practices preventing disseminated intravascular coagulation focus on preventing and promptly treating the severe conditions that trigger this syndrome. Aggressive early treatment of infections prevents progression to sepsis and endotoxemia. Prompt attention to wounds minimizes infection risk and tissue necrosis. Appropriate colic monitoring and early veterinary involvement when colic occurs improves outcomes and reduces endotoxemia risk from compromised bowel. Monitoring mares post-foaling and intervening promptly for retained placenta prevents the severe metritis that can trigger DIC. Essentially, any measure that prevents or quickly resolves severe illness reduces DIC risk.

Nutritional prevention of DIC relates indirectly to overall health maintenance that reduces disease susceptibility. Adequate nutrition supports immune function and recovery from illness. Maintaining good body condition provides reserves for handling health challenges. Balanced vitamin and mineral intake supports normal coagulation function. However, no specific nutritional intervention prevents DIC once severe triggering illness develops. The focus remains on disease prevention and management rather than nutritional prophylaxis against coagulopathy.

Exercise and conditioning considerations for DIC prevention are minimal since the syndrome develops secondary to illness rather than exercise-related factors. Appropriate conditioning reduces some injury risks that could lead to severe trauma triggering DIC, but this represents an indirect connection. Horses in intense training may face elevated gastric ulcer risk, and severe ulcer hemorrhage could theoretically contribute to conditions favoring DIC, but this is uncommon. The primary exercise-related consideration is simply maintaining overall health through appropriate activity levels.

Environmental factors in DIC prevention include biosecurity measures preventing infectious disease transmission, safe housing reducing injury risk, and appropriate management during weather extremes preventing heat stroke. In regions with venomous snakes, managing horse exposure to snake habitats reduces envenomation risk. Clean foaling environments reduce postpartum infection risk in mares. General environmental safety minimizes trauma risk. None of these directly prevents DIC, but all reduce risk of the severe conditions that may trigger coagulopathy.

Veterinary care protocols supporting DIC prevention include prompt attention to any concerning illness signs, appropriate perioperative monitoring and care for surgical patients, and vigilant postpartum management of broodmares. For horses at high risk of DIC-triggering conditions, such as those with known gastrointestinal disease predisposition or compromised immune function, proactive veterinary relationships enable early intervention. During hospitalization for conditions carrying DIC risk, monitoring coagulation parameters allows detection of subclinical changes before clinical coagulopathy develops. While DIC cannot always be prevented, the underlying conditions triggering it can often be controlled before they reach severity sufficient to initiate this catastrophic cascade.

Daily management during disseminated intravascular coagulation treatment requires intensive care best provided in hospital settings. Horses are typically hospitalized in intensive care units with continuous monitoring capabilities. Vital signs are checked frequently, often hourly or more during acute phases. IV fluid and medication administration continues around the clock. Transfusion products are administered as needed. Pain is managed to maintain comfort. Position changes in recumbent horses prevent pressure sores. Nutritional support begins as soon as the horse can tolerate feeding. The complexity of DIC management makes home care inappropriate during the acute phase, with hospitalization continuing until coagulopathy resolves and the horse is stable.

Housing considerations during DIC treatment center on the hospital environment. Affected horses require intensive care accommodations with appropriate footing, accessible monitoring, and facilities for managing recumbent patients if needed. After discharge, housing should minimize injury risk during the recovery period. Padded or well-bedded stalls reduce trauma from lying down and rising. Separation from aggressive herdmates prevents injury from normal herd dynamics until full recovery. Protection from environmental extremes reduces metabolic demands during convalescence. Gradual return to normal housing follows clinical recovery assessment.

Exercise during DIC treatment and recovery is strictly limited. Acutely affected horses are typically recumbent or on strict stall rest, moving only as necessary for care and treatment. Once coagulopathy resolves, gradual activity increases based on overall clinical status and the underlying condition's recovery requirements. Horses recovering from surgery require standard post-surgical exercise restrictions. Those recovering from sepsis need time to regain strength before resuming activity. No horse should return to exercise until coagulation parameters have fully normalized and veterinary assessment confirms readiness. Return to full work follows complete recovery and may take weeks to months.

Monitoring during recovery from DIC involves serial coagulation testing to confirm sustained normalization and detect any relapse. Complete blood counts track red blood cell recovery and platelet normalization. Chemistry panels assess organ function recovery. Vital sign monitoring continues more frequently than routine during convalescence. Owners learn to recognize signs of recurrence or complications, including any bleeding, weakness, or deterioration. Close communication with the veterinary team enables prompt response to concerning changes. The duration and intensity of monitoring depends on the original severity and the horse's recovery trajectory.

Quality of life considerations during and after DIC depend on the horse's response to treatment and residual effects. Horses that survive DIC and recover completely often return to normal quality of life and previous activities. Those with persistent organ damage may face limitations affecting their use or comfort. Decisions about appropriate activity levels, breeding soundness for mares, and athletic careers should be made in consultation with veterinarians familiar with the case. For horses that develop DIC but face poor prognoses despite treatment, quality of life assessment guides decisions about continuing treatment versus humane euthanasia. The severity of this syndrome means some cases do not survive despite intensive efforts.

No specific horse breed carries increased genetic susceptibility to disseminated intravascular coagulation, as the syndrome develops secondary to severe illness rather than through inherited predisposition. DIC occurs across all breeds when triggering conditions develop. Any variation in apparent incidence between breeds reflects differences in susceptibility to the underlying conditions that trigger DIC rather than differences in coagulation system function. Arabians may face slightly elevated DIC risk only because foals with severe combined immunodeficiency develop overwhelming infections, though this represents susceptibility to the triggering infection rather than the coagulopathy itself.

Use and discipline considerations for DIC risk relate to the activities and exposures that increase likelihood of triggering conditions. Horses undergoing abdominal surgery for colic face perioperative DIC risk regardless of breed, making this a concern across the sport horse, racing, and pleasure horse populations where colic occurs. Broodmares of any breed face reproductive-associated DIC risk from retained placenta and dystocia. Horses in regions with venomous snakes face envenomation risk. Foals of any breed can develop sepsis triggering DIC. The risk factors are situational rather than breed or discipline specific.

Genetic testing is not applicable for disseminated intravascular coagulation since the syndrome is entirely acquired rather than inherited. No genetic markers have been identified for DIC susceptibility. Testing for other conditions that might predispose horses to illnesses triggering DIC, such as immunodeficiency testing in Arabians, might be indirectly relevant by reducing risk of the predisposing conditions. However, the focus for DIC prevention remains on management and medical interventions rather than genetic selection.

Conditions commonly triggering or accompanying disseminated intravascular coagulation include sepsis and septic shock, which represent major causes of DIC in both foals and adults. Endotoxemia from gram-negative bacterial infection is a particularly potent DIC trigger. Gastrointestinal emergencies including strangulating colic, anterior enteritis, and colitis frequently lead to DIC through endotoxin absorption and tissue necrosis. Reproductive complications including retained placenta, metritis, and dystocia trigger DIC in mares. Heat stroke causes multi-organ dysfunction that may include coagulopathy. Severe hemolytic anemia can precipitate DIC. Neoplasia, particularly aggressive or widespread cancer, is associated with DIC in some cases.

Conditions with similar presentations or that may coexist with DIC include other causes of bleeding and multi-organ dysfunction. Severe thrombocytopenia from immune-mediated platelet destruction causes hemorrhage but without the coagulation factor depletion characteristic of DIC. Liver failure impairs coagulation factor production, causing similar bleeding tendencies but through reduced synthesis rather than consumption. Anticoagulant toxicity, though uncommon in horses, causes bleeding with specific coagulation test patterns. Sepsis and shock cause organ dysfunction that may precede or accompany DIC development. Multi-organ dysfunction syndrome from any cause shares clinical features with DIC. Accurate diagnosis requires integrating clinical findings with laboratory assessment.

Potential complications of disseminated intravascular coagulation include multi-organ failure from both microvascular thrombosis and hemorrhage. Acute kidney injury from renal microthrombi may require ongoing management or prove irreversible. Liver dysfunction impairs coagulation factor production, potentially worsening the coagulopathy. Pulmonary hemorrhage or microthrombosis causes respiratory compromise. Gastrointestinal hemorrhage from stress ulceration or underlying disease worsens blood loss. Laminitis may develop secondary to endotoxemia, hemodynamic compromise, or prolonged recumbency. Complications from intensive care including catheter-associated infections and pressure sores add morbidity. Survivors of DIC may experience long-term effects from organ damage incurred during the acute episode.