From the Guidelines
In a severely septic patient who develops coagulopathy, the expected laboratory values are low platelets, low fibrinogen, high fibrin split products, high prothrombin time, and high partial thromboplastin time. These laboratory findings reflect the pathophysiology of sepsis-induced coagulopathy, which involves excessive activation of coagulation pathways, impaired anticoagulant mechanisms, and suppressed fibrinolysis 1. The coagulopathy results from the systemic inflammatory response triggering tissue factor expression, leading to thrombin generation and fibrin formation, while simultaneously depleting coagulation factors and platelets.
Some key points to consider in the diagnosis and management of sepsis-induced coagulopathy include:
- Platelet count is usually decreased, often below 100,000/μL, due to consumption, sequestration, and decreased production 1.
- Fibrinogen levels may initially be elevated as an acute phase reactant but can later decrease to below 100 mg/dL as consumption exceeds production 1.
- Fibrin split products (FSPs) and D-dimer levels are markedly elevated, reflecting ongoing fibrin formation and breakdown 1.
- Both prothrombin time (PT) and partial thromboplastin time (PTT) are prolonged, typically greater than 1.5 times the normal control values 1.
Monitoring these parameters is essential for assessing the severity of coagulopathy and guiding appropriate interventions. The International Society on Thrombosis and Haemostasis (ISTH) has developed criteria for the diagnosis of sepsis-induced coagulopathy, which includes platelet count, prothrombin time, and sequential organ failure assessment (SOFA) score 1.
In terms of management, anticoagulant therapy with unfractionated heparin (UFH) has been shown to reduce 28-day mortality and hospital mortality without increasing the risk of serious hemorrhage in patients with sepsis-induced coagulopathy 1. However, the use of anticoagulant therapy should be individualized and based on the patient's specific clinical condition and laboratory findings.
Overall, the management of sepsis-induced coagulopathy requires a comprehensive approach that includes prompt recognition, laboratory monitoring, and individualized treatment to improve patient outcomes.
From the Research
Expected Laboratory Values in Severely Septic Patients with Coagulopathy
- Low platelets: This is expected due to the consumption of platelets in the formation of microthrombi 2, 3, 4, 5.
- Fibrinogen level: This can be decreased due to consumption in the coagulation process, but it can also be increased as an acute phase reactant 6, 3, 4, 5.
- Fibrin split products: These are expected to be high due to the breakdown of fibrin in the coagulation process 2, 3, 4.
- Prothrombin time (PT): This is expected to be high due to the consumption of coagulation factors in the formation of microthrombi 2, 3, 4, 5.
- Partial thromboplastin time (PTT): This is also expected to be high due to the consumption of coagulation factors in the formation of microthrombi 2, 3, 4, 5.
Laboratory Values in Specific Scenarios
- In sepsis, the coagulation system and platelets are fully activated, with increased markers of coagulation and platelet activation, but coagulation factors and global coagulation tests may not be changed 5.
- In severe sepsis and septic shock, coagulation factors are depleted, global coagulation tests are prolonged, and platelet count is reduced, indicating exhaustion of hemostasis 5.
- The expected laboratory values in a severely septic patient who develops a coagulopathy are low platelets, low fibrinogen, high fibrin split products, high prothrombin time, and high partial thromboplastin time 2, 3, 4, 5.