An 18-year-old woman collapsed while practicing for a marathon in hot, humid weather. The patient subsequently vomited 3 times and had a tonic-clonic seizure. She has no chronic medical conditions and takes no medications. The patient does not use alcohol or illicit drugs. Temperature is 40.8 C (105.4 F), blood pressure is 90/60 mm Hg, pulse is 130/min, and respirations are 22/min. The patient is profusely sweating and is confused. Pupils are sluggishly reactive to light. Cardiopulmonary examination reveals clear lungs and normal heart sounds. Laboratory results are as follows:
| Complete blood count | |
| Hemoglobin | 15.8 g/dL |
| Platelets | 90,000/mm3 |
| Leukocytes | 10,000/mm3 |
| Coagulation studies | |
| PT | 20 sec |
| Activated PTT | 43 sec |
Which of the following sets of hematologic findings is most likely to be present in this patient?
This patient with extreme hyperthermia and seizures has exertional heat stroke, a life-threatening multisystem disorder caused by inadequate body heat dissipation. Severe hyperthermia increases tissue oxygen demand and metabolic rate and shunts blood away from the central organs (eg, brain, kidneys, liver, GI tract) to the skin to dissipate heat. This can lead to tissue ischemia/necrosis and the release of procoagulant proteins (eg, tissue factor), which can trigger disseminated intravascular coagulation (DIC).
DIC is marked by the excessive activation of the extrinsic (tissue factor) coagulation cascade, leading to the generation of thrombin and cross-linked fibrin clots. Fibrinolysis is then activated to clear the intravascular thrombi; plasminogen is converted to plasmin, which cuts the cross-linked fibrin-fibers and generates fibrin-degradation products (eg, elevated D-dimer). Other anticoagulant proteins (eg, protein C, protein S) are also rapidly consumed.
Patients with acute DIC usually have bleeding (eg, oozing from venipuncture sites) and end organ damage (eg, confusion, lung injury, renal insufficiency); laboratory studies are diagnostic and show thrombocytopenia (due to consumption of platelets) and prolonged PT/PTT (due to consumption of coagulation factors).
Educational objective:
Disseminated intravascular coagulation is marked by widespread activation of the coagulation cascade, leading to excessive thrombin production and formation of microthrombi. Subsequent conversion of plasminogen to plasmin results in increased fibrinolysis to clear the thrombi. Laboratory studies show a consumption of clotting factors (prolonged PT/PTT) and platelets (thrombocytopenia) and signs of excessive fibrinolysis (eg, elevated D-dimer).