DIC Syndrome in the Practice of a General Practitioner: Clinical and Prognostic Aspects

Disseminated intravascular coagulation (DIC) syndrome is a polyetiological clinical and laboratory syndrome that is always secondary and accompanies the course of many internal diseases. The core mechanism of DIC syndrome involves pathological activation of the hemostatic system and thrombinemia, leading to generalized intravascular microthrombosis and microcirculatory disorders. Cases of sudden-onset DIC syndrome in previously healthy individuals are not described in the literature. Clinically, DIC syndrome can present in acute, subacute, or chronic forms. The pathological process progresses through four stages: hypercoagulation; consumption coagulopathy; severe procoagulant deficiency up to complete absence of fibrinogen; and a recovery stage. Depending on symptom severity, DIC syndrome is classified into compensated and decompensated forms, as well as overt and non-overt variants. Clinical Case Description. A 43-year-old male from a rural area was admitted to the intensive care unit with complaints of uncontrollable nasal bleeding, discolored urine ("meat slops"), subcutaneous hemorrhages, muscle weakness, headaches, and elevated blood pressure. The patient had no history of prior illnesses or trauma, and his epidemiological history was negative. Symptoms appeared during nighttime work on a farm, accompanied by episodic anxiety. Multiple consultations with an otorhinolaryngologist, urologist, and hematologist for nasal bleeding and hematuria failed to identify a primary cause. Blood tests revealed anemia, leukocytosis, lymphopenia, and an elevated erythrocyte sedimentation rate (ESR). Urinalysis showed proteinuria. Biochemical blood tests indicated hyperglycemia and signs of impaired renal nitrogen excretion. Acute infections, lymphoproliferative disorders, and liver pathology were ruled out. Hemostasis studies confirmed the absence of adequate blood clot formation. During the first days of hospitalization, nasal bleeding and macrohematuria persisted. Comprehensive therapy, including hemostatic agents, fresh frozen plasma, erythrocyte mass transfusion, and glucocorticoids, stabilized the patient’s condition, restored hemostasis, and normalized blood and urine parameters. The patient was discharged in an improved condition with stable hemodynamics. Conclusion. The sudden onset of DIC syndrome in a previously healthy patient was triggered by acute stress. The syndrome manifested as persistent hypocoagulation with renal involvement in the pathological process. Timely initiation of comprehensive pathogenetic therapy ensured a favorable clinical outcome.