Principles of conservative treatment
Patients with HFRS require strict monitoring and intensive care, as the disease is associated with a high probability of microcirculatory bed damage and the development of renal failure (uremia). The basis of conservative treatment consists of the following medical prescriptions:
- Intensive detoxification therapy: intravenous infusion solutions to correct severe hypovolemia and relieve intoxication syndrome.
- Transfusion support: use of fresh frozen plasma (FFP) to correct hemostasis.
- Microcirculation improvement: intravenous drip administration of Trental.
- Symptomatic and pathogenetic therapy: prescription of antihistamines and vitamin therapy.
- Hormonal therapy: the use of glucocorticoids is permissible, but exclusively in a short course and in the presence of strict clinical indications.
Indications for hardware treatment (hemodialysis)
In severe cases, conservative measures may not be sufficient. As the disease progresses, the vascular endothelium becomes increasingly damaged, leading to a sharp decrease in urine output (oliguria) and a critical accumulation of nitrogenous waste products.
If intensive drug therapy fails to bring an effect and the patient's condition steadily deteriorates, surgical (hardware) methods are indicated. The main life-saving method in such a situation is the immediate transfer of the patient to extracorporeal hemodialysis.
Laboratory and instrumental diagnostics
Adequate treatment is impossible without timely assessment of target organ status. Specific diagnostics are based on the detection of antibodies to hantaviruses using the indirect immunofluorescence assay (IFA).
The mandatory diagnostic minimum includes:
- Complete blood count (CBC): in the early stages, thrombocytopenia is typical, and leukopenia and signs of anemia may also be detected.
- Urinalysis (UA): to monitor diuresis and detect macrohematuria (cloudy dark red urine).
- Blood chemistry panel: screening with a focus on renal function markers (creatinine, urea, and residual nitrogen), as well as transaminases (ALT, AST).
- Assessment of acid-base balance (ABB).
- Instrumental methods: ECG is advisable to detect cardiac disorders (e.g., hypotension, muffled heart sounds, and relative bradycardia).
Pathogenesis and clinical features
HFRS is included in the broad group of viral hemorrhagic fevers (VHF). The key pathogenetic link is a critical increase in capillary permeability, which leads to hypovolemia and creates a high risk of pulmonary edema.
The disease debuts acutely: sudden temperature rise to 39–40°C, chills, severe myalgia (pain in the lower back, calf muscles), nausea, vomiting, facial hyperemia, and scleral injection. Patients often complain of "floaters" before the eyes.
Interestingly, hemorrhagic syndrome itself (from petechial rash to massive bleeding) is predominantly characteristic of severe disease courses and appears strictly during the peak period of the disease, rather than at its onset, indicating the development of thrombohemorrhagic complications.
Briefly: answers to topical questions
What are the strict clinical indications for prescribing glucocorticoids in HFRS?
Glucocorticoids in HFRS are prescribed for severe disease courses.
Specific clinical situations (emergency conditions) for their use:
- Septic shock (SS) with multiple organ dysfunction.
- Brain edema.
- Pronounced inflammatory syndrome with multiple organ dysfunction.
Stress (low/medium) doses of systemic glucocorticoids are used to exert an anti-inflammatory effect.
Which specific infusion solutions are used for intensive detoxification therapy in HFRS?
Crystalloid and colloid solutions are used for intensive detoxification therapy in HFRS.
The volume and nature of administered solutions depend on the stage of the disease and must correspond to daily fluid losses.
What consecutive periods are distinguished in the clinical course of HFRS?
HFRS is characterized by a cyclic course with successive periods.
The following periods are distinguished:
- Incubation period.
- Initial period (prodromal period is not typical).
- Peak period (development of renal and hemorrhagic syndromes), which includes oliguric and polyuric periods.
- Convalescence period.
What is the mechanism of development of acute renal failure at the organ and cellular levels in HFRS?
The morphological substrate of acute renal failure in HFRS is necrotizing nephrosis.
At the organ level, serous-hemorrhagic edema of the interstitium occurs, leading to tubular compression. The kidneys are enlarged, the capsule is tense, and multiple hemorrhages are observed in the pyramids and pelvis.
At the cellular level, dystrophy, necrotic changes, and desquamation of the tubular epithelium develop, along with protein and fibrin leakage into the tubular lumen. This causes tubule and collecting duct obstruction by fibrin plugs with impaired tubular reabsorption of urine.
Class and exam questions
Is a patient with HFRS contagious to medical staff and others?
No, not contagious. Human infection occurs upon accidental intrusion into the pathogen's ecological niche, after which the person becomes a "biological dead end." Nosocomial spread is uncharacteristic of HFRS.
During which period of the disease does hemorrhagic syndrome usually develop?
The appearance of hemorrhagic syndrome (petechiae, bleeding) strictly corresponds to the peak period of the disease and indicates progressive damage to the microcirculatory bed.
What change in the complete blood count is an early marker of infection?
In the early stages of the disease, thrombocytopenia is classically detected in the peripheral blood.
What is the main indication for transferring an HFRS patient to hemodialysis?
Lack of clinical effect from conservative intensive therapy against the background of progressive renal failure (increasing uremia).
What else to study on this topic
- Etiological structure and geography of viral hemorrhagic fevers (VHF).
- Differential diagnosis of HFRS with meningitis and acute abdomen.
- Hantavirus pulmonary syndrome (HPS): differences from renal syndrome.
- Features of natural focal zoonotic infections and their transmission routes.
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