bubble_chart Overview

Epidemic hemorrhagic fever is an acute infectious disease caused by viral infection, primarily characterized by fever, hemorrhage, and kidney damage. It is a natural focal disease commonly occurring in forested areas, mountainous regions, swamps, grasslands, or low-lying wetlands. Wild rodents (mice and rat mites) are the main sources of this infection. The disease is more prevalent in winter, with some areas also experiencing outbreaks between May and June. It mainly affects young adults, though children can also contract the disease, and there are occasional reports of infants and toddlers being infected.

bubble_chart Auxiliary Examination

1. Blood Picture White blood cell count is initially lower than normal, but can reach 10-20×10⁹/L by days 4-7 of the disease course; in severe cases, it may rise as high as 50-60×10⁹/L, presenting as a leukemoid reaction. Neutrophils show a left shift and toxic granules. Atypical lymphocytes increase daily, and in severe cases, may exceed 15%. In severe cases with hypotensive shock, hemoconcentration occurs due to plasma extravasation. Platelet counts show mild (Grade I) reduction in mild cases, while in severe patients, they may drop below 60-100×10⁹/L by days 4-8 of the disease course, or even below 20×10⁹/L.
2. Urine Protein, red and white blood cells, and various casts may appear early in the disease. Some patients may pass membrane-like substances containing red and white blood cells and shed epithelial cells. Urine specific gravity increases during the oliguric phase and decreases during the polyuric phase, returning to normal as renal function fully recovers.
3. Changes in Blood Generation and Transformation Due to kidney damage, azotemia and electrolyte imbalances occur. Blood urea nitrogen increases, while carbon dioxide combining power decreases. Blood sodium, potassium, and calcium levels also decrease.
4. Coagulation function tests, such as fibrinogen and prothrombin time, may show abnormal changes indicative of DIC (see DIC section). 5. Serological Tests Early in the disease course (days 4-5), detection of IgM antibodies by indirect immunofluorescence can aid in diagnosis.

bubble_chart Diagnosis

Epidemiology: Endemic areas, seasons, and a history of contact with rodents or visiting epidemic areas 1–6 weeks before the onset of illness.

Clinical symptoms:

Most patients experience an abrupt onset, with prodromal symptoms such as vertigo, headache, lack of strength, fatigue, and loss of appetite. The clinical course can be divided into five stages, though sometimes the stages are not clearly distinct.

1. Fever stage: The early phase is primarily characterized by fever, which can reach 39–40°C, often presenting as a remittent fever, with a few cases showing continuous or irregular fever, lasting 5–6 days. The face and orbital area exhibit marked congestion, resembling a drunken appearance. Concurrently, the skin of the neck, shoulders, and chest becomes flushed (the "three reds"), with petechial hemorrhages on the skin and mucous membranes, needle-sized and arranged in a cord-like pattern, mainly distributed in the armpits, chest, neck, back, upper limbs, oral soft palate, and conjunctiva. Plasma extravasation may lead to conjunctival edema and eyelid swelling. The "three pains" symptoms include headache, orbital pain, and lumbago. Most patients experience gastrointestinal symptoms such as loss of appetite, nausea, vomiting, and diarrhea. Severe cases may exhibit dysphoria, drowsiness, delirium, etc.
2. Hypotensive stage: This appears around days 4–6 of the illness, sometimes as early as the fever stage, when blood pressure fluctuates and drops, leading to shock. The patient's limbs become cold, lips cyanotic, and complexion dull. The pulse is thready and rapid, with cardiac enlargement, arrhythmia, and tachycardia, potentially leading to heart failure. Conjunctival, eyelid, and facial edema worsen. Persistent hiccups, nausea, vomiting, diarrhea, abdominal distension, and fullness are common gastrointestinal symptoms. Dysphoria, restlessness, confusion, delirious speech, and even agitation or spasms may occur.
3. Oliguric stage: Renal failure develops rapidly in this disease. The oliguric stage often follows the intermediate stage (second stage) or overlaps with the late stage (third stage), typically occurring around days 6–8 of the illness. Anuria lasts about 3–5 days, though it may be as short as 1 day or as long as over 10 days. Patients are extremely exhausted, with thirst, hiccups, persistent vomiting, and abdominal pain. Symptoms such as dysphoria, delirium, and spasms worsen. Epistaxis, hematemesis, hematochezia, and hematuria may occur, with membranous tissue expelled in the urine. Urine output significantly decreases or stops entirely. Severe complications such as pulmonary edema, heart failure, acidosis, uremia, hypertension, massive gastrointestinal bleeding, and secondary infections may arise.
4. Polyuric stage: As renal tissue recovers, the polyuric stage begins, usually around days 8–11 of the illness. Urine output increases, lasting about 3–5 days. Most patients gradually improve, though blood pressure remains elevated. A few still exhibit exhaustion, polydipsia, anorexia, and nausea. Massive bleeding may recur, and polyuria can lead to electrolyte imbalances, secondary shock, or even fatal exhaustion at this stage.
5. Stage of convalescence: Recovery begins in weeks 3–4 of the illness. Urine output normalizes, urine concentration function improves, and constitution gradually strengthens, with full recovery taking 1–3 months.

bubble_chart Treatment Measures

The key lies in early detection, early treatment, and early rest. (1) General Treatment Strengthen nursing care, ensure bed rest, and provide a semi-liquid diet that is nutritious and easy to digest, with adequate fluid intake. Patients should be strictly isolated, and their blood, urine, clothing, and utensils must be thoroughly disinfected.

(2) Symptomatic Management

1. For high fever, prioritize physical cooling methods and avoid or use antipyretics cautiously to prevent sudden drops in body temperature or profuse sweating, which may induce shock.
2. For obvious bleeding, medications such as Adrenobazone, Etamsylate, Vitamin K, and Vitamin C can be used. Severe cases may require fresh blood or platelet transfusions. Patients with severe DIC should receive anticoagulation and other corresponding treatments.
3. During oliguria, provide a high-sugar, high-vitamin, low-protein diet to control azotemia. For severely ill patients unable to eat, an appropriate amount of insulin can be added to intravenous glucose infusions.

(3) Maintaining Water, Electrolyte, and Acid-Base Balance Based on renal function changes, fluid intake should be restricted during oliguria, and attention should be paid to correcting electrolyte imbalances and acidosis. During the diuretic phase, daily fluid replacement should be calculated based on the previous day's urine output (approximately 1/3 to 2/3). Monitor infusion speed and volume to prevent heart failure and pulmonary edema.

(4) Treating Shock In cases of shock, in addition to expanding effective circulating volume and correcting metabolic acidosis, closely monitor urine output, blood gases, central venous pressure, heart rate, and rhythm to adjust the volume, composition, and speed of fluid infusion. Excessive fluid infusion may lead to heart failure, pulmonary edema, or cerebral edema. Vasoactive drugs such as Phentolamine or Tangut Anisodus alkaloids can also be used. Norepinephrine is not recommended for routine use due to its tendency to constrict renal blood vessels and exacerbate renal failure.

(5) Use of Diuretics During oliguria, 20% Mannitol, Furosemide, or Ethacrynate Sodium can be administered.

(6) Application of Immunosuppressants (Cyclophosphamide) and Immunostimulants (Transfer Factor) The effects are considered acceptable.

bubble_chart Prevention

(1) Isolate patients until symptoms disappear, and strictly disinfect contaminated clothing, utensils, as well as the patient's blood and urine. (2) Improve environmental and housing conditions, and enhance rodent and mite control. (3) Educate children not to play with rodents, cats, dogs, etc., and not to eat food bitten by rodents. (4) Strengthen protective measures for disease prevention personnel to prevent rodents and mites from entering clothing. At the same time, take care to avoid skin damage.

bubble_chart Differentiation

(1) Acute Rebing should be differentiated from upper respiratory tract infection, epidemic cerebrospinal meningitis, leptospirosis, cold-damage disease, septicemia, acute hepatitis, etc. (2) Hematological diseases should be differentiated from thrombocytopenic purpura, allergic purpura, leukemia, etc. (3) Renal diseases should be differentiated from acute nephritis, pyelonephritis, etc.