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Emergency And Acute Medicine – Hemorrhagic Fevers
Basics And Description
Hemorrhagic fever refers to a multisystem syndrome characterized by vasocapillary permeability, hemorrhage, and organ dysfunction. Viral hemorrhagic fevers (VHF) are caused by a distinct group of viruses and often begin with a nonspecific influenza-like illness. Hemorrhagic manifestations occur in a minority of patients and typically appear in later stages of disease.
Risk Factors
Travel to endemic regions
Exposure related to biologic warfare
Close contact with animals
Insect bites or ingestion
Pathophysiology
Viral hemorrhagic fevers cause endothelial injury leading to increased vascular permeability, hemorrhage, and progression to shock. The shock state is both hypovolemic and distributive and is often difficult to reverse. Rapid progression to hypotension indicates a very high mortality risk. Disseminated intravascular coagulation is commonly seen in Marburg and Crimean-Congo hemorrhagic fever but is less frequent in arenavirus infections. Dengue hemorrhagic fever is immune mediated and often results from secondary infection and is among the most common causes of VHF.
Etiology
Viral hemorrhagic fevers are caused by RNA viruses with zoonotic life cycles and short incubation periods of less than 10–21 days.
Filoviruses include Ebola and Marburg, with fruit bat reservoirs and transmission primarily in sub-Saharan Africa.
Arenaviruses include Lassa fever and South American hemorrhagic fevers, transmitted via aerosolized rodent excreta.
Flaviviruses include Dengue and Yellow fever, transmitted by mosquitoes, primarily in tropical regions.
Bunyaviridae include Rift Valley fever and Crimean-Congo hemorrhagic fever, transmitted by ticks or mosquitoes.
Hantaviridae include hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, transmitted via aerosolized rodent excreta.
Alert
Viral hemorrhagic fevers represent a potential biowarfare threat. With the exception of dengue, most are transmissible via aerosols and body fluids. Some have very high morbidity and mortality, and many replicate efficiently in cell culture, allowing weaponization.
Diagnosis – Signs And Symptoms
Common symptoms include acute fever, malaise, headache, nausea, vomiting, flushing, diarrhea, abdominal pain, and myalgias.
Less common manifestations include gingival bleeding, conjunctival hemorrhage, petechiae, hematemesis, melena, epistaxis, and ecchymoses.
Hemorrhagic features usually appear after day three and may involve skin, IV sites, gums, lungs, gastrointestinal tract, or uterus. Diffuse alveolar hemorrhage and ARDS may occur, particularly in Ebola, Marburg, Lassa, Crimean-Congo hemorrhagic fever, and hantavirus infections.
Characteristic rashes include nonpruritic centripetal maculopapular eruptions in Ebola and Marburg, jaundice in Yellow fever, and blanching maculopapular truncal rash in Dengue.
Late-stage disease may progress to shock, seizures, coma, and death.
History And Physical Examination
History should assess recent travel, exposure to sick contacts, animal or insect exposure, and clustering of cases.
Strict protection of healthcare workers is essential, using universal blood and body fluid precautions.
Vital signs should be monitored closely, as narrowed pulse pressure may signal impending cardiovascular collapse.
Physical examination may reveal hemorrhage, rash, hepatomegaly, right upper quadrant tenderness, and abnormal lung findings.
Essential Workup
The primary goal is to distinguish VHF from other acute febrile illnesses, especially malaria, in returning travelers. Lung involvement suggests systemic disease and poorer prognosis. Consider the possibility of a biologic attack if multiple patients present with similar unusual findings.
Diagnostic Tests And Interpretation
Laboratory studies may show leukocytosis, leukopenia, thrombocytopenia, pancytopenia, or hemoconcentration. Elevated hematocrit suggests third spacing and impending shock. Renal and hepatic dysfunction are common. Coagulation studies may reveal DIC, particularly in Ebola, Marburg, and Crimean-Congo hemorrhagic fever.
Definitive diagnosis requires specialized biosafety level 4 laboratories using RT-PCR, viral isolation, or immunohistochemistry, coordinated through the CDC.
Imaging such as chest radiograph or CT may identify ARDS, pneumonia, or internal hemorrhage.
Differential Diagnosis
Malaria
Dengue fever
Rickettsial infections
Typhoid fever
Meningococcemia
Sepsis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Leukemia
Pit viper envenomation
Treatment – Prehospital And Initial Stabilization
Early recognition is critical due to increased globalization and imported cases. Suspected cases must be reported to the CDC immediately.
Patients should be isolated, and healthcare workers must use full protective equipment, including HEPA-filtered respirators during aerosol-generating procedures.
Emergency Department Management
Treatment is primarily supportive. Empiric antimalarial therapy should be initiated until malaria is excluded. Secondary infections should be treated aggressively.
Bleeding is usually mild; if severe, manage with blood products and clotting factors.
Fluid resuscitation must be cautious due to third spacing and risk of flash pulmonary edema. Colloids or blood products should be reserved for impending shock.
Ribavirin is effective against Lassa fever, South American hemorrhagic fever, Crimean-Congo hemorrhagic fever, and hantavirus infections but is ineffective against filoviruses.
Convalescent plasma may benefit South American hemorrhagic fever if administered early.
Medications
Ribavirin intravenous loading dose of 33 mg/kg, followed by 16 mg/kg every 6 hours for 4 days, then 8 mg/kg every 8 hours for 3 days.
Oral prophylaxis consists of 500 mg every 6 hours for 7 days.
Vaccines are available for Yellow fever, while others remain under development.
Disposition And Follow-Up
All suspected cases require admission with isolation precautions. ICU care is indicated for shock or multiorgan failure. Discharge is not appropriate when VHF is suspected.
Coordination with the CDC is mandatory for patient management and postexposure prophylaxis of contacts.
Clinical Pearls And Pitfalls
Use extreme caution with fluid resuscitation.
Hemoconcentration and pulmonary involvement are critical warning signs.
Always consider viral hemorrhagic fever in febrile patients returning from endemic regions.
Strict isolation and universal precautions are essential to prevent transmission.
Notify the CDC immediately for all suspected cases.
Basics And Description
Hemorrhagic fever refers to a multisystem syndrome characterized by vasocapillary permeability, hemorrhage, and organ dysfunction. Viral hemorrhagic fevers (VHF) are caused by a distinct group of viruses and often begin with a nonspecific influenza-like illness. Hemorrhagic manifestations occur in a minority of patients and typically appear in later stages of disease.
Risk Factors
Travel to endemic regions
Exposure related to biologic warfare
Close contact with animals
Insect bites or ingestion
Pathophysiology
Viral hemorrhagic fevers cause endothelial injury leading to increased vascular permeability, hemorrhage, and progression to shock. The shock state is both hypovolemic and distributive and is often difficult to reverse. Rapid progression to hypotension indicates a very high mortality risk. Disseminated intravascular coagulation is commonly seen in Marburg and Crimean-Congo hemorrhagic fever but is less frequent in arenavirus infections. Dengue hemorrhagic fever is immune mediated and often results from secondary infection and is among the most common causes of VHF.
Etiology
Viral hemorrhagic fevers are caused by RNA viruses with zoonotic life cycles and short incubation periods of less than 10–21 days.
Filoviruses include Ebola and Marburg, with fruit bat reservoirs and transmission primarily in sub-Saharan Africa.
Arenaviruses include Lassa fever and South American hemorrhagic fevers, transmitted via aerosolized rodent excreta.
Flaviviruses include Dengue and Yellow fever, transmitted by mosquitoes, primarily in tropical regions.
Bunyaviridae include Rift Valley fever and Crimean-Congo hemorrhagic fever, transmitted by ticks or mosquitoes.
Hantaviridae include hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, transmitted via aerosolized rodent excreta.
Alert
Viral hemorrhagic fevers represent a potential biowarfare threat. With the exception of dengue, most are transmissible via aerosols and body fluids. Some have very high morbidity and mortality, and many replicate efficiently in cell culture, allowing weaponization.
Diagnosis – Signs And Symptoms
Common symptoms include acute fever, malaise, headache, nausea, vomiting, flushing, diarrhea, abdominal pain, and myalgias.
Less common manifestations include gingival bleeding, conjunctival hemorrhage, petechiae, hematemesis, melena, epistaxis, and ecchymoses.
Hemorrhagic features usually appear after day three and may involve skin, IV sites, gums, lungs, gastrointestinal tract, or uterus. Diffuse alveolar hemorrhage and ARDS may occur, particularly in Ebola, Marburg, Lassa, Crimean-Congo hemorrhagic fever, and hantavirus infections.
Characteristic rashes include nonpruritic centripetal maculopapular eruptions in Ebola and Marburg, jaundice in Yellow fever, and blanching maculopapular truncal rash in Dengue.
Late-stage disease may progress to shock, seizures, coma, and death.
History And Physical Examination
History should assess recent travel, exposure to sick contacts, animal or insect exposure, and clustering of cases.
Strict protection of healthcare workers is essential, using universal blood and body fluid precautions.
Vital signs should be monitored closely, as narrowed pulse pressure may signal impending cardiovascular collapse.
Physical examination may reveal hemorrhage, rash, hepatomegaly, right upper quadrant tenderness, and abnormal lung findings.
Essential Workup
The primary goal is to distinguish VHF from other acute febrile illnesses, especially malaria, in returning travelers. Lung involvement suggests systemic disease and poorer prognosis. Consider the possibility of a biologic attack if multiple patients present with similar unusual findings.
Diagnostic Tests And Interpretation
Laboratory studies may show leukocytosis, leukopenia, thrombocytopenia, pancytopenia, or hemoconcentration. Elevated hematocrit suggests third spacing and impending shock. Renal and hepatic dysfunction are common. Coagulation studies may reveal DIC, particularly in Ebola, Marburg, and Crimean-Congo hemorrhagic fever.
Definitive diagnosis requires specialized biosafety level 4 laboratories using RT-PCR, viral isolation, or immunohistochemistry, coordinated through the CDC.
Imaging such as chest radiograph or CT may identify ARDS, pneumonia, or internal hemorrhage.
Differential Diagnosis
Malaria
Dengue fever
Rickettsial infections
Typhoid fever
Meningococcemia
Sepsis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Leukemia
Pit viper envenomation
Treatment – Prehospital And Initial Stabilization
Early recognition is critical due to increased globalization and imported cases. Suspected cases must be reported to the CDC immediately.
Patients should be isolated, and healthcare workers must use full protective equipment, including HEPA-filtered respirators during aerosol-generating procedures.
Emergency Department Management
Treatment is primarily supportive. Empiric antimalarial therapy should be initiated until malaria is excluded. Secondary infections should be treated aggressively.
Bleeding is usually mild; if severe, manage with blood products and clotting factors.
Fluid resuscitation must be cautious due to third spacing and risk of flash pulmonary edema. Colloids or blood products should be reserved for impending shock.
Ribavirin is effective against Lassa fever, South American hemorrhagic fever, Crimean-Congo hemorrhagic fever, and hantavirus infections but is ineffective against filoviruses.
Convalescent plasma may benefit South American hemorrhagic fever if administered early.
Medications
Ribavirin intravenous loading dose of 33 mg/kg, followed by 16 mg/kg every 6 hours for 4 days, then 8 mg/kg every 8 hours for 3 days.
Oral prophylaxis consists of 500 mg every 6 hours for 7 days.
Vaccines are available for Yellow fever, while others remain under development.
Disposition And Follow-Up
All suspected cases require admission with isolation precautions. ICU care is indicated for shock or multiorgan failure. Discharge is not appropriate when VHF is suspected.
Coordination with the CDC is mandatory for patient management and postexposure prophylaxis of contacts.
Clinical Pearls And Pitfalls
Use extreme caution with fluid resuscitation.
Hemoconcentration and pulmonary involvement are critical warning signs.
Always consider viral hemorrhagic fever in febrile patients returning from endemic regions.
Strict isolation and universal precautions are essential to prevent transmission.
Notify the CDC immediately for all suspected cases.
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