Hantavirus Cardiopulmonary Syndrome (HCPS) Clinical Presentation

Updated: Jun 04, 2019
  • Author: Sally Lynne Westcott, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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The clinical course of Hantavirus cardiopulmonary syndrome (HCPS) advances through several sequential stages.

Following exposure, an incubation period of 2-3 weeks ensues. [32] The aerosolized virus enters the lung, is taken up by local phagocytes, and is subsequently transported to local lymph nodes where it prepares to disseminate. The prodrome/febrile phase lasts 3-10 days and is marked by the onset of fever, chills, and myalgias, often severe, and is the likely clinical correlate to viral dissemination. It is nearly impossible to distinguish HCPS from any other nonspecific viral syndrome during this period. Disease severity progresses quickly, and patients often develop nausea, vomiting, weakness, and sometimes diarrhea and headache. Andes virus HCPS of South America differs slightly, presenting with facial flushing, fine petechiae, and conjunctivitis. Though rhinorrhea, pharyngitis, otalgia, and coryza are notably absent in most Hantavirus infections, a dry cough often heralds sudden deterioration and progression to the cardiopulmonary phase of disease. [39, 40]

The cardiopulmonary phase lasts anywhere from 2-7 days and presents with sudden respiratory distress and, often, cardiovascular collapse within hours of arrival to the hospital. This phase of the illness correlates with massive capillary leakage into the pulmonary vascular bed, resulting in life-threatening pulmonary edema. [26] Clinical deterioration is precipitous and results in bronchorrhea, shock, coagulopathy (particularly with the Andes virus), and preterminal arrhythmias, in addition to the aforementioned pulmonary edema. Mean time from onset of first symptom to cardiopulmonary failure is 5 days. See the image below.

Clinical progression of hantavirus cardiopulmonary Clinical progression of hantavirus cardiopulmonary syndrome.

Survivors of the cardiopulmonary phase frequently experience a period of oliguria and then diuresis. This is less commonly described than hantavirus hemorrhagic fever with renal syndrome (HFRS). Finally, during the convalescent period, the patient typically recovers with little or no residual deficits. Recovery can occur as early as 24-48 hours after onset of cardiopulmonary symptoms. Several months of fatigue and decreased exercise tolerance are often the only sequelae. However, some patients can have residual renal complications and may even meet criteria for chronic kidney disease. [41]

Early diagnosis is difficult because the common presenting symptoms of HCPS overlap with those of other, less ominous, viral illnesses. Risk factors for rodent exposure must be sought and are often the only clue to an early diagnosis.

Consider diagnosis of HCPS in patients with the following:

  • Fever

  • Severe myalgias (often in the back and legs)

  • Exposure to mice or mouse droppings

Other symptoms may include the following:

  • Malaise

  • GI symptoms such as nausea and vomiting, diarrhea, and abdominal pain

  • Headache

  • Cough

Risk factors to seek in the history include the following:

  • Peridomestic rodent infestation

  • Entering or disturbing seasonally closed or infrequently opened buildings

  • Occupational exposure to rodents

Risk also varies with rodent abundance and distribution, which depends on several factors, including the following:

  • Geographic region (highest incidence in the Southwest United States)

  • Seasonality (increased incidence in spring and summer)

  • Weather patterns (Outbreaks may follow El Nino conditions of a temperate wet winter.)

The most common prodromal symptoms are the following:

  • Fever

  • Chills

  • Myalgias (often in the back and legs)

Other common prodromal symptoms include the following:

  • Nausea/vomiting

  • Diarrhea

  • Headache

  • Cough (usually nonproductive)

  • Malaise

  • Dizziness

  • Dyspnea (usually not observed at presentation but often heralds the cardiopulmonary phase of HCPS)

Consider another diagnosis in patients with the following symptoms:

  • Sore throat

  • Rhinorrhea

  • Conjunctivitis/coryza (except Andes virus)

  • Rash (except Andes virus where petechiae are common)

  • Otalgia



Physical findings vary substantially with the stage of disease at presentation.

The most frequent initial physical findings in Hantavirus cardiopulmonary syndrome (HCPS) are as follows:

  • Tachypnea

  • Fever

  • Tachycardia

Crackles or decreased breath sounds are noted in most patients on lung examination.

Abdominal tenderness is present in about 10% of patients and may be severe. One patient underwent an exploratory laparotomy before HCPS was recognized.

Petechiae are not observed despite thrombocytopenia (except Andes virus).

Hallmarks of the cardiopulmonary phase of HCPS include the following:

  • Hypotension

  • Respiratory distress with bilateral alveolar infiltrates on radiograph



In the United States, Hantavirus cardiopulmonary syndrome (HCPS) is primarily caused by the Sin Nombre virus (SNV) and is transmitted via inhalation of aerosolized virus from dried rodent excreta (see Background and Pathophysiology).

The vector of SNV is the deer mouse, P maniculatus (see image below). SNV causes no obvious harm to mice, and they therefore never develop immunity. Infected rodents thereby become chronic, persistent viral shedders.

Peromyscus maniculatus - The deer mouse. Peromyscus maniculatus - The deer mouse.

The incidence of HCPS closely parallels the distribution and number of infected deer mice in a geographic area. [8] Deer mouse populations are influenced by specific environmental conditions.

The El Nino conditions present during the 1993 Navajo outbreak increased the number of deer mice seen that year. The wet and mild conditions encouraged an unusually high population of pinons, a favorite source of food for mice. This, in turn, allowed for a 10-fold increase in the number of deer mice found that year in the Four Corners region of the United States.

Because of horizontal viral transmission via intra-rodent aggressive behaviors such as biting, high rodent density also increases the percentage of deer mice infected. [8] Thirty percent of deer mice in the Four Corners region tested positive for SNV in the 1993 outbreak.

All agree that some type of rodent exposure, whether occupational or sporadic, is the greatest risk factor for contracting Hantavirus. Some controversy exists as to whether occupational exposure on farms or in laboratories is as great a risk factor as sporadically entering rarely opened or seasonally closed rodent-infested buildings. [12, 42, 13]

Occupations at greatest risk for exposure are as follows:

  • Grain farmers

  • Agricultural workers

  • Feedlot employees

  • Field biologists



Potential acute complications of Hantavirus cardiopulmonary syndrome (HCPS) include death, cardiovascular collapse, respiratory failure, anoxic brain injury, renal failure, pulseless electrical activity (PEA), ventricular tachycardia, and ventricular fibrillation.

ECMO has its own set of significant and not infrequent complications, including massive hemorrhage, sepsis, renal failure, and limb ischemia. [43] ECMO remains a rescue therapy for patients who are deteriorating despite maximal conventional medical therapy.