key: cord-0035193-vbrrq76z authors: Greenberg, David E.; Greenberg, Stephen B. title: Viral Infections in ICU Patients date: 2005 journal: Tropical and Parasitic Infections in the Intensive Care Unit DOI: 10.1007/0-387-23380-6_4 sha: 81698fa0087f7be3d179f09e4ada66e58adc7ef7 doc_id: 35193 cord_uid: vbrrq76z nan Intensive care units (ICU) were used originally for mechanical ventilation of patients with poliomyelitis and for recovery of patients after anesthesia. Today, these units have been expanded to care for severely ill patients with a wide variety of clinical conditions requiring close monitoring and support. A variety of medical conditions and physiologic disturbances have benefited from this care. Many critically ill patients have underlying infections and of those with infections, viruses are the cause in a small but important percentage (1,2). The majority of viral infections which require care in an intensive care unit involve the respiratory or the central nervous system. However, other organ systems, such as the gastrointestinal tract, may be severely affected by viruses and require support or close monitoring. The conditions reviewed in this chapter are found in adults and do not include HIV infections. Table 1 is a summary of acute illnesses which may be caused by viruses and require treatment in an ICU in the Western Hemisphere. The syndromes and special hosts that are associated with severe viral infections may be diagnosed from epidemiologic clues and specific laboratory tests (3, 4) . Clinical signs and symptoms are rarely sufficient to make a specific diagnosis of a viral infection. Although severe community-acquired pneumonia is usually caused by bacteria, viruses account for approximately 3-10% of cases in large series (5, 6, 7, 8) . The usual viral causes of pneumonia in adults are influenzavirus type A and B, parainfluenzaviruses, respiratory syncytial virus (RSV), and adenoviruses (9,10,11). These pneumonias may be nosocomially acquired, especially during peak respiratory periods (12, 13, 14, 15, 16) . Viruses can cause an atypical pneumonia in otherwise healthy individuals or a pneumonia in immunocompromised hosts (17, 18, 19, 20 shortened the duration of respiratory support (81). An alternative treatment to plasma exchange appears to be IVIg. Even with treatment, the rehabilitation process is long and residual weakness is found in approximately 15%. Cardiogenic shock may develop following acute myocardial infarction or severe heart failure from any cause. Clinically, Cardiogenic shock is manifested by peripheral hypoperfusion, cold extremities, cyanosis, or hypotension. Viral infection of the myocardium can lead to clinical myocarditis which is severe enough to manifest Cardiogenic shock either due to myocardial failure or tachyarrhythmias (82,83). Although rarely proven, viruses are suspected as the major causes of acute myocarditis. A suspicion of viral myocarditis should be high in patients who had fever and myalgias preceding the development of cardiac symptoms. Evidence of myocardial damage with elevated creatine kinase and troponin levels is common. Patients may present with typical anginal chest pain and/or arrhythmias; making it difficult to rule out an acute myocardial infarction (84). Risk factors for DHF/DSS in the Americas include 1) secondary infection with a different serotype; 2) sequential serotypes in secondary infections; 3) association with dengue 2 virus and, less frequently, dengue 3 virus; 4) longer interval between first and second infection; 5) young age; 6) lower frequency in blacks; and 7) individuals with a history of asthma, diabetes mellitus, or sickle cell anemia (93). To consider a case, the travel history and local disease occurrence must be known. Diagnosis is made by detection of IgM antibody. Paired sera for the testing of specific rises in IgG antibody will give a more specific diagnosis. Treatment for DHF/DSS is supportive. . Viral hemorrhagic fevers (VHF) are caused by RNA viruses and transmitted by rodent or arthropod vectors. In the case of Marburg and Ebola viruses, the reservoir and mode of transmission remain unknown. Case-fatality rates vary from 1% to 90%. Clinical syndromes include hemorrhage secondary to capillary leakage, hepatitis, encephalitis, and/or nephropathy. Disseminated intravascular coagulopathy (DIC) is common to many but not all of these viruses. The viruses found naturally in the Western hemisphere include yellow fever, dengue, Sin Nombre virus (Hantavirus), and South American hemorrhagic fever viruses (Guanarito, Sabia, Junin, and Machupo) ( Table 2 ). Other viruses indigenous to Africa and Asia include Rift Valley fever, Crimean-congo hemorrhagic fever, Kyasanur Forest virus, Omsk hemorrhagic fever, hemorrhagic fever with renal syndrome, Lassa fever, and African hemorrhagic fever (Marburg and Ebola). The hemorrhagic fever viruses in Asia and Africa have the potential for introduction into the Western hemisphere or for use as biological warfare agents. The viruses causing hemorrhagic fever cause microvascular damage and alterations in vascular permeability (96,97). Fever, prostration, and myalgias are common initial symptoms. Physical examination will often reveal hypotension, facial flushing, and petechiae. With progression to shock and generalized bleeding, there is often hematopoietic, neurologic and pulmonary involvement. Hepatitis is common and severe with yellow fever but not with the other VHF agents of the Western hemisphere. Increasing vascular permeability, loss of intravascular volume, and multiorgan failure are often the final pathway to death. Routine laboratory tests yield nonspecific abnormalities, but thrombocytopenia and coagulation defects should suggest the diagnosis with the corresponding clinical presentation. Specific diagnosis requires isolation of the virus or staining of formalin-fixed tissue. Only the CDC and USAMRIID laboratories are under Biolevel safety 4 conditions which are necessary for attempting isolation of these viruses. RT-PCR assays for rapid diagnosis may become more widely available in the future. The care of patients with VHF is largely supportive. Patients in shock and actively bleeding will require close monitoring, fluid resuscitation as well as transfusion of red cells, platelets, and clotting factors (98, 99) . No aspirin or corticosteroids should be used. Dopamine may be the pressor of choice in unresponsive shock. Only ribavirin has been used successfully in VHF, especially for Lassa fever patients. Experimental use of ribavirin in Hantavirus pulmonary syndrome is being evaluated. Specific immune human plasma has been successful in treating Argentine hemorrhagic fever and may be useful in Bolivian hemorrhagic fever. All suspected VHF cases should be placed in isolation immediately. Respiratory precautions and placement in a negative pressure room should help reduce the spread to hospital personnel and close contacts. All specimens must be appropriately labeled. Decontamination of all areas where the patient has been is essential. Reporting all suspected cases to local, state, and federal authorities is necessary to alert the community of a possible outbreak. The differential diagnosis of viral meningitis and encephalitis includes a long list of viruses as well as bacteria and noninfectious conditions. Because the clinical presentation of viral meningitis and encephalitis overlaps with other infections and illnesses, the diagnostic evaluation and therapeutic management are complicated. The most common viral pathogens associated with meningitis or encephalitis and their epidemiology are listed in Table 3 (100-103). Viral meningitis and encephalitis cases occur worldwide. In the United States, echoviruses and coxsackie viruses (non-polio enteroviruses) are the cause of many cases of meningitis and some cases of encephalitis. (104). Although outbreaks are more common in the summer months, CNS enteroviral illness occurs throughout the year. The most common cause of sporadic cases of encephalitis in adults is HSV-1. Over 50% of the cases of encephalitis in adults older than 50 years are caused by HSV-1 (105 (110). Serum antibody assays are not helpful in diagnosis. EEG shows lateralized epileptiform discharges (PLEDs) over the temporal or frontal area in 85% of patients with HSE. In the first 5 to 6 days of illness, the CT scan maybe normal. MRI is more likely to be abnormal earlier than the CT scan. Brain biopsy, although the definitive diagnostic procedure, is only performed when there is an atypical clinical, radiologic, or laboratory picture. The mortality rate has been reduced to 20% with acyclovir therapy. However, the mortality rate is higher in those older than 30 years and in those who were comatose before treatment was initiated. West Nile virus had been a cause of encephalitis in Africa and the Middle East until 1999, when it was found in fatal cases of encephalitis in New York City (111,112). Over the next few years, hundreds of cases had been confirmed throughout most of the United States. West Nile virus is a member of the Flaviviridae family. Most infected patients are asymptomatic. Clinical illness is associated with fever, headache, anorexia and malaise. Lymphadenopathy has been reported in earlier epidemics. A maculopapular rash over the chest, back, and upper extremities is observed in approximately 50% of cases. Other signs and symptoms include conjunctivitis, nausea, abdominal pain, and diarrhea (113,114). Meningitis, encephalitis, and acute flaccid paralysis have been reported with West Nile virus (115-117). CSF examination usually reveals a lymphocytic pleocytosis and elevated protein level. Guillain-Barré syndrome has also been reported. Diagnosis can be made by serologic tests, but cross-reactive antibodies to other flaviviruses have been observed. Detection of virus by RT-PCR is positive in less than 50% of cases. Patients may need prolonged ventilation because of neurologic complications. No specific therapy has been found to be effective, although interferon, ribavirin and IVIg have been tested or proposed for clinical trials. Recovery may be prolonged with neurologic abnormalities being reported for up to one year following the illness. Specimens should be collected for viral isolation and PCR testing. CSF PCR tests are available for detecting HSV-1, CMV, EBV, VZV, HHV-6, HHV-7, and the enteroviruses. In HSV-1 encephalitis, the sensitivity of CSF PCR approaches 95% (118). Less information is available on the sensitivity of CSF PCR tests for the other viruses. For many patients with meningitis, admission to the hospital will not be necessary. Patients with suspected encephalitis should be admitted to the hospital and monitored closely. Initiation of empiric acyclovir intravenously should be considered. An MRI should then be reviewed for evidence of mass effect. If significant mass effect is present, then the CSF examination should be deferred and evidence of increased intracranial pressure (ICP) would require specific treatment (119). If no mass effect is found, then CSF examination should be performed and the appropriate tests ordered. If the HSV PCR test is negative, consider other diagnoses unless MRI is compatible with HSV. In 1% to 2% of patients with acute hepatitis, acute liver failure or fulminant hepatitis will occur (120). Patients with fulminant hepatitis will often manifest encephalopathic changes, jaundice, and a prolonged prothrombin time. Levels of elevated aminotransferases do not have prognostic value and may decrease as the liver failure becomes worse. The possible use of biological agents in a terrorist attack has become quite real since September 11, 2001 and the subsequent distribution of anthrax (161, 162) . Potential biological weapons have included both bacteria and viruses. The chief viral candidates with the greatest impact are smallpox, viral hemorrhagic fever agents such as Ebola virus, and equine encephalitis (163, 164) . Delivery of the virus weapon is likely to be by the respiratory route; contamination of food or water is less likely. A single case of smallpox would have significant impact on the health care system (165). Smallpox is caused by variola virus and is highly infectious. Spread may occur by person-to-person or by fomites. After a 12 to 14 day incubation period, a prodromal illness marked by fever, rigors, malaise, headache and backache will last approximately three days. During this time, the physician examining the patient will consider a "flulike" illness is most likely (166). A discrete centrifugal rash characterized by macules begins on the face, hands, and forearms (167). The macules become papules and then vesicles which spread over the whole body. Pustules and crusted lesions develop by the eighth day and thirteenth day, respectively. The rash can be distinguished from varicella (chickenpox) by being more peripheral and progressing at the same stage over the skin. Mortality may reach 30% and is highest during the second week of illness. Pulmonary edema and hemoptysis were commonly reported in earlier outbreaks. Renal failure and electrolyte abnormalities also contributed to the morbidity in smallpox patients. If a suspected case of smallpox were admitted to the hospital or ICU, the physician would need to notify local and national public health officials. Specimens should be sent for diagnosis to state and national laboratories where biosafety level 4 precautions are available. A suspected case of smallpox needs to be placed in strict airborne and contact isolation and in a negative-pressure room. Patient transport should be limited. Dedicated equipment should be used. Linens from the patient should be autoclaved before laundering (Table 4) . Isolation of the patient should be continued until all scabs separate. Smallpox patients will need monitoring and excellent skin care. There is no currently approved antiviral treatment, although cidofovir has been shown to be effective in vitro and in animal models (168,169). Vaccination of contacts should limit the development of clinical disease if administered within four days of exposure (170). VHF are caused by a diverse group of viruses that are transmitted by animal and arthropod vectors (171). VHF agents are potential biologic weapons because they are highly infectious, stable as aerosols, and cause high morbidity and mortality. These viral agents can infect by direct contact with needles, fluids and tissues of other infected patients, however aerosol infection in humans has not been reported with the exception of Hantavirus. All suspected cases of VHF should be placed in isolation in negativepressure rooms. Airborne, droplet and contact precautions should be instituted. Patient transport should be limited and masks should be placed if transport is essential. Dedicated equipment should be left in the patient's room. Disinfection of surfaces with 10% bleach solution or phenolic disinfectant is recommended. The patient should remain in isolation for the duration of the illness (Table 4 ). Burn patients have been reported to have a high incidence of herpes simplex virus (HSV) infections manifested as ARDS and occasionally as pneumonia (172) (173) (174) . Necrotizing tracheobronchitis, and facial rashes have also been found in these patients (175) (176) (177) (178) (179) . With acyclovir therapy, there has been reported clinical improvement. Isolation of HSV from bronchoalveolar lavage specimens is associated with the need for assisted ventilation in burn patients (180, 181) . However, there are conflicting studies on whether HSV activation is associated with increased mortality in these patients (182). A recent prospective study culturing for HSV in the respiratory tract of patients in critical care units showed HSV reactivation was frequent and associated with ARDS and increased length of stay in intensive care (183). This confirmed results from other older studies (184, 185) . Similar findings have also been found in critically ill surgical patients (186-188). There are numerous physiologic and immunologic changes in pregnancy that create a state of relative immunosuppression (189). Pregnant women are more susceptible to a variety of viral infections including pneumonia (189, 190) . Influenzavirus, VZV, and measles have all been reported as causes of pneumonia (191) (192) (193) (194) . Complications of VZV can be particularly devastating during pregnancy. Ninety percent of adults living in nontropical areas are immune to varicella, therefore most pregnant women are not susceptible (195) . Pneumonia can occur a few days after the development of rash and fever and can lead to respiratory failure. Both the mother and fetus can suffer morbidity and mortality from varicella. Patients with the complication of varicella pneumonia should be treated aggressively with antiviral therapy and close monitoring (194) (195) (196) (197) . Acyclovir is generally accepted as the treatment of choice despite the lack of safety studies (198) . In pregnant women with no history of VZV who have an exposure, the use of VZIG may be beneficial in preventing maternal infection (199) . Another virus that may lead to admission to the ICU is HSV. HSV infection can affect both the mother and the developing fetus (200) (201) (202) . HSV of the genital tract can be transferred to the newborn and result in severe and life-threatening disease (203). Although rare, HSV type 2 causing encephalitis following cesarean section has been reported (204). Finally, given recent concerns regarding bioterrorism, it is important to realize that smallpox has had high mortality in the pregnant woman compared to the non-pregnant woman (205). Viral infections can cause severe morbidity and mortality in both solidorgan and stem cell transplant patients (206) (207) (208) (209) (210) (211) (233). Solid organ transplant recipients also are at risk of developing severe lower respiratory tract viral infections. One study found a high incidence of influenza among lung transplant patients, but liver and kidney transplant patients also develop influenza (234). The Herpesviruses cause a variety of clinical syndromes in transplant patients. CMV, EBV, VZV, HSV, HHV-6 and HHV-8 have all been reported to cause disease (188, (235) (236) (237) (238) . CMV disease constitutes a serious problem in bone marrow transplant recipients with a 30-50% incidence of clinically significant infections (239, 240) . Pneumonitis is the most serious complication and was associated with high mortality prior to antiviral therapy (241). Ganciclovir and foscarnet have been frequently used for prophylaxis and treatment of CMV (242-245). Hyperimmune globulin in combination with antivirals has also been used for treatment of disease (246). Ganciclovir resistance in CMV has been reported and should be considered when clinical responses do not occur (247). EBV can reactivate in transplant recipients and lead to uncontrolled B-cell proliferation and post-transplant lymphoproliferative disorder (PTLD) (248). This can present as frank lymphoma with high mortality rates. Donor lymphocyte infusions and anti-CD20 antibody has been used for treatment (249). HSV can present as both severe mucocutaneous disease or in rare cases encephalitis (250 175. 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