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Critical Care Medicine

Library resources and services especially for critical care medicine

Approach to Fever in the ICU

The development of fevers in critically ill patients are a sign that the patient requires attention and management, as fevers are a common physiological response of a variety of infectious and non-infectious agents.

Table 1.2 Infectious and non-infectious causes of fever

Table 1.2 Infectious and non-infectious causes of fever

Pangtey, G.S., Prasad, R. (2020). Fever in Intensive Care Unit. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Table 1.5 Medicines associated with drug fever
Most common Barbiturates, phenytoin, antihistaminic, methyldopa, penicillin, salicylates, sulfonamides, amphotericin-B, procainamide, bleomycin
Less common Isoniazid, PAS, Streptomycin, rifampicin, propylthiouracil, streptokinase, vancomycin, nitrofurantoin, allopurinol, cephalosporin, hydralazine, azathioprine
Least common

Insulins, tetracycline, digitalis, chloramphenicol

Pangtey, G.S., Prasad, R. (2020). Fever in Intensive Care Unit. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Approach to Fever in the ICU

The systematic approach to patient with fever in critically illness in intensive care unit involves integration of following seven points:

  1. Medical history and review of records.
  2. Clinical examination.
  3. Interpretation of investigative data.
  4. Any chronic predisposing condition.
  5. Acute condition leading to ICU admission.
  6. Magnitude of fever.
  7. Any recent invasive procedure.

Empiric Antibiotic Therapy

If the fever is suspected to be caused by an infectious agent, broad spectrum antibiotics should be started as soon as possible after taking cultures. Empirical antibiotics should only be started on patients in shock, neutropenic, or those with suspected infection of a VAD. Infected catheters should be removed immediately in blood stream infections.

Febrile Neutropenia

Febrile neutropenia is defined by a single oral temperature of 101 °F or a temperature of more than 100.4 °F sustained over a period of 1 hour with ANC <500 cells/mm3 or an ANC which is expected to reduce to <500 cells/mm3 over the next 48 hours. Risk of infections secondary to neutropenia begins to rise with an absolute neutrophil count (ANC) of <1000 cells/mm3.

Risk Assessment

Figure 14.1:Risk assessment model for planning work-up and treatment, from Chakrabarti, P., Jitani, A.K. (2020). Approach and Management of Severe Infections in Neutropenic Patients. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.


Approach to diagnosis and monitoring

Figure 14.2: Approach to diagnosis and monitoring, from Chakrabarti, P., Jitani, A.K. (2020). Approach and Management of Severe Infections in Neutropenic Patients. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.


Approach to management

Figure 14.3: Approach to management, from Chakrabarti, P., Jitani, A.K. (2020). Approach and Management of Severe Infections in Neutropenic Patients. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.


Sepsis is clinical clinical syndrome resulting from dysregulated physiologic, pathologic and biochemical response to an infection that can lead to multi-organ dysfunction and death. The definition has evolved over the years, with the most recent coming from the Sepsis-3 Consensus Document in 2016. Sepsis-3 defines sepsis as “a life-threatening organ dysfunction caused by a dysregulated host response to infection”. Organ dysfunction and mortality are prognosis are determined by Sequential Organ Failure Assessment (SOFA) scoring.

Approach to a Case of Sepsis
Figure 2.1: Approach to a Case of Sepsis, from Mittal, A., Soneja, M. (2020). Clinical Approach to Sepsis. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Sepsis-3 Criteria for Sepsis/Septic Shock (Adapted from Singer et al. (2016)
  • Sepsis: qSOFA ≥2 plus evidence of infection
  • Septic shock: Sepsis plus persistent hypotension requiring administration of vasopressors to maintain a MAP>65 mmHg and a lactate >2 mmol/L despite adequate fluid resuscitation

Commonly used Biomarkers for Sepsis:

Since the current SOFA scoring can lead to misdiagnosis from non-infectious causes of organ dysfunction, its important to other other biomarkers to reliably differentiate infectious from non-infectious causes as well as bacterial from viral/fungal causes of sepsis.

  • C-reactive protein (CRP)
  • procalcitonin (PCT) -- one of the most popular and commonly used biomarkers used to initiate/escalate/de-escalate antibiotics, but recent meta-analyses have called into question it's use in sepsis
  • Presepsin -- advantage over PCT or IL-6 is that it rises earlier in sepsis
  • CD64
  • Soluble-urokinase-type-plasminogen-activator-receptor (suPAR)
  • Soluble triggering receptor expressed on myeloid cells 1 (sTREM-1)

There is no single symptom or sign or investigation that can reliably diagnose sepsis. It is usually an diagnosed based on the composite of history, examination and relevant investigations (laboratory, microbiological and radiological).

Management of Sepsis

Figure 2.2: Overview of management of sepsis, from Mittal, A., Soneja, M. (2020). Clinical Approach to Sepsis. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Surviving Sepsis Campaign 1-h Bundle (Levy et al. 2018)
  • Measure lactate level (follow serial measurements if initial level >2 mmol/L)
  • Obtain blood cultures prior to administering antibiotics
  • Administer broad-spectrum antibiotics
  • “Begin” rapid administration of 30 mL/kg of crystalloid for hypotension or lactate ≥4 mmol/L
  • Start vasopressors if patient is hypotensive during or after fluid resuscitation to maintain a MAP _65 mmHg

Goals in the management of sepsis:
  • MAP ≥ 65mm Hg
  • Lactate < 2mmol/L
  • P/F ratio >200
  • SpO2 88–92%
  • Urine output > .5ml/kg/h
  • Hemoglobin > 7g/dl
  • Blood glucose < 180mg/dl
  • No dyselectrolytemia
  • No acid base disbalance
  • Place a central venous catheter
  • Peptic ulcer prophylaxis
  • Venous thrombosis prophylaxis
  • Nutritional support
  • Pain management
  • Sedation vacation

Community-Acquired Pneumonia

Community-acquired pneumonia refers to an infection of the lung parenchyma acquired outside a healthcare setting. CAP forms a part of a larger group of diseases known as lower respiratory tract infections (LRTIs). The term severe CAP (SCAP) signifies a more serious form of community-acquired pneumonia that requires admission to the intensive care unit and has a high risk of mortality.

The pathogenesis of CAP involves establishment of an infection of the lung parenchyma by a virulent micro-organism by overwhelming the host defense. Cytokine levels (both pro-inflammatory and anti-inflammatory) in the plasma and the lungs are far higher in SCAP patients and are associated with both ICU admission and mortality. The reasons for this exaggerated response in some individuals are not well known. The administration of the first dose of antibiotics may also cause a massive surge in cytokine levels in some patients.

Etiology of SCAP

Around 11% of SCAP patients may have a polymicrobial etiology, especially when they present with ARDS or when they have underlying COPD.

Bacterial Pneumonia

The most common organism implicated in SCAP remains pneumococcus (Streptococcus pneumoniae), which is also the commonest organism isolated in any severity of CAP. The other common organisms causing SCAP include Hemophilus influenzae, atypical organisms, viruses, Staphylococcus aureus, Pseudomonas aeruginosa, other gram-negative bacilli (GNB), and anaerobes. About 6% of cases are caused by the so-called PES (Pseudomonas aeruginosa, extended-spectrum β-lactamase producing Enterobacteriaceae, and methicillin resistant Staphylococcus aureus) pathogens. Infections with atypical organisms such as Legionella, Mycoplasma, and Chlamydia species are also common and often co-exist with simultaneous typical bacterial infection in SCAP. Together, these pathogens may be responsible for 22% of cases of CAP.

Viral Pneumonia

Viruses also form a large group among microbes causing SCAP; the commonly implicated ones being influenza, rhinovirus, respiratory syncytial virus (RSV), metapneumovirus (HMPV), and the coronaviruses.

Risk Factors for Developing SCAP
  • Delayed diagnosis and absence of antibiotic therapy before hospitalization
  • Advanced age
  • Co-morbid illness (e.g., chronic respiratory illness like COPD, cardiovascular disease, diabetes mellitus, neurologic illness, renal insufficiency, malignancy)
  • Cigarette smoking
  • Alcohol abuse
  • Increased pathogen load or virulence
  • Pharmacological or pathological immunosuppression
  • Host genetic polymorphisms affecting the inflammatory and immunological response

Risk Factors for Unusual Pathogen/Drug Resistant CAP
Organism Risk factors
Drug-resistant pneumococcus Elderly
β-lactam or macrolide therapy within 3 months
Day-care centers
Medical co-morbidities
Gram-negative bacilli Recent hospitalization/antibiotics
Cardiopulmonary co-morbidities
Underlying malignancy
Community-acquired methicillin resistant Staphylococcus aureus Elderly
End-stage renal disease/renal replacement therapy
Prior MRSA infection/colonization
Recent hospitalization/antibiotics (particularly fluoroquinolones)
Contact sports
Men who have sex with men
Medical co-morbidities
Pseudomonas spp Chronic obstructive pulmonary disease
Structural lung disease like bronchiectasis
Immunosuppression/recent steroid exposure
Recent antibiotics/recent hospitalizatio

 Table 4.3 Risk factors for unusual pathogens and drug resistance, Saxena, P., Sehgal, I.S., Agarwal, R., Dhooria, S. (2020). Severe Community-Acquired Pneumonia. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.


Approach to Management of SCAP

Algorithm 4.1 Approach to Management of SCAP, Saxena, P., Sehgal, I.S., Agarwal, R., Dhooria, S. (2020). Severe Community-Acquired Pneumonia. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.\

Drug-Resistant Gram-Negative Bacteria

Gram negative infections are responsible for causing both community and healthcare associated infections, however in recent years the number of infections caused by resistant gram negative species has increased, mostly in hospitalized patients. Drug resistant gram negative bacteria are some of the most difficult infections to treat in the ICU. Resistance to most commonly used drugs leads to delay in treatment, which increases the risk of morbidity and mortality in these patients. The often-indiscriminate use of broad spectrum antibiotics in intensive care further increases the prevalence of resistance in these organisms, creating a vicious circle.

Clinical syndromes associated with gram negative infections
Clinical syndrome Common microorganisms Clinical features Diagnosis Treatment
Bacteremia Community acquired—Escherichia coli (most common)
Hospital acquired—Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli
Fever, shaking chills, features of sepsis.
Usually secondary to infection at other site (e.g. community acquired bacteremia is usually secondary to UTI)
Blood culture (plus catheter tip in CLABSI)
Rapid diagnostic tests such as MALDI-TOF and multiplex PCR can be used
Sepsis/ septic shock + risk features of MDR—Two anti-pseudomonal agents
Sepsis/ septic shock but no risk features of MDR—One anti-pseudomonal agentrisk factors of MDR but no sepsis/ septic shock—one anti-pseudomonal agent
No sepsis/ no risk factors of MDR—Broad spectrum antibiotic (no anti-pseudomonal coverage required)
Duration—7 to 14 days
Nosocomial pneumonia
[hospital acquired pneumonia (HAP) and ventilator associated pneumonia (VAP)]
Acinetobacter baumannii,
Klebsiella pneumoniae,
Pseudomonas aeruginosa
New or progressive infiltrates on a chest radiograph with fever>100.4° F; leucocytosis (>12,000/μl) or leucopenia (<4000/ μl); altered mental status; new onset purulent sputum or change in sputum character; worsening gas exchange HAP: Expectorated sputum: Culture growth is to be considered significant if ≥105 CFU/mL
VAP: Endotracheal aspiration or mini bronchoalveolar lavage (BAL): Culture growth is considered to be significant if ≥105 CFU/mL for tracheal aspirate and ≥ 103 CFU/mL for BAL.
Risk factors of MDR or shock—2 anti-pseudomonal
No risk factors of MDR or shock—1 anti-pseudomonal
Duration—7 days
Complicated urinary tract infection (catheter associated UTI/ pyelonephritis) Escherichia coli, Klebsiella pneumoniae Fever, urinary symptoms (dysuria, burning micturition, supra-pubic pain, urinary frequency and urgency), flank pain/ costovertebral angle tenderness, features of sepsis Urine routine—for pyuria
Urine culture from mid—stream urine
Blood culture in pyelonephritis
Abdominal/pelvic imaging
Broad spectrum antimicrobial with ESBL coverage
Duration—5–14 days
Table 21.2: Clinical syndromes associated with gram negative infections, from Gupta, N., Soneja, M. (2020). Management of Gram Negative Multi-Drug Resistant Organisms in Intensive Care Units. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Coverage of Newer Antimicrobials

Newer antimicrobials ESBL KPC NDM OXA48 MDR Pae MDR Aba
Cefiderocol Yes Yes Yes Yes Yes Yes
Ceftolozane-Tazobactam (CWSI) Yes       Yes Yes
Ceftazidime-Avibactam (CWSI) Yes Yes   Yes Yes  
Aztreonam-Avibactam (CWSI) Yes Yes Yes Yes Yes  
Imipenem-Relebactam (CWSI) Yes Yes        
Meropenem-Vaborbactam (CWSI) Yes Yes        
Plazomicin (aminoglycoside) Yes Yes   Yes Yes  
Eravacycline (Fluorocycline) Yes Yes Yes Yes  


Table 21.4 Newer antimicrobials and their coverage, from Gupta, N., Soneja, M. (2020). Management of Gram Negative Multi-Drug Resistant Organisms in Intensive Care Units. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.


Methicillin-resistant Staphylococcus aureus (MRSA) was described by Barber M in 1961, soon after its introduction in October 1960, and outbreaks of MRSA were reported in the early 1960s). Methicillin resistance in S. aureus is defined as an oxacillin minimum inhibitory concentration (MIC) of ≥4 mcg/mL. Since that time, MRSA has spread worldwide, and the prevalence of MRSA has increased in both health care and community settings.


The prevalence of MRSA isolates in intensive care units in the USA is 60 percent, and more than 90,000 invasive infections due to MRSA occurred in the USA in 2005.

Mechanisms of Resistance

Methicillin resistance is mediated by PBP-2a, a penicillin-binding protein encoded by the mecA gene that permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics. The mecA gene is located on a mobile genetic element called staphylococcal chromosome cassette (SCCmec). A single clone probably accounted for most MRSA isolates recovered during the 1960s; by 2004, six major MRSA clones emerged worldwide, labeled as SCCmec I to VI.

Risk Factors
Recent hospitalization HIV infection
Recent surgery Infection drug use
Residence in long-term care facility Prior antibiotic use
Hemodialysis Incarceration
Indwelling catheters Military services
  Sharing needles, razors, and other sharp objects
  Men who have sex with men
  Sharing sports equipment

Table 22.1 Risk Factors for HA- MRSA and CA-MRSA, Anand, R. (2020). Management of MRSA, VRE. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Drugs Used for MRSA Infection
Drug Group Mechanism of action Dose Side effects
Vancomycin Glycopeptide
Inhibits cell wall synthesis LD25–30 mg/kg IV (especially in septic shock) 15–20 mg/kgof actual BW IV q8–12 h Red neck syndrome, DRESS, fever, thrombocytopenia, Neutropenia hearing lose, nephrotoxicity
Daptomycin Lipopeptide Depolarization of the bacterial cell membrane 6 mg/kgTBW IV over 30 min q24 h myopathy, peripheral neuropathy, and eosinophilic pneumonia. Serial measurements of serum creatine kinase should be monitored at least weekly, and daptomycin should be discontinued in patients with symptomatic myopathy and creatine phosphokinase (CPK) ≥5 times the upper limit of normal (ULN) or in asymptomatic patients
With CPK ≥10 times the ULN
Teicoplanin Glycopeptide
Inhibits cell wall synthesis LD 6 mg/kg IV 12 h for 3doses, then MD of 6 mg/kg IV 12 h.
Severe Infection
higher doses have been used LD 12 mg/kg iv 12 h 3 doses the MD 12
Hypersensitivity, fever, skin reaction marked thrombocytopenia, anemia and neutropenia
Red neck syndrome and nephrotoxicity lesser than vancomycin
Inhibits initiation of protein synthesis at the 50S ribosome 600 mg/kg PO/IV q12h Thrombocytopenia, anemia, lactic acidosis, peripheral neuropathy, serotonin toxicity, and ocular toxicity
Can reversibly inhibit monoamine oxidase

Table 22.2 Drugs used for MRSA infection,Anand, R. (2020). Management of MRSA, VRE. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Respiratory Viruses

Viral respiratory infections can have nonspecific clinical presentations which may be difficult to differentiate from bacterial or fungal infections. Even the severity and clinical course of viral respiratory infections is comparable to that of bacterial and fungal infections.

Non-Specific Symptoms of Viral Respiratory Infections
  • Fever
  • Chills
  • Arthralgia
  • Myalgia
  • Headache
  • Vomiting
  • Diarrhea
  • Otitis
  • Tonsillitis
  • Keratinitis
  • Conjunctivitis
Respiratory Symptoms of Viral Respiratory Infections
  • Cough
  • Rhinorrhea
  • Shortness of breath

Immunocompromised patients have a more complicated course of illness as compared to immunocompetent. Whereas, an “atypical” pneumonia presentation may be seen in immunocompetent, severe lobar or bilateral pneumonia may be seen in immunocompromised hosts. These infections may be acquired either in community or nosocomial settings.

Respiratory virus profile in community acquired and nosocomial settings
Community acquired Endogenous HSV, CMV
Exogenous Influenza, parainfluenza, adenovirus, rhinovirus, RSV, coronavirus, metapneumovirus
Nosocomial Endogenous HSV, CMV
Endogenous Mimivirus, CMV (transfusion), H1N1 pandemic influenza

Table 15.2 Respiratory virus profile in community acquired and nosocomial settings, Gulati, S., Maheshwari, A. (2020). Management of Viral Infections in ICU. In: Soneja, M., Khanna, P. (eds) Infectious Diseases in the Intensive Care Unit. Springer, Singapore.

Role of corticosteroids in Respiratory Infections

Corticosteroids have been used in influenza, SARS and VZV pneumonitis in order to decrease damage induced by inflammation in severe pneumonia. Dexamethasone is being currently used with evidence of benefit in COVID-19.


Role of immunotherapies in Respiratory Infections

Among the immunotherapies palivizumab, IVIg, plasma exchange and combination ganciclovir-CMV immunoglobulins have been approved for high risk pediatric RSV infection, influenza, GBS, and CMV pneumonitis, respectively.

Therapies for Specific Respiratory Infections

Influenza (H1N1/H5N1)
  • Out of neuraminidase inhibitors (NAI) and amantadine groups of antivirals, the latter are no longer preferred on account of high resistance to these drugs.
  • Oseltamivir 
    • Indicated in severe infections or in areas endemic with strains having high mortality (e.g., H5N1).
    • In severe cases, antiviral therapy may be provided on clinical suspicion alone even without any laboratory confirmation. But their use in non-severe patients is discouraged due to risk of resistant strains.
    • If oseltamivir is instituted within 48 h of onset of illness, then it has a chance to reduce complications/disease severity along with illness duration.
    • It is given in a dose of 75 mg twice daily for 5 days, which may be extended for 10 days in severe infections.
    • Higher doses of oseltamivir (150 mg twice a day for 10 days) may be used in seriously ill patients, influenza B strains, H5N1, resistant/reduced susceptibility strains of influenza A and infection at sites with reduced drug penetration (e.g., central nervous system). However there is not much evidence in support of it and there are concerns regarding antiviral resistance with high dose oseltamivir.
    • Treatment of oseltamivir resistant H5N1/H1N1 strains may be challenging
  • Intravenous zanamivir, inhaled laninamivir or combination antivirals such as oseltamivir-zanamivir and NAI-ribavirin-favipiravir
    • May be utilized for treating resistant influenza.
  • Low dose corticosteroids
    • Have been used in septic shock due to severe influenza and SARS/VZV pneumonitis so as to decrease the inflammatory tissue injuries. However, its use may lead to slower clearance of viral particles, increased rates of nosocomial infectious complications and mortality.
  • Plasma and hyperimmune globulins
    • May be beneficial in severe avian influenza (H5N1) and swine flu (H1N1) has been suggested by few case control studies and randomized controlled trials.
  • The most potent intervention is to vaccinate the elderly and the high risk individuals against seasonal influenza with the available vaccines.


  • Aerosolized ribavirin
    • Only recommended for immunosuppressed and children
  • Corticosteroids and immunotherapy
    • May be combined along with ribavirin.
  • Intramuscular palivizumab
    • May be considered as prophylaxis in high risk patients.
VZV pneumonitis
  • Acyclovir
    • May be efficacious if utilized early in the course of infection.


Parainfluenza virus
  • Aerosolized ribavirin
    • Only in immunosuppressed patients
    • Not to be used in immunocompetent patients


Human Metapneumovirus
  • Treatment is largely supportive with no specific antivirals
  • Aerosolized ribavirin
    • May be utilized only for immunosuppressed patients.
    • The efficacy and safety of ribavirin in humans are not well established


  • Treatment is largely supportive, with antivirals only for immunosuppressed patients and those with severe infections.
  • Cidofovir
    • Small case reports and non-randomized studies support the use in immunosuppressed patients.
    • Immunosuppressed individuals may need preemptive cidofovir therapy based on weekly virological surveillance.
  • Pooled IVIg
    • May be used as complementary therapy as it has neutralizing antibodies against adenovirus.
  • Ganciclovir and lipid ester derivatives of cidofovir are under evaluation for efficacy against adenovirus.


  • Intranasal interferon (IFN) a-2b
    • Useful for decreasing the symptoms and in primary prevention of rhinovirus infections.
    • Further role in treatment of critically ill patients with severe rhinovirus infections is still not clear.


  • The drugs available to treat CMV infections include:
    • Ganciclovir
    • Valganciclovir
    • Acyclovir
    • Valacyclovir
    • Maribavir
    • Foscarnet
    • Cidofovir
  • These drugs have been used prophylactically, preemptively or when the critically ill patients demonstrate CMV viremia.
  • All these management strategies aim to start the therapy early so as to avoid development of end organ disease.
  • Therapy is started universally in preventive strategy in comparison to preemptive therapy, where it is started only in high risk patients.
  • The treatment should be started in immunosuppressed individuals, who may have severe manifestations of disease, and in patients with end organ involvement attributable to CMV infection.
  • Severe CMV-CAP is one such example where treatment is required in immunocompromised patients or in severe pneumonia associated with hypoxemia in immunocompetent patients.
  • Important side effects of the antivirals used in managing CMV infections include bone marrow suppression and teratogenicity.
  • Though there is enough evidence to not advise CMV therapy in immunocompetent patients, the experts feel that the same may not be held for critically ill immunocompetent patients.
  • As against a complete course of antivirals in immunocompromised patients, only a limited duration of therapy may be required in immunocompetent patients just enough to bear the crisis of the acute phase.
  • Pending convincing evidence, the experts advice that critically ill patients should be subjected to a clinical evaluation and those with high risk factors to acquire CMV infection should be offered treatment. Even though such an approach met with success in animal studies, only a handful of human studies have shown a decrease in rates of CMV infection and its sequelae. Well-designed trials are needed to draw conclusions on the role of periodic viral load monitoring to trigger antiviral therapy in critically ill immunocompetent patients.
  • Dosages for CMV therapy:
    • Ganciclovir -- 5 mg/kg 12 hourly for the duration of infection.
    • Valganciclovir -- 900 mg 12 hourly, to be given for 21 days.
      • Valganciclovir is the oral equivalent of ganciclovir, which may be given for the entire duration with the same efficacy or may be started after the initial intravenous ganciclovir to complete the entire course of therapy.
  • Immunocompetent individuals may not require the complete course as they may become better after receiving therapy for 1–2 weeks. The experts opine that the antiviral may be continued for an additional 1 week after the patient shows improvement in order to prevent a relapse.
  • Foscarnet is an additional option, but it may not be preferred because of its nephrotoxicity.
    • Foscarnet may be recommended in Ganciclovir resistant CMV


  • Acyclovir and valacyclovir
    • Been used in patients with HSV related bronchopneumonitis or ARDS because of their good pulmonary bioavailability.
    • However, the evidence of their safety and efficacy has been provided only by case reports or cohort studies.
    • Studies have shown that even though acyclovir had the ability of restraining activation of herpes virus in ARDS patients, it did not have any additional benefit of decreasing duration of mechanical ventilation or mortality rates in immunocompetent patients with HSV bronchopneumonitis or ARDS.