Research progress of viral sepsis: etiology, pathophysiology, diagnosis, and treatment : Emergency and Critical Care Medicine

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Research progress of viral sepsis: etiology, pathophysiology, diagnosis, and treatment

Li, Jianping; Luo, Yiqi; Li, Hao; Yin, Yunhong; Zhang, Yi*

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Emergency and Critical Care Medicine ():10.1097/EC9.0000000000000086, April 25, 2023. | DOI: 10.1097/EC9.0000000000000086
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Sepsis is a fatal organ malfunction caused by an abnormal host response to multiple infections.[1] There were 48.9 million cases of sepsis worldwide in 2017, with a morbidity rate of 677.5 cases per 100,000 people.[2] It is expected to cause approximately 11 million deaths worldwide.[3] Sepsis can result from infection by multiple pathogens, such as bacteria, viruses, and fungi. Several recent studies have focused on sepsis. However, there are few studies on viral sepsis, most of which have focused on bacterial sepsis.[4–6] In a study on the global epidemiology of severe pediatric sepsis, 54.4% of patients had bacterial infections, while viruses and fungi accounted for 21% and 13.4%, respectively.[7] Among 700 samples collected from children hospitalized with severe acute respiratory infection (SARI), 547 (78.1%) tested positive for viral infection.[8]

Because of the lack of a definition, diagnosis, and detection of viral sepsis, the reported proportion of viral infections among adults with sepsis is very low. Viral infections should be considered in patients who lack evidence of bacterial, parasitic, or fungal infections. A study found that 61% of patients admitted with viral sepsis were diagnosed with pure viral community-acquired pneumonia according to the Sepsis-3 criteria.[9] Viral sepsis can be caused by viral infections and combined with, or secondary to, bacterial infections. Influenza virus infections are often associated with Streptococcus pneumoniae and Staphylococcus aureus. The cytomegalovirus, Epstein-Barr virus, and other viruses may be reactivated after bacterial sepsis.[10]

Viral sepsis lacks specific clinical manifestations, particularly during the early stages. If sepsis is combined with respiratory or digestive tract symptoms, it can be easily misdiagnosed as a focal infection. Patients with viral sepsis may have focal positional symptoms or signs of infection during the early course of the disease. Studies have shown that the most common site of infection is the respiratory system, which accounts for 68.2% of infections.[11] The early symptoms in patients infected with the influenza virus are mainly in the respiratory tract, followed by acute respiratory distress syndrome.[12] Most patients with enterovirus infections experience show early gastrointestinal symptoms.[13] Dengue virus infection in its early stages is characterized by high fever, systemic muscle pain, and joint pain.[14] Clinical treatments are centered on identifying the pathogen that causes sepsis as soon as possible. Understanding the common types of viral sepsis and the main characteristics of its pathogenesis, clinical manifestations, and effective diagnostic and treatment strategies can improve patient prognosis. Early identification of the causative agents of viral sepsis can help reduce the overuse of broad-spectrum antibiotics. In this article, we review the common viruses of sepsis, their potential pathophysiology, targets of diagnosis, and remedies for viral sepsis.

The common viruses of viral sepsis

Influenza virus

The influenza virus is the most common pathogen that causes viral sepsis. Children younger than 5 years, pregnant women, immunosuppressed individuals, and older adults are at high risk for influenza. The incidence and mortality of influenza gradually increase with age in adults.[15] The influenza virus in the respiratory tract causes extensive damage to the airways and alveolar epithelial cells, which seriously affects gas exchange.[16] Severe infections can manifest as diffuse infiltration in lungs, refractory hypoxemia, and even acute respiratory distress syndrome.[17] A study on sepsis in infants reported that the detection rate of influenza virus was 7.8%.[18]

Respiratory syncytial virus

Respiratory syncytial virus (RSV) usually causes lower respiratory tract infections in children.[19] Premature children delivered by cesarean section, those with immune dysfunction, and those with bronchopulmonary dysplasia are at a high risk of RSV infection.[20] Respiratory syncytial virus infections mainly cause minor symptoms that manifest as bronchiolitis or viral pneumonia.[21] Respiratory syncytial virus–associated sepsis and septic shock are serious complications of RSV infection and usually occur in neonates with low immunity. The main manifestations include multiple systemic symptoms such as dyspnea, central apnea, status epilepticus, ventricular tachycardia, and myocarditis.[22]


Severe acute respiratory syndrome coronavirus 2 and Middle East respiratory syndrome coronavirus usually lead to an epidemic of serious respiratory syndromes among people, whereas human coronavirus NL63 (HCoV-NL63), HCoV-OC43, and HCoV-229E mainly cause infections in infants and the older people.[23] The number of patients with severe sepsis has increased with the outbreak of the novel coronavirus disease 2019 (COVID-19). The immune system of patients with severe COVID-19 is abnormally activated, showing typical characteristics of sepsis, such as cytokine storm, circulation disorder, weak pulse, severe lung injury, as well as liver, kidney, and other multiple organ dysfunctions. A meta-analysis showed that the prevalence of COVID-19–related sepsis was 77.9%, and acute respiratory distress syndrome (ARDS) was the most common clinical presentation.[24]


Adenoviruses are common DNA viruses that primarily infect the respiratory tract, digestive system, and conjunctiva. Severe patients present with hepatitis, gastroenteritis, myocarditis, pneumonia, pancreatitis, meningoencephalitis, hemorrhagic cystitis, and acute conjunctivitis.[25–27] Because of their low immunity, adenovirus infections are more common in young children.[28] One study reported 3 cases of fatal neonatal sepsis related to human adenovirus type 56.[29] Another study showed that 2 patients infected with human adenovirus C2 after allogeneic hematopoietic stem cell transplantation (allo-HSCT) developed bacterial septicemia.[30]

Other viruses

Enteroviruses usually cause mild symptoms; however, neonates are prone to serious complications and even sepsis.[31] Human parechoviruses (HPeVs) cause serious infections in neonates and young infants.[32] A study reported that the detection rates of HPeV-1 and enteroviruses in young infants diagnosed with sepsis were 5% and 38%, respectively.[33] Li et al. reported a case in which a young Chinese man was diagnosed with herpes simplex virus-associated sepsis using next-generation sequencing.[34] Rhinoviruses cause common viral infections of the upper respiratory tract that primarily cause flu-like illnesses.[35] Patients with premature birth, congenital heart disease, and noninfectious respiratory diseases are more likely to have severe symptoms. A recent study reported that a patient infected with human rhinovirus A45 had viral sepsis and central nervous system involvement.[36]Table 1 summarizes the susceptible populations and clinical manifestations of common viruses.

Table 1 - Common Viruses Causing Sepsis
Virus Susceptible Population Clinical Manifestation References
Influenza virus Children younger than 5 y, pregnant women, old adults, immunosuppressed individuals Influenza pneumonia, influenza sepsis, acute encephalitis, acute myocarditis, myositis and rhabdomyolysis [ 10]
Respiratory syncytial virus Infant, young children with preterm birth, cesarean section and bronchopulmonary dysplasia, immunocompromised children Bronchiolitis, viral pneumonia, central apnea, status epilepticus, ventricular tachycardia, myocarditis [ 21,22]
Coronaviruses Infants and the elderly (human coronavirus NL63 [HCoV-NL63], HCoV-OC43, and HCoV-229E), all humans (SARS-CoV-2 and MERS-CoV) Pneumonia, ARDS, thromboembolism and hypercoagulopathy, AKI, liver dysfunction, CNS dysfunction [ 24,37,38]
Adenoviruses Young children Hepatitis, gastroenteritis, myocarditis, pneumonia, pancreatitis, meningoencephalitis, hemorrhagic, cystitis and acute conjunctivitis [ 25–27]
Enteroviruses Neonates, pregnant woman Myocarditis, hepatitis, coagulopathy, meningoencephalitis, pneumonia [ 39]
Human parechovirus Neonates, young infants Gastroenteritis, respiratory tract infections, fever, rash and severe irritability, encephalitis, seizures, acute flaccid paralysis [ 32,40–43]
AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; CNS, central nervous system; MERS-CoV, Middle East respiratory syndrome coronavirus; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.

Pathophysiology of viral sepsis

Cytokine storm of viral sepsis

The specific pathogenesis of sepsis is unclear, but some consensus suggests that the balance between the systemic inflammatory response syndrome and compensatory anti-inflammatory response syndrome is disrupted in sepsis.[4] Cytokine storms are processes in which various tissues and cells (mainly immune cells) lose their negative feedback mechanisms to the immune system under the influence of external stimuli (such as viruses and bacteria) and oversecrete inflammatory cytokines. Viral infections can induce severe cytokine storms.[44]

Inflammatory cytokines are produced during the virus-activated innate immune response. Innate immunity is activated via pattern recognition receptors (PRRs). Pattern recognition receptors can recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).[45] Common PRRs include toll-like receptors (TLRs), retinoic acid-induced gene 1, and NOD-like receptors (NLRs), which initiate innate immune responses.[46] Toll-like receptors are the most researched PRR and are expressed in various cellular compartments such as dendritic cells, neutrophils, macrophages, and T and B cells. Transmembrane proteins include TLR1, TLR2, TLR4, TLR5, TLR6, and TLR11.[47] Toll-like receptors recognize viral proteins and induce NF-κB activation through adaptor proteins such as myeloid differentiation protein 88 (MyD88), TIR receptor-inducing interferon-β (TRIF), TIR domain-containing adaptor protein, and TRIF-related adaptor molecule (TRAM).[48] Activated NF-κB promotes the production of inflammatory cytokines. NOD-like receptors are intracellular receptors that recognize PAMPs and DAMPs. NOD-like receptor family pyrin domain-containing proteins, which consist of NLR proteins, apoptosis-associated speck-like proteins, and pro-caspase-1, participate in inflammasome.[49] Activation of the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome is a widely researched medium that plays an essential role in both inflammatory and antiviral responses. The NLRP3 inflammasome participates in the activation of caspase-1 and the generation of interleukin-1β (IL-1β) and IL-18[50] (Fig. 1). Activated cytokines lead to systemic inflammation and multiple organ dysfunction. Acute lung injury (ALI), acute renal injury, and acute gastrointestinal injury (AGI) are common clinical manifestations (Fig. 2).

Figure 1:
Pathophysiological features of cytokine storm. TLR and NLRP3 can recognize PAMP and DAMP to induce the production of inflammatory cytokines. ASC, apoptosis-associated speck-like protein; DAMP, damage-associated molecular patterns; IL-1, interleukin-1; IL-6, interleukin 6; IL-8, interleukin-8; MyD88, myeloid differentiation protein 88; NLRP3, NOD-like receptor family pyrin domain-containing protein 3; PAMP, pathogen-associated molecular patterns; TIRAP, toll/interleukin-1 receptor (TIR) domain-containing adapter protein; TLR, toll-like receptors; TNF-α, tumor necrosis factor α; TRAM, TRIF-related adaptor molecule; TRIF, toll/interleukin 1 receptor domain-containing adapter-inducing interferon β.
Figure 2:
Clinical manifestations of major organ systems in viral sepsis. ARDS, acute respiratory distress syndrome; GFR, glomerular filtration rate.

Lung injury in viral sepsis

The respiratory system is the most commonly infected system and the most common system to fail in sepsis.[51] Exposure of the respiratory tract to the environment increases the risk of viral infection. Viruses causing respiratory tract injury include influenza virus, coronavirus, and RSV.[52] Most patients with sepsis present with ALI and ARDS.[53] The interaction between multiple inflammatory cytokines is key to promoting the progression of lung injury. Interleukin 1β, IL-6, and tumor necrosis factor α (TNF-α) are considered as crucial proinflammatory mediators.[54] A study revealed that IL-1β suppression of vascular endothelial-cadherin transcription was the determining factor of endotoxemia-induced lung vascular injury.[55] Interleukin 5 can reduce lung injury by modulating the immune response and inhibiting sepsis-induced systemic inflammation.[56] Tumor necrosis factor α is involved in the early pathogenesis of sepsis induced ALI. Using TNF-α Ab prophylactically can decrease serum cytokines and lung myeloperoxidase activity.[57] Inflammatory factors directly damage the endothelium and increase vascular permeability. Studying the mechanism of injury and the biological function of cytokines in sepsis will provide a new strategy for the prevention and treatment of ALI.

Acute kidney injury in viral sepsis

Acute kidney injury (AKI) is characterized by a rapid decrease in renal function due to different causes. Sepsis-associated AKI refers to meeting the diagnostic criteria for both sepsis and AKI, excluding other causes that can explain AKI.[58] It was reported that approximately 60% of sepsis patients in the intensive care unit develop AKI.[59,60] The pathophysiology of sepsis-associated AKI is complex and has not been fully elucidated. Existing research has mainly focused on the following aspects: inadequate fluid resuscitation in sepsis, septic cardiomyopathy, microvascular dysfunction, and maladaptive redistribution of tissue blood flow may trigger ischemic renal injury.[61] Sepsis causes the release of PAMPS and DAMPS, which interact with PRR in immune, endothelial, and renal tubular epithelial cells. This process initiates downstream signaling cascades and triggers the release of many proinflammatory factors.[62,63] These inflammatory reactions eventually lead to damage to the tubular epithelial cells.

Gastrointestinal tract injury in viral sepsis

As a part of multiple-organ function disability syndrome, AGI is the most common symptom of critical patients and can be caused by a variety of factors. Gastrointestinal dysfunction is associated with a high mortality rate in patients with sepsis.[64] Another study showed that 86.7% of critically ill patients with COVID-19 had AGI.[65] The gastrointestinal tract is one of the earliest and most seriously affected organs in the pathogenesis of sepsis. Damage to the gastrointestinal mucosal barrier and intestinal microecology disorders can cause the displacement of intestinal bacteria and endotoxins and aggravate the condition of critical patients.[66] When AGI occurs in patients with sepsis, studies have confirmed that ghrelin levels and the serum gastrointestinal hormone motilin are significantly decreased, which affects gastrointestinal motility and means that harmful metabolites cannot be removed in time. These reactions further aggravate the damage to gastrointestinal function.[67]


Because of the lack of specific clinical manifestations, viral sepsis is often difficult to detect in its early stages. The first step involved establishing a diagnosis of sepsis using the sequential organ failure assessment score. Patients with sepsis may present with an abnormal body temperature, respiratory distress, circulatory changes, abnormal consciousness, and other symptoms. Patients with suspected sepsis should undergo microbiological analysis within the first 45 minutes.[68] It has been reported that 42% of sepsis cases are culture negative, suggesting that many cases are caused by nonbacterial infections.[69] In the search for evidence of sepsis etiology, relevant tests, such as antigenic testing, molecular testing, serological tests, histopathology, and immunohistochemistry, should be completed. Many biomarkers have been used to diagnose sepsis and predict outcomes. Common biomarkers include procalcitonin, C-reactive protein, lactate, cytokines, and immunoglobulins.[68,70,71] In recent years, next-generation sequencing has been used to identify potential bacterial and viral infections in sepsis.[72] A retrospective study based on metagenomic next-generation sequencing illustrated that concurrent viral load was closely related to the survival rate of patients with sepsis.[73]Table 2 summarizes the common diagnostic methods used for viral sepsis. When a patient with sepsis has no evidence of bacterial, parasitic, or fungal infection, viral sepsis should be considered, and the virus type should be determined as soon as possible.

Table 2 - Common Diagnostic Methods for Viral Sepsis
Diagnostics Value of Diagnosis Disadvantage
Polymerase chain reaction Rapid, simple, inexpensive Due to its target specificity, unselected viruses may be missed; requiring auxiliary testing and virus identification by trained personnel[ 74]
Next-generation sequencing High sensitivity, fast turnaround time.
Drug resistance gene information can be identified; can detect several different targets simultaneously; discovery of new or unexpected viral infection; ability to detect any portion of the genome; the detection rate is significantly higher for bacterial, mixed, viral, and pneumocystis infections[ 75,76]
Expensive, time consuming, not all genomes are available, prone to contamination with environmental species
Lactate Screen clinically suspected patients,[ 77] guide resuscitation to reduce mortality[ 78] Low sensitivity and specificity[ 78]
Procalcitonin Not increased in viral infection[ 68]
Early diagnosis, inexpensive, and easy to obtain
Limited specificity[ 79]
C-reactive protein Detect the presence of inflammatory or infectious agents[ 80] Reaching the peak levels slowly and last for several days, limited specificity, having no correlation with the severity of sepsis[ 71]
Cytokines Have correlation with the severity of the process; IL-6 has better diagnostic and prognostic value than those of PTX3 and PCT[ 81] Nonspecific
Pancreatic stone protein The only biomarker with the ability to discriminate between clinical severity and predict mortality (compared with CRP, PCT, IL-6, and WBC).[ 82,83]
CRP, C-reaction protein; IL-6, interleukin 6; PTX3, pentraxin 3; WBC, white blood cell.

Treatment of viral sepsis

Supportive treatment

Many deaths in patients with sepsis occur in the first 48–72 hours of treatment; therefore, early identification, reasonable resuscitation, and treatment are crucial for improving the condition of patients with sepsis.[84–86] Supportive treatments for sepsis include monitoring vital signs, fluid resuscitation, lung-protective ventilation, nutrient supply, glucose management, and maintaining the balance between electrolytes and acid base.[87] Early fluid resuscitation is necessary to maintain the balance of water, electrolytes, acids, and bases. However, excess fluid can cause a net positive fluid balance that increases intracardiac pressure, organ edema, and arterial vasodilation.[88] The use of an oxygen mask or tracheal intubation in the early stages can reduce oxygen consumption and protect the airway.[89] Metabolic abnormalities are commonly observed in patients with sepsis. The current consensus for the management of serum glucose is to maintain a serum glucose level of 180 mg/dL.[90] The nutritional treatment of hypermetabolic patients with sepsis remains challenging. Many studies have indicated that, although purposeful underfeeding during sepsis may seem counterintuitive, it may benefit patients with hypermetabolism by preventing hyperglycemia and hyperlipidemia.[91] A previous study reported that vitamin C reduced mortality in patients with sepsis. Daily vitamin C supplementation is recommended for patients at high risk of viral infection and sepsis.[92] Early supportive care in sepsis patients is beneficial for preserving vital organ function and reducing mortality.

Antivirus treatment

Antiviral therapy is a top priority in sepsis management, and antiviral drugs should be administered as early as possible in patients with viral sepsis. Antiviral therapy should be initiated to suppress viral replication and reduce the viral load in the early stages of viral sepsis. Broad-spectrum antiviral drugs such as ribavirin and arbidol can target viral entry and replication or modulate cellular defense systems.[93] Ribavirin is recommended for patients with rhinovirus and RSV infections as well as for those with rhinovirus, RSV, adenovirus, and parainfluenza virus infections.[94] Prophylactic use of acyclovir can reduce mortality in patients with herpes simplex virus type 1.[95] Pleconaril is an antiviral drug that fights enteroviruses and rhinoviruses by binding to viral capsids to prevent their adsorption and cell penetration. In a clinical trial of neonatal enterovirus sepsis, the pleconaril group showed lower overall mortality than the placebo.[96] Although the diagnosis of viral sepsis is helpful in reducing the use of unnecessary antibiotics, it should also be noted that severe viral infections can be complicated by or secondary to bacterial infections in clinical practice. Antibiotics should also be selected according to the situation of patients with sepsis.


In recent years, immunomodulatory therapy, which aims to promote the clearance of pathogens, thereby preventing severe infections caused by rapid pathogen proliferation, has become increasingly popular for the treatment of sepsis. There have been many studies on immunoregulatory therapy for sepsis; however, there is little consensus regarding the use of immunomodulatory drugs. Immunotherapy should be targeted at suppressing exaggerated inflammation while retaining moderate inflammatory.[97] Corticosteroids, which are traditional anti-inflammatory drugs, are a double-edged sword in the treatment of sepsis. Corticosteroids are recommended only when septic shock cannot be corrected with adequate fluid resuscitation and vasopressors.[98] Antibodies against IL-6 have become effective drugs for the treatment of COVID-19. Tocilizumab, an IL-6 receptor antagonist, reduces the risk of progression to severe ARDS.[99] Many studies have reported that recombinant IL-7 can reverse the basic immune deficiency in sepsis and significantly improve the survival rate.[100–102] PD-1 and PD-L1 are broadly expressed in immune, endothelial, and bronchial epithet.[103] A continuous increase in PD-1 levels in patients with sepsis is closely associated with mortality.[104] PD-1 is involved in the development of the immunosuppressive phase of sepsis by inducing apoptosis of effector T lymphocytes, and its ligand is an ideal target for the treatment of viral sepsis.[105,106]Table 3 summarizes the treatments for COVID-19–related viral sepsis. The principle of immunotherapy is to reduce damage to immune function and avoid rebound inflammation.

Table 3 - Treatment of COVID-19 Viral Sepsis
Drugs Indications Dosage Adverse Effects References
Corticosteroids (strong recommendation)
Dexamethasone Severe and critically ill cases 6-mg intravenous injection for 10 d or equivalent Hyperglycemia, secondary infection, psychiatric disorders, avascular necrosis [90]
Remdesivir (weak recommendation) For adults with severe COVID-19 who do not require mechanical ventilation Intravenous injection, 200 mg on day 1 followed by 100 mg daily for up to 9 d Elevation of liver enzymes, increased oxygen requirement, hyperglycemia [107,108]
Tocilizumab Severe COVID-19 400- to 800-mg intravenous injection Infections, nausea, abdominal pain, mouth ulceration and gastritis [109,110]
Baricitinib Patients with COVID-19 4-mg daily dose for 14 days Infections, thrombotic events [90,111]
Anticoagulant therapy (strong recommendation)
Enoxaparin For adults with severe or critical COVID-19 40-mg subcutaneous injection once a day Ecchymosis and skin necrosis due to vasculitis, urticaria, angioedema and erythema [112,113]
Apixaban For adults with severe or critical COVID-19 2.5 mg, oral twice daily The increased risk of bleeding, thrombocytopenia and nausea, vasculitis and skin necrosis [113,114]
COVID-19, coronavirus disease 2019.


Viral sepsis is difficult to diagnose. There is little difference in the clinical manifestations of the different causes of sepsis. Because of its complex manifestations, viral sepsis can cause serious damage to multiple organs. Modern etiological identification methods that effectively distinguish viral from bacterial sepsis will facilitate the development of a new generation of drugs to treat sepsis in the future. In addition, the prognosis of patients with viral sepsis should be a primary concern in future studies.

Conflict of interest statement

The authors declare no conflict of interest.

Author contributions

Zhang Y conceived the topic and scope of the study. Li J and Luo Y wrote the manuscript. Li H and Yin Y critically revised the manuscript. All the authors have read and approved the final version of the manuscript.



Ethical approval of studies and informed consent

Not applicable.




1. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical criteria for sepsis: for the third international consensus definitions for sepsis and septic shock (Sepsis-3). JAMA. 2016;315(8):762–774. doi:10.1001/jama.2016.0288
2. Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990–2017: analysis for the Global Burden of Disease Study. Lancet. 2020;395(10219):200–211. doi:10.1016/S0140-6736(19)32989-7
3. Trzeciak A, Mongre RK, Kim MR, et al. Neutrophil heterogeneity in complement C1q expression associated with sepsis mortality. Front Immunol. 2022;13:965305. doi:10.3389/fimmu.2022.965305
4. Bosmann M, Ward PA. The inflammatory response in sepsis. Trends Immunol. 2013;34(3):129–136. doi:10.1016/
5. Delano MJ, Ward PA. Sepsis-induced immune dysfunction: can immune therapies reduce mortality?. J Clin Invest. 2016;126(1):23–31. doi:10.1172/JCI82224
6. Iba T, Levy JH. Sepsis-induced coagulopathy and disseminated intravascular coagulation. Anesthesiology. 2020;132(5):1238–1245. doi:10.1097/ALN.0000000000003122
7. Weiss SL, Fitzgerald JC, Pappachan J, et al. Global epidemiology of pediatric severe sepsis: the sepsis prevalence, outcomes, and therapies study. Am J Respir Crit Care Med. 2015;191(10):1147–1157. doi:10.1164/rccm.201412-2323OC
8. Zhao Y, Lu R, Shen J, Xie Z, Liu G, Tan W. Comparison of viral and epidemiological profiles of hospitalized children with severe acute respiratory infection in Beijing and Shanghai, China. BMC Infect Dis. 2019;19(1):729. doi:10.1186/s12879-019-4385-5
9. Cilloniz C, Dominedo C, Magdaleno D, Ferrer M, Gabarrus A, Torres A. Pure viral sepsis secondary to community-acquired pneumonia in adults: risk and prognostic factors. J Infect Dis. 2019;220(7):1166–1171. doi:10.1093/infdis/jiz257
10. Kalil AC, Thomas PG. Influenza virus-related critical illness: pathophysiology and epidemiology. Crit Care. 2019;23(1):258. doi:10.1186/s13054-019-2539-x
11. Xie J, Wang H, Kang Y, et al. The epidemiology of sepsis in Chinese ICUs: a national cross-sectional survey. Crit Care Med. 2020;48(3):e209–e218. doi:10.1097/CCM.0000000000004155
12. Chow EJ, Doyle JD, Uyeki TM. Influenza virus–related critical illness: prevention, diagnosis, treatment. Crit Care. 2019;23(1):214. doi:10.1186/s13054-019-2491-9
13. Abzug MJ, Michaels MG, Wald E, et al. A randomized, double-blind, placebo-controlled trial of pleconaril for the treatment of neonates with enterovirus sepsis. J Pediatric Infect Dis Soc. 2016;5(1):53–62. doi:10.1093/jpids/piv015
14. Muller DA, Depelsenaire AC, Young PR. Clinical and laboratory diagnosis of dengue virus infection. J Infect Dis. 2017;215(suppl 2):S89–S95. doi:10.1093/infdis/jiw649
15. Iuliano AD, Roguski KM, Chang HH, et al. Estimates of global seasonal influenza-associated respiratory mortality: a modelling study. Lancet. 2018;391(10127):1285–1300. doi:10.1016/S0140-6736(17)33293-2
16. Herold S, Becker C, Ridge KM, Budinger GR. Influenza virus-induced lung injury: pathogenesis and implications for treatment. Eur Respir J. 2015;45(5):1463–1478. doi:10.1183/09031936.00186214
17. Smith RE, Shifrin MM. Critical care considerations in adult patients with influenza-induced ARDS. Crit Care Nurse. 2020;40(5):15–24. doi:10.4037/ccn2020746
18. Aykac K, Karadag-Oncel E, Tanir Basaranoglu S, et al. Respiratory viral infections in infants with possible sepsis. J Med Virol. 2019;91(2):171–178. doi:10.1002/jmv.25309
19. Jartti T, Gern JE. Role of viral infections in the development and exacerbation of asthma in children. J Allergy Clin Immunol. 2017;140(4):895–906. doi:10.1016/j.jaci.2017.08.003
20. Haerskjold A, Kristensen K, Kamper-Jørgensen M, Nybo Andersen AM, Ravn H, Graff Stensballe L. Risk factors for hospitalization for respiratory syncytial virus infection: a population-based cohort study of Danish children. Pediatr Infect Dis J. 2016;35(1):61–65. doi:10.1097/INF.0000000000000924
21. Smith DK, Seales S, Budzik C. Respiratory syncytial virus bronchiolitis in children. Am Fam Physician. 2017;95(2):94–99.
22. Bakalli I. Liver dysfunction in severe sepsis from respiratory syncytial virus. J Pediatr Intensive Care. 2018;7(2):110–114. doi:10.1055/s-0037-1612609
23. Su S, Wong G, Shi W, et al. Epidemiology, genetic recombination, and pathogenesis of coronaviruses. Trends Microbiol. 2016;24(6):490–502. doi:10.1016/j.tim.2016.03.003
24. Karakike E, Giamarellos-Bourboulis EJ, Kyprianou M, et al. Coronavirus disease 2019 as cause of viral sepsis: a systematic review and meta-analysis. Crit Care Med. 2021;49(12):2042–2057. doi:10.1097/CCM.0000000000005195
25. Lynch JP 3rd, Kajon AE. Adenovirus: epidemiology, global spread of novel serotypes, and advances in treatment and prevention. Semin Respir Crit Care Med. 2016;37(4):586–602. doi:10.1055/s-0036-1584923
26. Shauer A, Gotsman I, Keren A, et al. Acute viral myocarditis: current concepts in diagnosis and treatment. Isr Med Assoc J. 2013;15(3):180–185.
27. Echavarria M. Adenoviruses in immunocompromised hosts. Clin Microbiol Rev. 2008;21(4):704–715. doi:10.1128/CMR.00052-07
28. Lynch JP 3rd, Fishbein M, Echavarria M. Adenovirus. Semin Respir Crit Care Med. 2011;32(4):494–511. doi:10.1055/s-0031-1283287
29. Otto WR, Lamson DM, Gonzalez G, et al. Fatal neonatal sepsis associated with human adenovirus type 56 infection: genomic analysis of three recent cases detected in the United States. Viruses. 2021;13(6):1105. doi:10.3390/v13061105
30. Engelmann I, Coiteux V, Heim A, et al. Severe adenovirus pneumonia followed by bacterial septicaemia: relevance of co-infections in allogeneic hematopoietic stem cell transplantation. Infect Disord Drug Targets. 2016;16(1):69–76. doi:10.2174/1871526516666160407114623
31. Tapparel C, Siegrist F, Petty TJ, Kaiser L. Picornavirus and enterovirus diversity with associated human diseases. Infect Genet Evol. 2013;14:282–293. doi:10.1016/j.meegid.2012.10.016
32. Olijve L, Jennings L, Walls T. Human parechovirus: an increasingly recognized cause of sepsis-like illness in young infants. Clin Microbiol Rev. 2017;31(1):e00047–e00017. doi:10.1128/CMR.00047-17
33. Makvandi M, Teimoori A, Pirmoradi R, et al. Parechovirus and enteroviruses among young infants with sepsis in Iran. Iran J Microbiol. 2021;13(3):312–318. doi:10.18502/ijm.v13i3.6393
34. Li S, Jiang W, Peng JM, Du B, Weng L. Herpes simplex virus associated sepsis in an immunocompetent adult: the value of next-generation sequencing. Chin Med J (Engl). 2020;133(14):1727–1728. doi:10.1097/CM9.0000000000000893
35. Winther B. Rhinovirus infections in the upper airway. Proc Am Thorac Soc. 2011;8(1):79–89. doi:10.1513/pats.201006-039RN
36. Liu J, Zhao H, Feng Z, et al. A severe case of human rhinovirus A45 with central nervous system involvement and viral sepsis. Virol J. 2022;19(1):72. doi:10.1186/s12985-022-01799-x
37. Koçak, Tufan Z, Kayaaslan B, Mer M. COVID-19 and sepsis. Turk J Med Sci. 2021;51(SI-1):3301–3311. doi:10.3906/sag-2108-239
38. Ahmadian E, Hosseiniyan Khatibi SM, Razi Soofiyani S, et al. COVID-19 and kidney injury: pathophysiology and molecular mechanisms. Rev Med Virol. 2021;31(3):e2176. doi:10.1002/rmv.2176
39. Chuang YY, Huang YC. Enteroviral infection in neonates. J Microbiol Immunol Infect. 2019;52(6):851–857. doi:10.1016/j.jmii.2019.08.018
40. Benschop KS, Schinkel J, Minnaar RP, et al. Human parechovirus infections in Dutch children and the association between serotype and disease severity. Clin Infect Dis. 2006;42(2):204–210. doi:10.1086/498905
41. Sharp J, Bell J, Harrison CJ, Nix WA, Oberste MS, Selvarangan R. Human parechovirus in respiratory specimens from children in Kansas City, Missouri. J Clin Microbiol. 2012;50(12):4111–4113. doi:10.1128/JCM.01680-12
42. Khatami A, McMullan BJ, Webber M, et al. Sepsis-like disease in infants due to human parechovirus type 3 during an outbreak in Australia. Clin Infect Dis. 2015;60(2):228–236. doi:10.1093/cid/ciu784
43. Alam MM, Khurshid A, Shaukat S, et al. Identification of human parechovirus genotype, HPeV-12, in a paralytic child with diarrhea. J Clin Virol. 2012;55(4):339–342. doi:10.1016/j.jcv.2012.08.008
44. Fajgenbaum DC, June CH. Cytokine storm. N Engl J Med. 2020;383(23):2255–2273. doi:10.1056/NEJMra2026131
45. Chousterman BG, Swirski FK, Weber GF. Cytokine storm and sepsis disease pathogenesis. Semin Immunopathol. 2017;39(5):517–528. doi:10.1007/s00281-017-0639-8
46. Gu Y, Zuo X, Zhang S, et al. The mechanism behind influenza virus cytokine storm. Viruses. 2021;13(7):1362. doi:10.3390/v13071362
47. Oviedo-Boyso J, Bravo-Patiño A, Baizabal-Aguirre VM. Collaborative action of toll-like and NOD-like receptors as modulators of the inflammatory response to pathogenic bacteria. Mediators Inflamm. 2014;2014:432785. doi:10.1155/2014/432785
48. Rassa JC, Ross SR. Viruses and toll-like receptors. Microbes Infect. 2003;5(11):961–968. doi:10.1016/s1286-4579(03)00193-x
49. Man SM, Kanneganti TD. Converging roles of caspases in inflammasome activation, cell death and innate immunity. Nat Rev Immunol. 2016;16(1):7–21. doi:10.1038/nri.2015.7
50. Kim S, Bauernfeind F, Ablasser A, et al. Listeria monocytogenes is sensed by the NLRP3 and AIM2 inflammasome. Eur J Immunol. 2010;40(6):1545–1551. doi:10.1002/eji.201040425
51. Costa EL, Schettino IA, Schettino GP. The lung in sepsis: guilty or innocent?. Endocr Metab Immune Disord Drug Targets. 2006;6(2):213–216. doi:10.2174/187153006777442413
52. Ljungstrom LR, Jacobsson G, Claesson BEB, Andersson R, Enroth H. Respiratory viral infections are underdiagnosed in patients with suspected sepsis. Eur J Clin Microbiol Infect Dis. 2017;36(10):1767–1776. doi:10.1007/s10096-017-2990-z
53. Park I, Kim M, Choe K, et al. Neutrophils disturb pulmonary microcirculation in sepsis-induced acute lung injury. Eur Respir J. 2019;53(3):1800786. doi:10.1183/13993003.00786-2018
54. Sui X, Liu W, Liu Z. Exosomes derived from LPS-induced MHs cells prompted an inflammatory response in sepsis-induced acute lung injury. Respir Physiol Neurobiol. 2021;292:103711. doi:10.1016/j.resp.2021.103711
55. Xiong S, Hong Z, Huang LS, et al. IL-1β suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury. J Clin Invest. 2020;130(7):3684–3698. doi:10.1172/JCI136908
56. Wei B, Chen Y, Zhou W, Li X, Shi L, Liao S. Interleukin IL-5 alleviates sepsis-induced acute lung injury by regulating the immune response in rats. Bioengineered. 2021;12(1):2132–2139. doi:10.1080/21655979.2021.1930746
57. Bhargava R, Altmann CJ, Andres-Hernando A, et al. Acute lung injury and acute kidney injury are established by four hours in experimental sepsis and are improved with pre, but not post, sepsis administration of TNF-α antibodies. PLoS One. 2013;8(11):e79037. doi:10.1371/journal.pone.0079037
58. Godin M, Murray P, Mehta RL. Clinical approach to the patient with AKI and sepsis. Semin Nephrol. 2015;35(1):12–22. doi:10.1016/j.semnephrol.2015.01.003
59. Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005;294(7):813–818. doi:10.1001/jama.294.7.813
60. Poston JT, Koyner JL. Sepsis associated acute kidney injury. BMJ. 2019;364:k4891. doi:10.1136/bmj.k4891
61. Antonucci E, Fiaccadori E, Donadello K, Taccone FS, Franchi F, Scolletta S. Myocardial depression in sepsis: from pathogenesis to clinical manifestations and treatment. J Crit Care. 2014;29(4):500–511. doi:10.1016/j.jcrc.2014.03.028
62. Peerapornratana S, Manrique-Caballero CL, Gómez H, Kellum JA. Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology, prevention and treatment. Kidney Int. 2019;96(5):1083–1099. doi:10.1016/j.kint.2019.05.026
63. Fani F, Regolisti G, Delsante M, et al. Recent advances in the pathogenetic mechanisms of sepsis-associated acute kidney injury. J Nephrol. 2018;31(3):351–359. doi:10.1007/s40620-017-0452-4
64. Reintam Blaser A, Jakob SM, Starkopf J. Gastrointestinal failure in the ICU. Curr Opin Crit Care. 2016;22(2):128–141. doi:10.1097/MCC.0000000000000286
65. Sun JK, Liu Y, Zou L, et al. Acute gastrointestinal injury in critically ill patients with COVID-19 in Wuhan, China. World J Gastroenterol. 2020;26(39):6087–6097. doi:10.3748/wjg.v26.i39.6087
66. Yang H, Song Z, Jin H, Cui Y, Hou M, Gao Y. Protective effect of rhBNP on intestinal injury in the canine models of sepsis. Int Immunopharmacol. 2014;19(2):262–266. doi:10.1016/j.intimp.2014.01.023
67. Santacruz CA, Quintairos A, Righy C, et al. Is there a role for enterohormones in the gastroparesis of critically ill patients? Crit Care Med. 2017;45(10):1696–1701. doi:10.1097/CCM.0000000000002625
68. Esposito S, De Simone G, Boccia G, De Caro F, Pagliano P. Sepsis and septic shock: new definitions, new diagnostic and therapeutic approaches. J Glob Antimicrob Resist. 2017;10:204–212. doi:10.1016/j.jgar.2017.06.013
69. Phua J, Ngerng W, See K, et al. Characteristics and outcomes of culture-negative versus culture-positive severe sepsis. Crit Care. 2013;17(5):R202. doi:10.1186/cc12896
70. Meisner M. Update on procalcitonin measurements. Ann Lab Med. 2014;34(4):263–273. doi:10.3343/alm.2014.34.4.263
71. Ayazi P, Mahyar A, Daneshi MM, Jahanihashemi H, Esmailzadehha N, Mosaferirad N. Comparison of serum IL-1beta and C reactive protein levels in early diagnosis and management of neonatal sepsis. Infez Med. 2014;22(4):296–301.
72. Brenner T, Decker SO, Grumaz S, et al. Next-generation sequencing diagnostics of bacteremia in sepsis (Next GeneSiS-Trial): study protocol of a prospective, observational, noninterventional, multicenter, clinical trial. Medicine (Baltimore). 2018;97(6):e9868. doi:10.1097/MD.0000000000009868
73. Duan LW, Qu JL, Wan J, et al. Effects of viral infection and microbial diversity on patients with sepsis: a retrospective study based on metagenomic next-generation sequencing. World J Emerg Med. 2021;12(1):29–35. doi:10.5847/wjem.j.1920-8642.2021.01.005
74. Garcia-Arroyo L, Prim N, Marti N, Roig MC, Navarro F, Rabella N. Benefits and drawbacks of molecular techniques for diagnosis of viral respiratory infections. Experience with two multiplex PCR assays. J Med Virol. 2016;88(1):45–50. doi:10.1002/jmv.24298
75. Li N, Ma X, Zhou J, et al. Clinical application of metagenomic next-generation sequencing technology in the diagnosis and treatment of pulmonary infection pathogens: a prospective single-center study of 138 patients. J Clin Lab Anal. 2022;36(7):e24498. doi:10.1002/jcla.24498
76. Kozel TR, Burnham-Marusich AR. Point-of-care testing for infectious diseases: past, present, and future. J Clin Microbiol. 2017;55(8):2313–2320. doi:10.1128/JCM.00476-17
77. Contenti J, Corraze H, Lemoël F, Levraut J. Effectiveness of arterial, venous, and capillary blood lactate as a sepsis triage tool in ED patients. Am J Emerg Med. 2015;33(2):167–172. doi:10.1016/j.ajem.2014.11.003
78. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43(3):304–377. doi:10.1007/s00134-017-4683-6
79. Saikant R, Ravindran S, Vijayan A, et al. Response of letter to the editor on procalcitonin: a promising diagnostic marker for sepsis and antibiotic therapy. J Intensive Care. 2017;5:68. doi:10.1186/s40560-017-0260-x
80. Gunsolus IL, Sweeney TE, Liesenfeld O, Ledeboer NA. Diagnosing and managing sepsis by probing the host response to infection: advances, opportunities, and challenges. J Clin Microbiol. 2019;57(7):e00425–e00419. doi:10.1128/JCM.00425-19
81. Gaini S, Koldkjaer OG, Pedersen C, Pedersen SS. Procalcitonin, lipopolysaccharide-binding protein, interleukin-6 and C-reactive protein in community-acquired infections and sepsis: a prospective study. Crit Care. 2006;10(2):R53. doi:10.1186/cc4866
82. Fidalgo P, Nora D, Coelho L, Povoa P. Pancreatic stone protein: review of a new biomarker in sepsis. J Clin Med. 2022;11(4):1085. doi:10.3390/jcm11041085
83. Gukasjan R, Raptis DA, Schulz HU, Halangk W, Graf R. Pancreatic stone protein predicts outcome in patients with peritonitis in the ICU. Crit Care Med. 2013;41(4):1027–1036. doi:10.1097/CCM.0b013e3182771193
84. Morin L, Ray S, Wilson C, et al. Refractory septic shock in children: a European Society of Paediatric and Neonatal Intensive Care definition. Intensive Care Med. 2016;42(12):1948–1957. doi:10.1007/s00134-016-4574-2
85. Weiss SL, Balamuth F, Hensley J, et al. The epidemiology of hospital death following pediatric severe sepsis: when, why, and how children with sepsis die. Pediatr Crit Care Med. 2017;18(9):823–830. doi:10.1097/PCC.0000000000001222
86. Cvetkovic M, Lutman D, Ramnarayan P, Pathan N, Inwald DP, Peters MJ. Timing of death in children referred for intensive care with severe sepsis: implications for interventional studies. Pediatr Crit Care Med. 2015;16(5):410–417. doi:10.1097/PCC.0000000000000385
87. Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021;47(11):1181–1247. doi:10.1007/s00134-021-06506-y
88. Marik P, Bellomo R. A rational approach to fluid therapy in sepsis. Br J Anaesth. 2016;116(3):339–349. doi:10.1093/bja/aev349
89. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580–637. doi:10.1097/CCM.0b013e31827e83af
90. Levy MM, Evans LE, Rhodes A. The surviving sepsis campaign bundle: 2018 update. Crit Care Med. 2018;46(6):997–1000. doi:10.1097/CCM.0000000000003119
91. Arabi YM, Aldawood AS, Haddad SH, et al. Permissive underfeeding or standard enteral feeding in critically ill adults. N Engl J Med. 2015;372(25):2398–2408. doi:10.1056/NEJMoa1502826
92. Holford P, Carr AC, Jovic TH, et al. Vitamin C—an adjunctive therapy for respiratory infection, sepsis and COVID-19. Nutrients. 2020;12(12):3760. doi:10.3390/nu12123760
93. Geraghty RJ, Aliota MT, Bonnac LF. Broad-spectrum antiviral strategies and nucleoside analogues. Viruses. 2021;13(4):667. doi:10.3390/v13040667
94. Gu X, Zhou F, Wang Y, Fan G, Cao B. Respiratory viral sepsis: epidemiology, pathophysiology, diagnosis and treatment. Eur Respir Rev. 2020;29(157):200038. doi:10.1183/16000617.0038-2020
95. Traen S, Bochanen N, Ieven M, et al. Is acyclovir effective among critically ill patients with herpes simplex in the respiratory tract?. J Clin Virol. 2014;60(3):215–221. doi:10.1016/j.jcv.2014.04.010
96. Hernández M. A randomized, double-blind, placebo-controlled trial of pleconaril for the treatment of neonates with enterovirus sepsis. Rev Chilena Infectol. 2016;33(3):359. doi:10.4067/S0716-10182016000300021
97. Lin HY. The severe COVID-19: a sepsis induced by viral infection? And its immunomodulatory therapy. Chin J Traumatol. 2020;23(4):190–195. doi:10.1016/j.cjtee.2020.06.002
98. Russell JA, Williams MD. Trials in adult critical care that show increased mortality of the new intervention: inevitable or preventable mishaps?. Ann Intensive Care. 2016;6(1):17. doi:10.1186/s13613-016-0120-1
99. Trifi A, Abdennebi C, Mehdi A, et al. Beneficial of adding tocilizumab to standard care in critical forms of COVID-19 pneumonia: study on paired series. Tunis Med. 2022;100(4):309–312.
100. Hotchkiss RS, Monneret G, Payen D. Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Nat Rev Immunol. 2013;13(12):862–874. doi:10.1038/nri3552
101. Unsinger J, McGlynn M, Kasten KR, et al. IL-7 promotes T cell viability, trafficking, and functionality and improves survival in sepsis. J Immunol. 2010;184(7):3768–3779. doi:10.4049/jimmunol.0903151
102. Ge Y, Huang M, Yao YM. Biology of interleukin-17 and its pathophysiological significance in sepsis. Front Immunol. 2020;11:1558. doi:10.3389/fimmu.2020.01558
103. Boomer JS, To K, Chang KC, et al. Immunosuppression in patients who die of sepsis and multiple organ failure. JAMA. 2011;306(23):2594–2605. doi:10.1001/jama.2011.1829
104. Tomino A, Masanobu T, Ruri A, et al. Increased PD-1 expression and altered T cell repertoire diversity predict mortality in patients with septic shock: a preliminary study. PLoS One. 2017;12(1):e0169653. doi:10.1371/journal.pone.0169653
105. Lin GL, McGinley JP, Drysdale SB, Pollard AJ. Epidemiology and immune pathogenesis of viral sepsis. Front Immunol. 2018;9:2147. doi:10.3389/fimmu.2018.02147
106. Peters van Ton AM, Kox M, Abdo WF, Pickkers P. Precision immunotherapy for sepsis. Front Immunol. 2018;9:1926. doi:10.3389/fimmu.2018.01926
107. Gandham R, Eerike M, Raj GM, Bisoi D, Priyadarshini R, Agarwal N. Adverse events following remdesivir administration in moderately ill COVID-19 patients—a retrospective analysis. J Family Med Prim Care. 2022;11(7):3693–3698. doi:10.4103/jfmpc.jfmpc_2468_21
108. Alhazzani W, Evans L, Alshamsi F, et al. Surviving sepsis campaign guidelines on the management of adults with coronavirus disease 2019 (COVID-19) in the ICU: first update. Crit Care Med. 2021;49(3):e219–e234. doi:10.1097/CCM.0000000000004899
109. RECOVERY Collaborative Group. Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2021;397(10285):1637–1645. doi:10.1016/S0140-6736(21)00676-0
110. Sheppard M, Laskou F, Stapleton PP, Hadavi S, Dasgupta B. Tocilizumab (Actemra). Hum Vaccin Immunother. 2017;13(9):1972–1988. doi:10.1080/21645515.2017.1316909
111. Jorgensen SCJ, Tse CLY, Burry L, Dresser LD. Baricitinib: a review of pharmacology, safety, and emerging clinical experience in COVID-19. Pharmacotherapy. 2020;40(8):843–856. doi:10.1002/phar.2438
112. Villanueva CA, Najera L, Espinosa P, Borbujo J. Bullous hemorrhagic dermatosis at distant sites: a report of 2 new cases due to enoxaparin injection and a review of the literature. Actas Dermosifiliogr. 2012;103(9):816–819. doi:10.1016/
113. Cuker A, Tseng EK, Nieuwlaat R, et al. American Society of Hematology 2021 guidelines on the use of anticoagulation for thromboprophylaxis in patients with COVID-19. Blood Adv. 2021;5(3):872–888. doi:10.1182/bloodadvances.2020003763
114. Ozturk S, Can I, Erden I, Akyol H, Solmaz OA. Enoxaparin-induced hemorrhagic bullous dermatosis in a leprosy patient. Cutan Ocul Toxicol. 2015;34(3):254–256. doi:10.3109/15569527.2014.950381

Acute gastrointestinal injury; Acute kidney injury; Acute lung injury; Cytokine storm; Diagnosis; Treatment of viral sepsis; Viral sepsis

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