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SEVER Viral pneumonia last

Dr.Tarek Sabry
Dr.Tarek Sabry
Dr.Tarek SabryINTENSIVIST at FUJAIRAH HOSPITAL- MOH- UAE

Diagnosis and management of sever viral pneumonia in ICU

SEVER Viral pneumonia last

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MANAGEMENT OF Sever VIRAL PNEUMONIA IN
ICU
1
2
Sever VIRALPNEUMONIA
3
Introduction
 Severe pneumonia in intensive care
unit (ICU) patients represents a
major concern for intensivists
because of the high mortality and
morbidity rate attributable to these
episodes.
 During past decades many
strategies have been implemented
with the aim to optimize the outcome
of patients with severe lung
infections.
4
Introduction
 Acute respiratory distress
syndrome (ARDS) and
pneumonia are closely correlated
in the critically ill patient.
Whereas ARDS is often
complicated by nosocomial
pneumonia, pulmonary infection
is also the most frequent single
cause of ARDS.
5
Introduction
 Causative agents of severe pneumonia may
widely differ, mainly depending upon
epidemiological and clinical factors.
 Up to 10% of hospitalized patients with CAP
need intensive therapies because of respiratory
failure requiring mechanical ventilation and/or
septic shock.
 The frequency of microbiologically documented
CAP is around 25%among in-patients, but the
percentage of isolated pathogens in SCAP may
be higher, due to the availability and extensive
use of more reliable diagnostic tools in ICU.
6
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SEVER Viral pneumonia last

  • 1. MANAGEMENT OF Sever VIRAL PNEUMONIA IN ICU 1
  • 3. 3
  • 4. Introduction  Severe pneumonia in intensive care unit (ICU) patients represents a major concern for intensivists because of the high mortality and morbidity rate attributable to these episodes.  During past decades many strategies have been implemented with the aim to optimize the outcome of patients with severe lung infections. 4
  • 5. Introduction  Acute respiratory distress syndrome (ARDS) and pneumonia are closely correlated in the critically ill patient. Whereas ARDS is often complicated by nosocomial pneumonia, pulmonary infection is also the most frequent single cause of ARDS. 5
  • 6. Introduction  Causative agents of severe pneumonia may widely differ, mainly depending upon epidemiological and clinical factors.  Up to 10% of hospitalized patients with CAP need intensive therapies because of respiratory failure requiring mechanical ventilation and/or septic shock.  The frequency of microbiologically documented CAP is around 25%among in-patients, but the percentage of isolated pathogens in SCAP may be higher, due to the availability and extensive use of more reliable diagnostic tools in ICU. 6
  • 7. Introduction  Viral infections are common causes of respiratory tract disease in the outpatient setting but much less common in the intensive care unit.  However, a limited number of viral agents cause respiratory tract disease in the intensive care unit. . 7
  • 8. Respiratory viruses  Some viruses, such as Influenza, respiratory syncytial virus (RSV), cytomegalovirus (CMV), and varicella-zoster virus (VZV), are relatively common.  Others, such as adenovirus, severe acute respiratory syndrome (SARS)-coronavirus, Hantavirus, and the viral hemorrhagic fevers (VHFs), are rare but have an immense public health impact. 8
  • 9.  Respiratory viruses have received particular attention  infections with coronavirus (SARS) and influenza viruses (H1N1 , H5N1) are associated with a high incidence of ARDS 9
  • 10. viral respiratory infections  Most viral respiratory infections in the ICU are community-associated cases with severe lower respiratory disease that can progress into respiratory failure and acute respiratory distress syndrome (ARDS).  The remainder are infections seen in immunocompromised patients, such as transplantation . 10
  • 11. viral respiratory infections  In some instances (severe acute respiratory syndrome [SARS], influenza, and adenovirus), viral respiratory infections present with fulminant respiratory failure and ARDS, alarming a larger community outbreak  In these situations, the newly recognized illness in an ICU patient might be the first presentation of a larger public health emergency. 11
  • 12. Past Pandemics 1918 H1N1 “Spanish Influenza” 20-40 million deaths 1957 H2N2 “Asian Flu” 1-2 million deaths 1968 H3N2 “Hong Kong Flu” 700,000 deaths 1977 H1N1 Re-emergence No pandemic 2003 Corona V SARS 260 deaths 2009 H1N1 “Swine Flu Mild Pandemic 12
  • 13. 13
  • 14.  Recognizing these viral etiologies becomes paramount in treatment, infection control, and public health measures.  Therefore, a basic understanding of the pathogenesis of viral entry, replication, and host response is important for clinical diagnosis and initiating therapeutic options. 14 Pathophysiology
  • 15. Influenza RSV SARS-CoV Virus family Orthomyxovirdae Paramyxovirdae Coronaviridae Epidemiologic link Seasonal epidemic Seasonal epidemic, immunocompromised and transplant Laboratory exposure on known infected individual Pulmonary clinical findings Primary Alveolar Pneumonia Upper respiratory tract infection, bronchiolitis, pneumonia Rapid progressive pneumonia, ARDS Lipid envelope Yes Yes Yes Major receptor for cell entry Sialic acid RSV glycoprotein G CD209L ACE 2 Primary cell of infection Type 1 respiratory epithelium Type 1 respiratory epithelium Type 1 respiratory epithelium 15
  • 16. VZV Adenovirus CMV VHF Virus family Herpesvirdae Adenoviridae Herpesviridae Filoviridae Epidemiologic link Contact with infected individual Military camps, mental health facilities Transplantation, immunosuppressi ve medications Endemic area or contact with infected individual Pulmonary clinical findings Primary alveolar pneumonia Alveolar pneumonia with bronchiolitis Interstitial pneumonitis, bronchiolitis Alveolar edema Lipid envelope Yes No Yes Yes Major receptor for cell entry Glycoprotein C and D Coksackie- adenovirus receptor Unknown, involves integrens Folate receptor Alpha Primary cell of infection Macrophage and dendritic cells Type 1 respiratory epithelium Multiple Macrophages and dendritic cells 16
  • 17. Pathophysiology 17  In general, when viruses cause pneumonia, it initially affects the parenchyma adjacent to terminal and respiratory bronchioles and subsequently progresses to involve the entire lobule.  With rapidly progressive pneumonia, diffuse alveolar damage is seen, consisting of intra- alveolar hemorrhage, interstitial lymphocyte infiltration, edema, fibrin deposition, type 2 pneumocyte hyperplasia, and formation of hyaline membranes.
  • 18. Pathophysiology  pathophysiological changes occurring during severe infections (increased cardiac output; leaky capillaries/altered protein binding; end-organ dysfunctions) .  These changes modify drug clearance (Cl) and volume of distribution (Vd) according to their hydrophilic or lipophilic nature.[55. 18
  • 19. SARS pathology in the respiratory tract. Gu J et al. J Exp Med 2005;202:415-424 19
  • 20. 20
  • 21. Clinical picture in viral infection Exposure to viral infection Fever ,Myalgia,Dry cough,Headach (early symptoms) Non productive cough – Shortness of breath Incubation peroid Prodrome Lower respiratory phase 2- to 10 days up to 13 days 1- to 2 days From day 4 onwards 21 Non / very Low Low Very High Recovery aprox 90% Acute respiratory distress syndrome 10%INFECTIVTY
  • 22. Viruses Associated with Respiratory Infections Syndrome Commonly Associated Viruses Less Commonly Associated Viruses Corza Rhinoviruses, Coronaviruses Influenza and parainfluenza viruses, enteroviruses, adenoviruses Influenza Influenza viruses Parainfluenza viruses, adenoviruses Croup Parainfluenza viruses Influenza virus, RSV, adenoviruses Bronchiolitis RSV Influenza and parainfluenza viruses, adenoviruses Bronchopneum onia Influenza virus, RSV, Adenoviruses Parainfluenza viruses, measles, VZV, CMV 22
  • 23. 23
  • 24. Chest xray 24  None of the viral etiologies of pneumonia result in pathognomonic findings on chest radiographs, and bacterial pneumonia cannot be differentiated from viral pneumonia based on radiographic findings. Chest radiography may reveal the following findings:  Patchy interstitial or alveolar infiltrate, which may be bilateral or involve 2 or more lobes  Peribronchial thickening  Consolidation  Pleural effusion
  • 25. 25
  • 26. 26
  • 27. Computed tomography (CT) scannig  CT scanning is sensitive in showing differences in tissue attenuation and parenchymal changes associated with inflammation. HRCT has limited value for making a specific diagnosis.  CT findings should be corroborated with epidemiologic and clinical data to narrow the differential diagnosis. 27
  • 28. 28
  • 29. Laboratory Diagnosis 29  Rapid Diagnosis – nasopharyngeal aspirates, throat and nasal swabs are normally used. ◦ Antigen Detection – can be done by IFT or EIA. ◦ RNA Detection – RT-PCR assays give the best sensitivity and specificity. It is the only method that can differentiate the 2009 pandemic H1N1 strain from the seasonal H1N1 strain. However, it is expensive and technically demanding.
  • 30. Lung Biopsy  Infrequently, lung biopsy (ie, transbronchial via a bronchoscope, transthoracic via a thoracoscope, or open lung) is required to make a diagnosis in very ill patients, who often are immunocompromised. 30
  • 31. Bronchiolar lavage  Bronchiolar lavage may be useful to obtain material for cytopathologic analysis and microbiologic studies. 31
  • 32. 32
  • 33. Managment  Patients affected by severe pneumonia need to be treated urgently and appropriately, given the importance of rapid pathogens' clearance in reducing infection- driven systemic inflammatory activation and preventing multiorgan dysfunction. 33
  • 34. Management Acute care may involve use of the following: • Oxygen, if the patient has hypoximia • Beta-agonists, if bronchospasm is present • Fluids, if dehydration is present • Resuscitation bundle if septic shock is present • Appropriate anti viral according to guidelines • Respiratory isolation • Antibiotics, if infiltrate is seen on the chest radiograph • Mechanical ventilation if respiratory failure is present or impending 34
  • 35. Resuscitation  When severe pneumonia is complicated by severe sepsis and septic shock, adherence to a resuscitation interventions bundle  within the first 6h (measure of serum lactates, control of hypotension, early antibiotic administration after performing cultures)  and 24 h (low-dose steroids administration, glucose control, maintenance of inspiratory plateau pressure<30cmH2O for mechanically ventilated patients) is associated with improved outcome 35
  • 36. 36 INFECTION CONTROL • Isolation with General and strict percussions. • Avoid interventions which may cause aerosolisation of respiratory secretions:  Bronchoscopy  Nebulized bronchodilators  Chest physiotherapy  Gastroscopy  Any procedure / intervention that may release respiratory secretions Managment
  • 37. Antiviral therapy Virus Treatment Prevention Influenza virus Amantadine Influenza vaccine Rimantadine Amantadine Oseltamivir Oseltamivir Zanamivir Zanamivir Respiratory syncytial virus Ribavirin RSV immunoglobulin Palivizumab 37
  • 38. Antiviral therapy Virus Treatment Prevention Parainfluenza virus Ribavirin Herpes simplex virus Acyclovir Varicella-zoster virus Acyclovir Varicella-zoster immunoglobulin Adenovirus Ribavirin Measles virus Ribavirin Intravenous immunoglobulin Cytomegalovirus Ganciclovir Foscarnet Intravenous immunoglobulin 38
  • 39. H1N1 influenza  In the 2009-2010 H1N1 influenza epidemic, the US Centers for Disease Control and Prevention (CDC) recommended oseltamivir or zanamivir for treatment of all hospitalized patients with suspected or confirmed cases and for outpatients at increased risk for complications of H1N1 infection.  As of September 2009, only 28 of 10,000 H1N1 isolates tested were resistant to oseltamivir (11 from the United States), and all were susceptible to zanamivir. 39
  • 40. H1N1 influenza  Although intravenous peramivir had not been formally FDA approved for the treatment of influenza during the 2009-2010 H1N1 pandemic, the FDA issued an emergency use authorization (EUA) for its use in hospitalized patients who had potentially life-threatening suspected or laboratory confirmed infection with H1N1.  Under the EUA, treatment with IV peramivir was approved for patients who had not responded to either oral or inhaled antiviral therapy and/or drug delivery by a route other than IV that was not expected to be dependable or feasible. ] 40
  • 41. Coronavirus Pneumonia  Protease inhibitors (eg, lopinavir/ritonavir) demonstrated antiviral activity against severe acute respiratory syndrome coronavirus (SARS-CoV) infection.  Interferon alfa and interferon beta have activity against SARS-CoV in vitro and in animal models.  Limited human data seemed to demonstrate some beneficial effect.  Ribavirin is not active against SARS-CoV in vitro, and studies have not shown clinical efficacy,Therefore, this medication is not recommended for this infection. 41
  • 42. Systemic Corticosteroids  High-dose corticosteroids have not been shown to be beneficial in ARDS and septic shock unrelated to A(H1N1) virus infection in reducing mortality.  However, stress-dose corticosteroids (hydrocortisone 200-300 mg/d) may be beneficial in improving hospital mortality and morbidity outcomes. 42
  • 43. Systemic Corticosteroids  Although low-dose corticosteroids may be considered in the management of refractory septic shock, the precise role of systemic steroids in the setting of ARDS and refractory shock due to severe influenza pneumonitis requires further investigation  meta-analyses to date have mainly derived from data related to bacterial-induced sepsis, and data specific for pandemic A(H1N1) are limited.  It is important to use systemic corticosteroids with caution in the treatment of respiratory viral diseases. 43
  • 44. Systemic Corticosteroids  Early use of corticosteroids might prolong viral replication in severe acute respiratory syndrome (SARS) and H3N2 influenza.  prolonged use of systemic corticosteroids in SARS led to severe adverse effects, including fatal disseminated Aspergillus infection and osteonecrosis.  During the SARS period in the ICU, the use of systemic steroids was associated 44
  • 45. OXYGENATION  A major challenge that physicians attending to patients with severe pneumonia have to face is the management of acute respiratory failure (ARF) requiring mechanical ventilation.  Sequential supportive interventions aimed to manage severe ARF in patients with pneumonia are summarized in Fig. 1 45
  • 46. NON INVASIVE VENTILATION (NIV)  NIV, delivered through a facial mask or a helmet, represents a possible first-line intensive treatment for ARF, both in hypoxemic and hypercapnic patients.  Although the main reason for choosing NIV in patients with severe pneumonia and ARF is to avoid the complications associated with invasive mechanical ventilation, clinicians have to carefully consider those elements that may predict NIV failure, thus preventing dangerous delays in performing ETI. 46
  • 47.  a NIV Contra Indications  Severe central neurological disturbances.  unstable hemodynamic conditions.  organ dysfunction other than neurological.  inability to protect the airway or clear respiratory secretions.  severe gastrointestinal bleeding.  inability to fit the interface.  undrained pneumothorax. 47
  • 48. b Failure Of NIV Trial  Failure to maintain PaO2 : FiO2 ratio above 100.  neurological impairment.  persistence of dyspnea and tachypnea.  hemodynamic instability and intolerance of the interface. c Considered in patients with high recruitment potential.  ECMO, extracorporeal membrane oxygenation.  HFOV, high-frequency oscillatory ventilation.  iNO, inhaled nitric oxide. 48
  • 49. 49
  • 50. Stratgy in ARDS  Patients with severe pneumonia and severe ARF evolving into ARDS [acute onset, bilateral infiltrates and edema on chest X-ray, pO2/FiO2 ratio ≤ 300 mmHg and absence of clinical evidence of left atrium hypertension] commonly need invasive ventilation.  In these patients, a lung protective ventilation strategy with a tidal volume of 4–8 ml/kg of ideal body weight (IBW) and a plateau pressure (P plat) of 30cmH2O or less is required to avoid more lung injury. 50
  • 51.  Currently, the optimal positive end-expiratory pressure (PEEP) value has not been clearly established.  However, a recent meta-analysis of studies comparing different PEEP values for the management of ARDS (50% of patients were affected by severe pneumonia) observed that higher PEEP (around 15cmH2O) values were associated with improved survival rate (P = 0.03.  Additionally, conservative fluid strategies and early use of short term neuromuscular blocking agents are being associated with improved outcome. 51 Stratgy in ARDS
  • 53. PRONE POSITION  Patients whose gas exchanges are not adequately maintained are candidates for nonconventional ventilatory supportive strategies.  One of these interventions is represented by the prone position in patients with ARDS. The principal pathophysiological mechanisms that would improve oxygenation during prone positioning include redistribution of ventilation and perfusion matching, alveolar recruitment and avoidance of heart compression upon the lungs.  In a recent meta-analysis of randomized controlled trials (RCTs) upon prone positioning in ARDS patients, Sud et al observed that, in patients with a PaO2/FiO2 below 100, the use of this ventilator-supportive strategy was 53
  • 54. High-frequency oscillatory ventilation (HFOV)  High-frequency oscillatory ventilation (HFOV)is a ventilator mode which provides a small tidal volume by oscillating a bias gas flow in the airway.  The delivery of a small tidal volume at a high respiratory frequency (generally 3–15 Hz; 3–6 Hz in adults) and high mean airway pressure (mPaw) may result in improved alveolar recruitment with less risk of over distension.  Primary determinants of oxygenation are the fixed mPaw and the fraction of inspired oxygen, whereas the pressure amplitude of oscillation and the respiratory frequency are the main determinants of CO2 elimination 54
  • 55. NITRIC OXIDE  With the aim of reducing ventilation/perfusion mismatch, refractory hypoxemic ARDS patients may benefit from the use of inhaled vasodilators.  Inhaled nitric oxide (iNO) has been shown to improve oxygenation in ARDS patients and, despite a lack of evidence to support its benefits with regards to mortality rate and duration of mechanical ventilation, its use may be a rescue intervention for the management of ARDS patients. 55
  • 56. Extracorporeal membrane oxygenation (ECMO)  For those patients with severe hypoxemia unresponsive to the above mentioned unconventional ventilatory strategies, extracorporeal membrane oxygenation (ECMO) may be considered.  ECMO consists of extracting a large amount of venous blood from a central vein and returning it to venous or arterial circulation through an oxygenator and heat exchanger.  In CESAR trial Cases allocated to the ECMO group showed a significantly lower mortality rate compared with the control group (47 vs. 63%; P = 0.03).. 56
  • 57. Extracorporeal membrane oxygenation (ECMO)  confirmed a lower mortality rate (23.7 and 32 vs. 52.5%; P = 0.006) in patients with H1N1 ARDS who were transferred to an ECMO center in comparison with non-ECMO referred controls.  There is possibility of severe complications (i.e. bleeding, thromboembolism) and the intrinsic difficulty of extracorporeal circulation techniques.  Treatment with ECMO needs well trained clinicians and adequate hospital centers.  Hence, a network organization aimed at centralizing ARDS patients who may benefit from ECMO should be available in each country. 57
  • 58. Conclusion  Severe viral pneumonia is uncommon reason for ICU admission.  Given the importance of early treatment of critically ill patients, a prompt recognition of those conditions that require ICU management is crucial.  Rapid microbiological diagnosis is essential in order to avoid inappropriate empirical treatment and early clinical failures.  Patients with severe pneumonia often develop severe ARF needing invasive or noninvasive mechanical ventilation.  In addition to standard supportive ventilatory strategies, innovative measures, such as extracorporeal oxygenation, are now available and 58
  • 59. 59

Editor's Notes

  1. SARS pathology in the respiratory tract. (A) Lung of a SARS victim. The cut surface showed severe edema, consolidation, and hemorrhage. (B) LM of hematoxylin and eosin preparation of a SARS lung. The interstitial tissue was thickened with fibrin exudation and organization. Many alveoli were collapsed, filled with fluid, and exhibited hyaline membranes. Cellular infiltration was not obvious. Bar, 50 μm. (C) In situ hybridization of SARS genomic sequence of the lung from a SARS victim who died 62 d after the onset of high fever detected a large number of pulmonary epithelial cells (small arrows) that contained the virus. Multinuclear giant syncytial cells found in the alveoli contained a large amount of SARS viral sequences (large arrows). Bar, 80 μm. (D) In situ hybridization of SARS genomic sequence of the lung from a SARS victim who died 35 d after the initial symptoms showed macrophages (large arrows) in an alveolus, and many pulmonary epithelial cells (small arrows) contained the virus. Bar, 100 μm. (E) Blood vessel in SARS lung—double labeling, immunohistochemistry of CD68—brown (thin arrows). In situ hybridization of SARS viral sequence—black (thick arrows). A mixed color (arrowheads) indicates that monocyte was infected by SARS virus. The black color also may overshadow the brown color when both are present in the same blood cells and the in situ hybridization signal is very strong. Bar, 100 μm. (F) Negative control for in situ hybridization of SARS genomic sequence of the lung. No positive signal was detected. Bar, 100 μm. (G) EM in situ hybridization with colloidal gold labeling (10 nm gold; arrows) of viral sequence demonstrated that type II epithelial cells of the lung contained the virus. Bar, 0.2 μm. (H) EM image of a portion of an epithelial cell in the lung of a patient who had SARS. The region indicated by the arrow is enlarged in I. Bar, 2 μm. (I) Enlargement of the region in H. A large number of SARS virus–like particles (arrows) was observed. Bar, 0.5 μm. (J) In situ hybridization of SARS viral sequence demonstrated that most of the ciliated epithelial cells (arrows) of the trachea from a patient who had SARS were infected by the virus. Bar, 50 μm. (K) Negative control for in situ hybridization of SARS genomic sequence of the trachea from a patient who had SARS. No positive signal was detected. Bar, 50 μm.