PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of abfdLink to Publisher's site
 
Ann Burns Fire Disasters. 2012 September 30; 25(3): 135–139.
Published online 2012 September 30.
PMCID: PMC3575144

Review article: ventilator-associated pneumonia in major burns

Summary

Major burns victims are particularly susceptible to pneumonia, especially ventilator-associated pneumonia (VAP). VAP remains a prominent cause of morbidity and mortality, despite improvements in intensive care and burns surgery in recent times. Length of ventilation, type and size of burn (especially inhalational burns) are related to the incidence of VAP. Other risk factors (number of re-intubations, theatre visits) are also important. Effective preventative strategies should be adhered to, and protocols should be implemented to aid in the diagnosis and treatment of VAP. Clinical criteria, radiology, and broncho-alveolar lavage should be used to determine the causative organism, and there should be a low threshold for the early initiation of empiric therapy, based on the prevailing resistance patterns in the unit. Major burns should be managed in centres where there is ready access to multidisciplinary resources and expertise.

Keywords: ventilator associated pneumonia, nosocomial infections, major burn injuries, mechanical ventilation, mortality and morbidity in burns

Résumé

Les patients grands brûlés sont très vulnérables à la pneumonie et en particulier à la pneumonie sous ventilation assistée (PVA). La PVA reste une cause importante de morbidité et de mortalité, en dépit de l’amélioration des soins intensifs et de la chirurgie dans ces derniers temps. La longue durée de la ventilation, le type et l’extension des brûlures (les brûlures par inhalation en particulier) sont liés à la fréquence de la PVA. Autres facteurs de risque (nombre d’interventions, de ré-intubations et chirurgicales) sont également importants. Des stratégies efficaces de prévention doivent être respectées, et les protocoles doivent être mis en oeuvre pour faciliter le diagnostic et le traitement des la PVA. Les critères cliniques et radiologiques et la lavage bronchoalvéolaire doivent être utilisés pour déterminer le germe en question, et il faut avoir un seuil bas pour l’initiation précoce de la thérapie empirique, basée sur les profils de résistance en vigueur dans l’unité de brûlures. Les brûlures graves devraient être traitées dans des centres ayant accès à des ressources et à des connaissances multidisciplinaires.

Background

Severe burns are one of the most devastating forms of trauma. In South Africa, burn injuries are the third commonest external cause of fatal injuries up to the age of 15 years and the main cause under the age of 4 years. In the Cape Town region, at least six out of 10 000 children are seriously burnt every year, and as many as 15 out of 10 000 toddlers and infants.1,2

A number of advances have been made in recent times with regard to fluid resuscitation protocols, dressings, infection control strategies and antimicrobials, surgical techniques, intensive care, and nutrition. There is now widespread recognition that specialist burns units or centres deliver the best care for these patients. As a result of these measures, mortality and morbidity rates have declined significantly over the last few decades.3,4

Significant thermal injuries induce a state of immunosuppression; three-quarters of all severe burn related deaths are consequence of infection, most notably burn wound infections, sepsis, pneumonia and urinary tract infections, many of which are nosocomial.4-8 There are a number of mechanisms for the development of pneumonia in the severely burnt. Pulmonary complications are common with inhalational injury, but burnt patients have more pulmonary complications even without direct lung injury. Atelectasis and hypostatic pneumonia are common due to altered ventilation and reduced lung expansion that may occur in patients with chest or abdominal burns. These patients may also have a high risk of aspirating, and respiratory physiotherapy with regular airway suctioning of upper airway secretions and expectoration of sputum may be critical to maintaining pulmonary function.5,9

Patients who require prolonged ventilation are also at risk of developing ventilator-associated pneumonia (VAP). Prior to 2007, VAP could only be diagnosed after 48 h of mechanical ventilation. No minimum time of ventilation is now required to make the diagnosis.10 Despite this change in definition, there may still be some utility in considering patients in early or late groups, because causative organisms and their resistance patterns vary in relation to this.

In the paediatric intensive care setting, VAP is responsible for significant morbidity and mortality, and ranks as the second commonest hospital acquired infection. In fact, a large European trial in a variety of paediatric settings showed that VAP accounted for over half of hospital acquired infections in the PICU.11 The prevalence of nosocomial pneumonia in the ICU ranges from 10 to 65% and mortality rates exceed 25%. Those who develop VAP are twice as likely to die compared to those without VAP, and spend longer in intensive care. The nosocomial bacteria that cause VAP tend to be more resistant.11-15

There is a paucity of literature on VAP in children, particularly within the context of major paediatric burns. International guidelines for the prevention and management of VAP have largely been extrapolated from adult experience with VAP. Burns patients, and particularly paediatric patients with burns, are a special group, with peculiar demands and predispositions, and should be managed by burns surgeons, anaesthetists, specialist nursing staff, paediatric intensivists, physiotherapists and occupational therapists with special interest and experience.

Prevention

Much has been written in the critical care literature about the prominent role that VAP plays in respect of mortality and morbidity in the ICU. Burns victims have the highest relative risk of any category of ventilated patients. Several studies have demonstrated that the incidence of VAP in burns patients is more than 22 per 1000 ventilator days, more than double that seen in either surgical or medical cohorts. The rate in our paediatric unit is as high as 30 per 1000 ventilator days.5-8 VAP usually results from pathogens colonizing the lower respiratory tract and parenchyma by sustained micro aspiration. A number of factors in the burns patient facilitate the development of pneumonia (Table I).

Table I
Factors predisposing the burns patient to pneumonia in an ICU

Strategies to prevent VAP in burns patients have largely been adapted from studies focusing on other patient groups. Many of these have been incorporated into socalled ‘care bundles’ for ventilated patients. Table II lists some of the preventative strategies.

Table II
Strategies identified to prevent VAP

Daily interruptions and weaning protocols are now fundamental tenets of good adult ICU care. The role in children is less well established, but the principle of reducing ventilation duration to shortest possible is obviously paramount. 9,11,1616 Adaptations to the endotracheal tube have been examined in an attempt to reduce the incidence of VAP. The NASCENT trial, for instance, showed a 35.9% risk reduction when a silver impregnated endotracheal tube was used.17 Techniques to continuously aspirate subglottic secretions have been shown to be effective and should be implemented.17,18 At present intermittent open suctioning techniques are the norm in ICUs in developing countries.

Stress ulcer prophylaxis and early enteral nutrition are now well-established in both burns care and in the ICU scenario. However, they may also be responsible for raising the pH and gastric bacterial colonization, which predisposes to VAP. Gastritis is rare in the well-resuscitated child burn victim and many units may choose not to make use of stress ulcer prophylaxis. Sucrulphate may be a sensible alternative to other agents that raise gastric pH. In addition, post-pyloric feeding rather than gastric feeding, may reduce the incidence of VAP.9,19 Placing the patient in the semi-recumbent position is effective and easily applied in the adult patient, but may prove difficult in the paediatric population, where there may be marked size differences between patients.9

Meta-analyses have shown a significant reduction in the incidence of pneumonia with the use of selective decontamination of the GIT.20,21 Prophylactic antibiotics may also be justified in certain circumstances, but applied with an awareness of the prevailing resistance patterns.22 Chlorhexidine mouth-wash is a cost-effective and easily applied strategy for reducing VAP.23,24 Contact precautions and hand hygiene are now well-established tenets of critical care, and adherence to these and other elements in the ventilator care bundles need to be regularly reviewed.25

Burns patients frequently require blood transfusions during their course of treatment. A restrictive policy should be adhered to, as each unit of blood received is associated with a 13% increased risk of infection, presumably by exacerbating the state of immunosuppression.26,27 Intense insulin therapy and tight glucose control, despite initial optimism, need to be re-evaluated in a major trial, and particularly in major paediatric burns. The consequences of hypoglycaemia are potentially catastrophic, and more significant than the potentiation of infection during periods of high normoglycaemia, or even hyperglycaemia.28,29

Diagnosis

VAP remains one of the greatest challenges to the ICU clinician. This difficulty is illustrated by the fact that VAP represents the dominant indication for empiric antibiotic agents in the ICU. Scoring systems like the CPIS and the CDC criteria have been compiled to improve the accuracy by combining clinical, microbiological and radiological criteria. Scores of more than six are regarded as diagnostic30-33 (Table III). Scoring systems, however, have not been validated in the paediatric burns victims, and a number of problems have been identified. For instance, the burn patient frequently exhibits pulmonary dysfunction due to inhalational injury, overwhelming systemic inflammation, pulmonary oedema and ARDS. Fever, sputum, leukocytosis or leukopaenia, deranged oxygenation, and abnormal chest radiographs may all be present in a burns patient without pneumonia.6,9,30-34

Table III
The Clinical Pulmonary Infection Score

The traditional 48 h of ventilation required to make the diagnosis has now been removed from the definition of VAP.10 The ventilator is recognized as a major risk factor for the development of pneumonia in the ICU. The spectrum of bacteria responsible (community acquired vs nosocomial) and the efficacy of preventative and therapeutic measures, make time an important component. VAP is a prominent cause of morbidity and mortality in burns patients, but patients who developed pneumonia prior to 48 h of ventilation were also at high risk, particularly if they had large body surface burn wounds. Of the organisms responsible for VAP, Acinetobacter baumannii infections, in particular, have proved to be a virulent cause of ventilator associated pneumonia in our setting.6,9,11 Bronchoalveolar lavage, protected specimen brush or non-bronchoscopic lavage are the best means of obtaining reliable quantitative cultures. By combining one of these techniques with clinical features of pulmonary infection, the sensitivity and specificity may be optimized.6,9,11,34-38

Treatment

Several studies have demonstrated that a delay in initiating appropriate antibiotics may result in increased morbidity and mortality. Consequently units should be aware of their local bacterial milieu and resistance patterns, so that appropriate empiric antibiotic choices can be made.6,9,11,37 Pneumonias that occur early are more likely community acquired, most notably Streptococcus pneumonia and Haemophilus influenzae. Later onset VAPs are more likely a consequence of MRSA and gram negative organisms like Pseudomonas aeruginosa, E. coli, Klebsiella pneumonia, and Acinetobacter baumannii.

P. aeruginosa remains the most invasive pathogen in our patients, but Acinetobacter baumannii is now also a major problem, not least because of growing resistance. MRSA has not yet proved as significant a problem as experienced in other parts of the world. Because many of our patients are immunocompromised and malnourished prior to burn injury, several of our patients are particularly susceptible to fungal infections.

Many ICUs are still dependent on alternatives to invasive quantitative microbiological techniques like sputum cultures and tracheal aspirates. The results of these tests are relatively unreliable and treatment should be initiated and de-escalated with this is mind. If possible, empiric therapy should be limited to 48 h: this period of use should not increase resistance.38,39 Antibiotics may safely be stopped once clinical features of infection have resolved. There is probably no difference in outcomes if an eight or fifteen day course of treatment is implemented, unless the organism responsible is P. aeruginosa or Acinetobacter, where a longer course is necessary to reduce recurrence.39 Table IV lists some of the principles of antibiotic use for VAP.

Table IV
Principles of antibiotic use for VAP treatment

References

1. National Injury Mortality Surveillance System. MRC/UNISA; 2005.
2. Rode H. Burn research and clinical practice. 23rd DJ du Plessis Lecture, Surgical Research Society Meeting, Cape Town. SAJS. 2007;45:4. [PubMed]
3. Karpelowsky JS, Wallis L, Madaree A, et al. South African Burn Stabilisation protocol. S Afr Med J. 2007;97:574–7. [PubMed]
4. Rogers AD, Karpelowsky J, Argent D, et al. Fluid resuscitation in major burns. The problem of fluid creep. S Afr Med J. 2009;99:512–3.
5. Mosier MJ, Tam NP. American Burn Association practice guidelines for prevention, diagnosis and treatment of ventilator-associated pneumonia (VAP) in burn patients. J Burn Care Res. 2009;30:910–28. [PubMed]
6. Santucci S, Gobra S, Santos C, et al. Infections in the burns intensive care unit: experience of seven years. J Hosp Infect. 2003;53:6–13. [PubMed]
7. Wibbenmeyer L, Danks R, Faucher L, et al. Prospective analysis of nosocomial infection rates, antibiotic use, and patterns of resistance in the burns population. J Burn Care Res. 2006;27:152–60. [PubMed]
8. Lazarus H, Fox J, Lloyd J, et al. A six year descriptive study of hospital-associated infection in trauma patients: demographics, injury features, and infection patterns. Surg Infect (Larchmt) 2007;8:463–73. [PubMed]
9. Morrow BM, Argent AC, Jeena PM, et al. Guideline for the diagnosis, prevention and treatment of paediatric ventilator-associated pneumonia. SAMJ. 2009;99(4):255–67. [PubMed]
10. Centers for Disease Control and Prevention. The National Safety Network (NHSN) Manual: Patient Safety Component Protocol 2007: [accessed April 10 2011]. (NIDA research report series). http://www.cdc.gov/ncidod/dhqp/pdf/nhsn/NHSN_Manual_Patient_safety_protocol_Current.pdf .
11. Foglia E, Meier MD, Elward A. Ventilator-associated pneumonia in neonatal and pediatric intensive care unit patients. Clin Micro Review. 2007;20:409–25. [PMC free article] [PubMed]
12. Almuneeef M, Memish ZA, Balkhy HH, et al. Ventilator associated pneumonia in a paediatric intensive care unit in Saudi Arabia. A 30 month prospective surveillance. Infect Control Epidemiol. 2004;25:753–8. [PubMed]
13. Wright ML, Romano MJ. Ventilator-associated pneumonia in children. Semin Paediatr Infec Dis. 2006;17:58–64. [PubMed]
14. Safdar N, Defulian C, Collard HR, et al. Clinical and economic consequences of ventilator-associated pneumonia: a systematic review. Crit Care Med. 2005;33:2184–93. [PubMed]
15. Rello J, Ollendorf , Oster G, et al. VAP Outcomes Scientific Advisory Group. Epidemiology and outcomes of ventilator associated pneumonia in a large US database. Chest. 2002;122:2115. [PubMed]
16. Celis R, Torres A, Gatell JM, et al. Nosocomial pneumonia. A multivariate analysis of risk and prognosis. Chest. 1988;93:318–24. [PubMed]
17. Kollef MH, Afessa B, Anzueto A, et al. Silver coated endotracheal tubes and incidence of ventilator associated pneumonia, The NASCENT randomised trial. JAMA. 2008;300:805–13. [PubMed]
18. Mahul P, Auboyer C, Jospe R, et al. Prevention of nosocomial pneumonia in intubated patients: respective role of mechanical subglottic secretions drainage and stress ulcer prophylaxis. Intensive Care Med. 1992;18:20–5. [PubMed]
19. Cook D, Walter S, Cook R, et al. Incidence and risk factors for ventilator associated pneumonia in critically ill patients. Ann Intern Med. 1998;129:433–40. [PubMed]
20. Silvestri L, van Sacne HK, Thomann C, et al. Selective decontamination of the digestive tract reduces pneumonia and mortality without resistance emerging. Am J Infect Control. 2007;35:354–7. [PubMed]
21. Liberati A, D’Amico R, Pifferi S, et al., editors. Antibiotic prophylaxis to reduce respiratory tract infections and mortality in adults receiving intensive care. Cochrane Database Syst Rev 2004: CD000022. [PubMed]
22. Gastinne H, Wolff H, Delatour Faurisson F, et al. A controlled trial in intensive care units of selective decontamination of the digestive tract with nonabsorbable antibiotics. The French Study Group on Selective Decontamination of the Digestive Tract. N Eng J Med. 1992;326:594–9. [PubMed]
23. Houston S, Hougland P, Anderson JJ, et al. Effectiveness of 0.12% chlorhexidine gluconate oral rinse in reducing prevalence of nosocomial pneumonia in patients undergoing heart surgery. AM J Crit Care. 2002;11:567–70. [PubMed]
24. Koeman M, van der Ven AJ, Hak E, et al. Oral decontamination with chlorhexidine reduces the incidence of ventilator associated pneumonia. Am J Respir Crit Care Med. 2006;173:1348–55. [PubMed]
25. Landrum ML, Murray CK. Ventilator associated pneumonia in a military deployed setting: the impact of an aggressive infection control program. J Trauma. 2008;64:S123–7. [PubMed]
26. Palmieri TL, Caruso DM, Foster KN, et al. American Burn Association Multicenter Trials Group. Effect of blood transfusion on outcome after major burn injury: a multicenter study. Crit Care Med. 2006;34:1602–7. [PubMed]
27. Leal-Noval SR, Rincon-Ferrair MD, Garcia-Curiel A, et al. Transfusion of blood products and postoperative infection in patients undergoing cardiac surgery. Chest. 2001;2001:1461–8. [PubMed]
28. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med. 2001;345:1359–67. [PubMed]
29. Hemmila MR, Taddonio MA, Arbabi S, et al. Intensive insulin therapy is associated with reduced infectious complications in burns patients. Surgery. 2008;144:629–35. [PMC free article] [PubMed]
30. Chastre J, Fagon JY. Diagnosis of ventilator associated pneumonia. N Eng J Med. 2007;356:1469–70. [PubMed]
31. Pham T, Neff M, Simmons J, et al. The clinical pulmonary infection score poorly predicts pneumonia in patients with burns. J Burn Care Res. 2007;28:76–9. [PubMed]
32. Schurink CA, Van Niuwenhoven CA, Jacobs JA, et al. Clinical Pulmonary Infection Score for ventilator associated pneumonia. Accuracy and inter-observer variability. Intensive Care Med. 2004;30:217–24. [PubMed]
33. Gauvin F, Dassa C, Chaibou M, et al. Ventilator associated pneumonia in intubated children: comparison of different diagnostic methods. Paediatr Crit Care Med. 2003;4:437–43. [PubMed]
34. Fagon JY, Chastre J, Wolff M, et al. Invasive and noninvasive strategies for the management of suspected ventilator associated pneumonia: a randomised trial. Ann Intern Med. 2000;132:621–20. [PubMed]
35. Chastre J, Fagon JY. Invasive diagnostic testing should be routinely used to manage ventilated patients with suspected pneumonia. AM J Respir Crit Care Med. 1994;150:570–4. [PubMed]
36. Wahl W, Ahrns K, Brandt M, et al. Bronchoalveolar lavage in diagnosis of ventilator associated pneumonia in patients with burns. J Burn Care Rehabil. 2005;26:57–61. [PubMed]
37. Kollef MH, Ward S. The influence of Mini BAL cultures on patient outcomes: implications for the antibiotic management of ventilator associated pneumonia. Chest. 1998;113:412–20. [PubMed]
38. Rello J, Palva JA, Baraibar J, et al. International conference for the development of consensus on the diagnosis and treatment of ventilator associated pneumonia. Chest. 2001;120:955–7. [PubMed]
39. Chastre J, Wolff M, Fagon JY, et al. Pneum A Trial Group Comparison of 8 vs 15 days of antibiotic therapy for ventilator associated pneumonia in adults: a randomised trial. JAMA. 2003;290:2588–98. [PubMed]

Articles from Annals of Burns and Fire Disasters are provided here courtesy of Euro-Mediterranean Council for Burns and Fire Disasters (MBC)