Search Journal-type in search term and press enter
Social Media-Follow Southwest Journal of Pulmonary and Critical Care on Facebook and Twitter

Critical Care

Last 50 Critical Care Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

July 2019 Critical Care Case of The Month: An 18-Year-Old with
   Presumed Sepsis and Progressive Multisystem Organ Failure 
An Observational Study Demonstrating the Efficacy of Interleukin-1 
   Antagonist (Anakinra) in Critically-ill Patients with Hemophagocytic
Which Half Are You? Almost Half of Pediatric Oncologists and Intensivists
   Are Burnt Out……
Management of Refractory Hypoxemic Respiratory Failure Secondary to
   Diffuse Alveolar Hemorrhage with Venovenous Extracorporeal Membrane
Amniotic Fluid Embolism: A Case Study and Literature Review
April 2019 Critical Care Case of the Month: A Severe Drinking
Ultrasound for Critical Care Physicians: An Unexpected Target Lesion
January 2019 Critical Care Case of the Month: A 32-Year-Old Woman
   with Cardiac Arrest
The Explained Variance and Discriminant Accuracy of APACHE IVa 
   Severity Scoring in Specific Subgroups of ICU Patients
Ultrasound for Critical Care Physicians: Characteristic Findings in a 
   Complicated Effusion
October 2018 Critical Care Case of the Month: A Pain in the Neck
Ultrasound for Critical Care Physicians: Who Stole My Patient’s Trachea?
August 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Caught in the Act
July 2018 Critical Care Case of the Month
June 2018 Critical Care Case of the Month
Fatal Consequences of Synergistic Anticoagulation
May 2018 Critical Care Case of the Month
Airway Registry and Training Curriculum Improve Intubation Outcomes in 
   the Intensive Care Unit
April 2018 Critical Care Case of the Month
Increased Incidence of Eosinophilia in Severe H1N1 Pneumonia during 2015
   Influenza Season
March 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Ghost in the Machine
February 2018 Critical Care Case of the Month
January 2018 Critical Care Case of the Month
December 2017 Critical Care Case of the Month
November 2017 Critical Care Case of the Month
A New Interventional Bronchoscopy Technique for the Treatment of
   Bronchopleural Fistula
ACE Inhibitor Related Angioedema: A Case Report and Brief Review
Tumor Lysis Syndrome from a Solitary Nonseminomatous Germ Cell Tumor
October 2017 Critical Care Case of the Month
September 2017 Critical Care Case of the Month
August 2017 Critical Care Case of the Month
Telemedicine Using Stationary Hard-Wire Audiovisual Equipment or Robotic 
   Systems in Critical Care: A Brief Review
Carotid Cavernous Fistula: A Case Study and Review
July 2017 Critical Care Case of the Month
High-Sensitivity Troponin I and the Risk of Flow Limiting Coronary Artery 
   Disease in Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)
June 2017 Critical Care Case of the Month
Clinical Performance of an Interactive Clinical Decision Support System for 
   Assessment of Plasma Lactate in Hospitalized Patients with Organ
May 2017 Critical Care Case of the Month
Management of Life Threatening Post-Partum Hemorrhage with HBOC-201 
   in a Jehovah’s Witness
Tracheal Stoma Necrosis: A Case Report
April 2017 Critical Care Case of the Month
March 2017 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Unchain My Heart
February 2017 Critical Care Case of the Month
January 2017 Critical Care Case of the Month
December 2016 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: A Pericardial Effusion of Uncertain 
Corticosteroids and Influenza A associated Acute Respiratory Distress 


For complete critical care listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles directed to those who treat patients in the ICU, CCU and SICU including chest physicians, surgeons, pediatricians, pharmacists/pharmacologists, anesthesiologists, critical care nurses, and other healthcare professionals. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.



Analysis of Overall Level of Evidence Behind The Institute of Healthcare Improvement Ventilator-Associated Pneumonia Guidelines 

Reference as: Padrnos L, Bui T, Pattee JJ, Whitmore EJ, Iqbal M, Lee S, Singarajah CU, Robbins RA. Analysis of overall level of evidence behind the Institute of Healthcare Improvement ventilator-associated pneumonia guidelines. Southwest J Pulm Crit Care 2011;3:40-8. (Click here for PDF version of manuscript)

Leslie Padrnos1,4(

Tony Bui1,4 (

Justin J. Pattee2,4 (

Elsa J. Whitmore2,4 (

 Maaz Iqbal1,4 (

Steven Lee3,4 (

Clement U. Singarajah2,4 (

 Richard A. Robbins1,4,5 (


1University of Arizona College of Medicine

2Midwestern University-Arizona College of Osteopathic Medicine

3Kirksville College of Osteopathic Medicine

4Phoenix VA Medical Center

5Phoenix Pulmonary and Critical Care Research and Education Foundation


None of the authors report any significant conflicts of interest.




Clinical practice guidelines are developed to assist in patient care but the evidence basis for many guidelines has recently been called into question.


We conducted a literature review using PubMed and analyzed the overall quality of evidence and made strength of recommendation behind 6 Institute of Health Care (IHI) guidelines for prevention of ventilator associated pneumonia (VAP). Quality of evidence was assessed by the American Thoracic Society levels of evidence (levels I through III) with addition of level IV when evidence existed that the guideline increased VAP. We also examined our own intensive care units (ICUs) for evidence of a correlation between guideline compliance and the development of VAP.


None of the guidelines could be given more than a moderate recommendation. Only one of the guidelines (head of bed elevation) was graded at level II and could be given a moderate recommendation. One was graded at level IV (stress ulcer disease prophylaxis). The remainder were graded level III and given weak recommendations. In our ICUs compliance with the guidelines did not correlate with a reduction in VAP (p<0.05).


Most of the IHI guidelines are based on level III evidence. Data from our ICUs did not support guideline compliance as a method of reducing VAP. Until more data from well-designed controlled clinical trials become available, physicians should remain cautious when using current IHI VAP guidelines to direct patient care decisions or as an assessment of the quality of care.



The growth of guideline publications addressing nearly every aspect of patient care has been remarkable. Over the past 30 years numerous medical regulatory organizations have been founded to improve the quality of care. Many of these organizations have developed medical regulatory guidelines with 6870 listed in the National Guideline Clearinghouse (1). Many of these guidelines were rapidly adopted by healthcare organizations as a method to improve care.

Interest has grown in critically appraising not only individual clinical practice guidelines but also entire guideline sets of different medical (sub)specialties based on their rapid proliferation and in many instances an overall lack of efficacy in improving care (2,3). We assessed the quality of evidence underlying recommendations from one medical regulatory organization, the Institute for Healthcare Improvement (IHI), regarding one set of guidelines, the ventilator associated pneumonia (VAP) guidelines or VAP bundles (4). This was done by senior medical students during a month long rotation in the Phoenix Veterans Administration ICU. 



The study was approved by the Western Institutional Review Board.

Literature Search

In each instance PubMed was searched using VAP which was cross referenced with each component of the VAP bundle (as modified by the Veterans Administration) using the following MESH terms: 1. Elevation of the head of the bed; 2. Daily sedation vacation; 3. Daily readiness to wean or extubate; 4. Daily spontaneous breathing trial; 5. Peptic ulcer disease prophylaxis; and 6. Deep venous thrombosis prophylaxis. In addition, each individual component of the term was cross referenced with VAP. We also reviewed “Related citations” as listed on PubMed. Additional studies were identified using the “Related citations” in Pubmed from studies listed as supporting evidence on the IHI website and from the references of these studies.

Each study was assessed for appropriateness to the guideline. Studies were required to be prospective and controlled in design. Only studies demonstrating a reduction in VAP were considered, i.e., surrogate outcomes such as reduction in duration of mechanical ventilation were not considered. 

The American Thoracic Society grading system was used to assess the underlying quality of evidence for the IHI VAP guidelines (5) (Table 1). Only evidence supporting a reduction in VAP was considered. We added category IV when there was literature evidence of potentially increasing VAP with the use of the recommendation. A consensus was reached in each case. 

Table I. Levels of Evidence

Level of Evidence


Level I (high)


Evidence from well-conducted, randomized controlled trials.


Level II (moderate)


Evidence from well-designed, controlled trials without randomization (including cohort, patient series, and case-control

Studies). Level II studies also include any large case series in which systematic analysis of disease patterns was conducted, as well as reports of data on new therapies that were not collected in a randomized fashion.

Level III (low)


Evidence from case studies and expert opinion. In some instances, therapy recommendations come from antibiotic susceptibility data without clinical observations.

Level IV

No evidence of improvement with some evidence of an increase in a negative outcome.


Guideline Compliance and VAP Incidence

We also assessed our ICUs for additional evidence of the effectiveness of the VAP bundle. Data was collected for a period of 50 months from January, 2007 through February, 2011. This was after the Veterans Administration requirements for VAP reporting and IHI compliance was instituted. Diagnosis and compliance were assessed by a single quality assurance nurse using a standardized protocol (6). Statistical analysis was done using a Pearson correlation coefficient with a two-tailed test. Significance was defined as p<0.05.



Literature Review

Numbers of articles identified by PubMed search and used for grading the level of evidence and strength of recommendation are given in Table 2. Also included are the level of evidence and the strength of the recommendation.

Table 2.



Total Articles

No. of Articles Used (references)

Level of Evidence

Strength of Recommendation


Elevation of the head of the bed


8 (7-14)



Daily sedation vacation


4 (15-18)



Daily readiness to wean or extubate


3 (19-21)



Daily spontaneous breathing trial


1 (22)



Peptic ulcer disease prophylaxis


9 (23-29)



Deep venous thrombosis prophylaxis.


2 (30-31)



Head of Bed Elevation

A literature search identified 31 articles of which 8 were used in evaluating this guideline (7-14). However, only 2 specifically studied head of bed elevation with one supporting and another not supporting the intervention (7,8). Consequently it was graded as level II and the strength of recommendation was graded as moderate.

Daily Spontaneous Breathing Trial, Daily Readiness to Wean, and Daily Sedation Vacation

From 1-4 studies were identified for each of these interventions, however, none demonstrated a reduction in VAP. Consequently, it was judged that the evidence basis was level III and the strength of recommendation was graded as weak.

Stress Ulcer Disease Prophylaxis

We found no evidence that stress ulcer disease prophylaxis decreased VAP (23-29). There was some evidence that acid suppressive therapy increased pneumonia and VAP. Consequently, it was judged to be a level IV (possibly increasing VAP). 

Deep Venous Thrombosis Prophylaxis

We could find no evidence that deep venous thrombosis prophylaxis decreased VAP (30,31).

Guideline Compliance and VAP Incidence

Beginning in the first quarter of fiscal year 2007 there was a significant decrease in the incidence of VAP in our hospital (33). This coincided with the requirement for the monitoring of VAP, compliance with the VAP bundles and our adoption of endotracheal aspiration with nonquantitative culture of the aspirate as opposed to bronchoalveolar lavage which had been out standard practice. We changed practices because bronchoalveolar lavage with quantitative cultures appeared to offer no improvement in clinical outcomes to endotracheal aspiration (34). In our medical and surgical ICUs, 5097 audits representing 5800 ventilator-days were assessed. Nineteen cases of VAP were identified with an average of 2.1 VAP infections/1000 ventilator-days.  We assessed our surgical and medical ICUs, combined and separately, for a correlation between total bundle compliance and each component of the VAP bundle with VAP incidence (Appendices 1-3). There was no significant correlation between compliance with the bundles and VAP (p<0.05).



This manuscript questions the validity of the VAP bundles as proposed by the IHI. We found that a systematic review of the literature revealed predominately weak evidence to support these guidelines. Only one guideline (head of bed elevation) was supported by a randomized trial (7), but an additional, larger trial showed no decrease in VAP (8). Furthermore, data from our own ICUs showed no evidence of IHI VAP guideline compliance with a reduction in VAP.

Head of bed elevation is a relatively simple and easy to perform intervention which may reduce VAP. Studies examining aspiration have shown a reduction in critical care patients with the head of bed elevation but it is unclear whether this translates into a reduction in VAP (36,37). Drakulovic et al. (7) reported a randomized controlled trial in 86 mechanically ventilated patients assigned to semi-recumbent or supine body position.  The trial demonstrated that suspected cases of ventilator-associated pneumonia had an incidence of 34 percent while in the semi-recumbent position suspected cases had an incidence of 8 percent (p=0.003).  However, another study in 221 subjects demonstrated that the target head elevation of 45 degrees was not achieved for 85% of the study time, and these patients more frequently changed position than supine-positioned patients (8). The achieved difference in treatment position (28 degrees vs. 10 degrees) did not prevent the development of ventilator-associated pneumonia. The other 5 articles identified either did not identify head of bed elevation directly or as part of a bundle. Most were a before and after design and not randomized. Therefore, it is difficult to draw any meaningful conclusions.

The IHI groups daily "sedation vacations" and assessing the patient’s “readiness to extubate.” The logic is that more rapid extubation leads to a reduction in VAP. Kress et al. (15) conducted a randomized controlled trial in 128 adult patients on mechanical ventilation, randomized to either daily interruption of sedation irrespective of clinical state or interruption at the clinician’s discretion. Daily interruption resulted in a reduction in the duration of mechanical ventilation from 7.3 days to 4.9 days (p=0.004). However, in a retrospective review of the data, the authors were unable to show a significant reduction in VAP (16).

Stress ulcer prophylaxis and deep venous thrombosis prophylaxis are routine in most ICUs. However, stress ulcer prophylaxis with enteral feeding is probably as effective as acid suppressive therapy and acid suppressive therapy may increase the incidence of VAP (38). Deep venous thrombosis prophylaxis has been shown to decrease the incidence of pulmonary emboli but not improve mortality (32). Although we use these interventions in our ICU, we would suggest that these would be more appropriate for recommendations rather than guidelines.

The diagnosis of VAP is difficult, requiring clinical judgment even in the presence of objective clinical criteria (6). The difficulty in diagnosis, along with the negative consequences for failure to follow the IHI guidelines, makes before and after comparisons of the incidence of VAP unreliable. Therefore, we sought evidence for the effectiveness of VAP prevention guidelines reasoning that the better the compliance with the guidelines, the lower the incidence of VAP. We were unable to show that improved VAP guideline compliance correlated with a reduced incidence of VAP.

The IHI guidelines would not meet the criteria outlined earlier in an editorial in the Southwest Journal of Pulmonary and Critical Care for a good guideline:

Our study has several limitations. No literature review is totally comprehensive. It is possible that studies relevant to the IHI VAP guidelines, especially those written in a foreign language, were not identified. Second, the Phoenix VA data may be underpowered to show a small beneficial effect despite having over 5000 patient audits. Third, as with other healthcare facilities, the VAP guidelines at our institution were mandated and monitored. The threat of negative consequences may have compromised the objective assessment of the data, likely invalidating a before and after comparison. Fourth, correlation between guideline compliance and VAP incidence is not a substitute for a randomized trial. Unfortunately, the later is not possible given that guideline compliance is mandated.

It is unclear why the IHI guidelines have received such wide acceptance given their weak evidence basis. Agencies involved in guideline writing should show restraint in guideline formulation based on opinion or weak or conflicting evidence. Only those interventions based on strong evidence which can make a real difference to patients should be designated as guidelines.



The authors acknowledge Janice Allen, MSN, RN who collected the VAP data reported from the Phoenix VA.


  1. Accessed 3-16-2011.
  2. Lee DH, Vielemeyer O. Analysis of overall level of evidence behind infectious diseases society of America practice guidelines. Arch Intern Med 2011;171:18-22.
  3. Kett DH, Cano E, Quartin AA, Mangino JE, Zervos MJ, Peyrani P, Cely CM, For KD, Scerpella EG, Ramirez JA. Implementation of guidelines for management of possible multidrug-resistant pneumonia in intensive care: an observational, multicentre cohort study.  Lancet Infect Dis 2011 Jan 19. [Epub ahead of print].
  4. Accessed 3-16-2011.
  5. Schünemann H, Jaeschke R, Cook DJ, et al. An Official ATS Statement: Grading the Quality of Evidence and Strength of Recommendations in ATS Guidelines and Recommendations. Am J Resp Crit Care Med 2006;174:605-14.
  6. Horan TC, Andrus M, Dudeck MA. CDC/NHSN surveillance definition of health care-associated infection and criteria for specific types of infections in the acute care setting. Am J Infect Control 2008;36:309-32.
  7. Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S, Ferrer M. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: A randomised trial. Lancet 1999;354:1851-8.
  8. van Nieuwenhoven CA, Vandenbroucke-Grauls C, van Tiel FH, Joore HC, van Schijndel RJ, van der Tweel I, Ramsay G, Bonten MJ. Feasibility and effects of the semirecumbent position to prevent ventilator-associated pneumonia: a randomized study. Crit Care Med 2006;34:396-402.
  9. Baxter AD, Allan J, Bedard J, Malone-Tucker S, Slivar S, Langill M, Perreault M, Jansen O. Adherence to simple and effective measures reduces the incidence of ventilator-associated pneumonia. Can J Anaesth 2005;52:535-41.
  10. Muscedere J, Dodek P, Keenan S, Fowler R, Cook D, Heyland D; VAP Guidelines Committee and the Canadian Critical Care Trials Group. Comprehensive evidence-based clinical practice guidelines for ventilator-associated pneumonia: prevention. J Crit Care 2008;23:126-37.
  11. Wip C, Napolitano L. Bundles to prevent ventilator-associated pneumonia: how valuable are they? Curr Opin Infect Dis. 2009;22:159-66.
  12. Laux L, Dysert K, Kiely S, Weimerskirch J. Trauma VAP SWAT team: a rapid response to infection prevention. Crit Care Nurs Q 2010;33:126-31.
  13. Bird D, Zambuto A, O'Donnell C, Silva J, Korn C, Burke R, Burke P, Agarwal S. Adherence to ventilator-associated pneumonia bundle and incidence of ventilator-associated pneumonia in the surgical intensive care unit.  Arch Surg 2010;145:465-70.
  14. Torres A, Serra-Batlles J, Ros E, Piera C, Puig de la Bellacasa J, Cobos A, Lomeña F, Rodríguez-Roisin R. Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: the effect of body position. Ann Intern Med 1992;116:540-3.
  15. Kress JP, Pohlman, AS, O'Connor, MF, Hall,JB. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med 2000; 342:1471-1477.
  16. Schweickert WD, Gehlbach BK, Pohlman AS, Hall JB,  Kress JP. Daily interruption of sedative infusions and complications of critical illness in mechanically ventilated patients. Crit Care Med 2004; 32:1272–6.
  17. Mehta, S. A randomized trial of daily awakening in critically ill patients managed with a sedation protocol: a pilot trial. Critical Care Medicine 2008; 36:2092-9.
  18. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled Trial): A randomized contolled trial.  Lancet 2008;371:126-34.
  19. Marelich GP, Murin S, Battistella F, Inciardi J, Vierra T, Roby M. Protocol weaning of mechanical ventilation in medical and surgical patients by respiratory care practitioners and nurses: Effect on weaning time and incidence of ventilator-associated pneumonia. Chest 2000;118:459-67.
  20. Jain M, Miller L, Belt D, King D, Berwick DM.  Decline in ICU adverse events, nosocomial infections and cost through a quality improvement initiative focusing on teamwork and culture change.  Qual Saf Health Care 2006; 15: 235–239.
  21. Resar RK. Making noncatastrophic health care processes reliable: learning to walk before running in creating high-reliability organizations. Health Serv Res 2006; 41: 1677–89.
  22. Liang JF, Tian R, Feng L. Clinical experience of spontaneous breathing trial in weaning mechanical ventilation.  Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2009;21:617-20.
  23. Yildizdas D, Yapicioglu H, Yilmaz HL. Occurrence of ventilator-associated pneumonia in mechanically ventilated pediatric intensive care patients during stress ulcer prophylaxis with sucralfate, ranitidine, and omeprazole. J Crit Care 2002;17:240-5.
  24. Lopriore E, Markhorst DG,  Gemke RJ. Ventilator-associated pneumonia and upper airway colonization with Gram negative bacilli: the role of stress ulcer prophylaxis in : the role of stress ulcer prophylaxis in children. Intensive Care Med 2002;28:763–767.
  25. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858-873.
  26. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005;171:388-416.
  27. Laheij RJ, Sturkenboom MC, Hassing RJ, Dieleman J, Stricker BH, Jansen JB. Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs. JAMA 2004;292:1955-60.
  28. Cook DJ, Laine LA, Guyatt GH, Raffin TA. Nosocomial pneumonia and the role of gastric pH: A meta-analysis. Chest 1991;100:7-13.
  29. Chua LC, Mehta M, MD, Bhutani S, Schorr C, Milcarek B, Gerber D.  Early ventilator-associated pneumonia in patients on outpatient acid-suppressive therapy.  Chest  2010;138:730A [Abstract].
  30. Wahl WL, Talsma A, Dawson C, Dickinson S, Pennington K, Wilson D, Arbabi S, Taheri PA. Use of computerized ICU documentation to capture ICU core measures Surgery 2006; 140:684-9.
  31. Pronovost PJ, Berenholtz SM, Ngo K, McDowell M, Holzmueller C, Haraden C, Resar R, Rainey T, Nolan T, Dorman T. Developing & pilot testing quality indicators in the intensive care unit. Journal of Critical Care 2003;18:145-55.
  32. Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA. Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients. Ann Intern Med 2007;146:278-88.
  33. Benneyan JC, Lloyd RC, Plsek PE. Statistical process control as a tool for research and healthcare improvement. Qual Safe Health Care 2003 ;12:458-64.
  34. Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med 2006;355:2619-30.
  35. Robbins RA, Thomas AT Raschke RA. Guidelines, recommendations and improvement in healthcare. Southwest J Pulm Crit Care 2011;2;34-37.
  36. Torres A, Serra-Batlles J, Ros E, Piera C, Puig de la Bellacasa J, Cobos A, Lomeña F, Rodríguez-Roisin R. Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: the effect of body position. Ann Intern Med 1992;116:540-3.
  37. Orozco-Levi M, Torres A, Ferrer M, Piera C, el-Ebiary M, de la Bellacasa JP, Rodriguez-Roisin R. Semirecumbent position protects from pulmonary aspiration but not completely from gastroesophageal reflux in mechanically ventilated patients. Am J Respir Crit Care Med 1995;152:1387-90.
  38. Marik PE, Vasu T, Hirani A, Pachinburavan M. Stress ulcer prophylaxis in the new millennium: A systematic review and meta-analysis. Critical Care Medicine 2010:38;2222-8.


Click here for Appendix 1. VAP rate in all ICUs

Click here for Appendix 2. VAP in medical ICU

Click here for Appendix 3. VAP in surgical ICU



Robert Raschke

Steven Curry

Silke Remke

Ester Little

Richard Gerkin

Richard Manch

Alan Leibowitz

Banner Good Samaritan Regional Medical Center, Phoenix, AZ

Reference as:  Raschke R, Curry S, Remke S, Little E, Gerkin R, Manch R, Leibowitz A. Arterial ammonia levels in the management of fulminant liver failure. Southwest J Pulm Crit Care 2011;2:85-92. (Click here for PDF version)


Previous studies have suggested that an arterial ammonia level greater than 150 mmol/L is highly sensitive for predicting subsequent development of cerebral edema in patients with fulminant liver failure. We performed a prospective cohort study to confirm this relationship. We enrolled 22 consecutive patients who presented to our transplant hepatology service with grade 3-4 encephalopathy associated with fulminant liver failure. All patients underwent placement of an intraparenchymal ICP monitor, and every 12 hourly arterial ammonia levels. The prevalence of intracranial hypertension (IHTN) in our population was 95% (21/22 patients), with 82 discrete episodes recorded. The sensitivity of arterial ammonia levels to predict the onset of IHTN was 62% (95% CI: 40.8 to 79.3) at a cut point of 150 mmol/L. Arterial ammonia levels preceding the first intracranial hypertension event were less than 150 mmol/L in 8 of 21 patients (39%). Fifty nine of 82 episodes of IHTN (73%) occurred when arterial ammonia levels were less than 150 mmol/L. We conclude that the arterial ammonia level is not useful in making decisions regarding management related to cerebral edema in patients with fulminant liver failure. In fact, since almost all our study patients with grade III or IV encephalopathy secondary to fulminant liver failure went on to develop intracranial hypertension, our study supports the contention that all such patients might benefit from ICP monitoring regardless of arterial ammonia levels.


Cerebral edema is the most common cause of death in fulminant liver failure (FLF) (1,2), occurring in 80% of patients with advanced encephalopathy (3). Cerebral edema causes brain injury by compromising cerebral perfusion pressure and/or by causing cerebral herniation. Intracranial hypertension (IHTN) is the most reliable sign of cerebral edema, and is defined as an intracranial pressure (ICP) greater than 20 mmHg (4-6). Many authors have recommended ICP monitoring in FLF to guide management of cerebral edema (7,8) although this procedure entails significant hemorrhagic risk (9,10).

The pathogenesis of cerebral edema in FLF is likely multifactorial, but substantial evidence supports a causal role for hyperammonemia. Elevated ammonia levels alter neurotransmitter synthesis, and interfere with mitochondrial function causing oxidative stress and neuronal apoptosis (4,5,6,11-16). Increased delivery of ammonia to astrocytes provides substrate for the accumulation of intracellular glutamine (17-18). The resulting osmotic effect causes astrocyte swelling and cerebral edema (6,7,19). Clinical studies have repeatedly shown that arterial ammonia levels around 150 mmol/L have a statistically significant association with the development of IHTN and cerebral edema in humans (8,20-22).

Clemmensen and colleagues (8) measured arterial ammonia levels at the onset of grade III encephalopathy in 44 patients with FLF. Fourteen of those patients subsequently developed cerebral herniation. The patients who developed cerebral herniation had significantly higher mean arterial ammonia levels (230 vs. 118 μmol/L P<0.001), and all had ammonia levels > 146 μmol/L. At this cut point, arterial ammonia had a sensitivity of 100%, a specificity of 73% and a PPV of 64% for the subsequent development of cerebral herniation (8).

The results of this study raised the possibility that arterial ammonia levels could be used to select FLF patients likely to benefit from ICP monitoring. If arterial ammonia levels above 146 μmol/L were highly sensitive for predicting the development of IHTN, patients with arterial ammonia levels below this threshold would not likely benefit from ICP monitoring, therefore the significant hemorrhagic risk of monitor placement could be avoided (20,23).

The primary aim of our study was to confirm this premise by reassessing the sensitivity of the arterial ammonia concentration for predicting the onset of intracranial hypertension (IHTN). We chose IHTN as our dependent variable since cerebral herniation is uncommonly seen in patients managed with our neuroprotective treatment protocol (24), and because intracranial hypertension can cause brain injury by compromising cerebral perfusion in the absence of herniation. The secondary aim of our study was to determine whether following serial arterial ammonia levels are valuable in predicting the timing of recurrent IHTN episodes before and after liver transplantation.


A prospective case series was approved by the Institutional Review Board at Banner Good Samaritan Regional Medical Center, a 650 bed community teaching hospital in Phoenix Arizona. The Transplant Hepatology service identified consecutive patients admitted with FLF, as defined by standard criteria (20) between May 2004 and September 2006. All patients underwent serial neurological examinations by an intensivist, and those who developed grade 3-4 encephalopathy were evaluated for study participation. Eligible patients’ families were asked to provide informed consent.

Serial arterial ammonia levels were obtained in study patients. An arterial catheter was placed and 5 cc of arterial blood was drawn into a sodium heparin-containing tube every 12 hours. These samples were transported to the chemistry laboratory on ice within 30 minutes. Quantitative plasma ammonia concentrations were performed using an enzymatic kinetic assay (Roche Diagnostics, Mannheim Germany). This assay has a reportable range of 5.87-587 mmol/L and a coefficient of variability of 2%.

An intraparenchymal ICP monitor (Codman MicroSensor® - Codman/Johnson & Johnson Professional, Inc., Randolph, MA) was placed in the non-dominant frontal lobe under local anesthesia by a neurosurgeon. The ICP was monitored continuously thereafter. Hemostatic therapy and ICP management used in the study have been previously described (24). ICP monitors were removed post-transplantation when the patient could tolerate lowering of their head to zero degrees without precipitating IHTN. In patients who did not undergo transplantation, ICP monitors were removed upon clinical recovery or death.  

Our main independent variable was the arterial plasma ammonia level. Our main dependent variable was intracranial hypertension, defined as an ICP > 20 mmHg for > 20 mins.  We performed 3 separate sets of analyses to examine the relationship between arterial ammonia levels and IHTN: 1) we analyzed the arterial ammonia level that most closely preceded the onset of the first episode of IHTN in each patient; 2) we analyzed all arterial ammonia levels in relation to all episodes of IHTN; and 3) we analyzed all arterial ammonia levels in relation to all episodes of IHTN occurring post liver transplantation. The second and third analyses involved data values that were not independent of each other, therefore standard statistical techniques were not appropriate and time series analysis was performed. Statistical analyses were performed using SPSS 13.0 (SPSS Inc. Chicago IL.) Operating characteristics of arterial ammonia levels were calculated at a cut point of 150 mmol/L.  


Twenty two patients were entered – their clinical characteristics at study entry are listed in Table 1.

Table 1:  Patient Characteristics:

Mean age:

32.7 years (S.D. 10.3 yrs, range 15-56)


17/22 (77%) female


acetaminophen toxicity (12 patients)

hepatitis A (3)

hepatitis B (1)

anticonvulsant hypersensitivity syndrome (1)

sulfa hypersensitivity syndrome (1)

Wilson’s disease (1)

Cryptogenic (3)

Encephalopathy grade:

8 patients (36%) Grade III

14 patients (64%) Grade IV


Our 22 patients cumulatively underwent 3252 hours of ICP monitoring. Mean monitor duration was 147.8 +/- 143.3 hours. Monitors were left after liver transplantation in nine patients for 85.6 +/- 60.6 hours.

The prevalence of IHTN in our population was 95% (21/22 patients). Eighty-two discrete episodes of intracranial hypertension occurred. 62 occurred prior to, 4 during, and 16 after liver transplantation. The peak ICP during IHTN events was 33 +/- 13 mmHg (mean +/- S.D.) and the median duration was 60 minutes.

Relationship between arterial ammonia levels and the first episode of IHTN: The mean arterial ammonia level preceding the first intracranial hypertension event in each patient was 185 +/- 67 mmol/L (range: 96 – 337 mmol/L). The sensitivity of arterial ammonia levels to predict the onset of IHTN was 62% (95% CI: 40.8 to 79.3) at a cut point of 150 mmol/L. Arterial ammonia levels preceding the first intracranial hypertension event were less than 150 mmol/L in 8 of 21 patients (39%). We could not accurately calculate specificity or area under the receiver operator curve (AUROC) since only one patient did not develop IHTN.  

Relationship between arterial ammonia levels and all episodes of IHTN: The mean arterial ammonia levels just prior to each of the individual 82 episodes of IHTN were 122 +/- 80 mmol/L (range: 15 – 270 mmol/L). Fifty nine of 82 episodes of IHTN (73%) occurred when arterial ammonia levels were less than 150 mmol/L.

Relationship between arterial ammonia levels and all episodes of IHTN occurring post liver transplantation: Nine patients underwent liver transplantation. Seventy-nine ammonia levels were obtained post-liver transplantation in these patients. Four transplant recipients experienced 16 post-operative IHTN events. The mean arterial ammonia just prior to each of these events was 70 +/- 48 mmol/L (range: 15 – 161 mmol/L). The sensitivity of the arterial ammonia level preceding each IHTN event was 13% and the specificity was 100% at a cut point of 150 mmol/L. Arterial ammonia levels were statistically lower in post-transplant IHTN episodes than in pre-transplant episodes (P<0.001).


Our study showed that almost all patients with grade III or IV encephalopathy secondary to fulminant liver failure will develop intracranial hypertension – this supports the possible benefit of intracranial pressure monitoring in all such patients regardless of arterial ammonia levels. Although the high prevalence of IHTN in our study population prevented us from calculating the specificity of arterial ammonia levels, sensitivity is the key characteristic of this test in terms of our research question. Our study shows that arterial ammonia levels > 150 mmol/L are not sensitive for subsequent development of IHTN, and therefore should not be used to identify a subset of patients unlikely to benefit from ICP monitoring.

Our study did not confirm the clinical utility of arterial ammonia levels in predicting neurological injury in patients with FLF, as suggested by Clemmensen et al (8). This could be because the clinical event of interest in the two studies differed – Clemmensen focused on cerebral herniation, and we measured IHTN directly. Cerebral herniation occurred in 14 of Clemmensens’ 44 patients, but it was not observed in our patients. Our study utilized a management protocol specifically designed to prevent cerebral herniation (24). It is unknown how many of our patients with IHTN would have gone on to herniate if IHTN had not been detected and aggressively treated.           

Several other studies have examined the predictive value of arterial ammonia levels for cerebral edema and IHTN in patients with acute liver failure. Bernal and colleagues studied 165 patients with acute liver failure and grade 3-4 encephalopathy and found that arterial ammonia on admission was higher in those who later developed IHTN (121 vs 109 mmol/L p<0.05 (20). However, the sensitivity of an ammonia cut-point of 150 mmol/L was only 40%, and the positive predictive value (probability that a patient with ammonia > 150 mmol/L would develop IHTN) was only 16%.   

Bhatia and colleagues studied 80 patients with ALF, 58 of whom had grade 3-4 encephalopathy (21). They calculated an optimal cut-point for arterial ammonia for predicting mortality was 124 mmol/L by ROC analysis. Patients with ammonia levels above this cutpoint had a higher frequency of cerebral edema (47% vs. 22% P=0.02). Sensitivity and positive predictive values can be calculated from data presented in their paper, and are 71% and 48% respectively.  

Our results confirm those of Bernal and Bhatia in that all 3 studies showed that the operating characteristics of the arterial ammonia test are insufficient for triaging ALF patients in regards to invasive ICP monitoring. But our study has several important differences. IHTN or cerebral edema was detected in only 29% of Bernal’s patients and 35% of Bhatia’s. Both studies relied heavily on physical examination to diagnose these outcomes despite evidence that it lacks the sensitivity to do so (1,3,25-27). Our study utilized the gold standard (ICP monitoring) in all our patients. We found a much higher prevalence of IHTN – 95% in patients with grade 3-4 encephalopathy. This high prevalence explains the higher positive predictive value in our study, and suggests that previous studies may have suffered from significant underdetection of IHTN and cerebral edema.

Our study is also unique in that we performed repeated measures of arterial ammonia. This was important in terms of our hypothesis that patients’ risk for IHTN might change over time in response to treatments such as lactulose, continuous renal replacement therapy, and liver transplantation. Unfortunately, we found that repeated measures of arterial ammonia were no more clinically useful than the single levels used in previous studies.

Our study has several important limitations. Our limited sample size produced wide confidence intervals about our estimation of sensitivity. Our study only included patients with advanced encephalopathy - it’s possible that arterial ammonia levels might demonstrate improved prognostic significance earlier in the course of FLF. We did not attempt to analyze the effect of cumulative ammonia exposure over time.

 Our findings, and those of previous investigators, suggest that other factors besides peak ammonia levels are important in the pathogenesis of FLF-induced cerebral edema. Two other proposed causative factors are pathological alterations in cerebral blood flow (28-32) and systemic inflammatory response (30,33-34). The interplay of all three factors may be critical to the pathogenesis of cerebral edema in FLF and this might explain why simple measurement of serum ammonia is not sufficient to predict IHTN.

   Further work is needed to elucidate the pathogenesis of IHTN in FLF and identify variables that predict which patients will develop this life-threatening complication. Until then, we suggest that all patients with grade 3 or 4 encephalopathy secondary to FLF are at high risk. Our study shows that arterial ammonia levels in these patients cannot be relied upon to accurately triage patients in regards to their risk for IHTN. Thus, it is not helpful in determining which patients might benefit from ICP monitoring, nor determining when ICP monitoring can safely be discontinued.


An arterial ammonia level of 150 mmol/L is poorly sensitive for determining which patients with ALF will develop IHTN and should not be used to determine which patients are likely to benefit from ICP monitoring. The prevalence of IHTN in FLF patients with grade 3-4 encephalopathy is so high that no other predictive test is likely to be of added value. Although arterial ammonia levels are correlated with episodes of IHTN, most individual IHTN episodes occur when arterial ammonia levels are < 150 mmol/L. After successful transplantation IHTN events can continue to occur even as ammonia levels enter the normal range.


1. Lee WM. Management of acute liver failure. Semin Liver Dis 1996; 16:369-378.

2. Ellis AJ, Wendon J. Circulatory, respiratory, cerebral and renal derangement in acute liver failure: pathophysiology and management. Semin Liver Dis 1996; 16: 379-389.

3. Gill R., Sterling R, Acute Liver Failure. Journal of Clinical Gastroenterology 2001; 33 (3.:191-198.

4.Blei AT, Brain edema and portal-systemic encephalopathy. Liver Transplantation. 2000;6(Suppl 1.:S14-S20.

5. Kato M, Hughes RD, Keays RT, Williams R. Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure. Hepatology. 1992;15:1060-66.

6. Blei AT, Olafsson S, Therrien G, Butterworth RF. Ammonia-induced brain edema and intracranial hypertension in rats after portacaval anastomosis. Hepatology. 1994;19:1437-44.

7. Takahashi H, Koehler RC, Brusilow SW, Traystman RJ. Inhibition of brain glutamine accumulation prevetns cerebral edema in hyperammonemic rats. Am J Physiol. 1991;261:H825-H829.

8. Clemmessen JO, Larsen FS, Kondrup J, Hansen BA, Ott P. Cerebral herniation in patient with acute liver failure is correlated with arterial ammonia concentration. Hepatology 1999;29:648-653.

9. Lee WM. Acute liver failure. N England J Med 1993; 329: 1862.

10. Blei AT, Olafsson S, Webster S, Levy R. Complications of intracranial pressure monitoring in fulminant hepatic failure. Lancet. 1993;341: 157-8.

11. Vaquero J, Chung C, Blei AT. Brain edema in acute liver failure. A window to the pathogenesis of hepatic encephalopathy. Annals of Hepatology. 2003;2:12-22.

12. Tofteng F, Jorgensen L, Hansen BA, Ott P, Koadrap J, Larsen FS. Cerebral microdialysis in patients with fulminant hepatic failure. Hepatology. 2002;36:1333-40.

13. Kosenko E, Felipo V, Montolia C, Grisolia S, Kaminsky Y. Effectos of acute hyperammonemia in vivo on oxidative metabolism in nonsynaptic rat brain mitochondria. Metabolic Brain Diseases. 1996;12:69-82.

14. Norenberg MD. Oxidative and nitrosative stress in ammonia neurotoxicity. Hepatology. 2003;37:245-8.

15. Vaquero J, Chung C, Cahill ME, Blei AT. Pathogenesis of hepatic encephalopathy in acute liver failure. Seminars in liver disease. 2003;23:259-69.

16. Widmer R, Kaiser B, Engels M, Jung T, Grune T. Hyperammonemia causes protein oxidation and enhanced proteasomal activity in response to mitochondria-mediated oxidative stress in rat primary astrocytes. Arch Biochem Biophys. 2007;464:1-11.

17. Swain M, Butterworth RF, Blei AT. Ammonia and related amino acids in the pathogenesis of brain edema in acute ischemic liver failure in rats. Hepatology. 1992;15:449-53.

18. Cordoba J, Gottstein J, Blei AT. Glutamine, myo-inositol, and organic osmolytes after portocaval anastomosis in the rat: Implications for ammonia-induced brain edema. Hepatology. 1996;24:919-23.

19. Tofteng F, Hauerberg J, Hansen BA, Pedersen CB, Jorgensin L, Larsen FS. Persistant arterial hyperammonemia increases the concentration of glutamine and alanine in the brain and correlates with intracranial pressure in patients with fulminant hepatic failure. J Cereb Bood Flow Metab. 2006;26:21-7..

20. Bernal W, Hall C, Karvellas CJ, Auzinger G, Sizer E, Wendon J. Arterial ammonia and clinical risk factors for encephalopathy and intracranial hypertension in acute liver failure. Hepatology. 2007;46:1844-52.

21. Bhatia V, Singh R, Acharya SK. Predictive value of arterial ammonia for complications and outcome in acute liver failure. Gut. 2006;55:98-104.

22. Kundra A, Jain A, Banga A, Bajaj G, Kar P. Evaluation of plasma ammonia levels in patients with acute liver failure and chronic liver disease and its correlation with the severity of hepatic encephalopathy and clinical features of raised intracranial tension. Clin Biochem. 2005;38:696-9.

23. Bass NM. Monitoring and treatment of intracranial hypertension. Liver Transplantation 2000; 6(4. Supp1:S21-S26

23. Davern TJ. Predicting prognosis in acute liver failure: Ammonia and the risk of cerebral edema. Hepatology. 2007;46:1679-81.

24. Raschke RA, Curry SC, Rempe S, Gerkin R, Little E, Manch R, Wong M, Ramos A, Leibowitz AI. Results of a Protocol for the Management of Patients with Fulminant Liver Failure. Critical Care Medicine. 2008;36:2244-8.

25. Hoofnagle JH, Carithers RL, Shapiro C, Ascher N. Fulminant hepatic failure: Summary of a workshop. Hepatology. 1995;21:240-52.

26. Canalese J, Gimson AES, Davis C, Mellon PJ, Davis M, Williams R. Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure. Gut 1982;23:625-9.

27. Brajtbord D, Parks RI, Ramsay MA, Paulsen AW, Valek TR, Swygert TH, Klintmalm GB. Management of acute elevation of intracranial pressure during hepatic transplantation. Anesthesiology. 1989;70:139-141.

28. Wendon JA, Harrison PM, Keays R, Williams R. Cerebral blood flow and metabolism in fulminant liver failure. Hepatology. 1994;19:1407-13.

29. Sari A, Yamashita S, Ohosita S, Ogasahara H, Yamada K, Yonei A, Yokota K. Cerebrovascular reactivity to CO2 in patients with hepatic or septic encephalopathy. Resuscitation. 1990;19:125-34

30. Jalan r, Olde Damink SWM, Hayes PC, Deutz NEP, Lee A. Pathogenesis of intracranial hypertension in acute liver failure: Inflammation, ammonia and cerebral blood flow. Journal of Hepatology. 2004;41:613-20.

31. Kramer D, Aggarwal M, Darby J, Obrist W, Rosenbloom A, Murray G, Linden P, et al. Management options in fulminant hepatic failure. Transplant Proc. 1991;23:1895-8.

32. Jalan R, Olde Damink SWM, Deutz NEP, Hayes PC, Lee A. Restoration of cerebral blood flow autoregulation and reactivity to carbon dioxide in acute liver failure by moderate hypothermia. Hepatology. 2001;34:50-4.

33. Rolando N, Wade J, Davalos M, Wendon J, Philpott-Howard J, Williams R. The systemic inflammatory response syndrome in acute liver failure. Hepatology. 2000;32:734-9

34. Vaquero J, Polson J, Chung C, Helenowski I, Schiodt FV, Reisch J, Lee W, Blei AT, and the U.S. Acute Liver Failure Study Group. Infection and the progression of hepatic encephalopathy in acute liver failure. Gastroenterology.2003;125:755-64.     



Clement U. Singarajah

 Tyler Glenn

Richard A. Robbins

Phoenix VA Medical Center, Phoenix, AZ

Reference as: Singarajah CU, Glenn T, Robbins RA. Right pleural insertion of a small bore feeding tube. Southwest J Pulm Crit Care 2011;2:71-6. (Click here for PDF version)


We report a case of a 56 year old man who had a feeding tube inadvertently malpositioned into the right pleural space and had approximately 600 ml of tube feedings infused. After the malposition was recognized, the patient underwent chest tube placement, followed by video assisted thoracic surgery 5 days later. He made an uneventful recovery. The case illustrates the problems with identification and treating feeding tube insertion into the lung.  

Case Presentation

History of Present Illness

A 56 year old male was transferred from another hospital where he had been admitted 9 days earlier for severe community acquired pneumonia secondary to penicillin sensitive Streptococcus pneumoniae, respiratory failure and sepsis syndrome. He had a past medical history of morbid obesity, type 2 diabetes mellitus, hepatitis C, hypertension and had received a pneumococcal vaccination 8 years earlier. His course was complicated by prolonged mechanical ventilation, hypotension resulting in oliguric acute renal failure and atrial fibrillation with a fast ventricular response requiring cardioversion. He had sufficiently improved with antibiotics, hemodialysis and supportive therapy that he was able to be transferred to our hospital. He had a prolonged but uncomplicated course in our intensive care unit (ICU). He was initially unable to be weaned from mechanical ventilation and underwent tracheostomy but was eventually able to tolerate tracheostomy collar and intermittent use of a tracheostomy tube with a speaking valve. He was noted to be intermittently confused and agitated. After 17 days in our ICU, transfer was planned to a general medical floor.  However, prior to leaving our ICU he pulled his feeding tube and another small bore feeding tube was inserted. An abdominal film was performed and he was transferred to the medical floor. After transfer he complained through the night of chest pain and shortness of breath and required increasing inspired oxygen concentrations in order to maintain adequate oxygen saturation. .

Physical Examination

Physical examination was not markedly changed from the previous day. He had a tachycardia of 110, blood pressure of 139/97, respirations of 24, temperature of 36.3 degrees C and weight of 140.6 kilograms. He was not oriented to time or place and seemed to be in moderate discomfort. Pertinent findings including a small bore feeding tube in his left nostril, a tracheotomy in place and rhonchi over both lungs. Abdomen was protuberant but soft and there was no presacral or pretibial edema.

Laboratory Findings

Pertinent laboratory findings included arterial blood gases showing a pH of 7.44, pCO2 of 32 mm Hg, and pO2 of 65.3 on a FiO2 of 0.7. Blood glucose was elevated at 275 and his white blood cell count had increased from 6000/microL on the day of transfer to the floor to 11,400/microL with a left shift.


Initial abdominal films are show in figure 1.

Figure 1. Panel A and B are abdominal x-rays taken for feeding tube placement. Panel A shows the feeding tube below the diaphragm indicated by the arrow. Panel B, labeled at the same time and with the same acquisition number does not show the tube below the diaphragm but shows a tube apparently in the right chest. Panel C is an inverted image of Panel B.

A chest X-ray was taken on the patient’s return to the intensive care unit (Figure 2).


Figure 2. A. Chest X-ray shows feeding tube in trachea and right mainstem bronchus, looping in lower right chest and extending to upper right chest (arrows). B. Inverted image of A.

Hospital Course

Because of his high oxygen requirements and dyspnea, the patient was placed on mechanical ventilation. Bronchoscopy confirmed that the tube was in the lung. Due to concern for a pneumothorax should the tube be removed, a chest tube was placed first and directed to drain the pleural effusion. The feeding tube was removed and a follow up chest x-ray confirmed a pneumothorax that was treated with another chest tube. It was estimated that about 600 ml of feeding formula had been infused into the chest. Approximately 700 ml of milky fluid consistent with feeding was collected by the thoracostomy tube. Thoracic surgery consultation was obtained and recommended video-assisted thoracic surgery which was performed 5 days latter. A small amount of what appeared to be feeding formula was removed. He made a slow and uneventful recovery and was discharged to an extended care facility after a total duration of 43 days in our hospital.


Malposition of feeding tubes is relatively common (1,2). Given that the tubes are small, relatively flexible and blindly inserted this is not surprising. In a series of more than 2000 insertions, Sorokin and Gottlieb (1) reported a 2.4% rate of lung insertion while de Aguilar-Nascimento and Kudsk (2) found a 3.2% incidence of lung malposition. Most malpositions occurred in the intensive care unit with 95% of the patients having an abnormal mental status and more than half with an endotracheal tube. Therefore, our patient was typical of the patient prone for feeding tube malposition.

To prevent feeding tube malposition, many hospitals insert the tubes under fluoroscopic guidance (3). Perhaps more commonly, other hospitals require radiographic confirmation before beginning feeding (1,2) . The later is the policy at our hospital, but as this case illustrates, mishaps can occur even with this safeguard.

In our case, several errors were made leading to the adverse event. Although recorded at the same time, the initial abdominal films were actually taken at different times. The patient had pulled his first feeding tube and a second tube had been inserted by the ICU nurse into the lung. The medicine house officer who read the films was not informed that two films were taken and saw the tube below the diaphragm on the first film. The house officer missed the tube in the chest on the second film. However, on this and three subsequent films, all read by separate radiologists, the tube malposition was also not identified. It can be difficult with multiple densities, from chest cardiac leads, suction tubing, intravenous tubing, etc. to identify potentially misplaced feeding tubes.

Generally, feeding tube malposition is reasonably well tolerated although aspiration and pneumothorax may result (1-3). Removal of the tube usually results in little apparent clinical harm. Our case is unusual in that an enteral feeding formula was introduced into the pleural space. Although there are previous reports of pneumothorax complication feeding tube insertion, these are relatively uncommon and we were uncertain how to proceed (4).  Eventually we decided on video assisted thoracic surgery with removal of any residual fluid. In this case the patient made an uneventful but prolonged recovery.  

When a feeding tube is in the lung, it may or may not have punctured the pleura. If it has, as was clear in this case by the course it took, (multiple loops), the chance of a pneumothorax on removal may be high. It is a matter of opinion as to whether or not in this situation; a prophylactic chest tube should be placed prior to removal of the feeding tube. In this case, this was performed as he was on mechanical ventilation. In situations where the feeding tube is clearly in a mainstem bronchus, removal is probably safe without due concern for a pneumothorax.

The errors in the formal radiology readings may be reduced by inverting the images within the radiology viewing program, and making sure that the full course of the feeding tube from oropharynx to tip is noted. In some obese patients, such as this one, an abdominal x-ray and chest x-ray may be required to do this.


1. Sorokin R, Gottlieb JE. Enhancing patient safety during feeding-tube insertion: a review of more than 2,000 insertions. JPEN J Parenter Enteral Nutr 2006;30:440-5.

2. de Aguilar-Nascimento JE, Kudsk KA. Clinical costs of feeding tube placement. JPEN J Parenter Enteral Nutr 2007;31:269-73.

3. Huerta G, Puri VK. Nasoenteric feeding tubes in critically ill patients (fluoroscopy versus blind). Nutrition 2000;16:264-7.

4. Wendell GD, Lenchner GS, Promisloff RA. Pneumothorax complicating small-bore feeding tube placement . Arch Intern Med 1991;151:599-602.

Page 1 ... 26 27 28 29 30