Advertisement

Intensive Care Medicine

, Volume 41, Issue 5, pp 926–929 | Cite as

Rescue therapy for refractory ARDS should be offered early: no

  • Daniel Brodie
  • Claude Guérin
Editorial

Clinical vignette A previously healthy 51-year-old woman was admitted to the ICU with severe community acquired pneumonia. She required intubation and mechanical ventilation 6 h after admission. Her respiratory status declined continuously over the next few hours and her PaO2/FIO2 ratio was 65 with a PEEP of 8 cmH2O at 12 h after admission (plateau pressure was 28 cmH2O). She was hemodynamically stable and had normal renal function.

Despite the remarkable hypoxemia in this case of severe ARDS, there is no rush to ECMO for several reasons; each related to the fact that aspects of the patient’s current ventilator and non-ventilator management should be optimized prior to consideration of ECMO.

First of all, a low-volume, low-pressure ventilation strategy should be undertaken according to the protocols of the ExPress [1] or ARDSNet ARMA [2] trials. We are not given information about the selected tidal volume (VT). However, it should be based on predicted body weight (PBW). As the patient in this case is a woman, it should be mentioned that clinicians tend to use actual body weight instead of PBW for assigning VT and therefore over-ventilate women and people who are of shorter stature [3]. PEEP should be set initially according to the protocol used (standard or high PEEP strategy) [4, 5] and is almost certainly too low in this case. Titration of PEEP may benefit the patient. Bear in mind that after raising PEEP, plateau pressure (Pplat) may increase well above 30 cmH2O. However, should the lung be recruited by the increase in PEEP, Pplat would then decrease. Furthermore, the assessment of oxygenation response to PEEP also requires only a few minutes [6]. Is there room for Pplat greater than 30 cmH2O due to impairment of elastic properties of the chest wall? Grasso et al. [7] were able to avoid ECMO in seven severe influenza A(H1N1)-associated ARDS patients with high chest wall elastance that allowed the PEEP to be raised in order to reach a transpulmonary pressure of 25 cmH2O. Such measurements require the insertion of an esophageal balloon. A more common way of setting PEEP is to use a PEEP/FIO2 table. Suppose FIO2 is 0.80 in this case, PaO2 would be 52 mmHg and hence PEEP should range from 14 to 22 cmH2O depending on the PEEP/FIO2 table [4, 5]. Even though the current concept for setting PEEP is the prevention of the cyclical opening and closing of alveoli during tidal breaths, in a patient like this, the oxygenation response to PEEP is relevant. The post hoc analysis of the trials on PEEP observed that the oxygenation response to PEEP was associated with better outcomes in ARDS patients [8]. Chiumello et al. [9] found that the PEEP/FIO2 table was the only way to set lower PEEP in patients with low potential of recruitment and higher PEEP in patients with high potential of recruitment. In line with the above considerations, a recruitment maneuver should be considered in this patient [10] followed by a higher level of PEEP than prior to the procedure.

The second aspect of her care to optimize is sedation and neuromuscular blockade. Deep sedation should be provided to reduce oxygen consumption and improve ventilator synchrony and, once a level of deep sedation is reached, a neuromuscular blocking agent should be promptly started, ideally using cisatracurium for 48 h. With this medication, the oxygenation improves, the rate of pneumothorax is reduced, and the survival is improved [11].

The third item to consider is the fluid balance. With her normal renal function and stable hemodynamics, this patient is a good candidate for receiving early diuretics. Although a large randomized controlled trial failed to show a beneficial effect on mortality [12], a conservative fluid strategy was associated with improvement in the oxygenation index and improvements in ventilator- and ICU-free days. A separate randomized placebo-controlled trial showed that furosemide plus albumin significantly improved oxygenation in hypoproteinemic (plasma protein less than 6 g/dl) ARDS patients [13]. Should this patient be hypoproteinemic, this strategy is quite simple to improve oxygenation, and could be considered.

The fourth opportunity for optimization is in the use of prone positioning. The completion of previous steps should only require a couple of hours and, if the patient is still sufficiently hypoxemic, prone position should be instituted given that there are no known contraindications. Caution should be applied in centers that do not have extensive experience with prone positioning. In patients with ARDS and severity criteria (PaO2/FIO2 less than 150 mmHg with PEEP of at least 5 cmH2O and FIO2 of at least 0.6) a significant improvement in survival was demonstrated as compared to the supine position in the PROSEVA trial [14]. This benefit was also observed in the lowest quartile of PaO2/FIO2 at the time of randomization, which ranged from 45 to 87 mmHg. The current case in question is in this range. Proning should be performed in a complete prone position and for a prolonged session (16 consecutive hours or more as scheduled in PROSEVA).

The fifth item to consider would be inhaled pulmonary vasodilators: inhaled epoprostenol or inhaled nitric oxide. These medications can be used in severe hypoxemia to improve oxygenation by dilating pulmonary vascular beds in those areas of the lungs where ventilation is preserved, thereby decreasing the proportion of blood shunted through areas of poor ventilation. It can be started while the patient is still in the supine position but several studies found an additive effect of prone position and nitric oxide on oxygenation. That said, these medications do not change overall outcomes and, given that the degree of hypoxemia in this case is not immediately life-threatening, delaying the decision for ECMO in order to institute these medications may not be necessary.

Where in the course of treating this patient should we consider ECMO (Fig. 1)? In a patient without life-threatening hypoxemia, we would allow at least 6 h to decide whether or not ECMO should be undertaken. The following criteria for initiating ECMO in ARDS patients have been recently proposed [15]: PaO2/FIO2 ratio less than 80 despite high PEEP (15–20 cmH2O) for at least 6 h in patients with potentially reversible respiratory failure, or hypercapnia with acidemia (pH less than 7.15) or Pplat greater than 35–45 cmH2O, depending on the patient’s body habitus. A similar strategy is being tested in a multicenter randomized controlled trial and final results are expected in the near future.
Fig. 1

Management algorithm for patients with ARDS

Notes

Conflicts of interest

Dr. Brodie previously received research support and provided research consulting for Maquet Cardiovascular. He is on the medical advisory board of ALung Technologies and Kadence (Johnson & Johnson). All compensation for his consulting goes to Columbia University.

References

  1. 1.
    Mercat A, Richard JC, Vielle B, Jaber S, Osman D, Diehl JL, Lefrant JY, Prat G, Richecoeur J, Nieszkowska A, Gervais C, Baudot J, Bouadma L, Brochard L (2008) Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 299:646–655CrossRefPubMedGoogle Scholar
  2. 2.
    ARDSnet (2000) Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 342:1301–1308CrossRefGoogle Scholar
  3. 3.
    Fish E, Novack V, Banner-Goodspeed VM, Sarge T, Loring S, Talmor D (2014) The Esophageal Pressure-Guided Ventilation 2 (EPVent2) trial protocol: a multicentre, randomised clinical trial of mechanical ventilation guided by transpulmonary pressure. BMJ open 4:e006356CrossRefPubMedCentralPubMedGoogle Scholar
  4. 4.
    Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M, Schoenfeld D, Thompson BT (2004) Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 351:327–336CrossRefPubMedGoogle Scholar
  5. 5.
    Meade MO, Cook DJ, Guyatt GH, Slutsky AS, Arabi YM, Cooper DJ, Davies AR, Hand LE, Zhou Q, Thabane L, Austin P, Lapinsky S, Baxter A, Russell J, Skrobik Y, Ronco JJ, Stewart TE (2008) Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 299:637–645CrossRefPubMedGoogle Scholar
  6. 6.
    Chiumello D, Coppola S, Froio S, Mietto C, Brazzi L, Carlesso E, Gattinoni L (2013) Time to reach a new steady state after changes of positive end expiratory pressure. Intensive Care Med 39:1377–1385CrossRefPubMedGoogle Scholar
  7. 7.
    Grasso S, Terragni P, Birocco A, Urbino R, Del Sorbo L, Filippini C, Mascia L, Pesenti A, Zangrillo A, Gattinoni L, Ranieri VM (2012) ECMO criteria for influenza A (H1N1)-associated ARDS: role of transpulmonary pressure. Intensive Care Med 38:395–403CrossRefPubMedGoogle Scholar
  8. 8.
    Goligher EC, Kavanagh BP, Rubenfeld GD, Adhikari NK, Pinto R, Fan E, Brochard LJ, Granton JT, Mercat A, Marie Richard JC, Chretien JM, Jones GL, Cook DJ, Stewart TE, Slutsky AS, Meade MO, Ferguson ND (2014) Oxygenation response to positive end-expiratory pressure predicts mortality in acute respiratory distress syndrome. A secondary analysis of the LOVS and ExPress trials. Am J Respir Crit Care Med 190:70–76CrossRefPubMedGoogle Scholar
  9. 9.
    Chiumello D, Cressoni M, Carlesso E, Caspani ML, Marino A, Gallazzi E, Caironi P, Lazzerini M, Moerer O, Quintel M, Gattinoni L (2014) Bedside selection of positive end-expiratory pressure in mild, moderate, and severe acute respiratory distress syndrome. Crit Care Med 42:252–264CrossRefPubMedGoogle Scholar
  10. 10.
    Roeseler J, Sottiaux T, Lemiale V, Lesny M (2013) Prise en charge de la mobilisation précoce en réanimation, chez l’adulte et l’enfant (électrostimulation incluse). Réanimation 22:207–218Google Scholar
  11. 11.
    Papazian L, Forel J, Gacouin A, Penot-Ragon C, Perrin G, Loundou A, Jaber S, Arnal J, Perez D, Seghboyan J et al (2010) Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med 363:1107–1116CrossRefPubMedGoogle Scholar
  12. 12.
    Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, de Boisblanc B, Connors AF Jr, Hite RD, Harabin AL (2006) Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 354:2564–2575CrossRefPubMedGoogle Scholar
  13. 13.
    Martin GS, Moss M, Wheeler AP, Mealer M, Morris JA, Bernard GR (2005) A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. Crit Care Med 33:1681–1687CrossRefPubMedGoogle Scholar
  14. 14.
    Guerin C, Reignier J, Richard JC, Beuret P, Gacouin A, Boulain T, Mercier E, Badet M, Mercat A, Baudin O, Clavel M, Chatellier D, Jaber S, Rosselli S, Mancebo J, Sirodot M, Hilbert G, Bengler C, Richecoeur J, Gainnier M, Bayle F, Bourdin G, Leray V, Girard R, Baboi L, Ayzac L, Group PS (2013) Prone positioning in severe acute respiratory distress syndrome. N Engl J Med 368:2159–2168CrossRefPubMedGoogle Scholar
  15. 15.
    Brodie D, Bacchetta M (2011) Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med 365:1905–1914CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg and ESICM 2015

Authors and Affiliations

  1. 1.Division of Pulmonary, Allergy and Critical Care Medicine, New York-Presbyterian HospitalColumbia University College of Physicians and SurgeonsNew YorkUSA
  2. 2.Service de Réanimation MédicaleHôpital de la Croix-RousseLyonFrance
  3. 3.Hospices Civils de Lyon and Université de Lyon and INSERM UMR 955 Eq13LyonFrance

Personalised recommendations