Anestezjologia. Intensywna Terapia 1/2016-Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Still a spectrum of greys and whites

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Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Still a spectrum of greys and whites

Szymon Skoczyński1, Antonio M. Esquinas2

1Katedra i Klinika Pneumonologii Śląskiego Uniwersytetu Medycznego w Katowicach

2Intensive Care Unit, Hospital General Universitario Morales Meseguer, Murcia, Spain

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Skoczyński S, Esquinas AM: Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Still a spectrum of greys and whites. Anaesthesiol Intensive Ther 2016; 48: 61–62. doi: 10.5603/AIT.2016.0010.

Dear Editor,

Acute respiratory failure (ARF) and aspiration pneumonia were the most frequently observed respiratory complications after acute heroin overdose requiring endotracheal intubation (ETI) and intensive care unit (ICU) admission [1]. In some selected cases of drug overdose, noninvasive ventilation (NIV) could have avoided associated complications [2].

We were fortunate to have had a chance to read an article entitled “Swift recovery of acute hypoxemic respiratory failure under non-invasive ventilation” by Pichot et al. [3]. The authors present interesting evidence regarding the possible implementation of NIV in a patient presenting acute respiratory failure (ARDS) with extremely impaired PaO2/FiO2 ratio. It is important to underline that the report provides new potential indication in highly selected patients which, in special circumstances, it is possible to treat ARDS with the use of NIV with high positive end expiratory pressure (PEEP) and FiO2.

However, although the dynamic changes of clinical status during treatment were explained in the article, we consider that there are some factors to take into account in order to consolidate this observation in unconscious patients, those suspected of cocaine intake and with severe impairment of arterial blood gases (pH = 7.19, PaCO2 = 69 mm Hg, PaO2 = 57 mm Hg, SaO2 = 84%), precise more precisely the precautions that should have been considered by the authors.

Firstly, regarding equipment and interface, the patient was treated with the Drager Evita XL Ventilator, meaning an ICU-dedicated ventilator. From a clinical point of view, in this case it would have been more clinically valuable for readers if the authors had provided data on the interface used. Such features are of particular importance as differences in dead space between oro-nasal, full-face masks and a helmet could influence optimal synchronization and leakage in a patient with severe tachypnea of 30 breathes per minute as reported [4, 5].

Secondly, the authors have concluded that swift recovery was influenced by high PEEP-NIV strategy. However, this strategy has well known risks, namely: a) high PEEP levels induce leaks and gastric leaks and gastric distention and risk of aspiration, b) large tidal volumes not reported by the authors (800–1200 mL), associated with high airway resistance, low respiratory system compliance, and short inspiratory time, all increasing airway pressure and air entering the stomach [6] and c) the stability of oesophageal sphincter pressure (~20–25 cm H2O in adults) which, in turn, could vary by due to some pathways leading to gastric content aspiration possibly influenced by opiate toxicity. There is still controversy as to whether heroin-opioids may increase the risk of pulmonary aspiration by decreasing the pressure of oesophageal sphincter-intragastric pressure and hemodynamic compromise (supraventricular arrhythmia).

Thirdly, it is important to underline that the necessary high levels of FiO2 could also worsen alveolar damage and surfactant production. In this case, the FiO2 level was lower than 0.60, this figure being the lung toxicity cut off point after 08:45 hours of treatment [7].

Fourthly, the definition of “swift time period of 10 hours is still not broadly accepted. We know from previous studies, that an inability to improve PaO2/FiO2 after 1 hour of NIV was a predictor of treatment failure [8, 9]. We consider that for an appropriate extrapolation, it could be necessary to take into account other non-pulmonary factors as neurologic conditions and precise drugs.

Lastly, amiodarone infusion in a patient without severe cardiac arrhythmia with shock seems to be controversial. On the basis of the presented case history, we can assume that the patient was free of dangerous cardiac arrhythmia and the increased heart rate was probably caused by severe hypoxemia, dyspnoea, agitation and/or opiates reversed by naloxone treatment. In these circumstances, a heart rate (H R) of 171 and blood pressure (BP) of 141/71 mm Hg should have been diagnosed as physiological sinus tachycardia, indicating that the improvement of oxygenation should have been effective first line treatment [10]. Moreover, amiodarone with its alveolar toxicity may cause further lung damage and a poorer prognosis [11].

In conclusion, it is necessary to emphasize that although this case report gives one important data on ARDS treatment under strict supervision in the ICU, NIV is contraindicated in severe ARDS patients who are unable to protect their airways’ from aspiration. Finally, the swift time period is still controversial.

ACKNOWLEDGMENTS

  1. The authors declare no financial disclosure.
  2. The authors declare no conflict of interest.

References:

  1. Grigorakos L, Sakagianni K, Tsigou E, Apostolakos G, Nikolopoulos G, Veldekis D: Outcome of acute heroin overdose requiring intensive care unit admission. J Opioid Manag 2010; 6: 227–231.
  2. Ridgway ZA, PountneyAJ: Acute respiratory distress syndrome induced by oral methadone managed with non-invasive ventilation. Emerg Med J 2007; 24: 681.
  3. Pichot C, Petitjeans F, Ghignone M, Quintin L: Swift recovery of severe acute hypoxemic respiratory failure under non-invasive ventilation. Anaesthesiol Intensive Ther 2015; 47: 138–142. doi: 10.5603/AIT. a2014.0053.
  4. Nava S, Navalesi P, Gregoretti C: Interfaces and humidification for noninvasive mechanical ventilation. Respir Care 2009; 54: 71–84.
  5. Storre JH, Bohm P, Dreher M, Windisch W: Clinical impact of leak compensation during non-invasive ventilation. Respir Med 2009; 103: 1477–1483.
  6. De Keulenaer BL, De Backer A, Schepens DR, Daelemans R, Wilmer A, Malbrain ML: Abdominal compartment syndrome related to noninvasive ventilation. Intensive Care Med 2003; 29: 1177–1181.
  7. Aggarwal NR, Brower RG: Targeting normoxemia in Acute Respiratory Distress Syndrome may cause worse short-term outcomes because of oxygen toxicity. Ann Am Thorac Soc 2014; 11: 1449–1453. doi: 10.1513/AnnalsATS.201407–297PS.
  8. Antonelli M, Conti G, Moro ML et al.: Predictors of failure of noninvasive positive pressure ventilation in patients with acute hypoxemic respiratory failure: a multi-center study. Intensive Care Med 2001; 27: 1718–1728.
  9. Antonelli M, Conti G, Esquinas A et al.: A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med 2007; 35: 18–25.
  10. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM et al.: American College of Cardiology; American Heart Association Task Force on Practice Guidelines; European Society of Cardiology Committee for Practice Guidelines. Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias. ACC/AHA/ESC guidelines for the_management of patients with_supraventricular arrhythmias-executive summary: a_report_of the American_College_of_Cardiology/American_Heart_Association_Task Force_on_Practice Guidelines_and the_European_Society_of Cardiology_Committee_for_Practice Guidelines_(WritingCommittee to Develop Guidelines for theManagement of Patients with Supraventricular Arrhythmias). Circulation 2003; 108: 1871–1909.
  11. Dhokarh R, Li G, Schmickl CN et al.: Drug-associated acute lung injury: a population-based cohort study. Chest 2012; 142: 845–850.

Adres do korespondencji:
Szymon Skoczyński
Department of Pneumology, School of Medicine in Katowice,
Medical University of Silesia,

Medyków 14,40–752 Katowice
e-mail: simon.mds@poczta.fm

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