Anaesthesiology Intensive Therapy, 2010,XLII,4; 201-205

High frequency oscillation, extracorporeal membrane oxygenation and pumpless arteriovenous lung assist in the management of severe ARDS

*Marta Banach1,2, Jens Soukup1, Michael Bucher1, Janusz Andres2


1Klinik für Anästhesiologie und Operative Intensivmedizin der Martin-Luther-Universität, Halle


2Department of Anaesthesiology and Intensive Therapy, Collegium Medicum, Jagiellonian University in Kraków

  • Table1. Selected parameters of acid-base balance and haemodynamic indices at successive stages of treatment
  • Fig. 1. Chest radiogram after ITU admission
  • Fig. 2. Chest CT scan on day 7 of therapy
  • Fig. 3. Chest CT scan at week 3 of therapy
  • Fig. 4. CT scan by the end of ITU therapy

Background. The protective lung strategy for severe ARDS, has markedly decreased the associated morbidity and mortality. Sometimes, even the best instrumentation and therapeutic strategy may be insufficient, and extracorporeal gas exchange support is necessary. We describe a desperate case of ARDS, in which various modes of ventilation, combined with vigorous extracorporeal support, resulted in a successful outcome.

Case report. A 35-year-old man, a heavy smoker, was admitted to the hospital because of lobar pneumonia. Despite wide spectrum antimicrobial therapy, he developed ARDS and was placed on a ventilator. Standard ventilation was ineffective and veno-venous ECMO was instituted. The extravascular lung water index (EVLWI) was extremely high (over 30 mL kg-1) and signs of a hyperdynamic circulation (CI 6.1 L m-2 min-1) were observed. Modification of the inotropic support and continuous infusion of furosemide resulted in normalisation of the hydration status, and over a week of ECMO therapy, the patient’s general condition improved to the stage that he was scheduled to be weaned from extracorporeal treatment. On the 7th day however, he suddenly deteriorated. A lung CT-scan revealed bilateral pneumothoraces and diffuse pulmonary embolism. Three thoracic drains were inserted, but unfortunately, the drainage was complicated by massive bleeding and a subsequent thoracotomy. Two days later, a gastrointestinal haemorrhage occurred. Heparin dosage was reduced, and ECMO was discontinued and replaced with HFOV. This resulted in adequate oxygenation, however because of ineffective CO2 elimination, pumpless arteriovenous extracorporeal lung assist (PECLA) was instituted, allowing conventional ventilation to be resumed after 8 days. The further clinical course was complicated by persistent bilateral pneumothoraces, pleural effusion and Pseudomonas nosocomial infection. The man eventually recovered after 54 days in the ICU, and was transferred to a rehabilitation department.

Discussion and conclusion. ECMO has been recommended for severe ARDS since it avoids overdistension of the lungs and the use of high oxygen concentrations. Early institution of ECMO decreases mortality and morbidity in rapidly progressing ARDS. In the described case, ECMO was probably started too late, after volutrauma has already occurred. A combination of HFOV and PECLA may be recommended in selected cases, in which CO2 retention poses a serious problem.

Acute respiratory distress syndrome (ARDS) is still associated with high mortality rates. Aggressive mechanical ventilation due to severely impaired lung gas exchange, which accompanies ARDS, may lead to further lung damage and contribute to the development of systemic inflammatory response or even multi-organ failure [1, 2].

To avoid possible ventilator-associated lung damage, the current guidelines recommend to recruit and keep the pulmonary alveoli open, using the possibly lowest amplitude of airway pressures [3, 4]. This so-called lung protective ventilation strategy may substantially reduce mortality in ARDS [5]. The alternative method in accordance with the principles of protective ventilation is high frequency oscillation ventilation (HFOV). In HFOV, the patient`s blood saturation depends on the mean airway pressure and FIO2 whereas CO2 elimination – on pressure amplitude and oscillation frequency. Under such circumstances, extracorporeal gas exchange is required using extracorporeal membrane oxygenation (ECMO) or pumpless arteriovenous extracorporeal lung assist (PECLA).

ECMO is increasingly used to treat severe hypoxia and hypercapnia accompanying ARDS [6, 7, 8, 9]. Contrary to ECMO, a PECLA device, still less popular, does not use any external pump and the blood flow through it depends on mean arterial pressure, thus low cardiac output and shock are contraindications for this method [10]. At a low blood flow, 1-2 L min-1, which corresponds to about 1/3 of cardiac output, 95% of CO2 produced in the body is eliminated [11]. The study findings demonstrate that improvement in blood oxygenation with this method is not spectacular [12]. For this reason, many authors suggest the combined use of HFOV and PECLA in severe ARDS [11, 13, 14].

The present report describes a pioneer combination of HFOV, ECMO and PECLA in the treatment of a young patient with severe ARDS.

CASE REPORT

A 35-year-old male patient was hospitalized in ITU of the municipal hospital due to severe acute respiratory distress caused by right lower lobe pneumonia. The history revealed long-term nicotine addiction and possible job-related exposure to dust. During the 13-day ITU hospitalization, despite empiric broad-spectrum antibiotic therapy (meropenem, vancomycin, amoxicillin, fluoroquinolones), the patient developed the clinical and radiological picture of ARDS (Fig. 1) and haemodynamic instability. He was intubated and ventilated with BIPAP. The parameters of ventilation were increased (PEEP – 20 cm H2O/1.96 kPa, P insp to 40 cm H2O/3.92 kPa, f – 40 min-1, I:E 1.5:1, FIO2 0.8-1) and complete muscle relaxation was provided for three days yet hypoxia intensified. Due to lack of improvement in blood oxygenation (PaO2 – 60 mm Hg/ 8 kPa, PaO2/FIO2 – 70 mm Hg/9.33 kPa) and decreasing oxygenation index <38 over the further 6 h, on day 13 the decision was made to institute veno-venous ECMO through the right and left femoral vein and to transfer the patient to the teaching hospital ITU.

On ITU admission, lung ventilation was delivered through a tracheostomy using the BIPAP mode and arterial pressure maintained by the infusion of noradrenaline 0.2 µg kg-1 min-1, which ensured circulatory stability. The right pleural cavity was drained due to pneumothorax and a suspected pleural abscess. ECMO was started immediately after admission together with continuous infusion of heparin to obtain and maintain the recommended activated clotting time (ACT) of 130-160 s. Simultaneously, appropriate postural kinesitherapy was initiated using the RotoRest bed. The CO measurement by thermodilution on day 1 was 12.8 L min-1, CI – 6.1 L min-1 m-2. The extravascular lung water index (EVLWI) was markedly elevated to 30 mL kg-1.

Once dobutamine and furosemide continuous infusion was included during the successive days of treatment, the EVLWI gradually normalized (Table 1). The indices of inflammatory response, except for procalcitonine (0.17 ng mL-1), were elevated (CRP – 88 mg L-1, WBC – 15.5 G L-1, Il-6 – 24 pg mL-1). Since the inflammatory factor was not recognized and antibiotic therapy was ineffective, gentamicin and voriconazole were added and levofloxacin, administered earlier, continued.

During the ECMO therapy (blood flow − 4 L min-1, O2 − 6 L min-1, FIO2 – 0.8) and protective ventilation of the damaged lungs (PEEP − 15 cm H2O/1.47 kPa, inspiratory pressure − 20 cm H2O/1.96 kPa, FIO2 – 0.4, I:E − 1:2), the patient`s condition improved; thus, the ECMO support was reduced (blood flow − 2 L min-1, O2 − 2 L min-1, FIO2 – 0.3), the discontinuation of this therapy was considered. However, on day 7 of ECMO therapy, hypoxia and hypercapnia redeveloped (Table 1). Chest CT showed the typical ARDS picture with bilateral infiltrations of the pulmonary parenchyma, interstitial exudate and atelectasis in the posterior-basal region – bilateral pneumothoraces and bilateral pulmonary embolism (Fig. 2). For these reasons, two left-sided drainages and one right-sided drainage of the thorax were carried out. During 24 h, massive bleeding was observed at the site of right-sided drainage, which required mini-thoracotomy to secure it surgically as well as transfusion of red blood cells and fresh frozen plasma. On day 9 of ECMO therapy, symptoms of gastrointestinal bleeding developed. Under such circumstances, on day 10, it was decided to discontinue ECMO and initiate HFOV (mean airway pressure − 30 cm H2O/2.94 kPa, oscillation frequency − 7 Hz, FIO2 – 0.7). Blood heparinization was continued due to pulmonary embolism; the partial thromboplastin time (PTT) was kept within the range of 50-60 s. While searching for the cause of embolism, protein S deficiency was found, despite the supply of heparin.

The repeated microbiological tests of the bronchial secretion and pleural fluid excluded inflammatory causes of ARDS (Legionella, various types of influenza virus, mycoplasma, brucellosis, pneumocytosis, ornitosis, Acinetobacter, tuberculosis). The inflammatory parameters decreased yet were still slightly elevated (CRP-20 – 60 mg L-1, WBC-8 – 12 G L-1).

During the next days, hypoxia gradually subsided due to HFOV and kinesitherapy, which enabled us to reduce FIO2 to 0.45; however, hypercapnia persisted − 82 mm Hg (11 kPa) (Table 1). To eliminate CO2, the PECLA therapy was started using vascular catheters placed in femoral veins, which resulted in a reduction in PaCO2.

After 8 days of HFO, the BIPAP ventilation was re-instituted. Maintaining PECLA for 6 days, weaning from ventilator was started. Bilateral pneumothoraces persisted, therefore, multiple corrections of drain positions and 2 thoracotomies were necessary; a right-sided, and 7 days later a left-sided one with fibrin pleurodesis. The former was a life-saving procedure due to the development of tension pneumothorax (Fig. 3). Since lung fibrosis and emphysematous bullae with thinning and damage to the interalveolar septa were found intraoperatively (which was confirmed by histopatholgy) at negative bacteriological results, prednisolone was included with the initial dose of 1 mg kg-1, which was reduced to
0.5 mg kg-1 after ten days.

At week 5 of therapy during weaning from a ventilator, the patient was diagnosed with pneumonia, with increased values of CRP – 290 mg L-1, WBC – 13 G L-1, Il-6 – 47 pg mL-1, and body temperature 39.7oC. Microbiological examinations of bronchial secretion demonstrated the presence of Pseudomonas aeruginosa. After inclusion of doripenem and phosphomycin, according to the antibiogram, and everyday bronchial tree toilet, the symptoms of pneumonia subsided.

The CT scan performed on day 48 after the removal of drains from the thoracic cavity disclosed regressing residual pneumothoraces situated abdominally (a wider right-sided − to 2 cm) with persistent pulmonary parenchyma damage in this region with fibrotic lesions (Fig. 4). The thoracosurgical consultation did not consider further surgical treatment.

Until his discharge from ITU, the patient breathed spontaneously through a tracheotomy for 7 days; slight CO2 retention maintained (Table 1). He was ambulated to the standing position although his muscle power was markedly weakened. Oral analgesic therapy included hydromorfon. After 54 days in ITU, the patient, in good general condition, was transferred to the rehabilitation department.

DISCUSSION

Acute respiratory distress syndrome, both in adults and in the young population is still a serious therapeutic problem due to its high mortality rates. The priority objective of treatment in the acute stage of disease is maintenance of adequate gas exchange and prevention of further lung damage.

Many authors describe the successful use of ECMO, as a life-saving procedure, in the treatment of ARDS emphasizing the necessity of its earliest possible institution [6, 7, 9]. The assets of ECMO include immobilization of lungs and possibility to limit high therapeutic inspiratory concentrations of oxygen. The recovery of lungs results from reversal of hypoxic pulmonary hypertension and re-perfusion of the pulmonary vascular bed [6]. It has been demonstrated that the use of ECMO in severe yet potentially reversible respiratory failure markedly increases the long-term survival of patients without extensive disability [15].

In the case presented, the inclusion of ECMO to the treatment of ARDS enabled fast provision of adequate gas exchange and the use of artificial ventilation protecting the diseased lung. Despite such management, the patient developed bilateral pneumothoraces, which might have been caused by too long aggressive lung ventilation in the initial stage of disease. Moreover, massive bleeding was observed which necessitated the discontinuation of ECMO. According to the available literature data, such a complication is rare once clotting parameters are regularly monitored. They did not develop in 3 patients with ARDS, secondary to acute pancreatitis [8]; additionally, ARDS in a patient after pneumonectomy was reported, who underwent thoraco- and laparotomy during the ECMO therapy [6].

Other options of protective lung therapy in ARDS are HFO and PECLA. HFO ensures good blood oxygenation at lower amplitudes of airway pressures. Furthermore, it has been shown that during HFO, concentrations of inflammatory mediators in blood are lower than during conventional ventilation [3]. Elimination of CO2 may, however, be insufficient. The observation of 150 patients with ARDS treated with conventional ventilation or HFOV have demonstrated slight yet significantly higher CO2 retention in patients undergoing HFOV [3]. 

In the case described, high CO2 retention was observed, which led to respiratory acidosis with inadequate metabolic compensation (Table 1), most likely caused by pneumothorax. Once PECLA was instituted, the patient`s condition improved. These observations are in accordance with the reports suggesting the necessity of simultaneous use of HFOV and PECLA to provide adequate blood oxygenation and CO2 elimination [11, 13, 14].

Our case indicates the effectiveness of combined therapy consisting of ECMO, HFOV and PECLA to maintain gas exchange and to treat severe ARDS. Such management was supported by postural kinesitherapy, repeated bronchoscopic toilet of the bronchial tree, antibiotic therapy and therapy of complications.

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REFERENCES

1.    Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, Bruno F, Slutsky AS: Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA 1999; 282: 54-61.

2.    Imai Y, Parodo J, Kajikawa O, de Perrot M, Fischer S, Edwards V, Cutz E, Liu M, Keshavjee S, Martin TR, Marshall JC, Ranieri VM, Slutsky AS: Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA 2003; 289: 2104-2112.

3.    Derdak S, Mehta S, Stewart TE, Smith T, Rogers M, Buchman TG, Carlin B, Lowson S, Granton J: High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults. Am J Respir Crit Care Med 2002; 166: 801-808.

4.    Marini J: Recruitment maneuvers to achieve an “open lung”: whether and how? Crit Care Med 2001; 29: 1647-1648.

5.    The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301-1308.

6.    Dünser M, Hasibeder W, Rieger M, Mayr AJ: Successful therapy of severe pneumonia-associated ARDS after pneumonectomy with ECMO and steroids. Ann Thorac Surg 2004; 78: 335-337.

7.    Kuroda H, Masuda Y, Imaizumi H, Kozuka Y, Asai Y, Namiki A: Successful extracorporeal membranous oxygenation for a patient with life-threatening transfusion-related acute lung injury. J Anesth 2009; 23: 424-426.

8.    Peek GJ, White S, Scott AD, Hall AW, Moore HM, Sosnowski AW, Firmin RK: Severe acute respiratory distress syndrome, secondary to acute pancreatitis, successfully treated with extracorporeal membrane oxygenation in three patients. Ann Surg 1998; 227: 572-574.

9.    Madershahian N, Wittwer T, Strauch J, Franke UF, Wippermann J, Kaluza M, Wahlers T: Application of ECMO in multitrauma patients with ARDS as a rescue therapy. J Card Surg 2007; 22: 180-184.

10.    Matheis G: New technologies for respiratory assist. Perfusion 2003; 18: 171-177.

11.    Muellenbach RM, Wunder C, Nuechter DC, Smul T, Trautner H, Kredel M, Roewer N, Brederlau J: Early treatment with arteriovenous extracorporeal lung assist and high-frequency oscillatory ventilation in a case of severe acute respiratory distress syndrome. Acta Anaesthesiol Scand 2007; 51: 766-769.

12.    Zick G, Frerichs I, Schädler D, Schmitz G, Pulletz S, Cavus E, Wachtler F, Scholz J, Weiler N: Oxygenation effect of interventional lung assist in the model of acute lung injury: a prospective experiment. Crit Care 2006; 10: R56.

13.    Muellenbach RM, Kuestermann J, Kredel M, Johannes A, Wolfsteiner U, Schuster F, Wunder C, Kranke P, Roewer N, Brederlau J: Arteriovenous extracorporeal lung assist allows for maximization of oscillatory frequencies: a large-animal model of respiratory distress. BMC Anesthesiol 2008; 8:7.

14.    Brederlau J, Muellenbach R, Kredel M, Kuestermann J, Anetseder M, Greim C, Roewer N: Combination of arteriovenous extracorporeal lung assist and high-frequency oscillatory ventilation in a porcine model of lavage-induced acute lung injury: a randomized controlled trial. J Trauma 2007; 62: 336-346.

15.    Peek GJ, Mugford M, Tiruvoipati R, Wilson A, Allen E, Thalanany MM, Hibbert CL, Truesdale A, Clemens F, Cooper N, Firmin RK, Elbourne D: Efficacy and economic assessment of conventional ventilator support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomized controlled trial. Lancet 2009; 374: 1351-1363.

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address:

*Marta Banach
Klinik für Anästhesiologie und Operative Intensivmedizin
der Martin-Luther-Universität,
Ernst-Grube Str. 40
06120 Halle

received: 06.04.2010
accepted: 28.07.2010