Post-traumatic Acute Respiratory Distress Syndrome (ARDS) continues to be a major critical care challenge with a high associated mortality and extensive morbidity for those who survive. This paper explores the evolution in recognition and management of this condition and makes some recommendations for treatment of post-combat ARDS for military practitioners. It is aimed at the generalist in disciplines other than critical care, but will also be of interest to intensivists.
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In trauma patients with Acute Respiratory Distress Syndrome (ARDS) and continued respiratory deterioration despite using protective ventilator strategies, extracorporeal ventilator support (ECVS) offers potential benefit.
ECVS offers salvage ventilation to military trauma patients with severe ARDS facilitating their aeromedical evacuation to Role 4 facilities.
The ARDS net study suggests that all trauma patients should have protective ventilation.
Post-traumatic Acute Respiratory Distress Syndrome (ARDS) continues to be a major critical care challenge with a high associated mortality and extensive morbidity for those who survive. In the management of patients with ARDS due to war injury in a deployed hospital environment, difficulties in treatment can be compounded by the requirement for massive transfusion, extra-thoracic injuries and the need to evacuate a critically injured patient to an enhanced capability hospital in the home nation. This article reviews the strategies for ventilation in acute lung injury (ALI) after combat trauma, to inform the generalist, making aware the extent of support available and the importance for maintenance of such resources.
Clinical presentation, investigation and physiological disturbance
The mechanism of ARDS involves multiple pathways. An increased permeability of both capillary endothelium and alveolar epithelium allows protein-rich fluid to collect in the alveolar space. Stimulation of pro-inflammatory cytokines propagates leaky membranes and recruits neutrophils; activation of neutrophils allows their release of free radical mediators with subsequent extensive oxidative damage. Transcription errors in genes for many pro-inflammatory mediators are seen in ARDS lungs. Other factors, such as angiotensin-2, endothelin-1 and phospholipase A-2, also act to increase vascular permeability and enhance inflammation and lung damage.1
A patient will develop a progressive respiratory failure. Initially, a raised RR and increasing oxygen requirements may be apparent, while subsequent ABG analysis and CXR will provide evidence of the condition. In the ventilated patient, the increased oxygen requirements will be associated with a deterioration in lung compliance, prompting the consideration of ARDS.
The American-European Consensus Conference (AECC) in 1994 originally defined ARDS but limitations in the criteria directed revision. In 2011, the European Society of Intensive Care Medicine, endorsed by the American Thoracic Society and the Society of Critical Care Medicine, developed the Berlin Definition (Table 1). These criteria were evaluated using a meta-analysis of 4188 patients and provided better predictive validity for mortality than the AECC parameters. Limitations of the AECC definition included the definition of ‘acute’, clarity of radiographic findings and the use of the term ALI. The term ALI for less severe ARDS is subsequently no longer used, but appears in the literature and, therefore, is used in this article to discuss trials predating the revised definition of ARDS. The Berlin Definition grades the severity by the PaO2:FiO2 ratio: mild 26.7–40 KPa (201–300 mm Hg), moderate 13.4–26.6 KPa (101–200 mm Hg) and severe ≤13.3 KPa (<100 mm Hg).2 To reach the diagnosis, ABG analysis and a plain CXR must be obtained.
Although not required in the diagnostic criteria, CT scans of individual patients with ARDS have been evaluated to create three subgroups based on the appearances of lung morphology: diffuse attenuations in lungs (as a result of atelectasis), lobar attenuation in the lower lobes or patchy attenuations in both lungs. Although correlation of these radiological subgroups to the underlying cause of the patient's ARDS is generally poor,3 the radiological subgroups have been shown to respond differently to positive end expiratory pressure (PEEP), with the poorest response occurring in patients with a lobar distribution of atelectasis.4
ARDS after combat injury
Between 2008 and 2010, review of UK casualties from Afghanistan with injuries resulting from blast revealed five cases of ARDS from 412 patients (1.2%) who survived the initial blast and were received by the Role 3 Hospital at Camp Bastion.5 A total of 107 of these patients passed through the ICU at the UK Role 4 Hospital (Queen Elizabeth Hospital, Birmingham: QEHB) and radiological chest findings were identified in 66/107 (62%). Blast lung is therefore relatively common among this cohort of multiple injured military casualties. This report highlights that while the pulmonary effects of blast can evolve over time, they may be occult to the treating clinician, unless a high index of suspicion is maintained.5
Post-mortem CT of 121 improvised explosive devices (IED) blast fatalities in UK troops showed a 48% rate of primary blast lung injury,6 divided between those fatalities in mounted (on or in a vehicle with an external IED explosion) and dismounted (on foot) IED incidents; a significantly higher rate of primary blast lung injury was seen among the mounted troops.
After war injury, the aetiology of ARDS can be from a primary thoracic injury or as a result of a systemic inflammatory response to a major insult and/or massive transfusion or may be due to a combination of the two. An American study examining the incidence of ALI and ARDS over 21 hospitals ascertained that 79% were due to sepsis (46% pulmonary sepsis) and 3% secondary to pancreatitis showing a high prevalence due to systemic inflammatory response.7 The same study, which was in a peace time environment, attributed 7% of ARDS cases to severe trauma; unfortunately, the mechanism of trauma was not stated.
Blast lung injury is a primary blast injury, that is, it arises as a direct result of the blast wave which creates a rapid and extreme pressure disturbance (a form of barotrauma). Within the lung, this results in damage to the alveolar-capillary basement membrane allowing red cells to enter the alveolar cavity giving the picture of diffuse alveolar haemorrhage.5 ,8–10 The damaged alveolar-capillary basement membrane also allows a rapid fluid shift and formation of pulmonary oedema. Other injuries resulting from blast effects include pulmonary contusion, chest wall injury (including flail chest) and pneumothorax, as well as penetrating injuries from fragments associated with the blast, and also contribute to the morbidity of blast lung.
Transfusion related ALI
Transfusion related acute lung injury (TRALI) is the leading cause of transfusion related mortality in the USA, with an incidence of 1 in every 5000 transfused blood products. It can occur after the transfusion of any blood product, although most commonly with fresh frozen plasma. An immune antibody mediated mechanism is thought to be responsible for TRALI, with human leucocyte antigen implicated as the trigger. Some cases do not show an immune response and thus alternative, non-immune pathological mechanisms are under research.11 ,12
The Canadian Consensus Conference established diagnostic criteria for TRALI in 2004. Principal features of the criteria are hypoxia and bilateral pulmonary oedema occurring within 6 h of transfusion in the absence of cardiac failure or intravascular fluid overload. Transfusion associated circulatory overload is the main differential diagnosis.
Given that these diagnostic criteria are recent and many patients require blood products for concurrent underlying pathology, the incidence of TRALI could be underestimated. Separating the cause of an ALI to give a diagnosis of TRALI may also be difficult (as in trauma patients), and these criteria aim to make this clearer. There remains no reliable test for TRALI.11 ,12
Ventilator associated lung injury
Patients meeting the criteria for ARDS usually require management by mechanical ventilation. Ironically, the use of ventilation can result in further injury itself; ventilator associated lung injury (VALI) has been defined as: ‘lung injury that resembles ALI and that occurs in patients receiving mechanical ventilation’.13 Three main mechanisms are thought be responsible for VALI:14 volutrauma, cyclical airway closure and barotrauma (Table 2).
These underlying mechanisms also contribute to the inflammatory mediator response and the creation of a systemic inflammatory response.15 So-called ‘protective ventilator strategies’ have been developed to manage the ventilatory requirements of patients with ARDS and mitigate the effects of VALI.
Conventional protective ventilation strategies
Low Vt, low peak/plateau pressures
Since the 1980s, it had been known that high tidal volume (Vt) and high inspiratory pressures result in the development of hyaline membranes and inflammatory infiltrates in the lungs and subsequent respiratory failure.16 Following several conflicting studies, a large multicentre randomised controlled trial (RCT) compared conventional versus low Vt (6 mL/kg based upon ideal body weight) ventilation in ARDS patients.17 Following recruitment of 861 patients, the trial was halted prematurely due to a clear reduction in mortality using low Vt ventilation. The ventilation at lower Vt also used lower peak and plateau pressures.
High PEEP in ARDS aims to maintain alveolar patency by preventing collapse during expiration, thereby ensuring the delivered Vt is distributed to a greater number of alveoli and reducing the risk of barotrauma. This maintenance of open alveoli reduces intra-pulmonary shunting and enables improved oxygenation in patients with ARDS.1 Strategies using high PEEP in ARDS patients are now accepted as safe and likely beneficial.18
Protective ventilation using low Vts almost inevitably results in CO2 retention. Consequences of a raised CO2 include reduced cardiac contractility, reduced end systolic and end diastolic pressures, increased heart rate and an overall increase in cardiac output, the O2 dissociation curve shifts to the left and there is coronary and cerebral vasodilatation.19 Carvalho et al studied hypercapnia in young patients with ALI and noted no cardiac depression. The initial changes of increased cardiac output, decreased systemic vascular resistance and pulmonary hypertension reversed in 36 h.20 It is now accepted that aggressive ventilation to achieve a normal CO2 is not required and a PaCO2 of 6–7 KPa can be accepted unless contraindicated such as in patients with raised intra-cerebral pressure.
Inverse ratio ventilation
Inverse ratio ventilation is when the inspiratory to expiratory ratio (I:E) is >1. Prolonged inspiration is thought to allow a greater filling of alveoli while allowing the use of a lower Vt and lower inspiratory pressures. The risks with this technique are that, due to the low expiratory time, full expiration may not be allowed (especially with PEEP applied), a phenomenon known as ‘intrinsic PEEP’. When this occurs, each incomplete expiratory cycle leaves the lung a little more hyperinflated, eventually leading to markedly raised intra-thoracic pressure and reduced venous return and, if not recognised, eventually to a situation not dissimilar to tension pneumothorax. During positive pressure inspiration, cardiac output is reduced and in a patient with cardiac compromise this may have a noticeable effect.19
Conservative fluid management
Once resuscitation has been achieved and circulating volume restored, there are advantages proposed for promoting a negative fluid balance in patients with ARDS by infusing intravenous fluids in a ‘conservative’ rather than a liberal manner. In a study of conservative versus liberal fluid strategies in patients with ARDS or ALI, no statistically significant difference in 60-day mortality was found between the two groups 72 h after presentation with ARDS. However, patients treated with the fluid-conservative strategy had an improved oxygenation index and lung injury score and an increase in ventilator-free days, without an increase in extra-pulmonary organ failure.21
Other ‘bundles of care’ in the ventilated patient
Once ventilated on an ICU, patients are susceptible to ventilator associated pneumonia (VAP). Multifactorial elements contribute to the risk of VAP and to address this, an international study investigated the introduction of a multidimensional bundle of care.22 The bundle included 13 components including a hand hygiene protocol, semi-recumbent positioning, daily assessment of ability to wean and ventilator circuit care considerations. Internationally, this study included 55 507 patients with a total of 137 666 days of ventilation. On implementation of the bundle, some aspects were well adhered to such as semi-recumbent positioning, whereas others were less so like removal of condensate from ventilator circuits. The benefits of any one component of the bundle could not be measured, but as a combination a reduction in VAP was observed from 22/1000 to 17.2/1000 (p=0.0004).
Outcomes after ARDS
Despite these strategies for ventilation, mortality associated with ARDS remains high. A 1 year multicentre study in Spain from 2008 to 2009, in the era of protective ventilation, showed an overall hospital mortality of 47.8%.23 In a national study in Iceland, the trends in ARDS over a 23-year period (1988–2010) were plotted.24 This long term analysis confirmed a shift in ventilator technique to the use of lower Vt and inspiratory pressures but increasing PEEP. The short term outcome assessed by hospital mortality resulting from ARDS over time was significantly reduced.
A prospective cohort study over 13 ICUs in Baltimore examined 2-year survival with the use of protective ventilation strategies.25 A total of 475 consecutive ventilated patients were included in the study with twice daily computer recording of ventilator settings. At 2-year follow-up, 64% of the patients had died but the authors identified a 3% decrease in mortality risk over 2 years for each ventilator setting adhering to protective ventilation.
Longer term outcomes after ARDS were examined in a prospective cohort study of 109 patients in Toronto, 65 of whom were followed up for 5 years.26 At each follow-up visit, patients completed a 6 min walking distance test, pulmonary function testing and a medical component questionnaire. Neither young nor old groups returned to the full predicated physical function with a legacy of on-going medical costs. The worse outcomes occurred in those with greater co-existing morbidity; 77% of those who were employed prior to the ARDS did return to work, 94% of whom were in the same job despite the reduction in physical function.
Strategies beyond conventional protective ventilation in severe ARDS
High frequency ventilation
High frequency ventilation (HFV) uses a Vt less than that of the dead space at high frequency (>60 breaths per minute). HFV is believed to offer protection against barotrauma by ventilating in a manner to provide protective ventilation (high pressure to maintain recruitment and low volumes to avoid volutrauma). Most commonly, HFV is delivered by high frequency oscillatory ventilation (HFOV) with Vt of 1–4 ml/kg and frequencies of 3–15 Hz.1 Other methods include high frequency percussive or high frequency jet ventilation.
The role of HFOV in ARDS has been examined in two recent RCTs. These had slightly different outcomes, with the OSCILLATE trial showing increased mortality in patients treated with HFOV and a high PEEP strategy, and the OSCAR trial showing no difference between HFOV (with lower pressures than used in OSCILLATE) and conventional ventilation. The complexities involved are well covered in an accompanying editorial.27
Prone position ventilation
Lung compliance in ARDS is not uniform throughout the lung. Prone ventilation is a strategy which makes use of this principle, with an aim to improve oxygenation and reduce VALI.28 A systematic review of five RCTs that examined prone ventilation for ALI and ARDS in adults showed prone ventilation does offer benefit from improved oxygenation. However, the primary measure of the review was mortality, and no reduction was shown. From the five RCTs, ICU stay and the incidence of pneumonia were, likewise, not improved. A trend towards an increase in pressure sores gave a suggestion of increased harm with prone ventilation.29 Based on this evidence, prone position ventilation is often reserved as a rescue treatment to improve oxygenation.
Independent lung ventilation
In unilateral lung injury, independent ventilation has been used, although the evidence is sparse. One case report described its use in an 18-year-old road traffic accident patient with unilateral chest trauma.30 He required unilateral thoracotomy and lung resection. By using a double lumen endotracheal tube, independent ventilator settings were established on both lungs. Independent ventilation allowed improved ventilation rapidly on the non-injured side while more protective settings were maintained on the injured lung. In a military trauma patient, independent lung ventilation could be considered for suitable patients.
A meta-analysis examined three RCTs with a total of 431 patients assessing the role of neuromuscular blocking agents (NMBA) in ARDS.31 This showed that early use of NMBA reduced the mortality at 28 days (risk ratio 0.71, 95% CI 0.55 to 0.9), and reduced duration of ventilation and ICU stay.
A subsequent large multicentre RCT in France randomised 340 patients with ARDS to receive either 48 h of NMBA or placebo.32 No significant difference in mortality at 90 days between the two groups (NMBA group 31.6% vs 40.7% placebo) was found. Analysis of the more severe cases (FiO2:PaO2 ratio <150) revealed that there was a significant reduction in mortality in the NMBA group. This trial also found that the NMBA group was superior in terms of 28-day mortality, more ventilator-free days and more time outside the ICU. There was no difference in the ICU acquired weakness between the two groups.
Evidence for the use of NMBA early in ARDS from both a meta-analysis and a subsequent RCT with similar findings suggests that in patients being ventilated for ARDS, early neuromuscular blockade is advisable.
Inhaled nitric oxide (NO) has been used in patients with ALI or ARDS, primarily for its vasodilator property. By producing local pulmonary vasodilatation, inhaled NO improves the ventilation mismatch in well-ventilated alveoli, shunting away from those that are more poorly ventilated. This pulmonary vasodilatation causes a reduction in pulmonary vascular resistance and pulmonary hypertension.33 ,34 Additionally, NO is thought to act by modifying the release of cytokines, thus altering the immune response and inhibiting the inflammatory cascade.35 However, despite these theoretical benefits, a Cochrane review of 14 RCTs, including 1303 patients, reported transient improvement in oxygenation using inhaled NO in patients with ALI or ARDS, but no improvement in mortality and potential harm from the technique.33 From the 14 trials included, transient improvement in oxygenation was reported in the first 24 h with improvement in the FiO2:PaO2 ratio. However, throughout the trials, there was an increase in renal impairment in those receiving inhaled NO therapy.1
Topical factor VIIa for blast lung
Topical factor VIIa has been advocated to offer local haemostasis within the alveoli in patients with diffuse alveolar haemorrhage. Factor VIIa's action is produced after its interaction with a receptor on the air side of the alveolar basement membrane, therefore, favouring local rather than systemic administration8 and there are four case series that describe topical factor VIIa administration via bronchial lavage. The largest of these series reported success in all of its six cases;36 none died due to pulmonary haemorrhage and a significant improvement in oxygen saturations was achieved. This study, along with the three smaller series with similar successful results, were reported in a review of the therapy8 which detailed no adverse event as a result of topical factor VIIa administration.
Exogenous surfactant is routinely used in neonatal ARDS, resulting in improved lung compliance and increased oxygenation. Similar success has been reported in animal models of ARDS although this has not been replicated in studies with adult humans and no survival benefit has been found to date. In adult ARDS, there is a characteristic dysfunction of surfactant with abnormalities in the phospholipids and proteins produced by an inhibition of surfactant by plasma constituents. This is in contrast to neonates, where a reduction in the amount of surfactant produced is thought to be accountable for the ARDS. It is postulated that adult ARDS from direct causes (eg, aspiration or pneumonia) may be more responsive to exogenous surfactant than ARDS from indirect causes such as trauma, sepsis or pancreatitis.37 ,38
The theory of creating benefit from exogenous surfactant in ARDS is attractive; however, there are unknown factors at this time: the nature and dose requirement of exogenous surfactant, timings of administration and even the mode of delivery.38
Other medication in ARDS
Statins, inhaled prostacyclin and steroids have all been trialled in patients with ARDS, none of which have had a demonstrable benefit. An RCT examining statin use in ventilated ALI and ARDS patients assigned 30 patients to a control and 30 to a statin group.39 The study claims some benefit in terms of reduction in organ dysfunction and reduction in inflammation although no significant overall benefit was reported.
Prostacyclin is a potent pulmonary vasodilator and has been used to improve oxygenation, lower pulmonary vascular resistance and reduce pulmonary shunt when inhaled in ALI and ARDS but systematic review of the literature was unable to demonstrate any benefit.40
Corticosteroid (methylprednisolone) use in ALI and ARDS was studied using an RCT, with no benefit shown in the primary outcome of 60-day mortality.41 The study did demonstrate an increase in ventilator-free and shock-free days in the first 28 days with an improvement in oxygenation. The initiation of steroids in those greater than 14 days after the onset of ARDS was associated with significantly increased 60-day mortality.
Protective ventilator settings can be individualised with further monitoring.42 Neutrally adjusted ventilatory assist delivers airway pressures proportional to the inspiratory diaphragmatic electrical activity, monitored with a specific nasogastric device. This allows Vt delivery on a breath-by-breath basis according to demand. Another mechanism is targeted trans-pulmonary pressure and individualised PEEP, PEEP being guided by the difference between alveolar and pleural pressure. Alveolar pressure is approximated from the airway pressure and oesophageal pressure is used as an estimation of pleural pressure to avoid further invasive monitors.
Cytokine mediator therapy has been trialled in animals to protect against VALI.42 Interleukin (IL)-1 and IL-18 blockade or the use of anti-inflammatory cytokines IL-10 and IL-22 may reduce the effects of VALI.
The process of ARDS initiates a requirement for repair of the lung parenchyma. Stem cell therapy, predominantly trialled using bone marrow derived pluripotent cells administered in the circulation, is a consideration for accelerating the repair process.43 Mice studies demonstrated that following lethal irradiation up to 20% of the lung epithelium could be replaced with donor stem cells.
Extracorporeal ventilatory support
Extracorporeal ventilator support (ECVS) aims to achieve systemic oxygenation and removal of excess CO2 by an extracorporeal circuit that directly oxygenates and removes CO2 from the blood.44 Extracorporeal membrane oxygenation (ECMO) is the most common term used for this and can encompass several techniques. Typically, ECMO involves femoral venous cannulation via which blood is pumped into an oxygenator and travels along one side of a membrane that allows diffusion of gases across a blood–gas interface. Oxygenated blood is then returned to the patient via a second central venous cannula in the internal jugular vein; this is therefore a veno-venous (VV) ECMO technique.
Veno-arterial (VA) circuits can be used for ECMO, with blood being drawn from a vein and pumped arterially, with the added benefit of cardiac support. VA circuit use introduces an increased risk of thromboembolic stroke due to the mechanics of blood delivery back into the arterial circulation,45 so VV systems tend to be favoured for pure ventilatory support. Recently, a dual lumen cannula has been developed that can achieve ECMO via a single central venous puncture.46 When ECMO has been established, the patient's lungs continue to be ventilated, but at settings that aim to mitigate VALI; this is commonly known as ‘lung rest’.
The disadvantages of using a VA system are pump related: embolism, haemolysis, heparin-induced thrombocytopenia, risk of mechanical failure, or recirculation of oxygenated blood into the ECMO circuit if flow is too high and afferent and efferent catheters are close.44 The advantage of such a circuit, with a pump drive, is the ability to directly regulate flow over the oxygenation membrane without any additional strain to the heart. The pump also has the advantage of being able to assist a failing heart when used in a VA circuit.
Pumpless extracorporeal lung assist
Pumpless extracorporeal lung assist (PECLA) devices such as Novalung pass blood over an oxygenator membrane as in ECMO; however, no pump is involved in the circuit.45 PECLA uses a low resistance arterio-venous circuit using the patient's BP to drive flow. As the blood passing over the membrane is arterial, the difference in partial pressure is low, and under normal circumstance the oxygenation with such devices is minimal. The PECLA device does offer CO2 removal, which may be beneficial when using prolonged protective ventilator techniques. In extreme circumstances, when lung oxygenation is very low and the arterial PaO2 entering the circuit is reduced, the system can provide oxygenation support.
The advantage of PECLA over ECMO is the avoidance of all pump related complications. The disadvantages include the lack of direct control of flow, the subsequent potential for strain on the heart and the risk to oxygenation of tissue distal to the arterial cannulation. PECLA is limited by the patient requirement of a cardiac index greater than 3 L/min/m2 and a mean arterial pressure of greater than 70 mm/Hg; subsequently, heart failure is a contra-indication to PECLA and a pumped device would be required.45
Intra vascular oxygenator
The intravascular oxygenator (IVOX) is a technique involving the placement of an intravascular (normally vena caval) device which contains a membrane oxygenator. From the device leading externally are two tubes, an inlet for oxygenated air and an outlet. Studies in animals and humans have shown up to 30% CO2 removal using such devices with some ability for oxygenation.47 The device does not offer the same lung assist potential as PECLA or the ability to completely take over ventilation as in ECMO. The advantage of IVOX devices are a marked reduction in the exposure of blood to a foreign surface and the avoidance of extravasation into a foreign circuit with subsequent reduction in haemolysis and risk of embolus.
Clinical use of ECVS in trauma
The role of ECVS in the management of severe, reversible lung injury is controversial. ECVS is costly and demanding in terms of both human and logistic resources and evidence to support its use is somewhat scanty. Observational studies provide some anecdotal evidence of good outcomes after ECVS but genuine comparative data are hard to come by. Despite this, centres across the UK maintain ECVS capability as a contingency, including QEHB,5 when other ventilator strategies are ineffective.
The Conventional Ventilation or ECMO for Severe Adult Respiratory Failure (CESAR) study48 examined 180 patients with severe, potentially reversible ARDS who were randomised to continued conventional ventilation at their hospital or referred to a specialised centre where ECMO was available. Although outcomes at 6 months (in terms of death or severe disability) were significantly in favour of those patients referred to the ECMO centre, only 76% of those referred underwent ECMO and the control group did not have a protocol for ‘best practice’ conventional management of their ARDS with only a bare majority (70%) undergoing lung protective ventilation strategies. This raises the possibility that the effective intervention was protocolled care rather than ECMO.
A retrospective single centre study, at a regional ECMO centre, examined 28 trauma patients with a mean age of 27 years and minimal co-morbidities treated with ECMO between 1992 and 2000.49 All the patients were initiated on ECMO due to ARDS following failure of conventional ventilation techniques. The majority of these patients had a long bone fracture, blunt chest trauma or a combination. Overall, 20/28 (71%) survived to return to their referring hospitals. Unfortunately, no follow-up on whether the patient survived to discharge home was reported. This study demonstrated ECMO to be usable in trauma patients with ARDS and highlighted the need for an awareness of this technique among members of the trauma team.
Arlt et al50 retrospectively examined ECMO use in trauma patients who would previously have been excluded from ECMO use due to co-existing haemorrhagic shock. ECMO was initiated in 10 patients with a mean Injury Severity Score of 73 (±4). Due to concomitant bleeding, ECMO was initiated without heparinisation and the introduction of heparin was guided by laboratory results after correction of coagulopathies. Concurrent treatment to achieve haemorrhage control with damage control surgery was on-going. Despite the small number of subjects, cardiopulmonary benefit was reported within 2 h of ECMO in all patients; PaCO2 67 (36–89) mm Hg pre-ECMO improved to 41 (22–85) 2 h post-ECMO; and norepinephrine requirements improved from 3 (1–13.5) mg/h to 0.9 (0–5) mg/h 2 h after institution of ECMO. From a military viewpoint, this study has shown successful use of ECVS in patients with coagulopathies.
Over a 14-year period up to March 2011, a Scandinavian prospective observational trial examined the use of ECMO in 124 patients.51 A very favourable outcome of those meeting the criteria and treated with ECMO was reported. In total, 78% were weaned off ECMO and 72% were discharged alive from the ICU. Only 18 of the 124 were trauma patients, but outcomes were good with 72% survival in the trauma group. A principal finding from this study was the role of ECMO in transport of patients from referring hospitals to a specialist centre—106 (85%) were transported on ECMO; no patient was transferred for ECMO to be started at the specialist centre. Of those transported, there was no significant difference in outcome compared with those from within the specialist unit, with survival of 71% and 72%, respectively.
Following the introduction of Critical Care Air Transport Teams, critically ill casualties can be transported from theatre of military operations within hours of injury to a Role 4 medical facility. The hypobaric atmosphere on-board air transport produces difficulties in cases where ARDS is evident, with the potential for further respiratory deterioration in flight.52 ECMO capability for the International Security Assistance Force in Afghanistan is provided by the US Army based at Landstuhl Regional Medical Centre, Germany.53 This facility was established jointly with the US army and the Regional ‘Lung Failure’ centre at University Hospital Regensberg, a partnership which drove the development of ECVS technology providing smaller, transportable devices. Bein et al53 have recently reported on 10 combat casualties treated with both pumpless and pumped devices, detailing successful transportation of casualties out of operational environments using ECVS with a mortality of only 10%.
Over a 56-month period up to June 2010, US Central Command activated the Acute Lung Rescue Team (ALeRT) on 40 occasions (Table 3). ALeRT successfully evacuated patients on 24 of 27 missions launched (89%); three patients were too unstable for ALeRT evacuation. Of the 13 remaining activations, four patients died and nine patients improved sufficiently for standard Critical Care Air Transport Teams movement. ALeRT initiated pumpless extracorporeal lung assistance six times, but only once to facilitate evacuation. Two patients were supported with full ECMO support after evacuation due to progressive respiratory failure.54
ARDS is a major challenge in contemporary military critical care. Figure 1 provides a flow-diagram of how the authors interpret the evidence reviewed in this article suggesting how ARDS is best managed. Conventional protective ventilatory strategies are important and are associated with improved survival compared with historic cohorts of patients. As survivability of major military trauma continues to improve, we are likely to be faced with a small, but increasing number of patients with ARDS refractory to conventional strategies. While, as yet, there is little high quality evidence about long term outcomes, ECVS has a place in the management of these patients. The infrequent requirement for its use may preclude individual defence medical services maintaining independent capability. Coalition partners should continue to cooperate to establish and maintain the capability between nation states.
The authors would like to thank Dr David H Zonies, Director of Trauma, Landstuhl Regional Medical Centre, Landstuhl, Germany, for his helpful contribution to this manuscript. Opinions expressed in this manuscript are those of the authors and do not necessarily represent views of the UK Ministry of Defence or US Department of Defense.
Contributors TGB was the main author, having predominately researched and written the article. DMB is the senior author who initiated the idea and provided initial guidance and continued editorial input. JB, HK and JL were equally involved in the initial concept and provision of background research for the article. AMcJ gave further revision and intellectual content.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.