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Case Reports

Prolonged Use of Extracorporeal Membrane Oxygenation as a Rescue Modality Following Traumatic Brain Injury

Messing, Jonathan A.*; Agnihothri, Ritesh V.; Van Dusen, Rachel; Najam, Farzad§; Dunne, James R.*; Honig, Jacqueline R.; Sarani, Babak*

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doi: 10.1097/MAT.0000000000000103
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Abstract

Traumatic brain injury (TBI) is a leading cause of death following injury. Patients with TBI and adult respiratory distress syndrome (ARDS) pose an especially difficult challenge to clinicians. When patients with ARDS cannot be oxygenated despite conventional mechanical ventilation and other adjuncts, veno-venous extracorporeal membrane oxygenation (vv-ECMO) can be used as a rescue treatment modality.1,2 Traditionally, patients are systemically anticoagulated while on ECMO. This poses a problem in TBI patients as systemic anticoagulation to prevent circuit thrombosis can lead to recurrent cerebral hemorrhage and death.3 Only limited case reports are available addressing the successful use of ECMO in brain-injured patients with severe respiratory failure, and all reports involve a short duration of ECMO.4–7 In addition, there are currently no existing guidelines for the timing of therapeutic anticoagulation after TBI. Here, we report our experience with a 21-year-old male suffering from a severe TBI and ARDS not responding to conventional therapies. The patient survived neurologically intact after 20 days of ECMO.

Case Report

A 21-year-old white man suffered a high-speed rollover motor vehicle collision in which he was the belted driver. Prior to arrival at our level I trauma center, the patient was intubated with a King LT tube by emergency personnel due to an altered mental status and a witnessed massive aspiration. Upon arrival, he was endotracheally intubated and the aspiration was confirmed. Injuries included subdural and subarachnoid hemorrhage, diffuse axonal injury with early cerebral edema (Figure 1), large right-upper-lobe pulmonary contusion, and bilateral airspace opacities consistent with aspiration pneumonia. His injury severity score was 38. An intracranial pressure (ICP) monitor revealed an initial ICP of 15–22 mm Hg that responded to medical therapy. Despite chemical paralysis, initiation of inhaled prostacyclin and trials of various modes of mechanical ventilation, oxygenation deteriorated approximately 72 hours after injury such that the oxygenation saturation could not be kept above 80%. Chest x-ray was consistent with worsening ARDS (Figure 2). The patient was therefore placed on vv-ECMO on postinjury day 3 via an Avalon Elite Bi-Caval dual lumen catheter (Avalon, Rancho Dominguez, CA) inserted through the right internal jugular vein and using a Tandem-Heart (Cardiac Assist Inc., Pittsburgh, PA) pump, a heparin-bonded circuit, and a Quadrox-i adult oxygenator (Maquet Cardiovascular, Wayne, NJ). Flow rates were consistently 3–4 L/minute. The initial strategy for preventing thrombosis of the oxygenator was the use of a heparin-bonded circuit. Due to thrombi in the oxygenator prompting replacement of the oxygenator on three separate occasions, the decision was made to proceed with anticoagulation, given that each filter change contributed to desaturations down to 75–80%. Systemic heparin was administered on ECMO day 5 (post injury date 8) after a repeat computed tomography scan of the head confirmed that no new intracranial hemorrhage had occurred. The heparin was titrated to maintain an activated clotting time (ACT) target of 180–200 seconds. Heparin was chosen due to its ability to be easily titrated and monitored, a short half-life, and its reversibility in the event of clinical bleeding or for subsequent procedures. The goal ACT was adjusted to maintain adequate anticoagulation to prevent the appearance of thrombi in the oxygenator, balanced with limiting temporary oozing from the patient’s percutaneous endoscopic gastrostomy (PEG) site (ACT goal decreased to 160–180 seconds). Aside from minimal oozing at the PEG site requiring one unit transfusion of packed red blood cells, the patient experienced no bleeding complications. After 20 days of ECMO, the patient was successfully weaned once there was evidence of lung recovery, and was decannulated at the bedside. On postinjury day 34, the patient was discharged to a rehabilitation facility. He is now home with no clinically evident neurologic deficits.

F1-20
Figure 1:
Computed tomography scan of patient’s head demonstrates subdural hemorrhage, subarachnoid hemorrhage, and diffuse axonal injury.
F2-20
Figure 2:
Chest x-ray of patient’s progression to adult respiratory distress syndrome.

Discussion

Secondary brain injury significantly increases mortality and must be avoided.8 Factors contributing to secondary brain injury include hypoxemia, hypercapnea, and hypotension, to name a few. Concurrent ARDS and TBI pose an especially difficult challenge as they predispose the patient to secondary brain injury due to impaired gas exchange with resultant acidosis and cerebral hyperemia, and many of the treatments for the former directly conflict with the treatments of the latter. Prone positioning and ventilation strategies that may lead to hypercapnia contribute to increasing ICP. Similarly, ECMO, which successfully has been applied to patients with refractory ARDS,2 is often considered a contraindication in patients with TBI and/or intracranial hemorrhage due to its potential to worsen or actually cause hemorrhage.9,10 The risk of recurrent cerebral hemorrhage from trauma diminishes as time from injury increases, although the exact decrement in risk over time remains unknown. As such, we postulate that ECMO may be both efficacious and safe following TBI if sufficient time has lapsed from injury. We further postulate that once the head CT scan confirms that the cerebral hemorrhage is stable, the patient safely can be placed on ECMO and subsequently therapeutically anticoagulated.

The potential benefit of ECMO for oxygenation support following injury has been reported previously in patients with TBI and ARDS. However, survival probability is directly related to duration of mechanical ventilation prior to initiation of ECMO.11,12 Mortality is most impacted when ECMO is started prior to manifestation of multisystem organ failure. In our experience, ECMO was started when the patient had isolated respiratory failure and within 3 days of injury. Although advanced strategies such as airway pressure release ventilation, chemical paralysis, and inhaled prostacycline were used, ECMO was quickly utilized when these efforts were found to be ineffective. Therefore, the duration from onset of hypoxemia to initiation of ECMO was less than 8 hours.

One of the major concerns with ECMO in TBI is the need for systemic anticoagulation in a population where even prophylactic dosing is often debatable. Several studies exist arguing for or against deep vein thrombosis chemoprophylaxis in brain-injured patients. Kwiatt et al.,13 for example, found blunt TBI patients to be at greater risk for worsening intracranial hemorrhage when administered low-molecular-weight heparin. Scudday et al.,14 on the other hand, found a reduced incidence of venous thromboembolism and no increased progression of intracranial hemorrhage in TBI patients with a stable head CT 24 hours postinjury when receiving either enoxaparin twice daily or heparin three times daily. Dudley et al.15 also offer support for safe administration of prophylactic anticoagulation, defined as either enoxaparin 30 mg twice daily or dalteparin 5,000 units daily, in neurotrauma with stable head imaging and at least 48 hours of elapsed time. Considering the debate among clinicians for prophylactic doses of anticoagulation, caution must be exercised with therapeutic doses.

Although ECMO can be performed in a heparin-free fashion, this is usually only done for a short duration due to the thrombogenic nature of the tubing and oxygenator membrane. No guidelines for the timing of therapeutic anticoagulation after TBI currently exist. When resorting to ECMO as a rescue modality to maintain oxygenation and ventilation, one must consider the tradeoff between risks of anticoagulation, especially worsening intracranial hemorrhage, and benefits, including preventing thrombosis of the ECMO circuit and the risk of emboli. Muellenbach et al.5 reported three cases of patients with both severe TBI and ARDS where systemic anticoagulation was not used or delayed due to concerns of bleeding complications, yet they successfully achieved oxygenation goals without clinically significant thromboembolic events. The duration of ECMO applied in their patients was only 2–8 days, and when the patients did receive anticoagulation, it was of variable timing. Patients 1 and 2 started a heparin infusion with a targeted partial thromboplastin time of 40–50 seconds; patient 1 started on day 5 of ECMO and patient 2 started the day after initiating ECMO. Patient 3 started a heparin infusion once off of ECMO due to multiple areas of thrombi noted on a follow-up CT scan, possibly attributed to a combination of factor VIIa during the initial resuscitation and the subsequent use of ECMO. The longest duration of ECMO and anticoagulation together was 3 days.5 Of note, they did not experience complications related to worsening intracranial hemorrhage. Other studies on the role of heparin-free ECMO in TBI are limited by similar short durations of therapy. Reynolds et al.6 and Yen et al.7 did not use therapeutic anticoagulation and only heparin bonded circuits and did not have venous thromboembolism complications to share. Friesenecker et al.,4 on the other hand, started their patient on a heparin infusion with the initiation of ECMO, targeted an ACT of 150, and continued for a total of 15 days; their patient, however, incurred worsening intracranial hemorrhage prompting a craniotomy, though without clear relevance to the timing of the heparin infusion starting.

In our patient’s experience, we found that the oxygenator had to be changed nearly daily prior to the initiation of therapeutic anticoagulation due to thrombosis with impaired ability to exchange CO2, in particular, and a resultant rise in the ICP. This occurred despite maintaining adequate flow in the circuit. More important, we did not incur a hemorrhagic complication once the patient was therapeutically anticoagulated. Our patient started a systemic heparin infusion with a goal ACT of 180–200 seconds on day 5 of ECMO and continued for 15 days without worsening intracranial hemorrhage, which offers support for successful ECMO use in refractory ARDS and concomitant TBI.

Conclusion

The current case of severe aspiration pneumonitis with ARDS and TBI highlights the potential role of ECMO as a safe rescue method when conventional treatment maneuvers fail. An extended duration of ECMO with therapeutic anticoagulation following TBI is possible when sufficient time from injury elapses and the patient is closely monitored. Our case differs from previous reports of ECMO use in ARDS and TBI by demonstrating successful prolonged therapy without an adverse outcome. Further study is needed to better elucidate the safe interval from TBI to initiation of therapeutic anticoagulation.

References

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Keywords:

extracorporeal membrane oxygenation; traumatic brain injury; adult respiratory distress syndrome; anticoagulation

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