POCUS Case: Evaluation of Hypoxia in a Patient with Traumatic Brain Injury
Published on: July 01, 2021
A 34-year-old man presented with a high-grade traumatic brain injury (TBI) after being struck by a motor vehicle. In the emergency department he had a GCS of 3 and was intubated for airway protection. His initial CT showed bilateral frontal subarachnoid hemorrhage, left subdural hematoma and temporal contusion with effacement of his basilar cisterns, and 9mm of midline shift. He was given mannitol and taken to the OR for a left hemicrainectomy, followed by placement of a continuous ICP and PbtO2 monitor in the contralateral hemisphere and admission to the neurological intensive care unit (ICU).
Two days after admission, the patient developed a worsening oxygen requirement without significant change on chest X-ray. The neurocritical care fellow performed bedside POCUS of the patient’s lungs and heart to assess the etiology of his hypoxia. Lung ultrasound showed a predominant A-line pattern with normal lung sliding bilaterally. Bedside echocardiography revealed a dilated right ventricle (RV) on multiple views with flattening of the interventricular septum during diastole and systole, indicative of RV strain (Figure 1 and Videos 1 &2). These POCUS findings were concerning for an acute pulmonary embolus (PE), which was promptly confirmed with CT imaging. Given the patient’s evolving contusions, subsequent negative lower extremity duplex, and hemodynamic stability, therapeutic heparin was deferred for 5 days. The patient’s multimodality monitoring was discontinued and he was extubated and following commands 10 days following his injury.
Application of the POCUS skill set is particularly useful in evaluating unstable patients for whom transport for imaging may be precarious. Bedside ultrasound can be used to evaluate RV function with modest sensitivity and moderate to high specificity for the diagnosis of PE in the appropriate clinical context. In a meta-analysis examining the utility of ultrasonography in patients who presented with a clinical picture concerning for PE, an elevated RV end-diastolic diameter (>3.0cm) and a reduced tricuspid annular plane systolic excursion (normal >1.60) in the apical four-chamber view had the greatest sensitivity (86% and 61%, respectively) with moderate specificity (80% and 60%, respectively) for PE.1 Other bedside derived echocardiographic assessments, such as McConnell’s sign (RV dysfunction with akinesia of the mid free wall and hyperkinesia of the RV apex), abnormal interventricular septal motion, defined as bowing of the septum into the left ventricle (LV) on apical four-chamber or flattening of septum on parasternal short axis, and a RV:LV ratio >1, were shown to have poor sensitivity (22-55%) but high specificity (89-97%) for PE.1
Figure 1: Bedside echocardiography in the parasternal short axis (A&B) where the probe is positioned at the left sternal boarder around the second intercostal space, perpendicular to the chest wall with the indicator to the left shoulder. In the parasternal short axis, imaging at the level of the papillary muscles (white asterisks) allows for accurate assessment of ventricular function. The interventricular septum flattens during diastole (A) and systole (B), indicative of right ventricular (RV) volume and pressure overload, respectively. Images C&D depict the apical four chamber views where the probe is positioned at the xiphoid level in mid clavicular line, angled towards the patient’s right flank, with the indicator to the patient’s left. In the apical 4 chamber view as shown, the interventricular septum should be midline (black asterisk) and the free wall of the left ventricle (LV) should be visible to allow one to correctly estimate ventricular size. The RV:LV ratio (measured at the base) is greater >1:1, with the RV dominating the apex (C&D), both of which are suggestive of RV strain. Normal RV:LV ratio is ~0.6:1.
It is important to note that POCUS identifies right heart dysfunction, which can be a surrogate for PE. Moreover, the above findings are more likely to be seen in patients with larger, hemodynamically significant PEs.1 Thus, echocardiography should never be used in isolation to rule out a PE. Clinicians must consider the patient’s pre-test probability when performing POCUS, as echocardiography has limited sensitivity, and multiple factors, such as chronic lung disease, can cause pre-existing right heart strain. However, trauma patients are at an increased for venous thromboembolic events (VTE),2,3 and the incidence of post-traumatic PE in TBI has been reported to range from 0.1-6.0%.2 Though the pathophysiology is incompletely understood, experts suspect a combination of endothelial injury, enhanced inflammatory state, and prolonged immobility contribute to VTE in TBI and trauma.4 Given the increased incidence of PE in TBI, providers should maintain a high index of suspicion for this condition.
Video 1
Parasternal short axis at the level of the papillary muscles showing septal flattening or “D” sign during systole and diastole, indicating RV pressure and volume overload respectively.
Video 2
Apical four-chamber view with the interventricular septum midline and the LV free wall visible to allow for correct approximation of ventricular size. The RV:LV ration exceeds 1:1 and RV dominates the apex, concerning for right heart strain.
References
- Fields JM, Davis J, Girson L, Au A, et al. A Systematic Review and Meta-Analysis. J Am Soc Echocardiography. 2017; 30(7):714-723. doi: 10.1016/j.echo.2017.03.004.
- Bahloul M, Chelly H, Regaieg K, et al. Pulmonary embolism following severe traumatic brain injury: incidence, risk factors and impact outcome. Intensive Care Med. 2017; 43(9)/ doi: 10.1007/s00134-017-4815-z
- Cook D, Meade M, Guyatt G, et al. Dalteparin versus unfractionated heparin in critically ill patients. N Engl J Med. 2011; 364(14):1305-14. doi: 10.1056/NEJMoa1014475.
- Hamada SR, Espina C, Guedj T, Buaron R, Harrois A, Figueiredo S, Duranteau J. High level of venous thromboembolism in critically ill trauma patients despite early and well-driven thromboprophylaxis protocol. Ann Intensive Care. 2017 Sep 12;7(1):97. doi: 10.1186/s13613-017-0315-0.