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Point-of-Care Ultrasound in the Periarrest Setting—Lessons Learned: A Case Report

Juhl-Olsen, Peter, MD, PhD*,†; Aagaard, Rasmus, MD‡,§; Jeppesen, Anni, Nørgaard, MD, PhD*

doi: 10.1213/XAA.0000000000000678
Case Reports
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Point-of-care ultrasound may elucidate reversible causes of cardiac arrest, and its use is supported by international guidelines in the periarrest setting. We present a case in which the treatment of cardiac arrest caused tension pneumothoraces and cardiac tamponade by pneumopericardium. Both pneumothorax and tamponade were expected to be identified with ultrasound, but were not. Subcutaneous emphysema precluded the diagnosis of pneumothorax. Cardiac imaging was false negative for tamponade, because the latter was caused by air and not fluid. Diagnoses are not to be excluded with inconclusive point-of-care ultrasound examinations, which should prompt further clinical evaluation and imaging.

From the *Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus N, Denmark

Department of Clinical Medicine, Aarhus University, Aarhus C, Denmark

Department of Emergency Medicine, Aarhus University Hospital, Aarhus C, Denmark

§Department of Anesthesiology, Randers Regional Hospital, Randers NØ, Denmark.

Accepted for publication October 9, 2017.

Funding: None.

The authors declare no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website.

This case was presented at the Society of Critical Care Medicine’s annual meeting, January 24, 2017, Honolulu, HI, as a short verbal presentation.

Address correspondence to Peter Juhl-Olsen, MD, PhD, Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Palle Juul-Jensens Blvd 99, 8200 Aarhus N, Denmark. Address e-mail to peter.juhl-olsen@clin.au.dk.

Written consent has been obtained from the patient’s next of kin for publishing this case report. Point-of-care (POC) ultrasound is disseminating rapidly into clinical practice and is widely used in the fields of emergency medicine, anesthesiology, and critical care. A major indication for POC ultrasound is circulatory failure.1 Ultimate circulatory failure is cardiac arrest, and in this setting, POC ultrasound of the heart2 and lungs3 may elucidate reversible causes including cardiac tamponade, pulmonary embolism, and pneumothorax.4 Thus, POC ultrasound is supported both during cardiac arrest and after return of spontaneous circulation in the previous 2010 International Liaison Committee on Resuscitation guidelines as well as in the updated 2015 version5,6 as an adjunct to a thorough physical examination including auscultation. Whereas a physical examination can be performed by all physicians, the application of POC ultrasound in this time critical scenario is relatively new to most physicians. Few physicians have achieved substantial experience with its use, and it is a challenge to balance this against the potential diagnostic yield. This case report describes some of the pitfalls and diagnostic ambiguities encountered when using ultrasound in the periarrest setting.

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CASE STORY

An 87-year-old previously healthy man developed cardiac arrest in his home. Basic life support was initiated by family members and was continued when the primary ambulance arrived 6 minutes later (12:26 PM). The initial rhythm was asystole changing into a broad-complex pulseless electrical activity 7 minutes later (12:33 PM). A physician-staffed ambulance arrived within 30 minutes and administered a single dose (1 mg) of epinephrine intravenously, achieving return of spontaneous circulation at 1:03 PM. The initial blood pressure was 102/81 mm Hg, the electrocardiogram showed atrial fibrillation and right bundle-branch block, and the end-tidal carbon dioxide pressure was 4.67 kPa after intubation. En route to the hospital, mechanical compressions (LUCAS 2; Physio-Control, Lund, Sweden) were initiated repeatedly and titrates of epinephrine were administered due to very low blood pressure that was deemed incompatible with sufficient circulation. The patient arrived at the hospital at 1:34 PM where a coronary angiogram revealed a culprit lesion in the right coronary artery. A plain balloon angioplasty was performed with a good angiographic result. Subsequently, the patient’s blood pressure remained critically low despite bolus doses of epinephrine of up to 1 mg each. A renewed angiogram revealed reocclusion of the right coronary artery and a stent was placed, but the blood pressure did not increase subsequently. A physical examination revealed distant respiratory sounds and palpatory instability of the upper right-sided thorax compatible with multiple anterior rib fractures. There were no subcutaneous crackles and no apparent distension of the jugular veins. The respiratory-inspiratory pressure remained below the alarm threshold of 40 cm H2O. Special attention was given to lung expansion on the continuous x-ray examination (horizontal position) in the anterioposterior projection performed during the angiogram, but no pneumothorax could be identified. The abdomen was distended. In search of an explanation, a POC ultrasound examination was performed using a Vivid i ultrasound machine and an M3S cardiac probe (GE Healthcare, Horten, Norway) by the treating critical care physician. Subcostal cardiac ultrasound performed by a specialist in cardiology showed normal left ventricular ejection fraction and interventricular cavity size relationship. A critical care physician initiated an ultrasound evaluation of the lungs and right abdominal side. The critical care physician has >8 years of experience with POC ultrasound and regularly teaches courses on the subject nationally and internationally; however, no recognizable structures including the pleural line, diaphragm, and liver could be revealed. This puzzled the observers. Other abdominal views were inaccessible due to sterile dressings applied for the transfemoral coronary angiography.

An arterial blood sample revealed a slight metabolic acidosis (pH 7.29, lactate 11.9 mmol/L) and anemia (hemoglobin 5.2 mmol/L). Due to the patient’s unstable condition and the abdominal distension, abdominal trauma and hemorrhage secondary to automated external chest compressions were suspected, and blood products were ordered and infused, but without effect on the blood pressure.

Figure 1

Figure 1

Figure 2

Figure 2

As a last resort, the patient was rushed to a computed tomography scan (3:42 PM) revealing significant pneumopericardium, large bilateral pneumothoraces, and subcutaneous emphysema (Figure 1). No abdominal hemorrhage was seen. Chest tubes were inserted in both pleural cavities, but the circulation did not restore and the patient died a few hours later in multiorgan failure. Please see Figure 2 for a timeline of the case.

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DISCUSSION

The patient undoubtedly remained in circulatory failure, despite coronary reperfusion and high doses of epinephrine, due to tension pneumothoraces and cardiac tamponade. Both constitute well-known reversible causes of circulatory failure and cardiac arrest,7 but these conditions in this case were not identified by specialists in cardiology and critical care. Pneumothoraces may be difficult to see with x-ray,8 especially in the supine position, but both pneumothorax and cardiac tamponade are expected to be disclosed with ultrasound. In this case, these were not detected despite the sonographers’ considerable experience with POC ultrasound.

Pneumothorax can be ruled out with a very high negative predictive value if one of several signs is seen with ultrasound. These signs include pleural sliding,9 B-lines (comet tails),10 and lung pulse,11 which all rely on the juxtaposition of both parietal and visceral layers of the pleurae. However, in this case, the absence of these signs could not be determined because air in the subcutis reflected ultrasound beams and constituted an effective barrier for visualization of deeper structures. Subcutaneous emphysema also precluded evaluation of any intraperitoneal fluid. Please see Supplemental Video File 1 (Supplemental Digital Content 1, http://links.lww.com/AACR/A142, showing an experimental cine loop of the liver, diaphragm with pleural sliding clearly visible) and Supplemental Video File 2 (Supplemental Digital Content 2, http://links.lww.com/AACR/A143, showing an experimental cine loop of the same anatomical location, but after injection of 10 mL of air into the subcutis). Cine loops from the actual patient case were regrettably not stored despite current recommendations.12 Storage would have furthered subsequent review and quality assurance.

Fluid in the pericardium that causes tamponade is often easily identified with ultrasound as a uniform black mass surrounding the heart. In contrary, ultrasonographic signs of pneumopericardium are highly elusive. When air accumulates in the anterior part of the pericardium, myocardial visualization is hindered as air becomes interpositioned between the ultrasound probe and the myocardium. However, if the air is dispersed during expansion in diastole, the myocardium may be seen in a cyclic manner with structures being visible in diastole, but not in systole. This phenomenon is termed as the air gap sign.13 Although several case stories testify to its clinical presence,14,15 the diagnostic performance of the air gap sign has not been reported and it is likely missed, especially in time critical scenarios such as the pericardiac arrest setting. Imaging of the inferior vena cava may have yielded a distended vein with no respiratory fluctuation compatible with obstructive shock, although recent, albeit experimental, studies have shown that right-side dilation may also occur in hypoxia and hypovolemia.16,17

Furthermore, this case highlights the significance of a multimodal approach to elucidate reversible causes of circulatory failure or cardiac arrest. During severe hemodynamic compromise, POC ultrasound examination, continuous x-ray, and auscultation were inconclusive in regard to pneumothorax. It cannot be ruled out that this critical diagnosis might have been revealed if even further attention had been payed to classical clinical signs of tension pneumothorax such as jugular vein distension, the presence of high ventilator inspiratory pressures, or lung percussion. In analogy, tamponade remains a clinical diagnosis and a negative cardiac ultrasound, even when conducted by a specialist, does not exclude tamponade regardless of the etiology being gas or fluid.18 Inconclusive POC ultrasound examinations are to be expected in critical care and should prompt further imaging modalities if available, but not delay clinical decision making.

In conclusion, the patient probably developed cardiac arrest from coronary occlusion, but likely eventually died of tension pneumothoraces and cardiac tamponade. Diagnosis of reversible causes was attempted with POC ultrasound, but subcutaneous emphysema precluded evaluation of the pleura and abdomen, whereas cardiac imaging provided a false-negative result for tamponade. This case highlights important limitations of an otherwise powerful diagnostic modality in the periarrest setting that are relevant to all clinicians working with patients in circulatory failure. Especially, the presence of subcutaneous emphysema and pneumothorax should be suspected if no recognizable structures including the pleural line, diaphragm, and liver can be visualized with ultrasound.

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DISCLOSURES

Name: Peter Juhl-Olsen, MD, PhD.

Contribution: This author helped acquire data and draft the manuscript.

Name: Rasmus Aagaard, MD.

Contribution: This author helped interpret the data and revise the manuscript.

Name: Anni Nørgaard Jeppesen, MD, PhD.

Contribution: This author helped interpret the data and revise the manuscript.

This manuscript was handled by: Mark C. Phillips, MD.

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REFERENCES

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