Utilizing Point-of-Care Ultrasound for the Management of Massive Pulmonary Embolism in a Young Male: A Case Report

Abstract

Pulmonary embolism (PE) is a thromboembolic disorder characterized by obstruction of the pulmonary arterial circulation, most commonly due to embolization of thrombi originating from the deep venous system of the lower extremities. Massive PE is a critical condition marked by hemodynamic instability not caused by a new arrhythmia, cardiogenic shock, or circulatory collapse.

The patient is a 28-year-old male with no significant medical history who arrived at the Emergency Department with a self-inflicted neck wound. He received initial treatment, including securement of the airway, antibiotics, analgesia, and suturing. After neck exploration and tracheal repair, he was diagnosed with MRSA and ESBL + Klebsiella pneumoniae and treated with IV antibiotics. After 17 days of admission, the patient was discharged home but returned the same day with hypotension, shortness of breath, chest pain, and shock, with hypoxia. Point-of-care ultrasound (POCUS) revealed right ventricular dilatation suggestive of PE, which was finally confirmed with further testing. Echocardiogram confirmed substantial right ventricular and right atrial dilation with an estimated pulmonary artery pressure of 53 mm Hg and a positive McConnell's sign.

In conclusion, cardiac POCUS is a non-invasive, quick, and cost-effective imaging technique used in emergency settings to diagnose PE by identifying PE markers. This case report underscores the importance of POCUS in promptly diagnosing PE, emphasizing its role in preventing fatal outcomes due to delayed diagnosis.

Introduction

Pulmonary embolism (PE) is a condition where blood clots that arise from other areas of the body (most notably deep veins of the lower limbs) embolize to the pulmonary arteries, obstructing them and leading to a ventilation-perfusion mismatch [1]. In a minority of cases, embolism of fat, air, or tumor cells can cause PE, rather than blood clots [2]. In 2019, the incidence of PE in the United States was reported to be 120 per 100,000 [3]. In the same year, 393,000 individuals in the US were diagnosed with PE [3]. PE-related mortality is high, as it contributes to around 100,000 deaths annually in the US [4].

The most common symptoms of acute PE include dyspnea, pleuritic chest pain, hemoptysis, presyncope, and syncope in more severe cases [1]. Due to the nonspecificity of these symptoms, it is often challenging to diagnose PE. In addition to nonspecific symptoms, PE usually presents with nonspecific physical exam findings. Patients with acute PE may present with tachypnea or tachycardia, both nonspecific to PE [1]. Acute PE can manifest itself as sudden cardiac arrest in some patients. This occurs as a result of right heart strain due to PE (classified as massive PE), impairing left heart filling, resulting in low cardiac output and obstructive shock.

The gold standard for the diagnosis of PE remains computed tomography pulmonary angiography (CTPA), with a sensitivity of 83% and specificity of 96% in diagnosing PE [5]. However, CTPA still has its limitations in certain scenarios, particularly in settings where there are limited resources or when the patient is hemodynamically unstable [6]. Some of the limitations and challenges faced with CTPA include the limited availability and high cost, particularly in low-income countries, the challenge of transporting an unstable PE patient to the CT scan machine, and the risk of radiation in pregnant women [6]. This excludes the possible risk of nephrotoxicity due to the use of iodinated contrast material, especially in patients with baseline kidney impairment [7].

The occasional challenges and limitations faced when using CTPA to investigate PE prompt the need to identify a more readily accessible bedside investigation that can aid in diagnosing PE, especially in hemodynamically unstable patients or in poor-income areas. Point-of-care ultrasound (POCUS), a widely available and used method particularly in the Emergency Department (ED) setting, is a safe alternative that overcomes some of the mentioned limitations faced with CTPA, although it is less sensitive and specific than CTPA.

Diagnosing a pulmonary embolus using POCUS is notably challenging. In contrast to conditions such as pulmonary edema, pneumonia, or pleural effusion, the core issue in PE resides in the pulmonary arteries, which are not readily visible under normal circumstances. Nevertheless, by maintaining a high level of clinical suspicion, using a D-dimer test appropriately, and having an excellent understanding of the downstream effects of PE, clinicians can use POCUS to diagnose the condition with accuracy approaching that of CTPA [8].

Case presentation

A 28-year-old, previously healthy male with no significant past medical, surgical, or family history presented to the ED with a self-inflicted neck wound from a glass. On arrival, the patient was tachycardic, hypertensive, with a Glasgow Coma Scale of 11/15 and aphonic. On examination, an open transverse wound of the neck was noted, with the trachea being exposed and cut (Figure 1). The rest of the primary survey and other systems examination were unremarkable. Lab investigations are shown in Table 1. For initial management, the patient was intubated to secure his airway. The wound was approximated by suturing, followed by administration of analgesia, antibiotics, and tetanus toxoid. The patient was referred to the ENT & General Surgery services.

Table 1. Laboratory investigations on arrival to the ED.

ABG: Arterial Blood Gas; FBC: Full Blood Count; AST: Aspartate Aminotransferase; LFT: Liver Function Test; PT: Prothrombin Time; INR: International Normalized Ratio; ALT: Alanine Transaminase

Tests	Patient’s values	Reference range
ABG	pH 7.32	7.35-7.45
	PO2 282 mmHg	83-108 mmHg
	CTHB 11.7 g/dl	13.0-18.0 g/dl
	SO2 100.2	95-99%
	Cl 105 mmol/L	95-108 mmol/L
	Glucose 147 mg/dL	60-100 mg/dL
FBC	RBC count 3.86 x 106/uL	4.50-5.50 x 106/uL
	Hb 11.8 g/dL	13.0-17.0 g/dL
	Hematocrit 35.1%	40.0-50.0 %
	Absolute neutrophil 8.6 x 103/uL	2.0-7.0 x 103/uL
	Absolute monocyte 1.20 x 103/uL	1.0-3.0 x 103/uL
Urea & Electrolytes	HCO3 19.5 mmol/L	20-28 mmol/L
	Urea 78 mg/dL	12-40 mg/dL
	Anion gap 17 mmol/L	6-14 mmol/L
Blood Creatinine	1.57 mg/dL	0.7-1.2 mg/dL
AST	172 U/L	0-40 U/L
LFT	Bilirubin 1.38 mg/dL	0-1   mg/dl
	ALT 134 U/L	0-41 U/L
	Globulin 3.6 g/dL	2.8-3.4 g/dL
PT INR	PT 15.2 sec	12.2-14.6 secs
	INR 1.18	0.8-1.1

Figure 1. Open transverse neck laceration (arrow) with exposure and laceration of the trachea.

A polytrauma computed tomography (CT) scan protocol including brain, cervical spine, facial bones, chest, abdomen, pelvis, and dorsolumbar spine and pelvic bones was performed. The sagittal film of the cervical spine revealed pre-tracheal subcutaneous emphysema consistent with the mechanism of injury (Figure 2). A significant surgical emphysema in the cervical region was seen (Figure 3). The coronal CT scan of his chest (Figure 4) revealed bilateral multifocal predominantly centrilobular ground-glass opacification in all lobes of both lungs, which may be the result of a hemorrhage or aspiration. However, a contusion was not ruled out. A coronal CT scan of the neck also revealed evidence of pneumomediastinum (Figure 3).

Figure 2. Sagittal plane of the CT scan of the cervical spine demonstrating evidence of subcutaneous emphysema in the pre-tracheal area (yellow arrows) consistent with the penetrating injury mechanism.

Figure 3. Coronal plane of the CT scan of the neck revealing surgical emphysema at the site of laceration (blue arrows) and evidence of pneumomediastinum (yellow arrows).

Figure 4. Coronal CT scan of the lungs with contrast revealing centrilobular ground-glass opacification in all lobes (black arrows).

He was admitted under the General Surgery team as a case of deep self-inflicted anterior neck laceration in need of neck exploration & tracheal wound repair by the ENT service. A four-centimeter horizontal deep cut wound in the neck at the level of the upper part of the trachea, inferior to the cricoid cartilage, was discovered. Therefore, he was transferred to the Intensive Care Unit and remained intubated for seven days following the exploration. Respiratory culture on day 3 was positive for Methicillin-resistant Staphylococcus aureus, and on day 7, confirmed extended-spectrum beta-lactamases positive Klebsiella pneumoniae. A chest X-ray (CXR) done on day 11 demonstrated multifocal pneumonitis in the lungs bilaterally (Figure 5). After seven days of intravenous meropenem and linezolid, the patient improved clinically, and a CXR showed resolution of alveolar shadowing.

Figure 5. Chest X-ray demonstrating multifocal pneumonitis (black arrows) in both lungs.

A psychiatric evaluation performed after improvement revealed that he was suffering from major depression and chronic alcohol use. The patient was discharged on day 17 in a stable condition with instructions to follow up in the ENT clinic after two weeks.

On the same day of discharge, the patient returned to the ED with sudden shortness of breath with mild pleuritic chest pain associated with sweating and palpitations. On arrival, he had sinus tachycardia at a rate of 153 beats per minute, blood pressure of 88/76 mmHg, tympanic temperature of 36.3 °C, respiratory rate of 28 per minute with accessory muscle usage, and oxygen saturation of 84% on room air. The electrocardiogram indicated sinus tachycardia along with features suggestive of right bundle branch block (Figure 6). Laboratory investigations (shown in Table 2) revealed leukocytosis, thrombocytosis, slightly deranged ALT, and prolonged INR. His blood pressure and tachycardia did not improve with a fluid bolus and norepinephrine. A POCUS study was performed, which detected right ventricular dilatation and D sign on short axis with no tension pneumothorax. An echocardiogram revealed intact left ventricular function but a substantially dilated right ventricle and right atrium, with an estimated pulmonary pressure of 53 mmHg and a positive McConnell's sign (Video 1). A CXR showed normal heart size with both lungs, domes of the diaphragm and costophrenic angles being clear.

Table 2. Laboratory investigations on the second ED visit.

WBC: White Blood Cell; INR: International Normalized Ratio; ALT: Alanine Transaminase

Tests	Patient’s values	Reference range
WBC	25.7 x 103 U/L	3.6-11.0 x 103 U/L
Platelet count	575 x 103 U/L	150-410 x 103U/L
INR	1.13	0.8-1.1
ALT	175 U/L	0-41 U/L

Figure 6. ECG on second ED arrival demonstrating sinus tachycardia and a right bundle branch with a wide QRS complex duration (black lines), RSR' pattern in the V1 lead (black arrows), and wide, slurred S waves in lateral leads (violet arrows).

Video 1. Point-of-care ultrasound findings in pulmonary embolism.

Download video file ^{(1.5MB, mp4)}

Point-of-care ultrasound performed in the setting of acute pulmonary embolism (PE) demonstrating an elevated right ventricle (RV)/left ventricle (LV) ratio on the long axis along with D-sign in the short axis evident from flattening and pushing of the interventricular septum towards the LV.

CTPA revealed filling defects at the major pulmonary artery bifurcation bilaterally, as well as saddle-type thrombosis, which spread to the superior, inferior, segmental, and subsegmental pulmonary artery branches, more severe in both the lower lobes (Figure 7). The right ventricle/left ventricle ratio was elevated at 2.2. The main pulmonary trunk appeared normal with no filling defect, both lungs were clear with no focal lesions, and no evidence of pleural effusion was noted. 

Figure 7. CTPA on second ED arrival revealing bilateral filling defects (yellow arrows) in the main pulmonary arteries extending into the branches.

CTPA: Computed Tomography Pulmonary Angiography

A diagnosis of PE was made. Thrombolytic treatment was initiated with a 15 mg bolus of alteplase followed by an infusion of 85 mg over two hours. A therapeutic dosage of enoxaparin sodium was given for 48 hours, which was followed by direct oral anticoagulation on day 3. He was discharged with 15 mg rivaroxaban twice daily for 21 days, followed by 20 mg for 3-6 months, and scheduled for a follow-up echocardiogram appointment at the outpatient clinic after a month.

Discussion

Massive PE is a life-threatening condition caused by an abrupt blockage in the pulmonary arteries of the lungs, which may lead to right ventricular failure and hemodynamic instability [9]. Immediate diagnosis and intervention are crucial as the morbidity and mortality rates of untreated massive PE rapidly escalate with time [10]. POCUS is a well-recognized tool that aids in the diagnosis of acute PE in patients with hemodynamic instability who are not suitable candidates to undergo CTPA [9]. Therefore, this substantial tool leads to considerable acceleration in tailoring prompt personalized interventions and suitable individualized treatments [11]. As such, POCUS makes invaluable contributions to emergency physicians and raises the bar for patient care by miles and bounds [10].

In suspected cases of massive PE, POCUS evaluations frequently identify various changes indicative of RV dysfunction or strain (Figure 8).

Figure 8. POCUS findings in massive PE.

Figure illustrating POCUS findings observed in massive PE. Photos adapted from the patient's POCUS exam

POCUS: Point-of-Care Ultrasound; PE: Pulmonary Embolism

Diagnostic accuracy and clinical implications

When combined, these sonographic findings with the concomitant clinical presentation provide a strong indication of a diagnosis of massive PE [12]. It has been reported in the literature that RV dysfunction identified via POCUS has as high a specificity as 94% for the diagnosis of PE [12].

The early identification can make these POCUS findings have critical clinical implications [11]. Also, they enable emergency teams to rapidly commence appropriate management, including anticoagulation and consideration for thrombolytic therapy or other interventions based on hemodynamic status [11].

Limitations and considerations

Though POCUS can be a significant tool in aiding to diagnose massive PE, it should be noted that the absence of these findings does not exclude the diagnosis [12]. Some patients may present with less obvious and atypical presentations, making a comprehensive clinical assessment, including risk factor evaluation, laboratory testing, and possibly advanced imaging, crucial in establishing the diagnosis [12]. Also, acute RV strain needs to be distinguished from chronic causes like pulmonary hypertension [11]. Determining RV free wall diameter by echo (> 5mm suggests chronic etiology) helps differentiate between these conditions [11].

Rush protocol

RUSH (Rapid Ultrasound for Shock and Hypotension) protocol is an ultrasound examination focused on determining the prevalent causes of shock or hypotension [13]. It checks through the heart, inferior vena cava, abdomen, and lungs to find out if there is any cardiogenic, hypovolemic, obstructive, or distributive shock [13].

Management - thrombolytics

For massive PE, patients receive thrombolytic therapy, which may also be considered for submassive PE that shows adverse clinical signs [14]. However, thrombolytics are not recommended in cases of minor RV impairment and low-risk PE [15]. Catheter embolectomy and fragmentation and surgical embolectomy can also be used in those cases when needed [15].

Conclusions

POCUS is a non-invasive imaging technique that plays an important role in the quick diagnosis and management of massive PE in ED settings, especially when other imaging methods may cause delays or hinder prognosis. It identifies PE through signs of right heart strain, such as right ventricular systolic dysfunction, a positive McConnell’s sign, and the presence of D-sign. POCUS will enable emergency physicians to make prompt diagnoses, allowing early intervention and improved prognosis while decreasing mortality rates by enhancing quality of life. Nonetheless, POCUS must also be seen within its limitations concerning complete clinical assessment to ensure accurate diagnosis of patients with optimal care.