Analgesia & Resuscitation : Current ResearchISSN: 2324-903X

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Case Report, Analg Resusc Curr Res S Vol: 2 Issue: 0

An Uncommon Cause of Pulmonary Embolism Leading to a Cardiac Arrest

Walid Trabelsi*, Chihebeddine Romdhani, Anis Lebbi, Imen Naas, Haythem Elaskri, Iheb Labbene and Mustapha Ferjani
Department of Anesthesia and Intensive Care, Tunisian Military Hospital, Tunis, Tunisia
Corresponding author : Walid Trabelsi
Department of Anesthesia and Intensive Care, Tunisian Military Hospital, Tunis, Tunisia
Tel: 00-216-24091983; Fax: 00-216-71391099
E-mail: [email protected]
Received: April 17, 2013 Accepted: July 23, 2013 Published: July 26, 2013
Citation: Trabelsi W, Romdhani C, Lebbi A, Naas I, Elaskri H, et al. (2013) An Uncommon Cause of Cardiac Arrest. Analg Resusc: Curr Res S1. doi:10.4172/2324-903X.S1-011


An Uncommon Cause of Pulmonary Embolism Leading to a Cardiac Arrest

Compression of pulmonary arteries caused by mediastinal lymphadenopathy is an uncommon cause of pulmonary embolism: it is important that it is diagnosed correctly because its treatment and prognosis are different from that of pulmonary embolisms. Herein, we report the case of a young man with unknown mediastinal sarcoidosis and massive lymphadenopathy, which caused external compression of the pulmonary artery and led to rapidly fatal acute heart failure secondary to a massive pulmonary embolism.

Keywords: Sarcoidosis; Acute heart failure; Echocardiography


Sarcoidosis; Acute heart failure; Echocardiography

Case Report

A 23-year-old male, with no previous medical history, was admitted into the Department of Internal Medicine for deep-vein thrombosis of the left upper limb. He was a young military recruit and showed no symptoms except for having mild exertional dyspnea for 1 year. A Doppler ultrasound showed a thrombus in the left basilic vein, which confirmed the diagnosis and an etiological research was commenced (including for cancer, antiphospholipid syndrome, and for inflammatory, autoimmune, or inherited diseases (antithrombin deficiency, protein C, and protein S deficiency).
After two days of receiving curative unfractionated heparin at an initial dose of 80 UI/kg body weight as a bolus, followed by infusion of 18 U/kg per h, the patient suffered severe dyspnea. A chest x-ray showed a bilateral hilar and mediastinal enlargement, reticulonodular opacities and cardiomegaly (Figure 1). A full blood count and serum biochemistry were normal, except for D-dimer, which was high (3500; normal range <500).
Figure 1: Chest X-ray showing mediastinal lymphadenopathy and cardiomegaly.
A chest CT-scan and arteriography of the pulmonary vessels showed bilateral pulmonary embolisms with occlusion of the right pulmonary artery and the left posterior pulmonary artery, in addition to a hypodense mediastinal mass that encompassed the mediastinal vessels with multiple paratracheal and paravertebral lymph nodes (Figure 2 and Figure 3).
Figure 2: Non-contrast helical CT showing mediastinal paratracheal adenopathy (arrows). Small bilateral pleural effusions are also seen.
Figure 3: A) CT arteriograph showing occlusion of the right pulmonary artery due to external compression from a mass (white arrow). B) The left pulmonary artery is nearly completely occluded from the lymph-node mass (red arrow). Extensive mediastinal lymphadenopathy was also seen.
The patient was transferred to the Pulmonology Department, and a transthoracic echocardiograph showed normal left-ventricular (LV) function (LV ejection fraction, calculated using the modified Simpson’s rule, was equal to 55%), a severely dilated right ventricular (end-diastolic right-ventricular diameter of 80 mm/10 mm, and an end-diastolic left-ventricle diameter of 42 mm); a flat inferior vena cava with no respiratory variability and a diameter of 29 mm; Figure 4) and a tricuspid regurgitant jet velocity of 4.75 m/s (Figure 5). Also noted, was a high estimated pulmonary pressure of 105 mmHg (central venous pressure measured with a central-vein catheter at 25 mmHg). The patient also had abundant ascites, portal hypertension, and moderately bleeding esophageal varices as assessed by esophogastro- duodenal endoscopy.
Figure 4: Longitudinal view of the inferior vena cava.
Figure 5: Tricuspid velocity regurgitation.
Because of the presence of mediastinal lymphadenopathy, a mediastinoscopic and anatomopathological examination was performed (Figure 6). Based on clinical, radiological, and pathological findings, a diagnosis of lymphadenopathy sarcoidosis was made and intravenous corticotherapy (methylprednisolone 1 mg/kg daily) was started.
Figure 6: Histology images (intermediate-power; 400×) of a specimen from the lymphadenopathy biopsy. It showed well-formed, non-necrotizing epithelioid granuloma.
After being hospitalized for 4 days, the hemodynamic status of the patient worsened, with a sudden cardiac arrest caused by acute right-heart failure. In the intensive care unit, a Swan–Ganz catheter was applied and measured the following data: right atrial pressure of 41 mmHg, an end-diastolic right-ventricular diameter of 21 mm, systolic arterial pulmonary pressure of 120 mmHg, and a cardiac index of 0.9 L/min/m2. Also noted was the paradoxical motion of the interventricular septum, as assessed by transthoracic echocardiography (Figure 7 and Figure 8).
Figure 7: Parasternal short-axis view at the papillary-muscle level during cardiac systole.
Figure 8: Parasternal short-axis view at the papillary-muscle level during cardiac diastole.
The patient died a few hours later despite receiving cardiac vasopressors, NO, corticosteroids, and sildenafil.


Sarcoidosis is asymptomatic in 50% of cases. Its prevalence, incidence, and severity disease are higher among black patients (39 cases per 100,000 in black women vs. 12.1 in white women) [1]. Several hypotheses have been suggested for the association between sarcoidosis and a pulmonary embolism (PE). It could be a result of compression caused by extrinsic lymphadenopathy. Indeed, in sarcoidosis type I, bilateral lymphadenopathy may compress the tracheo-bronchial tree, but also may affect a vascular tree that has a perfusion defect [2].
Goffman et al. have reported on a patient with mediastinalpulmonary sarcoidosis, which was identified as an infusion disorder by scintigraphy with no ventilation disorder [3]. These authors considered a diagnosis of PE, but an angiograph found extrinsic compression without a defect in the vascular lumen (in contrast to our case where an intra-arterial thrombus was seen). This is why we started our patient on steroids and anticoagulant therapy, in contrast to Goffman et al.’s study where only steroids were given.
Thrombosis, secondary to vascular granulomas, has been described in sarcoidosis [4]. One study reported on 128 biopsies performed in patients with sarcoidosis [5]. A breach of the pulmonary vessel was found in 88 samples (69%). Of these positive samples, venous involvement was the most frequent incident (92%), it was isolated in 61% of cases, and was associated with arterial disease in 31%. Only 8% of the samples showed arterial disease alone.
In-hospital cardiac arrests (IHCA) are a relatively common occurrence: their reported incidence varies, but occurs within the range of 1–5 per 1000 admissions [6]. The European Resuscitation Council defines several causes for this event; some cases of are reversible and are often referred to as the six H’s (hypoxia, hypovolemia (associated with trauma, anaphylaxis, sepsis), hyperkalemia, hypokalemia, hypocalcemia (and other metabolic abnormalities) and hypothermia; and the four T’s: thrombosis (coronary or pulmonary), tamponade (cardiac), toxins, and tension pneumothorax) [7]. Theses causes can be treated and, thus, many patients recover. However, in our case, we think that death was the consequence of an “untreatable” etiology of PE (sarcoidosis). This represents a new facet to practitioners, if treatable causes of cardiac arrest are secondary to a non-treatable etiology.

Funding Source

Financial support was provided by departmental and institutional funding from the Tunisian Military Hospital.


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