Πληροφορίες άρθρου


Asteriou Ch.
Barbetakis N.
Chatzinikolaou F.
Gogakos A. S.
Lazopoulos A.
Paliouras D.
Rallis Th.


The Greek E-Journal of Perioperative Medicine 2014; 12(a): 72-76




POSTED: 07/31/14 2:29 PM
ARCHIVED AS: 2014, 2014a, Παρουσίαση περιστατικού

DOI: The Greek E-Journal of Perioperative Medicine 2014; 12(a): 72-76



Syncope is a common complaint in clinical medical care. Except of neurological disorder, most of the patients havea brief benign clinical course with spontaneous recovery. Etiology may range from benign disorders to severe life-threatening diseases.Syncope as the leading symptom in patients suffering from intrathoracic neoplasm is uncommon. A rare case of a giant pleural solitary fibrous tumor causing recurrent episodes of syncope is presented. Diagnostic considerations and therapeutic strategy are discussed.


Syncope is a common complaint in clinical medical care. It is defined as the transient loss of blood flow to the brain, secondary to hypo-tension after excessive vasopressor reflex. Drop in blood pressure caused by bradycardia or asystole results in transient conscious loss. In most cases syncope lasts for seconds to mi-nutes with spontaneous recovery, characterized by benign clinical course. Etiology includes a variety of disorders and although an extensive evaluation is always undertaken, it is difficult to identify its cause. A case of a solitary fi-brous pleural tumor associated with recurrent episodes of syncope is presented.


A 45 year-old male was admitted to our De-partment complaining for sudden conscious loss lasting 2-3 minutes with spontaneous recovery during last month. All the episodes oc-curred while being on ordinary activity. The patient experienced visual field darkness fol-lowed by cold sweat, vertigo and finally syn-cope. Findings on physical examination of he-art, lungs, abdomen and neurological system were normal. His medical record was clear without referring chest pain, shortness of bre-ath, or palpitation before the episodes. Blood glucose, electrolytes as well as the rest blood chemistry results were found within normal bounds. A carotid sinus test assessed by caro-tid massage did not produce syncope or pre-syncope.

Non-specific findings on electrocardiography study were recorded. However, transthoracic echocardiography revealed compression of the left cardiac chambers by an intrathoracic mass without intracardiac thrombus, emboli or peri-cardial effusion. Chest x-ray showed a large le-sion occupying almost completely the left pleural cavity (Figure 1). Chest Computed To-mography (CT) scans brought to light a giant tumor of the left hemithorax compressing both the left lung and heart without discrete media-stinal lymphadenopathy (Figure 2). The rest staging imaging studies [abdomen CT scans, brain Magnetic Resonance Imaging (MRI) and bone scan were negative for possible metasta-tic disease.

Figure 1. Chest x-ray depicting a large lesion occupying the left hemithorax.

Figure 1. Chest x-ray depicting a large lesion occupying the left hemithorax.


Figure 2. Chest Computed Tomography revealing a giant intrathoracic mass in the left pleural cavity. Compression of the left lung and heart is clearly indicated.

Figure 2. Chest Computed Tomography revealing a giant intrathoracic mass in the left pleural cavity. Compression of the left lung and heart is clearly indicated.

The patient underwent a left posterolateral tho-racotomy and complete excision of the tumor was achieved. Intraoperative findings were consistent with a large tumor originating from the parietal pleura and attaching with an adhe-sion to the visceral pleura of the left upper lo-be. The tumor was encapsulated without inva-ding the lung, heart or great vessels and remo-ved easily. Pathological diagnosis of a solitary pleural fibrous tumor with benign characteri-stics was reached (Figure 3).

Figure 3. Pathologic specimen. Tumor’s dimensions: 24x15x11cm.

Figure 3. Pathologic specimen. Tumor’s dimensions: 24x15x11cm.

Postoperative period was uneventful. Close one-year follow-up was negative for recurren-ce of syncope.


Syncope as the initial symptom regarding pati-ents with intrathoracic neoplasm is rare. In most published cases, it is associated with the presence of mediastinal tumors. The cause of syncope is related to pulmonary arteries or car-diac involvement. Pulmonary embolism, cardi-ac arrhythmia or pulmonary artery hypertensi-on appear as the possible mechanisms1.

A reduction of cardiac output by decreased ve-nous return could also induce syncope2. Glos-sopharyngeal syncope associated with tumor of the oropharynx or base of the skull has been demonstrated3. Neurally mediated syncope can be directly induced by an intrathoracic lesion stimulating the vagus or phrenic nerve4,5. Neu-rocardiogenic syncope is characterized by syn-copal episodes that are typically related to or-thostatism. The underlying mechanism may be suggested by the clinical history, but recently the mechanism has been found to be reliably documentable with the head-up tilt test4. Syn-cope usually is caused by a primary drop in blood pressure, by bradyarrhythmias or asysto-le, or by a combination of these complications. Resumption of the supine position typically re-solves the syncope and restores normal hemo-dynamic parameters.

Stimulation leading to syncope due to malig-nancy can be either mechanical or chemical6. The majority of these syndromes are seconda-ry to constitutional factors related to baseline hypotension, vagal hyperactivity, or, most fre-quently, an excessive vasodepressor reflex, o-riginating in the emptying but hypercontractile left ventricle. Most cases can be improved symptomatically by pharmacologic means (metoprolol, disopyramide, mineral cortico-ids), atrioventricular pacing, or both4,6. Para-neoplastic syndromes are infrequent and can involve any part of the nervous system, being degenerative, demyelinative, inflammatory, or necrotizing in nature7. They are associated wi-th certain malignant neoplasms, specifically small cell carcinomas of the lung7. Usually neurologic symptoms precede tumor diagnosis by about 4 months. Autonomic dysfunction oc-curs in 10% of patients with paraneoplastic en-cephalomyelitis and sensory neuropathy8.In our case possible pathophysiological mecha-nisms include both compression phenomena and decreased venous return, as well as stimu-lation of the left vagus nerve.


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  Author Disclosures: Authors Rallis Th, Asteriou Ch, Lazopoulos A, GogakosAS, PaliourasD, Chatzinikolaou F, Barbetakis N have no conflicts of interest or financial ties to disclose.

Corresponding author:
Christos Asteriou,
Al. Symeonidi 2, 54007,
Thessaloniki, Greece.
tel: +302310898314,
fax: +302310845514

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