Differential diagnosis between traumatic tricuspid regurgitation and infectious endocarditis

In the event of blunt chest trauma, identifying a mobile mass on the tricuspid valve presents the clinician with a dilemma: distinguishing infectious vegetation from a traumatic structural lesion. This case report documents the management of a patient in his sixties, suffering from pulmonary sarcoidosis, admitted after a five-meter fall that caused multiple fractures. Transthoracic echocardiography revealed a 7 mm mobile structure on the anterior tricuspid leaflet, associated with a flail motion and severe tricuspid regurgitation (TR).

The objective of this study is to illustrate the complexity of differential diagnosis when the clinical picture is obscured by a febrile state suggesting infective endocarditis (IE). The investigation is based on a traumatic etiological hypothesis — papillary muscle rupture — whose echocardiographic manifestations mimic endocardial vegetations with misleading precision. This case highlights the need for an exhaustive evaluation, including blood cultures and histopathological analysis, to rule out infection and guide towards surgical valve repair. The stakes are high: avoiding unjustified antibiotic therapy and preventing progression to long-term heart failure through targeted structural intervention.

Diagnostic pathway and intervention strategy

This case report describes the management of a male patient in his sixties, suffering from pulmonary sarcoidosis, admitted after a 5-meter fall resulting in multiple fractures. The diagnostic and therapeutic protocol was structured around the following steps:

• Initial evaluation: A transthoracic echocardiography (TTE) identified a 7 mm mobile structure located on the anterior tricuspid leaflet, associated with a flail movement and severe tricuspid regurgitation (TR).
• Clinical differentiation: In the presence of a febrile state, the hypothesis of infectious endocarditis (IE) was explored. The exclusion of IE was confirmed by negative blood cultures and complementary investigations, directing the diagnosis towards a traumatic rupture of the papillary muscle.
• Surgical protocol: The procedure was deferred for 4 months to allow for the consolidation of orthopedic repairs. The surgery consisted of a tricuspid valve repair through the implantation of artificial chords and annuloplasty.
• Pathological analysis: The ruptured papillary muscle was harvested for examination. The analysis looked for signs of inflammatory infiltration or coagulation necrosis to confirm the etiology.
• Postoperative follow-up: Hemodynamic stability and the absence of heart failure were evaluated over a 4-year period.

Clinical results and diagnostic investigations

Initial evaluation by transthoracic echocardiography (TTE) revealed a 7 mm mobile structure located on the anterior leaflet of the tricuspid valve. This mass, associated with a flail motion, resulted in severe tricuspid regurgitation (TR). Although a febrile state initially suggested a diagnosis of infectious endocarditis (IE), further investigations disproved this hypothesis.

Surgical confirmation and histopathological analysis

The surgical intervention was deferred for four months to allow for the consolidation of the patient's multiple fractures. Intraoperative findings confirmed the rupture of the papillary muscle, validating the traumatic etiological diagnosis. The repair strategy relied on two main techniques:

• Implantation of artificial chordae ;
• Tricuspid annuloplasty.

The histopathological examination of the ruptured papillary muscle revealed coagulation necrosis. The absence of significant inflammatory infiltration during this analysis definitively excluded an infectious origin in favor of a purely traumatic etiology following the blunt chest trauma.

Evolution and long-term follow-up

The patient remained hemodynamically stable under medical treatment during the preoperative phase. Following the valve repair surgery, the postoperative course was favorable. At the end of a 4-year follow-up, the patient remains stable, with no signs of heart failure exacerbation or recurrence of tricuspid regurgitation.

The diagnostic challenge: when trauma mimics endocarditis

This clinical case illustrates the complexity of differential diagnosis when faced with a mobile valvular mass following blunt chest trauma. The presence of a 7 mm structure on the anterior tricuspid leaflet, associated with severe tricuspid regurgitation (TR) and a febrile state, initially suggested infectious endocarditis (IE). The clinical challenge here is significant: diagnostic confusion can lead to unnecessary antibiotic therapy or delay necessary surgical management.

Negative blood cultures and additional investigations allowed the exclusion of an infectious cause in favor of a traumatic papillary muscle rupture. A key point of this study lies in the histopathological analysis of the ruptured papillary muscle, which revealed coagulation necrosis without significant inflammatory infiltration, thus confirming the purely traumatic etiology of the lesion.

An efficient and delayed surgical strategy

Unlike acute IE, which sometimes requires rapid intervention, the patient's hemodynamic stability under medical treatment allowed surgery to be deferred for four months, providing time to consolidate the multiple fractures. The technical choice of valve repair using artificial chordae and annuloplasty proved to be durable, with clinical stability confirmed during the four-year follow-up. This observation suggests that valve reconstruction remains a robust option, even after a period of extra-cardiac healing.

Although this report concerns only a single patient (n=1), it highlights that imaging alone can be misleading. The post-traumatic mobile structure can perfectly simulate a vegetation, requiring a rigorous evaluation integrating lesional kinetics and biological markers.

In practical terms, for the practitioner:

• Diagnostic differentiation: In the presence of a post-traumatic mobile valvular mass, do not initiate probabilistic antibiotic therapy without blood culture results, as traumatic lesions visually mimic vegetations.
• Surgical strategy: A delayed intervention (here 4 months after the trauma) using artificial chords and annuloplasty allows for lasting hemodynamic stability, with satisfactory follow-up documented at 4 years.
• Preventive indication: Even in a hemodynamically stable patient under medical treatment, surgery must be discussed by the Heart Team to prevent long-term right heart failure.

Technical Lexicon of the Clinical Case

Tricuspid flail motion: Abnormal and excessive movement of a valve leaflet that swings into the right atrium during systole, indicating a loss of structural support (often due to chordal or papillary muscle rupture).

Papillary muscle rupture: Traumatic or ischemic rupture of the muscular pillars anchoring the valve chordae; in this case, a direct consequence of blunt chest trauma.

Coagulative necrosis: Type of accidental cell death characterized by the preservation of tissue architecture for several days, identified here by pathological examination to confirm traumatic rather than infectious origin.

Artificial chordae: Synthetic sutures (generally made of PTFE) used during valve repair to replace ruptured native chordae and restore leaflet coaptation.

Annuloplasty: Surgical technique consisting of remodeling and strengthening the tricuspid annulus, often using a prosthetic ring, to treat functional or traumatic valvular insufficiency.

Blunt chest trauma: Non-penetrating thoracic trauma (direct impact), here secondary to a 5-meter fall, capable of generating sudden deceleration forces on cardiac structures.

Papillary muscle rupture after chest trauma: the pitfall of pseudo-endocarditis

The differential diagnosis between traumatic tricuspid regurgitation (TR) and infective endocarditis (IE) constitutes an immediate clinical challenge in emergency or intensive care units. Blunt chest trauma can generate mobile valvular lesions mimicking infectious vegetations almost perfectly on echocardiography, sometimes directing the practitioner toward erroneous therapeutic strategies.

Clinical case: a suspicious mobile mass following a fall

A 60-year-old man, followed for pulmonary sarcoidosis, is admitted after a 5-meter fall resulting in multiple fractures. Preoperative transthoracic echocardiography (TTE) reveals a 7 mm mobile structure on the anterior tricuspid leaflet, associated with a flail motion and severe TR. The presence of a febrile state in this trauma patient initially led to a suspicion of infectious endocarditis.

However, repeated blood cultures and additional investigations allowed the infectious etiology to be excluded. The diagnosis refocused on traumatic MI due to papillary muscle rupture. Although the patient remained hemodynamically stable under initial medical treatment, the multidisciplinary team (Heart Team) recommended surgical intervention to prevent long-term heart failure.

Surgical strategy and anatomopathological confirmation

The procedure was deferred for four months, allowing time to stabilize the orthopedic lesions. The procedure consisted of a tricuspid valve repair through the implantation of artificial chordae and an annuloplasty. Intraoperative findings fully confirmed the imaging diagnosis.

The histopathological examination of the ruptured papillary muscle was decisive. It revealed coagulation necrosis without significant inflammatory infiltration. This result confirms the traumatic etiology (deceleration injury or sudden compression) and definitively rules out any infectious or inflammatory process related to sarcoidosis.

Follow-up and perspectives

Four years after the procedure, the patient remains stable, with no signs of heart failure exacerbation. This case demonstrates that conservative repair using artificial chordae, even when delayed, offers excellent durability for traumatic tricuspid lesions.

Specifically for the practitioner:
• In the presence of any post-traumatic mobile valvular mass, systematically consider a papillary muscle rupture before initiating empirical antibiotic therapy, even in the event of fever.
• Imaging must track the flail motion, a pathognomonic sign of structural rupture rather than a simple vegetation.
• Reconstructive surgery (chordae and annuloplasty) remains the gold standard to prevent long-term right ventricular remodeling.

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