Acute mediastinitis is a life-threatening infection; mediastinal masses are characterized by anatomic compartment and patient age.
Also known as: mediastinitis, mediastinal mass, anterior mediastinal mass, descending necrotizing mediastinitis, post-sternotomy mediastinitis
Overview
Mediastinitis: acute or chronic infection of mediastinal connective tissue, most commonly post-cardiothoracic surgery or following esophageal perforation. Fibrosing (sclerosing) mediastinitis is a rare chronic fibroinflammatory form, in the US usually an exaggerated host response to prior Histoplasma infection (less often TB), in which invasive fibrous tissue encases mediastinal vessels, airways, and esophagus. Mediastinal mass: any abnormal expansion of mediastinal tissue, categorized by ITMIG-defined compartments (prevascular [anterior], visceral [middle], paravertebral [posterior]).
Epidemiology
Post-sternotomy mediastinitis complicates ~1-3% of cardiac surgeries with mortality 10-25%. Descending necrotizing mediastinitis from oropharyngeal infection is rare but carries mortality up to 40%. Mediastinal masses are found on just under 1% of adult screening chest CTs, most often thymic lesions; distribution shifts by age — anterior masses dominate in adults, posterior in children.
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Question 1PulmonaryMedium
A 55-year-old man with a remote history of pulmonary histoplasmosis 10 years ago presents with 3 months of progressive dyspnea, dysphagia to solids, facial swelling, and distended neck veins. Exam shows facial plethora, dilated chest wall venous collaterals, and bilateral upper extremity edema. Chest CT reveals a calcified, infiltrative mediastinal mass encasing the superior vena cava and right mainstem bronchus with extensive mediastinal calcifications. Bronchoscopy with biopsy is nondiagnostic for malignancy. Which of the following is the most likely complication of his prior infection?
AChronic pulmonary aspergilloma of a residual cavity
BHistoplasma pericarditis with constrictive physiology
CFibrosing mediastinitis from prior histoplasma infection
DBroncholithiasis from calcified histoplasma lymph nodes
Why Fibrosing mediastinitis from prior histoplasma infection is correct
Fibrosing (sclerosing) mediastinitis is the most feared late complication of pulmonary histoplasmosis
It is thought to reflect an aberrant host immune response to Histoplasma antigens leaking from mediastinal lymph nodes, which drives exuberant fibrosis; the exact pathogenesis is unknown
The result is a calcified mediastinal mass that compresses central airways, great vessels, and the esophagus
It presents years after an often-unrecognized primary infection, with superior vena cava (SVC) syndrome, pulmonary hypertension from pulmonary artery/vein obstruction, or central airway obstruction
Calcified mediastinal lymphadenopathy with vascular encasement on CT is the classic imaging finding
Why the others are wrong
Chronic pulmonary aspergilloma of a residual cavity — aspergilloma colonizes prior histoplasma cavities but produces hemoptysis with a fungus ball within a cavity, not a calcified infiltrative mediastinal mass
Reactivation chronic cavitary pulmonary histoplasmosis — chronic cavitary histoplasmosis is a parenchymal process, usually in patients with underlying emphysema/COPD, with upper-lobe cavities, productive cough, fever, night sweats, and weight loss. A remote infection with new symptoms years later invites a TB-style reactivation reading, but every localizing finding here is extrinsic compression of the SVC, bronchus, and esophagus by a calcified mass, which signals scarring, not active cavitary infection
Histoplasma pericarditis with constrictive physiology — constriction elevates jugular venous pressure but produces lower extremity edema, hepatomegaly, and ascites; it does not encase the SVC or explain facial plethora, bilateral upper extremity edema, and chest wall venous collaterals. Constriction after histoplasma pericarditis is also rare
Broncholithiasis from calcified histoplasma lymph nodes — calcified histoplasma nodes can erode into an adjacent airway, and his calcified nodes and bronchial involvement make this tempting, but broncholithiasis presents with cough, hemoptysis, expectorated stones (lithoptysis), or postobstructive pneumonia from an intraluminal calcified node; it does not encase the SVC or compress the esophagus, so it cannot explain SVC syndrome and dysphagia
Additional high-yield points
Treatment is supportive: intravascular stents help selected patients with SVC or pulmonary artery/vein obstruction, while airway stents are generally avoided because of the high risk of granulation-tissue growth. Surgery is high-risk and reserved for otherwise fatal obstruction (IDSA 2007 histoplasmosis guideline)
Antifungals and corticosteroids have not been shown to reverse established fibrosis
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Posterior masses: neurogenic tumors (schwannoma, neurofibroma, ganglioneuroma, and neuroblastoma in young children with elevated urine VMA/HVA), spinal lesions, extramedullary hematopoiesis
Pathophysiology
Acute bacterial mediastinitis spreads rapidly along fascial planes due to negative intrathoracic pressure and continuous tissue communication. Common pathogens after sternotomy: Staphylococcus aureus (including MRSA), coagulase-negative staphylococci, gram-negatives. Descending necrotizing mediastinitis is typically polymicrobial with oral anaerobes (Bacteroides, Fusobacterium, Peptostreptococcus) and Streptococcus species. Mediastinal masses cause local compression (SVC syndrome, tracheal compression, dysphagia) and systemic effects (paraneoplastic syndromes).
Clinical presentation
Symptoms
Mediastinitis: fever, chest pain, tachycardia, sternal instability or drainage after sternotomy, neck swelling and odynophagia in descending forms
Esophageal perforation (Boerhaave) — Severe chest pain after forceful emesis, subcutaneous emphysema, pneumomediastinum on CT, left pleural effusion with low pH and high amylase
Thymoma — Anterior mediastinal mass in adult 40-60 y; associated with myasthenia gravis (~30-40%), pure red cell aplasia, hypogammaglobulinemia
Germ cell tumor — Young men 20-40 y; elevated AFP (yolk sac/nonseminoma), beta-hCG (choriocarcinoma); pure seminomas never elevate AFP (beta-hCG may be mildly elevated)
Lymphoma — B symptoms (fever, night sweats, weight loss), bulky bilateral lymphadenopathy, biopsy for histology
Substernal thyroid — Continuity with cervical thyroid on imaging, iodine uptake on scintigraphy
Neurogenic tumor — Posterior mediastinal mass, often pediatric or young adult; CT shows widening of intervertebral foramen
Fibrosing mediastinitis — Years after histoplasmosis (less often TB); CT shows a calcified, infiltrative mediastinal mass encasing the SVC, pulmonary arteries or veins, bronchi, or esophagus; presents with SVC syndrome, dyspnea, hemoptysis, dysphagia, or pulmonary hypertension; biopsy is negative for malignancy
Diagnostic workup
Diagnostic criteria
Post-sternotomy mediastinitis (CDC/NHSN criteria), any one of: (1) organism identified from mediastinal tissue or fluid; (2) evidence of mediastinitis on gross anatomic or histopathologic exam; or (3) fever >38.0°C, chest pain, or sternal instability PLUS purulent drainage from the mediastinal area or mediastinal widening on imaging.
Labs
CBC, CMP, lactate, blood cultures for suspected mediastinitis
Procalcitonin and inflammatory markers (CRP, ESR) for trending
Tumor markers for anterior mass in young men: AFP, beta-hCG, LDH
Anti-AChR and anti-MuSK antibodies if myasthenia gravis suspected
TSH for suspected substernal thyroid
Imaging
Contrast-enhanced CT chest is the cornerstone imaging study for both mediastinitis and mediastinal masses
CT signs of mediastinitis: fluid collections, pneumomediastinum, fat stranding, mediastinal widening; in post-sternotomy patients, sternal dehiscence and retrosternal collections
Water-soluble contrast esophagogram if esophageal perforation suspected, followed by barium if initial study negative
MRI for posterior masses to assess spinal canal involvement
PET/CT and tissue diagnosis (CT-guided core biopsy, EBUS, mediastinoscopy, or VATS) for mass characterization
Treatment
First-line
Acute mediastinitis: hemodynamic resuscitation, broad-spectrum IV antibiotics initiated within 1 hour after blood cultures
Empiric coverage: vancomycin (MRSA) PLUS piperacillin-tazobactam or cefepime/metronidazole (gram-negatives and anaerobes); add antifungal if immunocompromised or prolonged ICU stay
Urgent surgical debridement and drainage; sternal rewiring with omental or muscle flap reconstruction for sternal wound infections
Esophageal perforation: NPO, NG decompression, broad-spectrum antibiotics, antifungals (Candida coverage), early surgical or endoscopic repair (stent, primary repair, esophagectomy in late presentations)
Thymoma
Surgical resection (thymectomy) for stage I-II disease
Adjuvant radiation for invasive disease; chemotherapy (cisplatin-based) for unresectable or recurrent
Manage associated myasthenia gravis with pyridostigmine, prednisone, and immunosuppressants
Germ cell tumor
Seminoma: cisplatin-based chemotherapy (BEP — bleomycin/etoposide/cisplatin) or radiation; surgery for residual mass
Nonseminomatous: BEP followed by resection of residual disease
Pre-induction airway and cardiac assessment is mandatory for large anterior mediastinal masses — supine positioning can precipitate fatal airway collapse.
Hamman crunch with subcutaneous emphysema after vomiting = Boerhaave until proven otherwise.
AFP elevation is incompatible with pure seminoma — the mass contains a non-seminomatous element.
Always check anti-AChR antibodies in adults with anterior mediastinal mass to detect occult myasthenia gravis.
Descending necrotizing mediastinitis arises from odontogenic or retropharyngeal infection — early CT neck/chest and aggressive surgical drainage save lives.
Fibrosing mediastinitis after histoplasmosis causes SVC syndrome and airway or pulmonary vessel encasement; antifungals and corticosteroids do not reverse it, so management is supportive: intravascular stents for selected SVC or pulmonary artery/vein obstruction, airway stents generally avoided because of granulation tissue growth, and surgery reserved for otherwise fatal obstruction (IDSA 2007).
References
RadioGraphics 2017 — Carter BW et al. ITMIG Classification of Mediastinal Compartments and Multidisciplinary Approach to Mediastinal Masses. RadioGraphics 2017;37:413-436
Ann Thorac Surg 1996 — El Oakley RM, Wright JE. Postoperative Mediastinitis: Classification and Management. Ann Thorac Surg 1996;61:1030-1036 (reference classification)
EACTS — Abu-Omar Y, Kocher GJ, Bosco P, et al. European Association for Cardio-Thoracic Surgery expert consensus statement on the prevention and management of mediastinitis. Eur J Cardiothorac Surg 2017;51(1):10-29
IDSA — Wheat LJ, Freifeld AG, Kleiman MB, et al. Clinical practice guidelines for the management of patients with histoplasmosis: 2007 update by the Infectious Diseases Society of America. Clin Infect Dis 2007;45(7):807-825
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