The patient’s blood counts told the first part of the story. He was severely anemic and profoundly neutropenic, with an absolute neutrophil count of just 150 cells per microliter—far below the threshold of 500 cells per microliter that clinicians regard as a major risk factor for invasive aspergillosis. Neutrophils are the body’s first line of defense against filamentous fungi, engulfing and destroying inhaled spores before they can germinate into invasive hyphae. When chemotherapy strips that defense away, ubiquitous environmental molds that most people breathe in daily without consequence can colonize and invade tissue with alarming speed. Prolonged neutropenia lasting more than 20 days is among the strongest known predisposing factors, and the cumulative risk of invasive aspergillosis climbs to roughly 70 percent after 34 days of persistent neutropenia in vulnerable patients.

What happened next is what makes this case remarkable. A chest computed tomography scan revealed a mass-like lesion along the posterior wall of the trachea, just below the suprasternal notch. Critically, the scan showed no evidence of involvement of the lung parenchyma itself—the tissue where pulmonary aspergillosis almost always announces itself. Invasive pulmonary aspergillosis, the most feared form of the disease, typically produces nodules, halos of hemorrhage, or cavitary lesions within the lung tissue, and radiologists use these patterns to guide early treatment. Here, the lungs appeared spared. The infection had instead declared itself as a solitary, obstructing lesion inside the central airway, a pattern that mimics an endobronchial tumor or an aspirated foreign body far more than a fungal infection.

Flexible bronchoscopy settled the question of what was occupying the trachea, though not before revealing how dangerous the situation had become. The scope encountered a whitish, irregular endoluminal mass with elongated, intertwined projections and a pseudomembranous appearance—classic visual features of fungal growth—situated in the mid-trachea. The lesion was obstructing enough that the bronchoscope could not be advanced beyond it, meaning the medical team could not visually assess the distal airways for further disease, mucus impaction, or more extensive tracheobronchial involvement. Notably, the visible mucosa showed no overt invasion, necrosis, or active bleeding, and biopsies were taken without complication.

Laboratory analysis of the sampled tissue provided the definitive answer. Microscopy demonstrated septate hyphae branching at acute angles of approximately 45 degrees—the morphological signature of Aspergillus species—and polymerase chain reaction testing confirmed Aspergillus fumigatus as the causative organism. That identification is hardly surprising from an epidemiological standpoint: A. fumigatus accounts for more than 90 percent of human aspergillosis cases. The fungus is found everywhere—soil, decaying vegetation, water, food, and air—and infects hosts almost exclusively through inhalation of airborne spores, which helps explain why the respiratory tract bears the brunt of disease. Research also suggests A. fumigatus adheres to airway epithelium more effectively than related species such as A. flavus or A. niger, potentially giving it a particular advantage in colonizing the tracheobronchial tree.

Treatment was initiated promptly with amphotericin B and voriconazole, the workhorse antifungals for invasive aspergillosis. It did not matter. The patient deteriorated rapidly and died of respiratory failure within 36 hours of diagnosis. The authors of the report acknowledge that the precise mechanism of this fulminant collapse remains uncertain. The obstructing tracheal lesion itself likely played a central role—endobronchial fungal proliferation can critically narrow the airway lumen and precipitate respiratory failure—but the inability to examine beyond the obstruction means distal airway spread could not be excluded. In a patient with essentially no neutrophil defense, the authors note, multiple converging factors may have driven the fatal outcome.

The rarity of this presentation underscores its diagnostic difficulty. Endobronchial aspergillosis, defined by endoluminal fungal growth within the tracheobronchial tree, is an uncommon manifestation of Aspergillus disease. A 2019 review by Ngu and colleagues identified only 28 documented cases worldwide, most occurring in Asian males with a mean age of 58 years, and a separate series described by Huang and colleagues found 17 cases with similar demographics. The condition is frequently discovered incidentally during bronchoscopy performed for other reasons, such as evaluating hemoptysis. Symptoms—fever, breathlessness, chest pain, cough, and bleeding—are nonspecific, and risk factors include any form of immunosuppression as well as underlying lung disease. In a 2011 series of ten patients reported by Ma and colleagues, all had identifiable predisposing conditions such as tuberculosis, lung cancer, or foreign body aspiration, and only two had concurrent parenchymal lung involvement, a pattern echoed by the present case.

The stakes of missing or delaying diagnosis are stark. Among patients with severe airway aspergillosis who require mechanical ventilation, mortality reaches 94 percent, compared with 25 percent among those who do not—a difference that reflects both advanced disease at presentation and the mechanical consequences of airway obstruction. Diagnosis itself is far from straightforward. The traditional gold standard, fungal culture, is limited by the difficulty of obtaining adequate samples from hemodynamically unstable patients, by coagulopathies such as thrombocytopenia that make biopsy risky, and by false-negative results in patients already receiving antifungal therapy. Indirect methods fill some of the gap: galactomannan detection in serum or bronchoalveolar lavage fluid shows reasonable reliability in hematologic malignancy, though its sensitivity ranges widely from 44 to 90 percent, and false positives occur with certain antibiotics and with dimorphic fungal infections. Beta-D-glucan testing, meanwhile, lacks specificity for aspergillosis altogether.

Treatment of endobronchial aspergillosis remains unstandardized, with management individualized case by case. Most clinicians favor combining systemic antifungal therapy with interventional bronchoscopy to debulk obstructing lesions, and favorable outcomes have been reported with bronchoscopically guided resection combined with drug therapy. Some experts have argued for conservative approaches, noting that systemic agents may penetrate airway lesions poorly, while intolerance or resistance to azoles, or competing infections, can push clinicians toward surgical resection. The pharmacology is also evolving: liposomal amphotericin B carries less nephrotoxicity than the deoxycholate formulation, but adverse effects including renal tubular acidosis, hypomagnesemia, and hypokalemia have shifted general clinical preference toward azoles and echinocandins for pulmonary disease.

The authors are candid about the limits of their own report. Histopathological assessment was confined to the obstructing endoluminal lesion; because of the patient’s critical condition and the risk of procedure-related complications, no biopsies were taken from the tracheal wall or cartilage. That means direct evidence of mucosal, submucosal, or cartilaginous invasion was never obtained, and the lesion could not be definitively classified as invasive or necrotizing tracheobronchitis rather than more superficial endobronchial disease. The pseudomembranous bronchoscopic appearance, the profound neutropenia, and the explosively fatal course all hint at a more aggressive process, but certainty was impossible. What the case establishes beyond doubt is the clinical lesson the authors emphasize: endobronchial Aspergillus infection belongs on the differential for any immunocompromised patient with airway obstruction, even when chest imaging shows the lungs themselves are clear. In this patient, an isolated tracheal lesion—invisible to the usual radiologic playbook—was enough to kill within two days of identification, a reminder that in the profoundly neutropenic host, the absence of parenchymal disease offers no reassurance at all.

Subject of Research: A fatal case of isolated endobronchial Aspergillus fumigatus infection in a neutropenic lymphoma patient without lung parenchymal involvement

Article Title: Endobronchial Aspergillosis Presenting as an Isolated Airway Lesion in an Immunocompromised Patient

Article References: Sadeghi, M., Sadat Hosseini Khajouei, F., GhanbarAliAkhavan, H., & Soleimani, A. M. (2026). Endobronchial Aspergillosis Presenting as an Isolated Airway Lesion in an Immunocompromised Patient. Respirology Case Reports, 14(9), Article e70701. https://doi.org/10.1002/rcr2.70701

Image Credits: AI Generated

DOI: 10.1002/rcr2.70701

Keywords: aspergillosis, Aspergillus fumigatus, endobronchial aspergillosis, neutropenia, immunocompromised, bronchoscopy, tracheal obstruction, invasive fungal infection, lymphoma, chemotherapy, respiratory failure, case report

The patient, a Nepalese man with well-controlled asthma and hypertension, first sought medical attention in 2017 after experiencing mild, intermittent hemoptysis—the coughing up of blood. A contrast-enhanced computed tomography (CT) scan revealed a large, compartmentalized collection along the right pleural space, the thin cavity between the lung and chest wall. The mass measured approximately 13.7 by 6.5 by 7 centimeters and appeared consistent with an organized pleural hematoma. Ultrasound-guided drainage produced altered, old blood rather than evidence of active hemorrhage. Tests found no acid-fast bacteria or other bacteria in the fluid, and cytological analysis showed no malignant cells. Because his symptoms were mild and his condition stabilized with oral tranexamic acid, a medication that helps prevent clot breakdown, he declined surgical removal.

The hematoma did not disappear. When the patient returned after another episode of hemoptysis in 2020, imaging showed new pockets of gas inside the otherwise blood-filled lesion. The finding was particularly concerning because he had undergone no intervening pleural procedure and had no documented infection that could readily explain gas formation. Clinicians suspected a bronchopleural fistula, an abnormal passage connecting the bronchial tree to the pleural cavity. Such a connection can allow air from the respiratory tract to enter the hematoma and, in the opposite direction, enable blood or infected material to reach the airways. The patient then returned to Nepal and was lost to medical follow-up for five years, leaving the suspected communication untreated while the encapsulated mass continued its slow evolution.

By late 2025, he re-presented with chest pain and severely elevated blood pressure. A CT angiogram ruled out an acute aortic dissection, but showed that the pleural hematoma had grown to 14.0 by 7.8 by 8.4 centimeters. Its outer capsule also contained more dystrophic calcification, a process in which calcium deposits accumulate in chronically damaged tissue. The increase in size was modest in some dimensions, but clinically important: a lesion occupying much of one side of the chest can compress adjacent lung tissue, restrict its expansion and impair the diaphragm’s movement. The patient also had new-onset atrial fibrillation, an irregular heart rhythm that increases the risk of stroke. After his blood pressure was controlled, clinicians began apixaban, an anticoagulant prescribed to reduce that risk.

Soon afterward, he developed life-threatening hemoptysis and type 2 respiratory failure, in which inadequate ventilation causes carbon dioxide to accumulate in the blood. Apixaban was immediately stopped, but the bleeding was severe enough to require emergency intubation and mechanical ventilation in an intensive-care unit. Bronchoscopy, in which a camera is passed through the breathing tube, showed blood oozing from the right lower-lobe bronchus—the airway anatomically closest to the hematoma. This localization strengthened the suspicion that the expanding pleural lesion had begun bleeding into or communicating with the bronchial system. Respiratory testing also detected Klebsiella pneumoniae and methicillin-resistant Staphylococcus aureus, prompting treatment with levofloxacin and vancomycin. However, CT bronchial arteriography did not show enlarged or abnormal bronchial arteries that could explain the hemorrhage, suggesting that the bleeding might have arisen from fragile vessels within the chronic inflammatory capsule rather than from a readily embolized arterial source.

The biology of CEH helps explain why such a mass can enlarge long after the original bleeding event. As hemoglobin and other blood products break down, they irritate surrounding tissues and maintain a low-grade inflammatory response. The body attempts to contain the collection by forming granulation tissue and a thick fibrous capsule. That capsule is not inert: it can develop a network of small, abnormal blood vessels. These newly formed capillaries are structurally fragile and vulnerable to repeated microhemorrhage. Each tiny bleed adds more blood to the lesion, while further inflammation and organization thicken the capsule, creating a self-perpetuating cycle. Over years, the result can be a heterogeneous pleural mass containing layers of different-aged clot, fibrous tissue, inflammatory cells and calcification. The same cycle has been proposed in other chronic expanding hematomas, including those occurring after tuberculosis-related pleural disease or old thoracic operations.

The clinical team considered the standard definitive treatment: surgical evacuation of the clot together with capsulectomy, or removal of the constricting fibrous shell. Surgery is generally favored because simply draining a CEH may leave behind the vascularized capsule that drives further bleeding and expansion. In some high-risk patients, selective arterial embolization may be performed before surgery to reduce blood loss. The operation, however, can itself be hazardous because the capsule may adhere tightly to the lung, chest wall and major vessels, and reports have described substantial intraoperative blood loss. In this patient, persistent type 2 respiratory failure, severely restricted lung volumes, poor diaphragmatic excursion and frailty made major thoracic surgery too dangerous. An attempt to aspirate the mass through a needle also failed: the blood had become so densely organized that no fluid could be withdrawn.

Mechanical ventilation introduced another complication. Positive pressure increased the pressure within the airways and apparently worsened the suspected bronchopleural air leak, producing subcutaneous emphysema—air trapped beneath the skin of the chest and neck. The swelling was managed conservatively and eventually resolved without insertion of an intercostal chest drain. Yet the underlying problem remained. Recurrent bleeding required frequent bronchoscopic suctioning and airway clearance, while the large hematoma continued to compromise respiratory mechanics. The patient repeatedly failed attempts to come off the ventilator and ultimately underwent an elective tracheostomy to provide longer-term ventilatory support. Two months later, despite intensive supportive treatment, he developed hospital-acquired pneumonia and died from progressive respiratory failure.

A post-mortem examination finally provided definitive confirmation. The pleural lesion contained dense fibrous tissue, dystrophic calcification, patchy chronic inflammation, mature fibroadipose tissue and organized blood clots—the characteristic mixture expected in a chronic expanding hematoma. There was no histological evidence of tuberculosis, cancer or acute infection. The authors emphasize that CEH should be considered when CT reveals a slowly enlarging, heterogeneous pleural mass surrounded by a thick, sometimes calcified capsule, particularly after more common explanations such as malignancy and active infection have been excluded. The case also demonstrates why early recognition matters: a patient with mild symptoms may later develop airway bleeding, bronchopleural fistula, infection, lung compression and respiratory collapse. Because treatment decisions involve radiologists, pulmonologists, intensivists and cardiothoracic surgeons, the report argues for multidisciplinary assessment and early consideration of definitive surgery before the lesion becomes too organized or the patient too medically fragile to survive it.

Subject of Research: Chronic expanding thoracic hematoma complicated by life-threatening hemoptysis, bronchopleural fistula and respiratory failure

Article Title: Chronic Expanding Hematoma Complicated by Life Threatening Hemoptysis and Respiratory Arrest—A Case Report

Article References: Yu A. S.-y., Cheung C. Y., Ng C. T., et al., “Chronic Expanding Hematoma Complicated by Life Threatening Hemoptysis and Respiratory Arrest—A Case Report,” Respirology Case Reports 14, no. 7 (2026): e70665. Original research article

Image Credits: AI Generated

DOI: 10.1002/rcr2.70665

Keywords: chronic expanding hematoma, thoracic hematoma, life-threatening hemoptysis, bronchopleural fistula, respiratory failure, pleural disease, organized blood clot, dystrophic calcification