United States

Introduction 
Allan Herndon Dudley syndrome (AHDS) is an X-linked neuropsychomotor disorder characterized by congenital hypotonia with progressive spasticity and psychomotor delay [2]. It is caused by mutations in MCT8 (monocarboxylate transporter 8) which is a transporter specific for thyroid hormone T3 [2]. These patients have elevated serum levels of T3, low to below normal levels of free T4 and TSH is within normal range [2]. We present an interesting case of a patient with AHDS leading to ventilator-dependent respiratory failure from severe tracheobronchomalacia and endobronchial polyposis which were evident on bronchoscopy. 
Case Presentation 
Our patient is a 22-year-old male with a past medical history of Allan Herndon Dudley Syndrome who presented to the hospital with complaints of productive cough, fever, and vomiting. The patient was febrile, tachycardic, and hypoxic requiring 2L oxygen supplementation via nasal cannula. Chest X-ray revealed perihilar infiltrates. Upon further questioning, the patient’s caregivers endorsed that the patient had been producing high-pitched squealing sounds with respirations for a prolonged period of time with ongoing issues of aspiration of oral secretions. Subsequently, the patient was started on Ampicillin/Sulbactam for aspiration pneumonia. The hospital course was complicated with worsening hypoxia and increased work of breathing. Despite steroids, the patient desaturated to 60% which prompted intubation. Repeat chest X-ray revealed worsening bilateral patchy airspace opacities. Multiple attempts were made to wean the patient off of the ventilator but failed and eventually tracheostomy was done. Hypoxic episodes persisted and the patient then underwent bronchoscopy which revealed severe tracheobronchomalacia with endobronchial polyposis requiring custom length bivona hyperflex tracheostomy acting as a tracheal stent. After bivona tracheostomy placement, the patient had no further hypoxia episodes and was eventually discharged to long-term acute care hospital.
Discussion 
AHDS causes decreased thyroid hormone uptake in the brain leading to developmental disabilities. The disease features include neurological, developmental, and psychomotor irregularities such as central hypotonia, ataxia, paralysis, aphasia, non-epileptic paroxysmal movement disorders, spastic paraplegia, and intellectual disability [1]. The syndrome also causes thyroid irregularities including poor weight gain, reduced muscle mass, cold intolerance, tachycardia, and constipation [1]. Per our review of the literature, there have been no reported cases of AHDS with pulmonary complications yet. Our patient was found to have severe tracheomalacia and endobronchial polyps requiring custom-made tracheostomy. Hence, bronchoscopic evaluation may be necessary for AHDS patients who have hypoxia despite medical management to evaluate for tracheobronchomalacia and endobronchial polyps as it can reduce the length of hospital stay with appropriate management. 
References 
1. Beheshti, R., Aprile, J., &amp; Lee, C. (2022). Allan-Herndon-Dudley Syndrome: A Novel Pathogenic Variant of the SLC16A2 gene. Cureus, 14(1), e21771. https://doi.org/10.7759/cureus.21771 
2. Sarret C, Oliver Petit I, Tonduti D. Allan-Herndon-Dudley Syndrome. 2010 Mar 9 [Updated 2020 Jan 16]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2024. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26373/

AMA Research Challenge 2024 

A Rare Case of Allan Herndon Dudley Syndrome Associated with Severe Tracheobronchomalacia and Endobronchial Polyposis

Introduction 
Allan Herndon Dudley syndrome (AHDS) is an X-linked neuropsychomotor disorder characterized by congenital hypotonia with progressive spasticity and psychomotor delay [2]. It is caused by mutations in MCT8 (monocarboxylate transporter 8) which is a transporter specific for thyroid hormone T3 [2]. These patients have elevated serum levels of T3, low to below normal levels of free T4 and TSH is within normal range [2]. We present an interesting case of a patient with AHDS leading to ventilator-dependent respiratory failure from severe tracheobronchomalacia and endobronchial polyposis which were evident on bronchoscopy. 
Case Presentation 
Our patient is a 22-year-old male with a past medical history of Allan Herndon Dudley Syndrome who presented to the hospital with complaints of productive cough, fever, and vomiting. The patient was febrile, tachycardic, and hypoxic requiring 2L oxygen supplementation via nasal cannula. Chest X-ray revealed perihilar infiltrates. Upon further questioning, the patient’s caregivers endorsed that the patient had been producing high-pitched squealing sounds with respirations for a prolonged period of time with ongoing issues of aspiration of oral secretions. Subsequently, the patient was started on Ampicillin/Sulbactam for aspiration pneumonia. The hospital course was complicated with worsening hypoxia and increased work of breathing. Despite steroids, the patient desaturated to 60% which prompted intubation. Repeat chest X-ray revealed worsening bilateral patchy airspace opacities. Multiple attempts were made to wean the patient off of the ventilator but failed and eventually tracheostomy was done. Hypoxic episodes persisted and the patient then underwent bronchoscopy which revealed severe tracheobronchomalacia with endobronchial polyposis requiring custom length bivona hyperflex tracheostomy acting as a tracheal stent. After bivona tracheostomy placement, the patient had no further hypoxia episodes and was eventually discharged to long-term acute care hospital.
Discussion 
AHDS causes decreased thyroid hormone uptake in the brain leading to developmental disabilities. The disease features include neurological, developmental, and psychomotor irregularities such as central hypotonia, ataxia, paralysis, aphasia, non-epileptic paroxysmal movement disorders, spastic paraplegia, and intellectual disability [1]. The syndrome also causes thyroid irregularities including poor weight gain, reduced muscle mass, cold intolerance, tachycardia, and constipation [1]. Per our review of the literature, there have been no reported cases of AHDS with pulmonary complications yet. Our patient was found to have severe tracheomalacia and endobronchial polyps requiring custom-made tracheostomy. Hence, bronchoscopic evaluation may be necessary for AHDS patients who have hypoxia despite medical management to evaluate for tracheobronchomalacia and endobronchial polyps as it can reduce the length of hospital stay with appropriate management. 
References 
1. Beheshti, R., Aprile, J., & Lee, C. (2022). Allan-Herndon-Dudley Syndrome: A Novel Pathogenic Variant of the SLC16A2 gene. Cureus, 14(1), e21771. https://doi.org/10.7759/cureus.21771 
2. Sarret C, Oliver Petit I, Tonduti D. Allan-Herndon-Dudley Syndrome. 2010 Mar 9 [Updated 2020 Jan 16]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2024. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26373/

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Abstract Title
A Rare Case of Bilateral Secondary Spontaneous Pneumothorax Due to Tuberculosis

Background
A secondary spontaneous pneumothorax (SSP) is defined as a pneumothorax occurring as a complication of underlying lung disease. We describe a rare case of bilateral SSP with tuberculosis.

Case Presentation
A 64-year-old male with PMH former smoker (100-pack year) and current alcohol use presented with 6-month history of progressively worsening shortness of breath and 1-month history of a productive cough with yellow sputum. He also reported dull chest pain, decreased appetite, and 10-pound weight loss. He denied fever, night sweats, hemoptysis, or sick contacts. On examination, he was afebrile, hypoxic (72% O2 saturation) and had increased respiratory effort with tripod posturing, along with bilateral wheezes and rhonchi. A chest x-ray demonstrated large bilateral pneumothorax; bilateral chest tubes were placed with lung re-expansion. A subsequent CT chest with contrast demonstrated diffuse bilateral consolidations with bilateral upper lobe cavitation; differentials included necrotizing pneumonia, malignancy, or tuberculosis. He was placed on airborne isolation and started on broad-spectrum antibiotics. The following day, AFB smear was positive for moderate acid-fast bacilli with subsequent PCR showing Mycobacterium tuberculosis (MTB). Upon further probing, he reported traveling extensively for work with multiple prolonged stays in Asia. MTB treatment was initiated with rifampin, isoniazid, pyrazinamide, and ethambutol. He was also started on clarithromycin for positive Mycobacterium avium intracellulare (MAI) infection in sputum. After four months, he was discharged (after obtaining three consecutive negative AFB samples) with instructions to complete MTB and MAI treatment.


Discussion
SSP is commonly seen in patients with COPD, cystic fibrosis, malignancy, infectious/interstitial lung diseases, or connective-tissue disease. SSP complicates between 0.6% and 1.5% of cases of tuberculosis, with most cases reported from developing nations. The mean age of TB-associated SSP is 35-45 years and about 90% of patients are male. The mechanism of pneumothorax development is progressive caseating necrosis and rupture of tuberculous cavities or blebs into the pleural space. The most common presenting features of SSP are cough, dyspnea, chest pain, and fever. Chest x-ray may demonstrate cavity, consolidation or infiltration. First-line management of patients with large or symptomatic SSP is chest tube placement. Surgical repair or pleurodesis may be indicated in cases complicated by persistent air leak following chest tube placement or in cases of bronchopleural fistula. Bilateral secondary spontaneous pneumothorax due to tuberculosis is very rare and seldom reported with most of the data from developing nations. Tuberculosis should be considered in the differential diagnosis of patients presenting with secondary spontaneous pneumothorax.





A Rare Case of Bilateral Secondary Spontaneous Pneumothorax Due to Tuberculosis




Introduction
Spontaneous pneumothorax is a condition that commonly affects young adults who may not have underlying lung diseases. There are several well-known risk factors contributing to the onset of spontaneous pneumothorax. They include cigarette smoking, particularly among adolescents and young male adults with lean physique. While smoking is a recognized risk factor for spontaneous pneumothorax, there is limited understanding regarding the role of electronic cigarettes (e-cigarettes) in its development (1, 2, 3, 4, 5).
Currently, the use of e-cigarettes has surged to epidemic proportions, particularly in the younger population, with about 21% of high school students and 5% of individuals aged 18–34 reported to be users. While the long-term health implications of e-cigarettes remain unclear, there is growing concern over acute adverse effects associated with vaping. Although there have been various presentations of pneumonitis linked to vaping, cases involving pneumothorax complications remain sparse in existing literature (1, 2, 4, 6).
Here we describe a case of a 25-year-old old male, who presented with a large, left – sided pneumothorax following the use of a vaping device. 

Case Report 
A 25-year-old male with a past medical history of attention-deficit and hyperactivity disorder presented to the hospital with a complaint of increasing shortness of breath. He reported that he was sitting in a chair, talking to his friends and vaping the day before presenting to the emergency department (ER). Suddenly, he felt sharp pain in the middle of his chest, radiating to his left side. He also experienced a tightness in his ribs followed by trouble breathing. Even though the patient was able to sleep that night, he noticed that his symptoms became progressively worse. The progression prompted him to come to the ER.
Upon detailed questioning, the patient reported a history of smoking cigarettes and vaping since he was 16 years old. He quit smoking cigarettes at the age of 20. Interestingly, around the time he quit smoking cigarettes, he presented to the ER with the complaint of progressive substernal chest pain. However, a CT chest at that time did not show anything of significance, including bullous or parenchymal lung disease. 
Though he quit smoking cigarettes, he continued vaping. He reported working as a waiter which he found to be very stressful; this led him to vape constantly throughout the day. At the exact time of chest pain onset significant to this case report, he was doing nothing other than sitting comfortably in a chair vaping; he was not experiencing stress at that present moment. 
It is also pertinent to include that during history taking, the patient reported no family history of pulmonary disease. Despite being 6 feet and 2 inches tall, he is the shortest amongst his brothers. Due to his tall and slender physique, he was tested for Marfan syndrome as a teenager; results were negative. The patient also reported a sedentary lifestyle with frequent social alcohol use. 
The patient went on to be admitted to the hospital. During his stay, a chest x-ray revealed a large, left pneumothorax measuring about 50%. Appropriate treatment was promptly initiated, including fluoroscopic guided chest tube placement. Over the next few days, the pneumothorax resolved without any complications. The patient was discharged home and subsequently quit using e-cigarettes. 

Discussion 
E-cigarettes were introduced to the United States market in the early 2000s. Since then, their usage has seen a significant rise. This increase can be attributed to the perception that e-cigarette users are spared from the traditional harmful effects associated with smoking cigarettes. Particularly among young adults, the adoption of vaping has grown sharply over the past decade (1).
Pneumothorax refers to the presence of air in the pleural space, which potentially leads to partial or complete lung collapse. It is characterized by the presence of air buildup in the pleural space, typically resulting from the rupture of subpleural blebs or bullae. Pneumothorax is broadly categorized as either traumatic or spontaneous. Spontaneous pneumothorax typically affects tall, slender males aged 10 to 30. Historically, cigarette smoking has been linked to an increased pneumothorax risk, and emerging evidence suggests that e-cigarettes may carry similar risks. The rise in e-cigarette use, especially among adolescents, has accompanied the increase in lung injuries, including pneumothorax (3, 6).
While e-cigarettes have been marketed as less harmful to lung tissue compared to traditional smoking, the increasing incidence of associated E-cigarette or Vaping Product Use-Associated Lung Injury suggests otherwise. It is hypothesized that e-cigarette use may augment pneumothorax risk through physiological mechanisms and exposure to the inhaled toxins. Pneumothorax often stems from the spontaneous rupture of subpleural blebs or bullae, or increased pleural porosity due to inflammation. In the case of e-cigarette use, this could be exacerbated by inhaled nicotine and other compounds linked to lung cell damage and inflammation (1, 4). Additionally, repeated inhalation through e-cigarette devices may create significant negative intrathoracic pressure swings, leading to airway barotrauma and lung collapse (4).
In our case report, we demonstrated a unique and rare association between vaping and pneumothorax. We uncovered a direct link between the time of e-cigarette use and the onset of respiratory symptoms related to pneumothorax in the patient. While the exact pathophysiology of vape-associated spontaneous pneumothorax remains unclear, it is crucial to raise awareness among healthcare providers and the general population, particularly adolescents, about the potential complications of vaping. Further investigation into vaping-related risk factors is warranted.

Conclusion
In the setting of e-cigarette use being on the rise, further investigation into its effects is needed, especially with its popularity growing in such young populations. While the long-term sequelae of vaping remain unknown, healthcare professionals need to be aware of vaping as a risk factor for pneumothorax. This association that has been supported through the case of this 25-year-old sheds light on the importance of collecting vaping history during patient interviews. Furthermore, the purpose of this report is to bring attention to risk factors that may be attributed to vaping; just one of which is spontaneous pneumothorax.

References
1. Alex Bonilla, Alexander J. Blair, Suliman M. Alamro, Rebecca A. Ward, Michael B. Feldman, Richard A. Dutko, Theodora K. Karagounis, Adam L. Johnson, Erik E. Folch, and Jatin M. Vyas. Recurrent spontaneous pneumothoraces and vaping in an 18-year-old man: a case report and review of the literature. J Med Case Rep. 2019; 13: 283. Published online 2019 Sep 9. doi: 10.1186/s13256-019-2215-4
2. Munish Sharma, Humayun Anjum, Chinthaka P Bulathsinghala, Mihir Buch, Salim R Surani. A Case Report of Secondary Spontaneous Pneumothorax Induced by Vape. Cureus. 2019 Nov 4;11(11):e6067. doi: 10.7759/cureus.6067.
3. Ellen Boakye, Olufunmilayo H Obisesan, Albert D Osei, Omar Dzaye, S M Iftekhar Uddin, Glenn A Hirsch, Michael J Blaha. The Promise and Peril of Vaping. Curr Cardiol Rep. 2020 Oct 9;22(12):155. doi: 10.1007/s11886-020-01414-x.
4. Joanna Wieckowska, Usama Assaad, Muhammad Aboudan. Pneumothorax secondary to vaping. Respir Med Case Rep. 2021; 33: 101421. Published online 2021 May 5. doi: 10.1016/j.rmcr.2021.101421.
5. Obaid Ashraf, Adeel Nasrullah, Rahul Karna, Ahmad Alhajhusaina. Vaping associated spontaneous pneumothorax – A case series of an enigmatic entity! Respir Med Case Rep. 2021; 34: 101535. Published online 2021 Oct 23. doi: 10.1016/j.rmcr.2021.101535.
6. Dietmar H Borchert, Hagen Kelm, Meghan Morean, Andrea Tannapfel. Reporting of pneumothorax in association with vaping devices and electronic cigarettes. BMJ Case Rep. 2021 Dec 17;14(12):e247844. doi: 10.1136/bcr-2021-247844.
7. Seth J Deskins, Samuel K Luketich, Saif Al-Qatarneh. Recurrent spontaneous pneumothorax in a 15-year-old female associated with electronic cigarettes. Pediatr Pulmonol. 2022 Oct;57(10):2568-2570. doi: 10.1002/ppul.26058. Epub 2022 Jul 29.
8. Ishan Garg, Aditi Vidholia, Ankita Garg, Shuchita Singh, Alireza Agahi, Archana Laroia, Sachin S Saboo, Alejandro P Comellas, Eric A Hoffman, Prashant Nagpal. E-cigarette or vaping product use-associated lung injury: A review of clinico-radio-pathological characteristics. Respir Investig. 2022 Nov;60(6):738-749. doi: 10.1016/j.resinv.2022.06.011. Epub 2022 Aug 11.
9. Mohsin Shah, Mary K Bryant, Gita N Mody, Rebecca G Maine, Judson B Williams, Trevor C Upham. The Impact of Vaping on Primary Spontaneous Pneumothorax Outcomes. Am Surg. 2023 Apr;89(4):825-830. doi: 10.1177/00031348211048849. Epub 2021 Oct 7.
10. Pitchaporn Yingchoncharoen, Jerapas Thongpiya, Sakditad Saowapa, Mahmoud Abdelnabi, Myrian Vinan-Vega, Kenneth Nugent. Severe Acute Respiratory Distress Syndrome Secondary to Concomitant Influenza A and Rhinovirus Infection Complicated by Methicillin-resistant Staphylococcus aureus Pneumonia in an Early Pregnancy Patient With Vaping-induced Lung Injury. J Community Hosp Intern Med Perspect. 2023 Jun 29;13(4):91-96. doi: 10.55729/2000-9666.1213. eCollection 2023. 


A Rare Case Of Vaping-Associated Spontaneous Pneumothorax

Background
Interstitial lung disease serves as an umbrella term to cover over 100 conditions causing scarring and inflammation of the lungs. Common offending agents include autoimmune disease such as lupus and rheumatoid arthritis, pneumoconiosis such as asbestosis, hypersensitivity pneumonitis, or adverse reactions to medications. Nitrofurantoin is one such medication that can cause pulmonary injury, with about 1 in 5000 having acute hypersensitivity presenting an average of 9 days after initiation, while chronic pneumonitis reactions take 6 months to several years. Risk factors include age over 60, pre-existing lung conditions and renal impairment. Commonly used to treat uncomplicated lower urinary tract infections, we present the case of a patient that is unique for developing lung toxicity while on this medication outside of the expected timeframe of this manifestation.

Case Presentation
An 86-year-old female with past medical history significant for hypertension, hypothyroidism, CKD stage 2, presented to the emergency department with exertional dyspnea and fatigue for 3 weeks. For 4 months leading up to this admission, the patient had been on daily UTI prophylaxis with nitrofurantoin. She is a former smoker with a 50-pack year and quit 3 years ago. Pertinent labs include positive ANA, RF and anti-CCRP antibodies. 2D Echo was unremarkable. CT chest was significant for diffuse dense ground glass opacities with scattered areas of consolidation worse at the peripheries. There was no evidence of honeycombing, traction bronchiectasis or pleural effusion. Pulmonology was consulted and a bronchoscopy was performed. BAL studies were negative for Aspergillus, PCP, Histoplasma, Blastomyces. The clinical history, CT imaging findings and further workup results were suggestive of nitrofurantoin lung toxicity. Nitrofurantoin was discontinued and patient was started on steroid taper of oral prednisone, 2L/min O2 supplementation to maintain SPO2>90% with plan for repeat CT chest in 6 weeks.

Discussion
As the 5-year survival rate for ILD is 48.1%, identifying the cause is key for overall prognosis. In our patient with infectious and cardiogenic causes ruled out, autoimmune work up was positive. It’s not unusual to have positive antibodies in nitrofurantoin toxicity, including RF and ANA having been reported. It would be unusual to develop acute RA- related lung disease at her age without any other systemic symptoms or signs. Improved function and imaging on repeat follow-up will confirm, with this case serving to illustrate the high index of clinical suspicion needed by the provider to implement timely interventions in cases that present in an atypical fashion.

Atypical Presentation of Nitrofurantoin-Induced Pulmonary Toxicity


Introduction
Co-infection with Influenza A and Methicillin-Resistant Staphylococcus aureus (MRSA) is a rare but devastating clinical scenario, especially in the elderly with multiple comorbidities. This case report describes a 77-year-old female who rapidly deteriorated from a co-infection of Influenza A and MRSA, resulting in fatal hemorrhagic pneumonia or diffuse alveolar hemmorhage (DAH). This case emphasizes the need for heightened clinical vigilance, prompt diagnosis, and aggressive management in such vulnerable populations (1).

Case Presentation
A 77-year-old female with a medical history notable for type 2 diabetes mellitus, hypertension, mild coronary artery disease (clean catheterization in 2021), and recently diagnosed dementia, was transferred to the Emergency Department (ED) from a psychiatric facility. The transfer to ED was prompted by hypoxia, with an oxygen saturation reading in the low 80s. The patient had been admitted to the psychiatric facility just 2 days before her ED admission for suicide evaluation. She did not attempt suicide, but her progressive cognitive decline was causing her significant distress, leading her to have suicide ideation. She had been experiencing mild cough and congestion for several days even prior to her transfer to pschiatric facility. However, on the morning of her admission to the ED, she complianed of significant dyspnea and chest tightness, leading to her transfer to the hospital. Patient was a former smoker but quit smoking several years ago. As per her daughter she had been upto date on her appointments with her PCP and was generally healthy and compliant with all her medications. She was taking baby aspirin but denied taking any blood thinners or chemotherapy medications.

Upon arrival at the ED, the patient was found to be confused and somnolent but arouseable. She was noted to be in significant distress due to her acute hypoxic respiratory failure and was immediately placed on BiPap. On admission, she was febrile with a temperature of 100 F, tachycardic with a heart rate of 99 beats per minute and a blood pressure of 123/66. Patient denied any hemoptysis or bloody emesis but was noted to have dried bloody secretions in her mouth. On lung examination, she had coarse crackles and wheezes bilaterally, more pronounced on the right side. Laboratory tests showed initial hemoglobin of 13.3 g/dL, severe leukopenia (with a total white blood count of 1.88 k/uL and absolute neutrophil counT of 0.60 k/uL) and bandemia (total band percentage of 19.0). The platelet count was 136 k/uL with initial lactate of 3.64 which trended upto 4.64 mmol/L and a procalcitonin level of 47.26 ng/ml. Coagulation profile showed an international (INR) of 1.36 and a prothrombin time (PT) of 16.5 and a partial thrombolastin time (PTT) of 29.4. Serum and urine toxicology were negative and salycilate, acetaminophen and alcohol levels were within normal limits. Radiological imaging revealed a complete whiteout of the right mid to lower lung lobe, concerning for right lobe pneumonia. The patient’s condition rapidly deteriorated; she became hypotensive and unresponsive, necessitating emergent intubation. During intubation, blood was observed in her lungs, prompting an emergent bedside bronchoscopy which confirmed active pulmonary hemorrhage.

The patient was septic on arrival but rapidly developed shock and was immediately transferred to the Intensive Care Unit (ICU) where she was started on two vasopressors to manage her hypotension. She was also started on broad spectrum antibiotics with vancomycin and meropenem. While attempts were being made to stop her alveolar hemorrage via bedside bronchoscopy, her Influenza A nasal swab came back positive. She was also started on oseltamivir. However, despite aggressive measures, including multiple runs of epinephrine and cold saline to control the alveolar bleeding, the hemorrhage continued unabated. The patient was deemed too unstable for transfer to Interventional Radiology for embolization. Her condition remained refractory to all interventions and she was eventually transitioned to comfort care, passing away shortly thereafter.

Postmortem laboratory investigations which included blood cultures, bronchoalveolar lavage (BAL), revealed a co-infection with Influenza A and MRSA. This combination is known to be particularly lethal due to the synergistic pathogenic mechanisms leading to severe necrotizing hemorrhagic pneumonia .(1,3) The presence of Influenza A likely predisposed the patient to a secondary bacterial infection with MRSA, creating a cascade of respiratory compromise and hemorrhagic manifestations and that proved impossible to halt with available medical interventions (1).

Discussion
The case of our patient illustrates the severe consequences of co-infection with Influenza A and MRSA, particularly in an elderly individual with multiple comorbid conditions. Influenza A infection can impair the respiratory epithelium, reduce immune responses, and create an environment conducive to secondary bacterial infections, such as MRSA (4) . Once established, MRSA can cause necrotizing pneumonia, characterized by rapid tissue destruction, extensive inflammation, and hemorrhage (3) .

Elderly patients, particularly those with underlying comorbidities like diabetes mellitus, hypertension, coronary artery disease, and cognitive impairments, are at higher risk of severe outcomes from respiratory infections (4). The immunosuppressive effects of diabetes and advanced age can exacerbate the severity of infections and impair the patient's ability to mount an effective immune response (4) . The pathophysiology involves several mechanisms: Influenza A virus damages the respiratory epithelium, reducing mucociliary clearance and creating a nidus for bacterial colonization and invasion (4). MRSA exploits this breach, leading to severe secondary infections. MRSA produces several virulence factors, including Panton-Valentine leukocidin (PVL), which can cause necrotizing pneumonia with tissue necrosis and hemorrhage (3) . The combination of these pathogens leads to a severe inflammatory response, often resulting in alveolar hemorrhage, rapid respiratory failure, and high mortality (1) . However, the absence of these virulence factors does not neceassary decrease the risk of developing complications. For instance, a young healthy 46-year-old woman succumbed to death within a few hours of arrival due to co-infection, even though the PCR assay did not detect PVL. ( number)

Managing such cases presents significant challenges. Early recognition and differentiation between primary viral pneumonia and secondary bacterial infections are crucial (4) . Empiric broad-spectrum antibiotics, including coverage for MRSA, are recommended in severe cases of community-acquired pneumonia during influenza season (4) . However, rapid progression to hemorrhagic pneumonia, as seen in this patient, limits the efficacy of medical management (3). Despite advanced medical interventions, the rapid progression and severe hemorrhagic manifestations in such co-infections often outpace therapeutic measures. The case underscores the need for aggressive early treatment strategies and the potential role of antiviral and antibacterial prophylaxis in high-risk populations (2) .

Prevention of such fatal outcomes requires a multifaceted approach. Influenza vaccination is critical in preventing primary viral infections. Annual vaccination can reduce the incidence and severity of influenza infections (4) . Strict infection control practices in healthcare settings, especially in long-term care and psychiatric facilities, are essential to prevent the spread of MRSA and other nosocomial pathogens (4). Prompt identification and isolation of infected individuals can prevent the spread of influenza and MRSA (4) . Early use of antiviral medications for influenza and empiric antibacterial therapy, including MRSA coverage, in suspected severe cases of respiratory infection can mitigate disease progression (2).

Further research is needed to better understand the synergistic effects of influenza and MRSA co-infection and to develop more effective treatment protocols (1). Increased awareness among clinicians about the potential for such severe co-infections can lead to earlier diagnosis and intervention, potentially improving outcomes (2) . The role of steriods in such cases also needs to be studied further. Despite administeration of stress-dose steriod in some cases patients condition continued to deteriorate. The same is true for the use of ECMO. Given the severity of pulmonary hemorrage and coagulopathy patients develop, they are not considered candidates for ECMO. 

Conclusion
This case highlights the lethal potential of co-infection with Influenza A and MRSA, particularly in elderly patients with multiple comorbidities. The rapid progression to hemorrhagic pneumonia, as demonstrated, poses formidable challenges to clinical management. Heightened vigilance, early diagnosis, and aggressive treatment are crucial. Preventive measures, including vaccination and strict infection control practices, are paramount in protecting vulnerable populations. Further research and increased clinical awareness are necessary to improve outcomes in such devastating cases (1) .

References
Toolsie, O., Tehreem, A., & Diaz-Fuentes, G. (2019). "Influenza A pneumonia associated with diffuse alveolar hemorrhage." American Journal of Case Reports, 20, 592-596.

Randolph, A. G., Vaughn, F., Sullivan, R., Rubinson, L., Thompson, B. T., Yoon, G., ... & Project, N. E. C. C. (2011). "Critically ill children during the 2009–2010 influenza pandemic in the United States." Pediatrics, 128(6), e1450-e1458.

Klugman, K. P., & Madhi, S. A. (2012). "Rapidly lethal necrotizing hemorrhagic pneumonia." Critical Care Medicine, 40(12), 1235-1244.

Chakrabarti, B., Davies, P. D. O., & Dewan, P. (2017). "How a mild influenza B infection can kill: A case of necrotizing pneumonia." Lung India, 34(5), 448-450.

Case Report: Rapidly Fatal Hemorrhagic Pneumonia in an Elderly Patient with Co-Infection of Influenza A and MRSA

Cryptococcal Pneumonia in a Patient with recent COVID19 infection 

Background 

COVID-19 has been linked to numerous opportunistic infections, including various fungal diseases such as Aspergillosis, Mucormycosis, Histoplasmosis, Blastomycosis, and Cryptococcus. Here we present a case of pulmonary cryptococcus infection in a patient who developed severe worsening cryptococcal infection with recent COVID-19 infection. 

Case Presentation 

A 77-year-old Caucasian male presented to the emergency department for shortness of breath, progressive generalized weakness, and hypotension. His past medical history is significant for diabetes mellitus II, polymyalgia rheumatica requiring prednisone use (5 mg daily), and hypertension. He was diagnosed with COVID-19 infection two weeks before these current symptoms, required admission to an outlying facility, and was treated for pneumonia. After discharge, he completed his antibiotic course, but one week later, he noticed worsening symptoms. He was seen a day prior at the clinic where it was revealed that the patient had an elevated white blood count, acute kidney injury, and a chest radiograph showing bilateral pulmonary infiltrates. Chest CT with contrast revealed extensive, severe bilateral airspace disease with necrotizing pneumonia. He was admitted to the hospital and started on antibiotics including anti-fungal coverage. Pulmonology was consulted, a bronchoscopy was performed, and serology testing came positive for cryptococcal antigen. He was started on fluconazole with improvement in symptoms. He was discharged home with pulmonology and infectious disease follow-up. 

Discussion 

Severe COVID-19 infection can cause ARDS and intense inflammation creating the need for corticosteroids. High-dose corticosteroids along with comorbidities like Diabetes Mellitus make the patients susceptible to opportunistic infections. Our patient has a history of Polymyalgia Rheumatica, for which he has been taking low-dose corticosteroids, as well as Diabetes Mellitus. In addition to this, he has been administered high-dose corticosteroids for treatment of recent COVID-19 infection. These factors made him susceptible to Cryptococcal infection. The literature review showed many cases of aspergillosis and COVID-19 infection, but pulmonary cryptococcal was less documented. In COVID-19 patients with rapidly worsening respiratory failure and not responding to traditional treatment suspicion of superimposed fungal infection should be considered. Diagnosis can be made with the detection of cryptococcal antigen as broncho-alveolar lavage cultures are not very sensitive or specific. The first-line treatment for pulmonary cryptococcus is fluconazole or amphotericin B/flucytosine in patients with CNS involvement. 

Pulmonary cryptococcal infection is difficult to diagnose as it can mimic multiple conditions including lung cancer, tuberculosis, and bacterial pneumonia with consolidation. Early recognition and diagnosis of pulmonary cryptococcal infection can prevent morbidity and mortality.

Cryptococcal Pneumonia in a Patient with Recent COVID19 Infection.

Abstract Title
Microscopic Polyangiitis and the Impact of Steroid Treatment on Lung Compliance 

Background
Microscopic polyangiitis (MPA) is a small-vessel vasculitis characterized by systemic infiltration, primarily targeting the renal and pulmonary systems. While diffuse alveolar hemorrhage (DAH) is among its most lethal pulmonary manifestations, the spectrum of lung pathology in MPA is extensive, necessitating immediate immunosuppressive therapy.
Our case study focuses on an elderly woman who initially presents with MPA-induced rapid progressive glomerulonephritis (RPGN) but subsequently develops an array of vasculitis-related pulmonary insults requiring endotracheal intubation. Following a brief course of immunosuppression, her lungs demonstrate rapid physiologic recovery. This case highlights the role of induction therapy with steroids in enhancing lung compliance, leading to a more profound respiratory recovery in MPA patients without DAH-related pulmonary symptoms.

Case Presentation
The patient, a woman in her mid-60s with a history of hypertension, chronic anemia, and Raynaud’s phenomenon, was referred to the emergency department by her primary care provider for a creatinine level of 16.53 and potassium level of 6.3. Immediate hemodialysis was initiated, and an autoimmune workup for acute renal failure was conducted. Labs and renal biopsy revealed RPGN induced by MPA.
Within two weeks, the patient's oxygen demand increased, and clinical presentation and imaging raised concerns for DAH, leading to intubation. A subsequent bronchoscopy and bronchoalveolar lavage showed no active hemorrhage. Induction therapy with two days of pulse-dose steroids (methylprednisolone [MTP]) followed by five days of low-dose steroids was initiated. The patient's ventilator settings rapidly improved post-MTP therapy, with decreased pressure support and FiO2 requirements. She was extubated within a week and discharged on MTP and rituximab.

Discussion
This case features an uncharacteristic pulmonary presentation of MPA, marked by acute hypoxemic respiratory failure not due to DAH but due to various small-vessel disease components. The patient's rapid recovery post-MTP induction was objectively measured through improved markers of lung compliance, including reduced daily driving pressures, decreased peak pressures, and increased dynamic compliance.
These findings suggest that current guidelines for induction therapy with steroids could benefit pulmonary MPA patients without DAH, especially in ventilated patients, by improving lung compliance.

Microscopic Polyangiitis and the Impact of Steroid Treatment on Lung Compliance 

Background
Pulmonary adenocarcinoma has become the most common histological subtype of non-small cell lung cancer. It originates in the glandular cells of lung tissue. It is characterized by slow growth and a tendency to metastasize. Early detection is crucial for prognosis and effective treatment. In its early stages, it typically appears on tomography as ground-glass nodular lesions; however, it can manifest in various ways, posing a diagnostic challenge.

Case Presentation
A 76-year-old female Jehovah's Witness, accountant, with controlled type II diabetes, arterial hypertension, and a hysterectomy for myomatosis at age 45. She began experiencing a dry cough in August 2021, which progressed over a year to the point of causing dyspnea,
accompanied by a weight loss of 10 kilograms, denying any fever or night sweats. She was referred to a tertiary hospital where an initial diagnosis of multinodular disease was made (Fig. 1 and 2), and a bronchoscopy was performed, revealing only a positive result for galactomannan in bronchoalveolar lavage. Treatment with itraconazole was started without improvement. Due to persistent symptoms, a new bronchoscopy was performed in August 2022, which
documented adenocarcinoma cells in bronchial fluid cytology but not in biopsy, leading to another biopsy via Video Assisted Thoracoscopic Surgery, with the following results:

Histopathological Report: Pulmonary adenocarcinoma with a lipidic, mucinous pattern,immunohistochemistry: TTF1 negative, CK7 and CK20 positive, enteric variety. Negative mutation panel. PDL1 0%.

Given the clinical stage IV due to multinodular pulmonary disease without mutations, chemotherapy with carboplatin/pemetrexed was decided upon. After the third cycle of chemotherapy, a new chest CT scan showed an unusual response pattern with multiple cystic lesions where the previous lesions had been (November 2022). Due to clinical stability, the same chemotherapy regimen was maintained, with a follow-up CT scan planned for February2023.

Discussion
The unusual change from nodules to cystic lesions in pulmonary adenocarcinoma represents a rare diagnostic challenge. This case provides valuable insight into the atypical variants of the disease and their clinical implications, addressing from the initial clinical presentation to diagnostic confirmation

Pulmonary Adenocarcinoma: Atypical Presentation and Unusual Tomoghraphic Patterns

Introduction: 
Tracheobronchopathia osteochondroplastica (TO) is a rare idiopathic benign disease of the large airways with a clinical prevalence of 0.2% to 0.7%. It is characterized by osteocartilaginous nodules that arise from the anterolateral aspects of the airway walls and project into the lumen of the trachea and bronchi. While typically asymptomatic, patients may experience dyspnea, excessive mucus production, or hemoptysis. The gold standard for diagnosis is a computed tomography (CT) scan and bronchoscopy, which often discover TO secondary to another condition. While no specific treatments exist for TO, the prognosis is generally favorable. This case report discusses a presentation of a male whose potential TO was incidentally discovered while evaluating his pleural effusion. 

Case Presentation:
A 70-year-old nonsmoker male with diabetes mellitus, end-stage renal disease on hemodialysis, and atrial fibrillation (not on anticoagulation) presented for continued evaluation of his unexplained bilateral pleural effusion.

The patient underwent a thoracentesis that confirmed an exudative pleural effusion (protein = 3.5 g/dl and LDH > 2/3 upper limit of normal). A follow-up CT scan of the chest revealed that the pleural effusion was more prominent on the left side, bibasilar atelectasis, compressive and rounded left lower lobe (LLL) atelectasis, scattered calcified granulomas, and left-sided pulmonary infiltrates.

To further evaluate, a bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy was conducted the following month. Although the BAL and transbronchial biopsy results were negative, the bronchoscopy revealed yellowish tracheal nodules and bronchial nodules in the right mainstem and left upper lobe bronchi, suggesting potential Tracheobronchopathia Osteochondroplastica.

Discussion:
TO is often a difficult condition to diagnose due to its benign nature and unknown etiology. This patient’s bronchoscopy revealing yellowish nodules along his tracheal and bronchial walls, CT showing potential calcifications, and biopsy indicating no malignancies collectively suggest a possible presentation of TO. There are no established follow-up guidelines, and it may be useful to see if the nodules increase in size or number over time and how this progression could affect the patient's symptoms and long-term outcomes. More work is needed to see if TOs are associated with or increase the risk for lung pathologies, such as pleural effusions, among other systemic diseases.

Conclusion:
As TOs have very few effects, a diagnosis of TO is often made incidentally when evaluating other primary conditions. This patient’s presentation suggestive of tracheobronchopathia osteochondroplastica contributes to the limited literature on how TO may present.


References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474380/
https://www.mayoclinicproceedings.org/article/S0025-6196(19)30101-6/fulltext

Unveiling Hidden Nodules: An Incidental Discovery of Tracheobronchopathia Osteochondroplastica

Title: Breaking Barriers in Amniotic Fluid Embolism Management with Interventional Radiology

Introduction: 
Amniotic fluid embolism (AFE) is a rare obstetric emergency with high mortality rates. Prompt recognition and supportive, multidisciplinary treatment is vital for enhancing patient outcomes. This case highlights the successful treatment of AFE with interventional radiology (IR). 

Background: 
Amniotic fluid embolism is a rare medical emergency that can occur during labor and postpartum. The pathogenesis is theorized to be due to a release of inflammatory cytokines reacting to amniotic fluid in the maternal bloodstream, causing cardiovascular collapse, respiratory failure, and disseminated intravascular coagulation (DIC) [1]. Diagnosis is based on clinical findings of hypoxia, hypotension, and coagulopathy in peripartum or postpartum women [2].

Treatment is supportive, including respiratory, cardiac, hemostatic, and hemodynamic resuscitation. This requires a multidisciplinary team to be heavily involved in the patient’s care, with primary contributions from obstetrics, critical care, cardiology, and pulmonology [3]. 

The prognosis is grim. Studies suggest maternal mortality ranges from 20% to 60% [4]. With placenta accreta spectrum disorder, mortality doubles [5]. 

Case: 
Our patient is a 27-year-old now G2P2 female with a history of placenta accreta who developed seizure-like activity, hypotension, and respiratory distress shortly after delivery, all concerning for AFE. Initial labs revealed a fibrinogen of 69 and INR of 1.2, findings consistent with disseminated intravascular coagulation (DIC). She developed pulseless ventricular tachycardia that spontaneously resolved and was transferred to our facility for further workup.

Upon arrival, she was cyanotic, tachypneic, tachycardic, and hypotensive. CXR revealed pulmonary edema. Bedside echocardiogram revealed an ejection fraction of 35-40%. Troponins were elevated at 50,000. MTP was subsequently activated. 

Plans were made to undergo CTA C/A/P to exclude a pulmonary embolism; however, due to hemodynamic instability, she was taken to the IR suite for embolization of the bilateral uterine and internal iliac arteries. Following the procedure, her vital signs normalized without vasopressor support. 

Later that evening, she became hypotensive and tachycardic. CXR was concerning for flash pulmonary edema. She developed two episodes of supraventricular tachycardia that responded to vagal maneuvers. Intubation was performed for hypoxemia and respiratory distress. 

After a multidisciplinary discussion, the decision was made to take the patient for a repeat diagnostic pelvic angiogram, which revealed brisk arterial extravasation from the left inferior epigastric artery which was not conspicuous on the initial angiogram. IR then performed coil embolization of the left inferior epigastric artery. A conventional pulmonary arteriogram was also performed to exclude a large pulmonary embolus given her worsening hypoxemia. 

She was subsequently stabilized and remained so for the duration of her admission, receiving a total of 14 pRBCs, 13 FFP, 3 platelets, and 3 cryoprecipitates.

Discussion:
IR’s prompt identification and treatment of arterial extravasation were monumental in stabilizing the patient and mitigating the risk of further deterioration. In obstetric emergencies, especially those involving severe hemorrhage, rapid and precise interventions are crucial. IR offers minimally invasive techniques that can effectively and quickly control emergent bleeding and provide patient stabilization without the need for vasopressor support or general anesthesia.

There is currently no specific research or case documentation highlighting the significance of IR procedures in managing AFE. Further studies are warranted to analyze the significance of incorporating IR into the standard management of AFE across medical facilities. 

While interventional radiology may not traditionally be a primary component of the management for AFE, its inclusion in this case demonstrates its ability to significantly optimize patient outcomes and warrants more frequent consideration in similar emergencies.

Conclusion: 
The prompt integration of IR into our multidisciplinary approach played a pivotal role in the successful management of AFE, highlighting the significant impact IR can have on optimizing patient outcomes. 

References:
Cavoretto PI, Rovere-Querini P, Candiani M. Toward Risk Assessment for Amniotic Fluid Embolisms. JAMA Netw Open. 2022;5(11):e2242850. Published 2022 Nov 1. doi:10.1001/jamanetworkopen.2022.42850
Sundin CS, Mazac LB. Amniotic Fluid Embolism. MCN Am J Matern Child Nurs. 2017;42(1):29-35. doi:10.1097/NMC.0000000000000292 
Pacheco LD, Clark SL, Klassen M, Hankins GDV. Amniotic fluid embolism: principles of early clinical management. Am J Obstet Gynecol. 2020;222(1):48-52. doi:10.1016/j.ajog.2019.07.036
Clark SL. Amniotic fluid embolism. Obstet Gynecol. 2014;123(2 Pt 1):337-348. doi:10.1097/AOG.0000000000000107
Mazza GR, Youssefzadeh AC, Klar M, et al. Association of Pregnancy Characteristics and Maternal Mortality With Amniotic Fluid Embolism. JAMA Netw Open. 2022;5(11):e2242842. Published 2022 Nov 1. doi:10.1001/jamanetworkopen.2022.42842

Breaking Barriers with Amniotic Fluid Embolism Management with Interventional Radiology

Abstract Title: Unique Presentation of Diabetic Striatopathy in an Elderly Female
Background:
Diabetic striatopathy (DS), also known as hyperglycemic chorea-ballism or nonketotic hyperglycemic hemichorea-hemiballism, is a rare neurological complication predominantly seen in individuals with type 2 diabetes experiencing poorly controlled hyperglycemia. Radiologically, DS is identified by specific hyperintensities in the basal ganglia on T1-weighted MRI, and striatal hyperdensity on CT scan; a hallmark of the disease's impact on central nervous system function. Management of DS primarily focuses on rapid correction of hyperglycemia and symptomatic control of chorea. Despite strict glucose control, recurrence rates have shown to be 18.2%, making the timely diagnosis of DS a crucial component in patient management.
Case Presentation:
This report is based upon the clinical case of a 79-year-old female with a medical history of type 2 diabetes mellitus, hypertension, hyperlipidemia and dementia who presented to the emergency department (ED) with altered mental status displaying confusion, but no evidence of chorea. Preliminary workup was performed in the ED and was significant for mild tachycardia, tachypnea, and elevated blood pressure. Pertinent laboratory findings revealed hyponatremia of 130 mEq/L, hyperkalemia of 6.5mEq/L, hypocarbia with CO2 of 8mEq/L, increased anion gap of 29, elevated glucose of 796 mg/dL, increased blood urea nitrogen and creatinine of 67 mg/dL and 2.7 mg/dL. Furthermore, brain CT was performed and revealed an acute left basal ganglia hemorrhage. The patient was first admitted to the intensive care unit and then stabilized and moved to the neurological step-down unit. Repeat brain CT confirmed the diagnosis of diabetic striatopathy. Lantus was initially administered aggressively to achieve rapid glucose control and was titrated down by 5 units nightly until appropriate serum glucose was achieved. In addition, the patient was started on Glipizide, Metformin, and 10 units of Humalog sliding scale as needed. The patient's blood glucose levels showed impressive improvement during the course of her hospitalization. She was hospitalized for 10 days and her condition gradually improved. 
Discussion:
This case is a unique presentation of DS in an elderly patient with uncontrolled type 2 diabetes mellitus. Awareness of the risk factors and clinical manifestations of DS is vital for accurate assessment and effective management. Furthermore, given the likelihood of recurrence, documenting a prior diagnosis of DS is imperative for optimizing future care in patients with a history of DS.

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