United States

Authors: Ruth Agwaze, Grace Ro, Aspen Ainsworth, Bradley Van HeuKelum, Margaret Puelle

Title: Challenges Faced Treating Severe Postpartum Psychosis when Standard of Care is Contraindicated

Background: Thyroid dysfunction is a perinatal complication associated with mood disorders, particularly postpartum depression (Schmidt, 2022). However, there are few accounts of thyroid disorders leading to postpartum psychosis treated with antipsychotic and antithyroid agents (Fulton, 2024) We present a case of postpartum thyrotoxicosis and psychosis in which these medications were ineffective/contraindicated.

Case: A 36-year-old Black female G4P4004 with multiple sclerosis, migraines and anxiety presented to her primary care physician with persistent asymptomatic sinus tachycardia five months after a postpartum pulmonary embolism, despite treatment with propranolol. A few weeks later, she developed palpitations, weight loss, and tremors. Blood work showed free T4 &gt; 4.4 ng/dL (reference range 0.9-1.7 ng/dL), antibodies to thyroglobulin and thyroid peroxidase, and undetectable TSH. She was diagnosed with Grave’s Disease and prescribed oral methimazole. Five months later, she presented to the hospital with diffuse abdominal pain and altered mental status. She had been self-treating with topical vitamin-infused oils instead of methimazole because she feared its side effects. For the next year, she had numerous hospitalizations due to paranoid and erratic behaviors, delusions of being married to a deceased rapper, and over 100-lb weight loss. In the hospital, she received IV methimazole which led to agranulocytosis. Higher antipsychotic and beta-blocker doses were ineffective. She had limited insight and made multiple attempts to leave against medical advice. Due to the need for consistent outpatient follow-up, social distancing, and concerns for future fertility, radioactive ablation was contraindicated. This left thyroidectomy as the only option, but she refused surgery when she was previously in a lucid state. Endocrinologists, psychiatrists, neurologists, and legal/ethical consultants concluded that treatment over objection was not acceptable because the patient was not in a life-threatening thyroid storm. Plasmapheresis was discussed, but this placed the patient at risk without guarantee that psychosis would resolve. One day, she spontaneously regained lucidity and consented to a thyroidectomy. She eventually returned to her baseline after weeks of levothyroxine treatment, and her tachycardia resolved. 

Discussion: This case demonstrates the diagnostic and therapeutic challenges of treating psychosis in the setting of postpartum thyroiditis, as well as ethical implications of treatment in patients with limited capacity. 

Conclusion/implications: This case provides further evidence that postpartum thyroid dysfunction can lead to postpartum psychosis. More research is necessary to understand the relationship between postpartum thyroiditis and psychosis, as well as guidelines for patients who may not respond to typical treatment regimens. 

References: 
1. Fulton, A., Mittal, N., &amp; Deb, A. (2024). Postpartum Psychosis as a Consequence of Thyroiditis Versus Relapse: A Diagnostic Dilemma. Cureus, 16(1), e52357. https://doi.org/10.7759/cureus.52357
2. Schmidt, P. M. D. S., Longoni, A., Pinheiro, R. T., &amp; Assis, A. M. (2022). Postpartum depression in maternal thyroidal changes. Thyroid research, 15(1), 6. https://doi.org/10.1186/s13044-022-00124-6

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Challenges Faced Treating Severe Postpartum Psychosis when Standard of Care is Contraindicated

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Authors: Ruth Agwaze, Grace Ro, Aspen Ainsworth, Bradley Van HeuKelum, Margaret Puelle

Title: Challenges Faced Treating Severe Postpartum Psychosis when Standard of Care is Contraindicated

Background: Thyroid dysfunction is a perinatal complication associated with mood disorders, particularly postpartum depression (Schmidt, 2022). However, there are few accounts of thyroid disorders leading to postpartum psychosis treated with antipsychotic and antithyroid agents (Fulton, 2024) We present a case of postpartum thyrotoxicosis and psychosis in which these medications were ineffective/contraindicated.

Case: A 36-year-old Black female G4P4004 with multiple sclerosis, migraines and anxiety presented to her primary care physician with persistent asymptomatic sinus tachycardia five months after a postpartum pulmonary embolism, despite treatment with propranolol. A few weeks later, she developed palpitations, weight loss, and tremors. Blood work showed free T4 > 4.4 ng/dL (reference range 0.9-1.7 ng/dL), antibodies to thyroglobulin and thyroid peroxidase, and undetectable TSH. She was diagnosed with Grave’s Disease and prescribed oral methimazole. Five months later, she presented to the hospital with diffuse abdominal pain and altered mental status. She had been self-treating with topical vitamin-infused oils instead of methimazole because she feared its side effects. For the next year, she had numerous hospitalizations due to paranoid and erratic behaviors, delusions of being married to a deceased rapper, and over 100-lb weight loss. In the hospital, she received IV methimazole which led to agranulocytosis. Higher antipsychotic and beta-blocker doses were ineffective. She had limited insight and made multiple attempts to leave against medical advice. Due to the need for consistent outpatient follow-up, social distancing, and concerns for future fertility, radioactive ablation was contraindicated. This left thyroidectomy as the only option, but she refused surgery when she was previously in a lucid state. Endocrinologists, psychiatrists, neurologists, and legal/ethical consultants concluded that treatment over objection was not acceptable because the patient was not in a life-threatening thyroid storm. Plasmapheresis was discussed, but this placed the patient at risk without guarantee that psychosis would resolve. One day, she spontaneously regained lucidity and consented to a thyroidectomy. She eventually returned to her baseline after weeks of levothyroxine treatment, and her tachycardia resolved. 

Discussion: This case demonstrates the diagnostic and therapeutic challenges of treating psychosis in the setting of postpartum thyroiditis, as well as ethical implications of treatment in patients with limited capacity. 

Conclusion/implications: This case provides further evidence that postpartum thyroid dysfunction can lead to postpartum psychosis. More research is necessary to understand the relationship between postpartum thyroiditis and psychosis, as well as guidelines for patients who may not respond to typical treatment regimens. 

References: 
1. Fulton, A., Mittal, N., & Deb, A. (2024). Postpartum Psychosis as a Consequence of Thyroiditis Versus Relapse: A Diagnostic Dilemma. Cureus, 16(1), e52357. https://doi.org/10.7759/cureus.52357
2. Schmidt, P. M. D. S., Longoni, A., Pinheiro, R. T., & Assis, A. M. (2022). Postpartum depression in maternal thyroidal changes. Thyroid research, 15(1), 6. https://doi.org/10.1186/s13044-022-00124-6

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Background
Malingering involves intentional falsification of symptoms for external gain, affecting 8% of medical cases and costing $150 billion annually. Detection is challenging due to its episodic nature. The DSM-IV- TR classifies malingering as a condition of clinical attention without precise criteria. Socio-economic factors contribute to its prevalence among prisoners, employees avoiding work, and homeless individuals seeking benefits.

Case Presentation
A 32-year-old homeless male was admitted from the ED under suicide precautions. He traveled from another state seeking a new start but lacked support. Previously hospitalized for hypoglycemia while on escitalopram and cyproheptadine for PTSD, he was admitted to our hospital's general medical floor. He was referred to our team for inpatient psychiatric consultation due to possible suicidal ideation. The patient reported a "medium" mood with lapses in medication adherence due to a TBI from an MVC three months ago. He denied current suicidal ideation, hallucinations, or mania, attributing suicidal thoughts to missed SSRI doses. His PTSD originated from the MVC that rendered him paraplegic and caused the death of the driver and the traumatic loss of his parents in the Iraq War in 2010. He experiences nightmares and flashbacks but denies hypervigilance. His history includes a suicide attempt in 2010 leading to hearing loss and several psychiatric admissions for suicidal ideation. He recounted an interrupted suicide attempt where a bullet struck metal and lodged in his leg, later removed surgically. Concerns arose due to dramatic and questionable details, further complicated by the attending physician recognizing him under a different identity. Physical therapy for paraplegia showed inconsistencies in sensory perception, with intact sensation in all extremities but claimed loss in the lower extremities.

Discussion
Factitious disorder and malingering were assessed through evaluations by the primary team, Neurology, and physical therapy. For example, factitious or malingered insulin use involves assessing insulin levels to differentiate between exogenous and endogenous sources. Managing these disorders involves confronting the patient with gathered information. In this case, when confronted with his prior name, he confirmed previous use. Regarding the falsification or malingering of paraplegia, the teams informed him that placement in a nursing home or subacute rehabilitation was not possible because his clinical exam did not indicate acute or subacute rehab needs Having a primary care physician can help mitigate malingering, though this is difficult for homeless patients. Hospital protocols should ensure thorough history evaluations and vigilance to manage malingering cases.



Challenges in Detecting and Managing Malingering Disorder

Gastroesophageal reflux disease (GERD) is a chronic gastrointestinal disorder characterized by the regurgitation of gastric contents into the esophagus. In this case, we describe a pediatric patient with a with a history of reflux symptoms that have been evaluated via endoscopy who presents to the clinic for evaluation of his anxiety. Upper GI endoscopy demonstrated mild inflammation with an unremarkable biopsy. However, reflux symptoms continue to persist as his anxiety has been increasing. The current base of knowledge regarding pediatric GERD and anxiety is small, and challenges remain in discovering a definitive causative link between the two.

Generalized Anxiety Disorder and Gastroesophageal Reflux Disease in a Pediatric Patient

Abstract Title
Psychosis Due to B12-Deficiency Followed by Steroid-Induced Psychosis Without Psychiatric History

Background
Both B12 deficiency and corticosteroid use can present clinically with neuropsychiatric manifestations like a manic episode, including personality changes, poor concentration, memory impairment, delirium and psychosis. Underlying mechanisms for such mental changes in B12 deficiency include alterations in one carbon metabolism, genetic vulnerability, and variability in folate metabolism. Neuropsychiatric symptoms of B12 deficiency typically improve with B12 supplementation, but may lead to irreversible cognitive impairment. For Corticosteroid-induced psychotic disorder (CIPD), there appears to be a dose-dependent relationship with prednisone doses greater than 40 mg per day and psychiatric manifestations. Termination of the steroid typically leads to neuropsychiatric symptom resolution within two weeks, but can last from days
to months. Severity of symptoms can be minimized with antipsychotics or mood-stabilizing medications.
This case discusses a rare scenario in which a patient with no known psychiatric history experiences two episodes of psychosis caused by different organic causes (B12 deficiency, corticosteroid use) within 7 months.

Case Presentation
A 61-year-old male with a past medical history of hypertension and hyperlipidemia, and no prior psychiatric history presents to the ED for mania-like symptoms including elevated mood, decreased need for sleep, pressured speech, grandiosity, and distractibility. Lab results revealed severely low B12 of 50 mcg/ml, and the patient was discharged with a diagnosis of Psychotic Disorder due to another Medical Condition. In the subsequent weeks, the patient’s psychiatric symptoms resolved with consistent B12 supplementation. 
Six months later, the patient presented outpatient for symptoms of left ear labyrinthitis and was prescribed 60mg prednisone daily for 20 days. 14 days into the course, the patient began to experience similar mania-like symptoms and presented to the ED. Laboratory workup was unremarkable including normal B12 levels, and he was transferred to inpatient psychiatry. The patient was diagnosed with Steroid-Induced Psychosis and started on Depakote 500mg BID and Zyprexa 10mg nightly. He was discharged 2 days later after considerable improvement in severity of symptoms

Discussion
Additional study of organic psychoses is needed to understand how to treat symptoms for acute stabilization vs. long-term prevention and describe the underlying predispositions to and mechanisms of psychotic symptoms in each context. There is no known link between prior psychosis due to B12 deficiency and risk of CIPD. More research is needed to explain the etiology of episodic neuropsychiatric symptoms in patients with no known psychiatric history, and whether primary psychiatric disorders such as Bipolar I better explain the symptoms.

Recurrent Psychosis without Prior Psychiatric History: B12-Deficiency Followed by Steroid-Induced Psychosis

Refractory Anti-NMDA Receptor Encephalitis Improved with Bilateral Salpingo-Oophorectomy 

Alyssa Jackson, Rachel Billingsly, Kristin Olson, Miguel Yerena, Lauren Stogner, Shefali Hegde, MD, Rizwan Hassan, DO, Taylor Wallace, MD, Alex LaFever, MD, David Spiegel, MD


Anti-NMDA Receptor (anti-NMDAR) encephalitis is the most common type of autoimmune encephalitis, characterized by antibodies directed at the NR1 subunit of NMDA receptors. Decreased NMDA signaling is thought to be the cause of the characteristic neuropsychiatric features. It is a paraneoplastic syndrome, most commonly associated with ovarian teratomas. The disease course involves a viral-like prodrome phase that rapidly progresses to psychiatric symptomatology within weeks to months of onset ranging from deficits in memory, speech, and cognition, to seizure, autonomic dysfunction, altered mental status, and disorganized movements. Prompt diagnosis and treatment is vital as 20% of patients develop focal deficits or die from the resultant encephalitis, with another 10% relapsing within 1-2 years. This novel case report describes a refractory case where empiric bilateral oophorectomy, with subsequent negative pathology, led to symptom resolution.

This was a case of a 32-year-old female with a past medical history of HSV and no past psychiatric history that presented after a witnessed tonic-clonic seizure. UDS was positive for cannabis and cocaine, initially concerning for substance-induced delirium, but with sustained confusion and agitation. Lumbar puncture revealed a mild lymphocytic pleocytosis. CSF studies were positive for anti-NMDA receptor antibodies. A malignancy work-up was negative. She received a course of IVIG and steroids, PLEX and steroids, and then rituximab with only modest improvement. Whole body PET scan was considered, but logistically difficult to obtain due to need for transportation to another facility and ongoing agitation requiring physical restraints. Diagnostic laparoscopy was unremarkable, and a right salpingo-oophorectomy was performed; the pathology report was negative for micro-teratoma. With only minimal symptomatic improvement after nearly 2 weeks, she returned to the OR for an empiric left salpingo-oophorectomy, which was also negative for micro-teratoma. Despite negative ovarian pathology, she demonstrated clinical improvement 2 days later and was discharged to long-term rehab shortly after. 

As in this case of refractory anti-NMDAR encephalitis, it is important to exhaust all non-invasive approaches to treatment prior to oophorectomy. Although controversial, bilateral salpingo-oophorectomy should be considered in patients with severe and treatment refractory anti-NMDA encephalitis despite negative imaging. There have been similar cases of anti-NMDA receptor encephalitis described in the literature which have shown improvement after oophorectomy despite negative pathology.


Refractory Anti-NMDA Receptor Encephalitis Improved with Oophorectomy

Background
In June 2023, the FDA released a First Draft Guidance on Clinical Trials with Psychedelic Drugs, reflecting a reemerging interest in using psychoactive compounds like psilocybin to treat conditions such as depression, PTSD, and substance use disorders. Psilocybin, specifically, has shown promising efficacy in treating unipolar depression, with ongoing studies exploring its safety in bipolar II depression. However, its significant serotonergic activity raises concerns about potentially triggering manic episodes in susceptible individuals. Existing clinical trials of psilocybin have historically excluded patients with bipolar disorder, and literature is scarce regarding psilocybin-induced mania.

Case Presentation
The patient is a 16-year-old male with a history of depression, was brought to the emergency department by police following erratic behavior reported by his family. He had new-onset decreased need for sleep, pressured speech, grandiosity, and paranoia. On exam, he reported high energy and made several grandiose statements, such as that he believed he could achieve anything and fly if he wanted to. He admitted to consuming chocolates infused with magic mushrooms and cannabis. Despite his regular cannabis use, there had been no recent change in frequency or type. Lab work, including urine drug screen (UDS) and liver panel, were positive for THC and mildly elevated LFTs, respectively. Due to safety concerns related to his high-rise living situation, he was hospitalized. The patient was initiated on risperidone due to signs of both mania and psychosis being present and was recommended for transfer to an inpatient psychiatric facility. On day three, he continued to demonstrate elevated mood, grandiosity, tangential speech, and distractibility, although there were improvements in his sleep. 
The patient was then accepted for transfer to an external psychiatric facility, and the remainder of his clinical course is not known.

Discussion
This case underscores the potential of psilocybin to induce manic episodes, especially in individuals with a personal or family history of bipolar disorder. Healthcare providers should prioritize obtaining comprehensive substance use histories and evaluating past medical and family histories when assessing patients presenting with acute manic or psychotic symptoms. Such practices are essential for assessing the risk of psilocybin-induced mania and formulating appropriate management strategies.
Future research is critical to elucidate the safety profile of psilocybin, particularly in populations with existing bipolar disorder or heightened susceptibility to mania. Understanding these risks is paramount for informing clinical decisions regarding the therapeutic use of psilocybin and mitigating potential adverse outcomes, as highlighted by this case.

Unmasking the Silent Danger: Manic Symptoms in an Adolescent Following Psilocybin Use

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/

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

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.

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