Management and Discussion of COVID-19 Related Tracheal Stenosis: A Single Center Retrospective Review.

SARS-CoV-2 virus has led to an unprecedented amount of tracheal stenosis. Rigid bronchoscopy can serve as a curative measure or bridge therapy to tracheal resection. We also briefly discuss the pathophysiology of tracheal stenosis from prolonged intubation and SARS-CoV-2 virus. This should be differentiated from other forms of airway obstruction such as tracheobronchomalacia which would be considered a pseudo-tracheal stenotic disease. The aim of this study is to evaluate stenosis that is unable to be improved with positive airway pressure or "PAP" therapies and required stenting and/or subsequent tracheal resection. By performing Rigid Bronchoscopy and subsequent stenting of airways, we demonstrated outcomes for long term airway patency regarding patients who were intubated secondary to the SARS-CoV-2 virus. We demonstrate superb outcomes in a consecutive case series of 6 patients managed with rigid bronchoscopy, airway stent and tracheal resection. The patients were all managed from a pulmonary perspective by the physicians mentioned in this study.

A rare case and review of pulmonary ossification.

Pulmonary ossification (PO) is a rare metastatic disease characterized by the formation of diffuse heterotopic bone units in the lung parenchyma. Herein, we describe a 45-year-old Filipino male with dendriform pulmonary ossification in combination with gastroesophageal reflux disease and chronic dust exposure, a notably unique association. Radiographic imaging and pathology findings are examined with discussion of various pulmonary disease entities from current literature. Further recognition of PO will facilitate appropriate treatment and better outcomes for patients diagnosed with this enigmatic condition.

Quantitative Pupillometry in the Intensive Care Unit.

Quantitative pupillometry provides a noninvasive and objective assessment within the neurological examination. This review details the physiology of the pupillary light response, the clinical significance of changes in pupillary reactivity, and the variables that compose the Neurological Pupil index or NPi are discussed. This article reviews the most recent applications and advances in quantitative pupillometry for noninvasive intracranial pressure monitoring, postcardiac arrest prognostication, and subarachnoid hemorrhage. Also discussed are the limitations and confounders of quantitative pupillometry in the modern neurological intensive care unit.

Multimodal management of giant cerebral aneurysms: review of literature and case presentation.

The pathophysiology of giant cerebral aneurysms renders them difficult to treat. Advances in technology have attempted to address any shortcomings associated with open surgery or endovascular therapies. Since the introduction of the flow diversion technique, the endovascular approach with flow diversion has become the first-line modality chosen to treat giant aneurysms. A subset of these giant aneurysms may persistent despite any treatment modality. Perhaps the best option for these recurrent and/or persistent giant aneurysms is to employ a multimodal approach-both surgical and endovascular-rather than any single technique to provide a curative result with favourable patient outcomes. This paper provides a review of the histopathology and treatment options for giant cerebral aneurysms. Additionally, an illustrative case is presented to highlight the unique challenges of a curative solution for giant cerebral aneurysms that persist despite initial treatment.

Elevations in High-Sensitive Cardiac Troponin T and N-Terminal Prohormone Brain Natriuretic Peptide Levels in the Serum Can Predict the Development of Anthracycline-Induced Cardiomyopathy.

BACKGROUND: Anthracyclines remain the cornerstone of the treatment in many cancers including lymphomas, leukemia and sarcomas, and breast cancer. The cardiomyopathy that develops from anthracyclines can lead to heart failure and decreased survival. Multiple mechanisms are involved in the pathophysiology of anthracycline-induced heart failure. STUDY QUESTION: We hypothesize that anthracycline-induced cardiac (AIC) pathology can be monitored using a panel of blood biomarkers including high-sensitive cardiac troponin T (hs-cTnT) for myocyte necrosis and N-terminal prohormone brain natriuretic peptide (NT-proBNP) for parietal stress. STUDY DESIGN: A prospective, institutionally approved study recruited all patients with cancer scheduled to start anthracycline chemotherapy in the Transylvania University cancer clinics. MEASURES AND OUTCOMES: Transthoracic 2D echocardiography and the measurements of NT-proBNP and hs-cTnT plasma levels were performed at the beginning of the study and 3 months and 6 months after anthracycline treatment initiation. RESULTS: The plasma levels of hs-cTnT at 3 months (rho = 0.439, P = 0.0001) and 6 months (rho = 0.490, P = 0.0001) are correlated with AIC occurrence. For a cutoff value of hs-cTnT at 3 months > 0.008 ng/mL, we obtained 66.7% sensitivity and 67.9% specificity for developing AIC at 6 months, with a 54.5% positive predictive value and a 87.8% negative predictive value. The NT-proBNP serum levels at 3 months (rho = 0.495, P = 0.0001) and 6 months (rho = 0.638, P = 0.0001) are correlated with an AIC diagnosis at 6 months. For a cutoff value of NT-proBNP at 3 months >118.5 pg/mL, we obtained 80% sensitivity and 79.2% specificity for evolution to AIC at 6 months, with 52.2% positive predictive value and 93.3% negative predictive value. CONCLUSIONS: In anthracycline-treated cancer patients, the increase in plasma levels of NT-proBNP and of hs-cTnT can predict the development of anthracycline-induced cardiomyopathy. Early identification of at-risk patients will potentially allow for targeted dose reductions and will diminish the number of patients developing cardiac pathology.

Refractory Central Neurogenic Hyperventilation: A Novel Approach Utilizing Mechanical Dead Space.

This report describes the successful management of a case of central neurogenic hyperventilation (CNH) refractory to high dose sedation by increasing the mechanical dead space. A 46-year-old male presented with a history of multiple neurological symptoms. Following an extensive evaluation, he was diagnosed with primary diffuse CNS lymphoma and started on high dose steroids. After initial symptomatic improvement, the patient developed increasing respiratory distress and tachypnea. He was intubated and transferred to the neurointensive care unit (neuro ICU). While in the ICU the patient remained ventilator dependent with significant tachypnea and respiratory alkalosis resistant to fentanyl and propofol. This prompted an attempt to normalize the PaCO2 via an increase of the mechanical dead space. This approach successfully increased PaCO2 and bridged the patient until ongoing therapy for the underlying disease resolved the pervasive breathing pattern typical of CNH. Further investigation is warranted to evaluate this strategy, which upon review of the literature appears underused.

Deep brain stimulation for obsessive compulsive disorder: A review of results by anatomical target.

Studies suggest deep brain stimulation (DBS) as a treatment modality for the refractory obsessive-compulsive disorder (OCD). It is unclear where to place the DBS. Various sites are proposed for placement with the ventral capsule/ventral striatum (VC/VS) among the most studied. Herein, we aim to summarize both quantitative Yale-Brown Obsessive-Compulsive Scale (YBOCS) data and qualitative descriptions of the participants' symptoms when given. A literature search conducted via PubMed yielded 32 articles. We sought to apply a standard based on the utilization of YBOCS. This yielded 153 distinct patients. The outcome measure we focused on in this review is the latest YBOCS score reported for each patient/cohort in comparison to the location of the DBS. A total of 32 articles were found in the search results. In total, 153 distinct patients' results were reported in these studies. Across this collection of papers, a total of 9 anatomic structures were targeted. The majority of studies showed a better response at the last time point as compared to the first time point. Most patients had DBS at nucleus accumbens followed by VC/VS and the least patients had DBS at the bilateral superolateral branch of the median forebrain bundle and the bilateral basolateral amygdala. The average YBOCS improvement did not seem to directly correlate with the percentile of patients responding to the intervention. Well-controlled, randomized studies with larger sample sizes with close follow up are needed to provide a more accurate determination for placement of DBS for OCD.

A Rare Presentation of Neuromyelitis Optica Spectrum Disorders.

Neuromyelitis optica spectrum disorders (NMOSDs) are a set of demyelinating disorders that primarily target the optic nerves and the spinal cord. Previously thought to be a subset of multiple sclerosis (MS), now is recognized as a distinct entity. We present a 59-year-old female patient who was admitted for acute upper and lower extremity weakness. The patient had woken up from sleep with sudden onset of weakness. Patient was initially diagnosed with a right hemispheric stroke; however, magnetic resonance imaging of the cervical spine later performed showed abnormal enhancement from C2-C4, representing transverse myelitis. Cerebrospinal fluid was negative for organisms and inflammatory biomarkers. An anti-aquaporin-4 receptor antibody titer was found to be elevated with titers >80 units/mL. The patient was treated with high-dose steroids and plasmapheresis. The NMOSD is a rare entity and, here, we present a rare presentation of the disease. Since its description in 1870, it was confused with MS for years. The advent of anti-aquaporin-4 antibody has been instrumental in differentiating the disease process from MS. This distinction is important, in terms of agents used for treatment and prognostication. The NMOSD is a set of debilitating disease, which requires prompt recognition and appropriate treatment, to avoid the disabling sequelae. Future prospects of the disease include development of novel biological treatment modalities which focus on restoring the loss of immune tolerance which is key to the pathogenesis of the disease.

A Case of Statin-Associated Autoimmune Myopathy.

A 70-year-old previously independent man developed progressive proximal leg weakness resulting in a fall at home suffering traumatic brain injury. He was prescribed a statin medication two years prior, but this was discontinued on admission to the hospital due to concern for statin myopathy. His weakness continued to progress while in acute rehabilitation, along with the development of dysphagia requiring placement of gastrostomy tube and respiratory failure requiring tracheostomy. Corticosteroids and intravenous immunoglobulin were administered without response. Nerve conduction study demonstrated no evidence of neuropathy; electromyography revealed spontaneous activity suggestive of myopathy. A muscle biopsy was performed and demonstrated myonecrosis. Serology was positive for autoantibodies to 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), verifying our diagnosis of statin-associated autoimmune myopathy (SAM). The patient was subsequently treated with rituximab and methotrexate and demonstrated mild clinical improvement. He was eventually liberated from the ventilator. However, later in the course of treatment, he developed respiratory distress and required ventilator support. The patient was discharged to long-term acute care two months after his initial presentation and died due to ventilator-acquired pneumonia three months later. Since their introduction 30 years ago, statin medications have been widely prescribed to prevent cardiovascular diseases. Myalgias and/or myopathic symptoms are among the most recognized side effects of the medication. Statin-associated autoimmune myopathy is a very rare complication of statin use and estimated to affect two to three for every 100,000 patients treated. Clinically, the condition presents as progressive symmetric weakness, muscle enzyme elevations, necrotizing myopathy on muscle biopsy, and the presence of autoantibodies to HMGCR. These findings will often persist and even progress despite discontinuation of the statin. Very few cases of SAM have been described in the literature. Describing this rare condition and the ultimately fatal outcome of our patient, we aim to further understanding of SAM, its presentation and clinical course to promote earlier diagnosis and prompt management.

Nodular Sarcoidosis Masquerading as Cancer.

Nodular lung disease is a rare pulmonary manifestation of sarcoidosis and resembles metastatic neoplasm disease. Nodular sarcoidosis is rare, varying from 1.6% to 4% of patients with sarcoidosis. Radiographic nodules measure from 1 to 5 cm in diameter that typically consist of coalescent granulomas. There is limited data on this form of sarcoidosis and its presentation can mimic primary or metastatic pulmonary neoplasms. Nodular sarcoidosis has a favorable prognosis, and resolution can be seen with oral corticosteroids. Herein, we present such a case of nodular pulmonary sarcoidosis with a lung nodule measured up to 6 cm.

Amiodarone-Induced Pulmonary Toxicity - A Frequently Missed Complication.

INTRODUCTION: Amiodarone is often used in the suppression of tachyarrhythmias. One of the more serious adverse effects includes amiodarone pulmonary toxicity (APT). Several pulmonary diseases can manifest including interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome, diffuse alveolar hemorrhage, pulmonary nodules or masses, and pleural effusion. Incidence of APT varies from 5-15% and is correlated to dosage, age of the patient, and preexisting lung disease. DESCRIPTION: A 56-year-old male with a past medical history of coronary artery disease and chronic obstructive pulmonary disease was admitted for a coronary artery bypass graft. Post-operatively, the patient was admitted to the ICU for ventilator management and continued to receive his home dose of amiodarone 400 mg orally twice daily, which he had been taking for the past 3 months. The patient was found to be hypoxemic with a PaO2 52 mmHg and bilateral infiltrates on chest x-ray. Patient also complained of new onset dyspnea. Physical exam found bilateral rhonchi with bibasilar crackles and subcutaneous emphysema along the left anterior chest wall. Daily chest x-rays showed worsening of bilateral interstitial infiltrates and pleural effusions. A chest high-resolution computed tomography on post-operative day 3 showed extensive and severe bilateral ground glass opacities. APT was suspected and amiodarone was discontinued. A course of oral prednisone without antibiotics was initiated, and after one week of treatment the chest film cleared, the PaO2 value normalized and dyspnea resolved. DISCUSSION: APT occurs via cytotoxic T cells and indirectly by immunological reaction. Typically the lungs manifest a diffuse interstitial pneumonitis with varying degrees of fibrosis. Infiltrates with a 'ground-glass' appearance appreciated on HRCT are more definitive than chest x-ray. Pulmonary nodules can be seen, frequently in the upper lobes. These are postulated to be accumulations of amiodarone in areas of previous inflammation. Those undergoing major cardiothoracic surgery are known to be predisposed to APT. Some elements require consideration: a baseline pulmonary function test (PFT) did not exist prior. APT would manifest a restrictive pattern of PFTs. In APT diffusing capacity (DLCO) is generally >20 percent from baseline. A DLCO was not done in this patient. Therefore, not every type of interstitial lung disease could be ruled out. Key features support a clinical diagnosis: (1) new dyspnea, (2) exclusion of lung infection, (3) exclusion of heart failure, (4) new radiographic features, (5) improvement with withdrawal of amiodarone. Our case illustrates consideration of APT in patients who have extensive use of amiodarone and new onset dyspnea.

Diagnostic and therapeutic considerations in idiopathic hypereosinophilia with warm autoimmune hemolytic anemia.

Hypereosinophilic syndrome (HES) encompasses numerous diverse conditions resulting in peripheral hypereosinophilia that cannot be explained by hypersensitivity, infection, or atopy and that is not associated with known systemic diseases with specific organ involvement. HES is often attributed to neoplastic or reactive causes, such as chronic eosinophilic leukemia, although a majority of cases remains unexplained and are considered idiopathic. Here, we review the current diagnosis and management of HES and present a unique case of profound hypereosinophilia associated with warm autoimmune hemolytic anemia requiring intensive management. This case clearly illustrates the limitations of current knowledge with respect to hypereosinophilia syndrome as well as the challenges associated with its classification and management.