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Background and Objective: Acute respiratory distress syndrome (ARDS) is a severe, life-threatening medical condition characterized by poor oxygenation due to non-compliant lungs secondary diffuse alveolar damage. Encouragingly, the incidence of ARDS has declined steadily recently, attributed mainly to implementation of keystone guidelines and continuous research efforts. Mechanical ventilation is the cornerstone of supportive care for ARDS patients. This review aims to consolidate the current knowledge on pneumothorax (PNX) and pneumomediastinum (PMD) and to enhance the understanding of the readers. The objectives are to (I) explore the etiology and risk factors of PNX and PMD, (II) discuss the various diagnostic modalities available, (III) evaluate management options, and (IV) recent advancements. Methods: A search of the literature was conducted using PubMed, MEDLINE, and Google Scholar for relevant articles pertaining to PNX and PMD in ARDS population. The clinical presentation, diagnostic and management strategies of PNX, PMD, and ARDS were summarized, and all authors reviewed the selection and decide which studies to include. Key Content and Findings: The adoption of lung-protective ventilation strategies, based on the review of literature from the recent years, shows that it has played a significant role in reducing the occurrence of barotrauma, such as PNX and PMD. However, PNX and PMD remains to be a challenging complication to manage. With a specific focus on PNX and PMD, this review provides valuable insights into effectively managing and understanding these critical complications among ARDS patients. Conclusions: ARDS, with its evolving definition, continues to pose a life-threatening threat. Despite the widespread adoption of lung-protective ventilation strategies, PNX and PMD present persistent challenges in management. Further research is imperative to enhance the risk assessment of ARDS patients prone to developing PNX and PMD and to institute more effective prevention and treatment measures.
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BACKGROUND: New onset hyperglycemia is common in patients with severe coronavirus disease 2019 (COVID-19) infection. Cytokine storm due to COVID-19 infection is an essential etiology for new-onset hyperglycemia, but factors like direct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced pancreatic ß-cell failure have also been postulated to play a role. AIM: We plan to investigate further the mechanisms underlying SARS-CoV-2 infection-induced hyperglycemia, particularly the rationale of the cytokine-induced hyperglycemia hypothesis, by evaluating the association between inflammatory markers and new onset hyperglycemia in non-diabetic patients with COVID-19 infection. METHODS: We conducted a retrospective case-control study on adults without diabetes mellitus hospitalized for COVID-19 infection. The serum levels of glucose and inflammatory markers at presentation before initiation of corticosteroid were collected. Hyperglycemia was defined as glucose levels ≥ 140 mg/dL. C-Reactive protein (CRP) ≥ 100 mg/L, ferritin ≥ 530 ng/mL, lactate dehydrogenase (LDH) ≥ 590 U/L, and D-dimer ≥ 0.5 mg/L were considered elevated. We used the χ 2 test for categorical variables and the Mann-Whitney U test for continuous variables and calculated the logistic regression for hyperglycemia. RESULTS: Of the 520 patients screened, 248 met the inclusion criteria. Baseline demographics were equally distributed between patients with hyperglycemia and those who were normoglycemic. Serum inflammatory markers in patients with or without new-onset hyperglycemia were elevated as follows: CRP (58.1% vs 65.6%, P = 0.29), ferritin (48.4% vs 34.9%, P = 0.14), D-dimer (37.1% vs 37.1%, P = 0.76) and LDH (19.4% vs 11.8%, P = 0.02). Logistic regression analysis showed LDH odds ratio (OR) = 1.623 (P = 0.256). We observed significantly higher mortality (24.2% vs 9.1%, P = 0.001; OR = 2.528, P = 0.024) and length of stay (8.89 vs 6.69, P = 0.026) in patients with hyperglycemia. CONCLUSION: Our study showed no association between CRP, ferritin, LDH, D-dimer levels, and new-onset hyperglycemia in non-diabetic patients with COVID-19 infection. It also shows an increased mortality risk and length of stay in patients with hyperglycemia. With new-onset hyperglycemia being closely associated with poor prognostic indices, it becomes pivotal to understand the underlying pathophysiological mechanisms behind the SARS-CoV-2 infection-induced hyperglycemia. We conclude that the stress hyperglycemia hypothesis is not the only mechanism of SARS-CoV-2 infection-induced hyperglycemia but rather a multicausal pathogenesis leading to hyperglycemia that requires further research and understanding. This would help us improve not only the clinical outcomes of COVID-19 disease and inpatient hyperglycemia management but also understand the long-term effects of SARS-CoV-2 infection and further management.
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A thorough history and identifying risk factors are pivotal in establishing the cause of pancreatitis and preventing recurrences to curb the incidence of chronic pancreatitis and/or pancreatic cancer.
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INTRODUCTION: Human granulocytic anaplasmosis (HGA) is a potentially fatal tick-borne disease caused by the obligate intracellular bacterium Anaplasma phagocytophilum. It is most commonly found in the Northeastern and Midwestern parts of the United States especially during spring and summer months. The clinical picture of anaplasmosis is varied ranging from common symptoms such as fever, headache and myalgia to rarer presentations such as pancytopenia. CASE PRESENTATION: We present a case of a 62 year old male who presented with watery diarrhea, fever, and pancytopenia. Although there is a broad differential for pancytopenia, a thorough history provides clues regarding the diagnosis. In our patient, a recent history of camping in Upstate New York was suggestive of an infectious etiology from a tick borne illness. CLINICAL DISCUSSION: A tick-borne panel guided us to identify the diagnosis of HGA. Although the exact underlying pathogenesis of tick-borne illnesses leading to pancytopenia is still unknown, the pancytopenia is postulated to be due to a multi-nodal mechanism involving immune and non immune platelet destruction, global bone marrow suppression, hemophagocytic lymphohistiocytosis and myelosuppressive chemokines release. CONCLUSION: We hope that this case report elucidates the importance of obtaining a meticulous history in guiding clinicians towards prompt diagnosis, even in instances where there may be an evolving clinical picture.
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The global pandemic of Coronavirus 2019 (COVID-19) or SARS-CoV-2 has numerous manifestations in different organ systems. It is known that SARS-CoV-2 infects the hepatobiliary system leading to presentations such as acute cholecystitis, choledocholithiasis and hepatitis. Although the exact mechanism of the underlying pathology is unknown, it is likely attributed by the tropism of the virus to the ACE2 receptors in the hepatocytes and bile duct cells resulting in a cytokine storm that precipitates as systemic symptoms from acute COVID-19 infection. In this case report we present a case of a 47-year-old male who presented with signs consistent with acute cholecystitis. It was confirmed on ultrasound and he was incidentally found to be positive for COVID-19 on routine surveillance testing. He was asymptomatic and was being prepped for cholecystectomy, but developed an acute elevation of liver enzymes suggesting choledocholithiasis. After endoscopic retrograde cholangiopancreatography (ERCP) and cholecystectomy the patient experienced a rapid normalization of liver enzymes and improvement of his abdominal symptoms.
