American journal of hospital medicine, volume 6, issue 4 (2022 October-December)

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https://hdl.handle.net/10355/94701

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    Acute chest syndrome : a narrative review to guide inpatient management
    (University of Missouri, Department of Medicine, Division of Hospital Medicine, 2022-10) Wang, Kevin; Das-Ireland, Monisha
    Introduction: Acute Chest Syndrome (ACS) is a leading complication of sickle cell disease (SCD) with significant morbidity and mortality. The current practice guidelines lack sufficient detail on the evidence behind our standard of practice. Materials and Methods: A comprehensive literature search was accomplished with PubMed with a particular focus on literatures published between 2015-2021 with the keywords ACS management, vaso-occlusive crisis, sickle cell, antibiotics, opioids, transfusion, fluid, steroids, bronchodilators, incentive spirometry, anticoagulation, oxygen, prevention, and SARS-CoV2. We included literatures both in the adult and pediatric population. Results/Discussion: ACS is defined as a new infiltrate in a chest radiograph involving at least one broncho-pulmonary segment in an individual with one additional clinical finding. There are multiple causes of ACS which include infections, pulmonary edema, hypoxemia, and hypoventilation. The goal is to quickly diagnose and treat this condition to prevent irreversible lung damage and mortality. In this narrative review, we discuss why a balanced approach to fluid and pain management will provide better outcomes for patients, and the evidence behind using antibiotics, steroids, bronchodilators, nitric oxide, incentive spirometry, as well as the current management of patients with concomitant ACS and SARS-CoV2. Conclusions: All patients admitted with ACS should be started on a third-generation cephalosporin and macrolide or a fourth-generation fluoroquinolone, incentive spirometry, thromboprophylaxis, oxygen, and simple or exchange transfusion if needed, with a balanced approach to fluid resuscitation and pain control.
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    Do no harm : health systems' duty to promote clinician well-being
    (University of Missouri, Department of Medicine, Division of Hospital Medicine, 2022-06) Agarwal, Anish K.; Gallagher, Thea
    Burnout and mental health disorders plague the health care workforce. Since the pandemic began, there has been an uptick in symptoms of anxiety, depression, and suicidality among health care professionals.1 These threats to the workforce existed before the pandemic. However, they have been exacerbated by the pandemic and are likely to persist for years ahead.2 The attention toward clinician well-being was heightened during the initial surges of COVID cases.3 The nation watched as these individuals struggled with patient acuity and volume, lack of resources, and difficult clinical and personal life decisions. The subsequent surges during various iterations of the pandemic only heightened these issues. Sadly, these problems only intensified with hiring freezes, a lack of salary increases, and a higher emotional burden for practitioners and patients.4 As a result, clinicians became more vocal (and were sometimes heard) across the globe as they discussed: moral injury in allocating care, the dangers of bringing COVID home with them, and frustrations around public policy and behavior, to name a few poignant topics. Due to the initial hiring-freeze policies, the system became overburdened at a time when it needed the most support. Many providers are now stressed by the lack of resources and the ultimate threats to their patients and their license to practice.
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    In-hospital mortality rate and predictors of 30-day readmission in patients with iron deficiency anemia and diastolic heart failure : a cross-sectional study
    (University of Missouri, Department of Medicine, Division of Hospital Medicine, 2022-07) Gangu, Karthik; Bobba, Aniesh; Patel, Parth S.; Vellanki, Sruthi; Trikannad, Anup Kumar; Basida, Sanket; Avula, Sindhu; Tripathi, Alok
    Introduction: There is currently strong evidence of the adverse effects of anemia on the prognosis of heart failure with reduced ejection fraction. Unfortunately, the data on the effects of anemia on a large sample of patients with diastolic heart failure (DHF) is lacking. In this study, we aimed to evaluate the effect of iron deficiency anemia on DHF readmission rates and its corresponding causes and burdens on the healthcare system. Methods: We utilized 2018 Nationwide readmission data and included patients aged ≥18 years with ICD-10 CM code indicating acute or acute chronic diastolic heart failure and iron deficiency anemia was included in the study. The primary outcome is 30-day readmission rates. Secondary outcomes were mortality rates, common causes of readmission, and healthcare utilization. Independent predictors for readmission were identified using cox regression analysis. Results: The total number of admissions in our study was 795,777. The mean age was 74.4 years (SD=13.7), and 63.54% were females. The 30-day readmission rate in patients with diastolic heart failure and iron deficiency anemia was 18.32 % vs. 16.01% in patients without anemia. The mortality rate at index admission and readmission was 3.62 % (2601) and 5.82 % (737), respectively. The most common cause of readmission was hypertensive heart and kidney disease with heart failure (17.74%). The independent predictors of readmission were age [less than] 85 years, household income [less than] 59000$/per year, Medicare and Medicaid insurance, higher Elixhauser comorbidities score, longer Length of stay during the index admission, discharge to a nursing home, hospital located in a large metropolitan area. The financial burden on healthcare for all the readmission was $837 million for 2018. Conclusion: The 30-day readmission rate in patients with diastolic heart failure and iron deficiency anemia is 18.32% in the year 2018. The mortality rate increased from 3.62 % to 5.82 % with readmission. The financial burden for readmission during that year was $837 million. Future studies are warranted to treat iron deficiency anemia to prevent readmissions in diastolic heart failure.
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    Partial anomalous pulmonary venous return mimics arterial positioning after central line placement for plasmapheresis
    (University of Missouri, Department of Medicine, Division of Hospital Medicine, 2022-10) Griffith, Alex J.; Ray, Victoria; Glazer, Joshua M.; Rose, William N.
    A 61-year-old male who was status post right single lung transplant complicated by grade three primary graft dysfunction was admitted and mechanically ventilated for hypoxic respiratory failure. Donor specific antibody testing to human leukocyte antigens was positive. The protocol for antibody-mediated transplant rejection was initiated. One aspect of the protocol was a series of plasmapheresis procedures. In advance of the first plasmapheresis, central line placement was attempted via the left internal jugular vein. A chest x-ray showed a line that terminated to the left of the midline and raised concern for arterial placement (Figure 1). Blood gases from the line were: pH 7.72, pCO2 21 mmHg, pO2 369 mmHg, bicarbonate 28.4 mmol/L. Vascular surgery was consulted and recommended CT imaging of the chest and neck that showed that the line entered the left internal jugular vein, continued to brachiocephalic vein, and then entered an anomalous vein connecting with the left upper lobe pulmonary vein (Figure 2). This anomalous connection suggested that the patient had an anatomic variant, referred to as partial anomalous pulmonary venous return (PAPVR). This anomalous connection explained the high pO2 on the blood gas drawn from the line. The central line was removed. Interventional radiology successfully placed a new central line via right femoral vein access. Usually, four main pulmonary veins drain oxygenated blood from the lungs into the left atrium of the heart. PAPVR refers to an anatomical variant where a pulmonary vein, instead of draining into the left atrium, drains into a systemic vein. The prevalence is 0.4-0.7% [1]. Left-sided PAPVR typically affects the venous drainage of the left upper lobe of the lung and is often an incidental (but potentially alarming) finding. It is often caused by an anomalous vertical vessel that branches off the upper left pulmonary vein and joins with the left brachiocephalic vein or coronary sinus. In right-sided PAPVR, an anomalous pulmonary vein drains into the superior vena cava, inferior vena cava, azygous vein, or coronary sinus [2]. Recognizing PAPVR is particularly important in critically ill patients, as a left-to-right shunt might become obvious only after stopping mechanical ventilation [3]. About 10 case reports describe strategies of keeping the line, removing it, or repositioning it [4]. Finally, while plasmapheresis is a relatively low-risk intervention by itself, the common requirement of central line placement confers risks of bleeding, thrombosis, infection, and misplacement [5].
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    Severe hypothyroidism presenting as cardiac tamponade
    (University of Missouri, Department of Medicine, Division of Hospital Medicine, 2022-10) Pathak, Prutha; Patel, Siddharth; Basu, Ashish; Antony, Mc Anto
    Wide-spread availability of thyroid stimulating hormone assays and routine screening have resulted in early diagnosis of hypothyroidism. Affordable thyroid hormone replacement therapy has ensured that the prevalence of complications of untreated hypothyroidism including cardiovascular complications remains extremely low. Although pericardial effusion can be seen in hypothyroidism especially in severe cases, cardiac tamponade is uncommon. Cardiac tamponade as the first presenting feature of hypothyroidism is a rarity. A 60-year-old man with a history of hypertension and stroke was brought to the hospital with chief complaints of fall and altered mental status. In the emergency room, he was found to have hypothermia and drowsiness, and his laboratory investigations showed severe hypothyroidism. CT scan of chest revealed a large pericardial effusion and an echocardiogram showed evidence of cardiac tamponade. He was taken for an emergent pericardiotomy with a pericardial window. Pericardial fluid and serum investigations confirmed untreated hypothyroidism as the cause of cardiac tamponade. The patient was treated with aggressive thyroid hormone replacement therapy and his clinical condition improved. This case highlights the importance of screening and treatment of hypothyroidism in at-risk populations. If untreated, hypothyroidism may rarely lead to a potentially life-threatening complication such as cardiac tamponade.