Background One of the rare complications of primary total knee arthroplasty is intra-operative fracture. Intra-operative fracture during revision knee arthroplasty has been well-documented but there is limited literature on fractures occurring during primary knee arthroplasty. We conducted a systematic review of the literature to compare and contrast the various studies to clearly define the predisposing factors, incidence, and characteristics of the fracture itself and to arrive at a consensus on the management and prevention of intra-operative fractures during primary knee arthroplasty. Methods The PubMed/Medline, Cochrane, Scopus and Embase databases were searched using keywords “intra-operative fracture”, “distal femoral fracture”, “tibial fracture”, “patella fracture” and “primary total knee arthroplasty”. A total of 158 articles were retrieved and after further filtration and exclusion processing, 10 articles that evaluated intra-operative fractures in primary total knee arthroplasty were included for the review. Results The reported incidence of intra-operative fractures varied from 0.2% to 4.4%. A higher incidence in female patients with a male to female ratio of 0.4 was reported. Posterior stabilized (PS) total knee arthroplasty was associated with higher risk of intra-operative femoral fractures by many authors in this review. Timing of occurrence and location of the intra-operative fractures can vary widely, with femoral fractures occurring more commonly during bone preparation, trialing and impaction of the final implant and tibial fractures occurring during preparation for the tibial keel and impaction of the tibial component. Conclusions Intra-operative fractures during primary total knee arthroplasty are rare with higher risk associated with osteoporosis, rheumatoid arthritis, advanced age, female gender, chronic steroid use, metabolic bone disorders, PS type of femoral implant and difficult surgical exposure of the knee joint due to severe deformities. A plethora of management options have been utilized according to surgeon preference. Standard principles of fracture fixation and arthroplasty principles should be followed to achieve stable internal fixation and any unstable fracture site should be bypassed with the utilization of stemmed components. Satisfactory radiographic and functional outcome can be expected with appropriate treatment.
Non-alcoholic fatty liver disease (NAFLD) progressing to non-alcoholic steatohepatitis (NASH), cirrhosis, end-stage liver disease (ESRD), and hepatocellular carcinoma (HCC) is emerging as a global epidemic. Obesity, diabetes, and metabolic syndrome are some of the leading risk factors for NAFLD. The most prevalent treatment to stop the progression is aimed at dietary modification and lifestyle changes. Bariatric surgery is indicated for patients with morbid obesity with NAFLD. The progression of NAFLD to NASH and HCC can be arrested at various stages of pathogenesis by the already prevalent drugs and the emerging newer molecular and genetic targets. This review article analyzed various preclinical animal trials and clinical trials and has summarized various groups of drugs that can be life-altering in patients diagnosed with NAFLD. This study also discusses the obstacles in taking these clinical trials to bedside treatment.
Sickle cell disease (SCD) is a genetically inherited hematological condition that predominantly affects the African-American subset of the population. It leads to the precipitation of multi-systematic manifestations throughout the course of the life of the patient leading to an increased rate of inpatient admissions and decreased quality of life. This article has reviewed some of the most common pulmonary complications of SCD with a brief overview of the clinical features and their management and has also highlighted the fatality of the complications placing a strong focus on screening, monitoring, and the treatment of the disease. The article has also discussed the management of SCD from a pulmonological perspective rather than hematological alone.
Thrombotic thrombocytopenic purpura (TTP) is caused by the deficiency of ADAMTS13, a von Willebrand factor cleaving protease, which results in thrombotic microangiopathy. It is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and microvascular thrombosis leading to organ damage. It has an extremely high mortality rate if left untreated, making early diagnosis and treatment of the utmost importance. We report a case of TTP that developed after vaccination with Ad26.COV2.S COVID vaccine.We present a case of a 50-year-old African American female who presented with dyspnea one week after receiving the first dose of Ad26.COV2.S vaccine. Initial labs showed anemia, thrombocytopenia, and markers of intravascular hemolysis. The suspicion for thrombotic thrombocytopenic syndromes (TTS), vaccine-induced thrombotic thrombocytopenia (VITT), TTP, and Immune thrombocytopenic purpura (ITP) was high based on the history and laboratory results. Computed tomography (CT) of the chest and ultrasound of bilateral lower extremities did not show any evidence of thrombosis. The absence of thrombosis in the presence of a high PLASMIC score increased the suspicion of TTP over the other differentials. Diagnosis of TTP was confirmed when the ADAMTS13 level was low with an elevated autoantibody inhibitor level. The patient underwent treatment with corticosteroids, plasmapheresis, and rituximab with improvement in symptoms and platelet count. TTP and VITT are the possible differential diagnosis for a patient presenting with anemia, thrombocytopenia, and signs of hemolysis after vaccination with Ad26.COV2.S. It is necessary to differentiate these two clinical entities as the management varies based on the diagnosis.
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