[Management of Patients With Kennedy Terminal Ulcer: Challenges and Best Practices].

Whether receiving acute, long-term, or home care, patients at the end of life may experience skin failure due to hemodynamic changes and insufficient perfusion of skin tissue. Skin failure begins as superficial ulcers that can quickly become full-thickness lesions, which are referred to as Kennedy terminal ulcers. Skin lesions commonly occur in the final 6 weeks of life and can occur even in the presence of a comprehensive care plan. The pathogenesis of Kennedy terminal ulcers is often misunderstood and these ulcers are commonly misdiagnosed as pressure injuries. This confusion may lead to aggressive care with subpar clinical outcomes that cause further psychological and emotional distress to patients and family members. Patients at the end of life must be provided care focused on their comfort rather than wound healing. To provide the highest quality of care to patients, four end-of-life strategies should be used, including: taking account of the preferences of patients and families, protecting the skin, describing the wound, and preserving a high quality of care. The terms, pathophysiological and clinical manifestations, and nursing treatments related to skin failure at the end of life described in the literature are introduced in this paper. Furthermore, monitoring indicators of nursing quality are provided.

Special presentation of bronchobiliary fistula after transcatheter arterial chemoembolization: A case report.

RATIONALE: Transcatheter arterial chemoembolization (TACE) is a widely adopted treatment for advanced stage hepatocellular carcinoma (HCC). Nevertheless, several complications may occur, such as hepatic artery injury, nontarget embolization, pulmonary embolism, hepatic abscess, biloma, biliary strictures, and hepatic failure. However, bronchobiliary fistula is rarely mentioned before. PATIENT CONCERNS: A 65-year-old man with HCC underwent the TACE procedure, and then he encountered fever, dyspnea, abdominal pain, and abundant yellowish purulent bronchorrhea. DIAGNOSIS: Bronchobiliary fistula was diagnosed based on the computed tomography (CT) scan of his chest, which revealed the right lower lobe of his lung was connected to a hepatic cystic lesion. INTERVENTIONS: Percutaneous transhepatic cystic drainage was performed, and we obtained yellowish bile, showing the same characteristics as the patient's bronchorrhea. OUTCOMES: We kept drainage of his biloma and provided supportive care as the patient wished. Unfortunately, the patient passed away due to progressive right lower lobe pneumonia 2 weeks later. LESSONS: This case exhibits a typical CT scan image that was helpful for the diagnosis of post-TACE bronchobiliary fistula. Post-TACE bronchobiliary fistula formation hypothesis includes biliary tree injuries with subsequent biloma formation and diaphragmatic injuries. Moreover, the treatment of bronchobiliary fistula should be prompt to cease pneumonia progression. Therefore, we introduce this rare complication of post-TACE bronchobiliary fistula in hopes that future clinicians will keep earlier intervention in mind.

Case Report: Factor VII Deficiency Presented With Cephalohematoma After Birth.

Introduction: Factor VII deficiency is a rare inherited autosomal recessive bleeding disorder with a global prevalence of 1/500,000. Most cases remain asymptomatic, and cases with severe clinical presentation are rarely reported. Case Presentation: A newborn male with no relevant maternal antenatal history, delivered via vacuum-assisted cesarean section, presented with a large cephalohematoma after delivery. Poor appetite, pale appearance, and bulging fontanelles were observed 2 days later, progressing to hypovolemic shock. Further imaging examination revealed a large intracranial hemorrhage. Serial laboratory examination revealed remarkable coagulopathy with prolonged prothrombin time and factor VII deficiency (<1%, severe type). The patient was genetically confirmed to have the FVII:c 681+1 G>T homozygous mutation. Brain hemorrhage was resolved with high-dose factor VII replacement therapy with recombinant activated factor VII. However, repeated hemothorax and intracranial hemorrhage were detected. Therefore, the patient was under regular factor VII supplementation with a rehabilitation program for cerebral palsy. Conclusions: A case of factor VII deficiency with large cephalohematoma and intracranial hemorrhage after birth is described herein, which was treated with high-dose replacement therapy. Variants of the FVII:c 681+1 G>T (IVS6+1G>T) homozygous genotype may present with a severe phenotype at the neonatal stage. We aim to share a unique neonatal presentation with a certain genotype and treatment experience with initial replacement therapy, followed by regular prophylactic dosage.

The protective effect of quercetin on retinal inflammation in mice: the involvement of tumor necrosis factor/nuclear factor-κB signaling pathways.

Quercetin is a natural flavonoid that occurs in fruits and vegetables. Retinal inflammation is an important cause of vision loss. This study was aimed to analyze the effects of oral administration of quercetin on retinal inflammation. Transgenic mice, carrying nuclear factor-κB (NF-κB)-driven luciferase genes, were injected with 1 mg per kg body weight of lipopolysaccharide (LPS). Various amounts (1, 10, and 100 mg per kg body weight) of quercetin were orally given to mice. LPS-induced retinal inflammation was evaluated by bioluminescence imaging and histological examination 4 hours later. RNA-Seq analysis of gene expression profiles was performed to explain the mechanisms of quercetin on eye inflammation. Our data showed that LPS enhanced luminescent signals on ocular tissues, while LPS-induced luminescence intensities were significantly suppressed by quercetin by 73.61 ± 21.74%. LPS significantly increased the thickness of retinal tissues by 1.52 ± 0.37 fold, in comparison with the mock, while quercetin reduced the LPS-induced retinal thickness and decreased the accumulation of infiltrating granulocytes. Biological pathway analysis showed that tumor necrosis factor (TNF), cytokine, and NF-κB signaling pathways were involved in the anti-inflammatory mechanisms of quercetin. Immunohistochemical staining further showed that quercetin reduced the activation of NF-κB, the expression of interleukin-1ß and TNF-α, and the infiltration of granulocytes in retinal tissues. In conclusion, this is the first study reporting the effects and mechanisms of orally administered quercetin against LPS-induced retinal inflammation in mice. Due to its safety, our study suggested that supplementation of quercetin has beneficial effects on the eyes.