Complications of Cranioplasty Following Decompressive Craniectomy: Risk Factors of Complications and Comparison Between Autogenous and Artificial Bones.

Objectives: Craniectomy is widely performed to lower the intracranial pressure in various conditions, such as traumatic brain injury, stroke, or brain swelling. Several complications can occur after craniectomy and cranioplasty, which significantly affect the prognosis of the patients after surgery. We studied the complications of craniectomy and cranioplasty and the factors affecting prognosis after the operation. Methods: Patients who underwent cranioplasty after craniectomy at Daejeon St. Mary's Hospital from 2015 to 2021 were included. We retrospectively reviewed their medical records and images. All patients were classified according to their sex, age, clinical grade, and diagnosis. Complications after craniectomy and cranioplasty were investigated for 1 year after surgery. The complications included postoperative hemorrhage, infection, hydrocephalus, and bone resorption. Results: This study included 104 patients. Complications after decompressive craniectomy were significantly frequent in patients with hypertension history (p=0.03). In contrast, complications of cranioplasty were significantly frequent in patients with history of diabetes mellitus, hepatic failure, or trauma (p=0.03, p<0.01, and p=0.01, respectively). Artificial bones were used more frequently than autologous bones in patients with trauma (p=0.03); however, there was no difference in the incidence of complications between them (p=0.64). Conclusion: Hypertension is a significant risk factor for decompressive craniectomy complications, especially rebleeding. Diabetes, hepatic failure, and trauma are significant risk factors for cranioplasty complications. There was no statistical difference in the incidence of complications between the use of autologous and artificial bones.

Complications and risk factors after digital subtraction angiography: 1-year single-center study.

OBJECTIVE: Digital subtraction angiography (DSA) is an imaging technique used to diagnose and confirm abnormal lesions of cerebral blood vessels in various situations. Several complications such as cerebral infarction, contrast-induced allergy, and angio-site hematoma or infection can occur after DSA. We investigated complication rates and risk factors related to DSA. METHODS: All patients who underwent DSA at Incheon St. Mary's Hospital from January to December 2021 were included. Those who underwent emergency DSA due to stroke or who underwent endovascular surgery within 1 week after DSA were excluded. Complications that occurred within 1 week after DSA were included in the study and was classified into three categories (neurologic complications, contrast-induced allergy, and wound complications). RESULTS: The mean age was 57.7±13.2 years old and the female was dominant at 63.9%. The overall complication rate was 5% (n=20/407). Regarding neurologic complications, the presence of malignancy (p<0.01), and a longer procedure time (>15 minutes, p=0.04) were statistically significant factors. Contrast-induced allergy did not show any statistically significant difference in any parameter. The wound complication rate was higher in men (p=0.02), trans-femoral approach (p=0.02), frequent alcohol drinkers (p=0.04), those taking anticoagulants (p=0.03), and longer procedure time (>15 minutes, p<0.01). CONCLUSIONS: DSA is an invasive diagnostic modality and can cause several complications. Patients with cancer should be more careful about the occurrence of cerebral infarction, and men taking anticoagulants or drinking frequently should be more careful about the occurrence of angio-site hematomas.

Granulocyte colony stimulating factor treatment in non-alcoholic fatty liver disease: beyond marrow cell mobilization.

Protective effects of granulocyte colony stimulating factor (G-CSF) in acute liver injury via marrow cell mobilization have been reported in several studies. But exact mode of action and optimal protocol of G-CSF has been still doubt in chronic disease. Here we investigated mode of action and optimization of G-CSF as a treatment for non-alcoholic fatty liver disease (NAFLD). Various doses of conventional G-CSF (30 µg/kg once weekly, once daily for 5 days, twice weekly) and long acting G-CSF (30 µg/kg once a month) were evaluated in two kinds of NAFLD animal models to optimize the G-CSF protocol. G-CSF receptor expression highest increased in NAFLD model among various liver diseases compare to control (NAFLD: 14.7 times, alcohol hepatitis: 7.1 times, cirrhosis: 2.4 times, and ischemia reperfusion: 6.8 times). G-CSF treatment reduced intrahepatic fat accumulation, and inflammation in two kinds of NAFLD animal models. G-CSF increased PI3K/Akt expression in hepatocyte as well as decreased apoptotic drive (increased Bcl-2 expression and decreased Bax expression) in animal model. Five day consecutive G-CSF treatment and once a month long acting G-CSF increased marrow derived stem cell marker in peripheral blood. But twice a week conventional G-CSF treatment did not increased CD34+ cell in peripheral blood and liver neither. Not only high dose G-CSF (once daily for 5 days) but also hepatotropic dose G-CSF (twice a week) significantly reduced hepatocyte apoptosis via PI3K and Akt pathway activation without marrow cell mobilization in NAFLD animal model.

Histologic and Metabolic Derangement in High-Fat, High-Fructose, and Combination Diet Animal Models.

BACKGROUND: We used high-fat (HF), high-fructose (HFr), and combination diets to create a dietary animal model of nonalcoholic fatty liver disease (NAFLD). Comparison of both clinical phenotypes has not been well defined. The purpose of this study was to compare histologic and metabolic characteristics between diets in an animal model of NAFLD. METHODS: NAFLD was induced in rats by feeding them HF, HFr, and combination (HF + HFr) diets for 20 weeks. The degree of intrahepatic fat accumulation, inflammation, and oxidative stress was evaluated. Metabolic derangements were assessed by the oral glucose tolerance test and the intrahepatic insulin signal pathway. RESULTS: Body weight gain and intrahepatic fat accumulation were more prominent in the HF feeding group than in the HFr group. The expressions of NOX-4 and TLR-4 were higher in the HF and HFr combination groups than in the HF-only group. Other intrahepatic inflammatory markers, MCP-1, TNF-α, and endoplasmic reticulum stress markers, were the highest in the HF + HFr combination group. Although intrahepatic fat deposition was less prominent in the HFr diet model, intrahepatic inflammation was noted. CONCLUSIONS: Intrahepatic inflammation and metabolic derangements were more prominent in the HF and HFr combination model than in the HF monodiet model.

Osthol attenuates hepatic steatosis via decreased triglyceride synthesis not by insulin resistance.

AIM: To evaluate the effects of osthol on intrahepatic fat synthesis, ß-oxidation, inflammation, and insulin resistance by multifaceted analysis. METHODS: Sprague-Dawley rats (n = 30) were randomly divided into control, non-alcoholic fatty liver disease (NAFLD), and osthol groups. NAFLD and osthol groups were fed with a high-fat diet for 14 wk. After 8 wk of the high-fat diet, the osthol group also received osthol 20 mg/kg orally 5 times/wk. To assess the insulin resistance, oral glucose tolerance was performed at the end of 14 wk. Immunohistochemical (4-HNE, F4/80) and hematoxylin and eosin (HE) staining were performed on liver tissue extracts after animal sacrifice at 14 wk. SREBP1c, FAS, SCD-1, PPAR-α, CROT, MCP-1, IRS-1, and IRS-2 mRNA expressions were assessed with reverse transcription-polymerase chain reaction. RESULTS: HE staining revealed that, compared with the NAFLD group, the osthol group showed significantly decreased intrahepatic fat content (39.4% vs 21.0%; P = 0.021). SREBP1c expression in the NAFLD group increased compared to controls (P = 0.0001), while osthol treatment decreased SREBP1c expression compared with the NAFLD group (P = 0.0059). In the osthol group, intrahepatic FAS and SCD-1, which act downstream of SREBP1c, decreased significantly compared with the NAFLD group. Moreover, PPAR-α expression in the osthol group was also significantly higher than in the NAFLD group (P = 0.0147). CONCLUSION: Osthol treatment attenuated liver steatosis by decreasing de novo liver triglyceride synthesis and had nominal effects on insulin resistance and liver inflammation.