Intra-abdominal pressure increases peri-operatively in patients undergoing deep inferior epigastric perforator flap reconstruction: A prospective study linking high intra-abdominal pressure to non-fatal lung embolism within one patient.

BACKGROUND: The deep inferior epigastric perforator (DIEP) flap is the gold standard for autologous breast reconstruction. The procedure and peri-operative period are associated with the risk of severe post-operative complications, like venous thromboembolic events (VTE) and lung embolism. Whether the intra-abdominal pressure (IAP) increases after the closure of the abdominal defect, thereby potentially affecting the venous backflow and the risk of VTE, is currently not known. AIM: The primary aim is to test if the closure of the abdominal donor site increases the IAP in women undergoing secondary DIEP flap breast reconstruction. MATERIALS AND METHOD: By using a Unometer, we measured the intravesical pressure as a surrogate marker for the IAP, at baseline, immediately after, and 24 h after abdominal skin closure, for 13 patients. RESULTS: The mean IAP increased from 6.1 mmHg (95% CI 4.6-7.7) at baseline to 9.0 mmHg (95% CI 8.0-10.0) immediately after skin closure [mean diff. 2.9 (95% CI 1.0-4.8) (p = 0.007)] and further up to 11.7 mmHg (95% CI 9.0-14.5) 24 h after closure [mean diff. 5.3 (95% CI 1.4-9.1) (p = 0.012)]. We found that IAP varies among the patients, regardless of the tightness of abdominal closure or rectus plication (n = 3). Immediately after closure, none of the isolated patients showed abnormal levels of IAP (>12 mmHg), while eight out of 12 isolated patients (67%) showed IAP levels above the normal range after 24 h. One patient developed a non-fatal lung embolism. CONCLUSION: The mean IAP increases significantly over the post-operative period after DIEP flap reconstruction, although abnormal IAP values are only seen 24 h after the closure of the skin.

Soccer and Benign Paroxysmal Positional Vertigo.

Introduction. Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo among adults. The etiology of BPPV is unknown in approximately 50 percent of cases. This condition is also termed primary BPPV, if the etiology is unknown, and secondary BPPV if patients have identified predisposing factors. A few studies suggest that there is a correlation between the development of BPPV and specific sports. Case Report. A 19-year-old male presented with recurrent episodes of vertigo during soccer play. Eight months prior to referral, the patient was involved in a car accident with a mild head trauma. The patient was later diagnosed with BPPV several times. Discussion. Soccer might be a plausible BPPV trigger, especially if there is a prehistory of head trauma. This is most likely due to the demands of the game such as the change of directions, repetitive head impacts (headers or head collisions), accelerations/decelerations, jumps, foot landings, and rapid head movements.

Inhibition of carnitine palmitoyl-transferase 1 is a potential target in a mouse model of Parkinson's disease.

Glucose metabolism is dysregulated in Parkinson's disease (PD) causing a shift toward the metabolism of lipids. Carnitine palmitoyl-transferase 1A (CPT1A) regulates the key step in the metabolism of long-chain fatty acids. The aim of this study is to evaluate the effect of downregulating CPT1, either genetically with a Cpt1a P479L mutation or medicinally on PD using chronic rotenone mouse models using C57Bl/6J and Park2 knockout mice. We show that Cpt1a P479L mutant mice are resistant to rotenone-induced PD, and that inhibition of CPT1 is capable of restoring neurological function, normal glucose metabolism, and alleviate markers of PD in the midbrain. Furthermore, we show that downregulation of lipid metabolism via CPT1 alleviates pathological motor and non-motor behavior, oxidative stress, and disrupted glucose homeostasis in Park2 knockout mice. Finally, we confirm that rotenone induces gut dysbiosis in C57Bl/6J and, for the first time, in Park2 knockout mice. We show that this dysbiosis is alleviated by the downregulation of the lipid metabolism via CPT1.

Children's distal forearm fractures: a population-based epidemiology study of 4,316 fractures.

AIMS: The aim of this study was to report a complete overview of both incidence, fracture distribution, mode of injury, and patient baseline demographics of paediatric distal forearm fractures to identify age of risk and types of activities leading to injury. METHODS: Population-based cohort study with manual review of radiographs and charts. The primary outcome measure was incidence of paediatric distal forearm fractures. The study was based on an average at-risk population of 116,950. A total number of 4,316 patients sustained a distal forearm fracture in the study period. Females accounted for 1,910 of the fractures (44%) and males accounted for 2,406 (56%). RESULTS: The overall incidence of paediatric distal forearm fractures was 738.1/100,000 persons/year (95% confidence interval (CI) 706/100,000 to 770/100,000). Female incidences peaked with an incidence of 1,578.3/100,000 persons/year at age ten years. Male incidence peaked at age 13 years, with an incidence of 1,704.3/100,000 persons/year. The most common fracture type was a greenstick fracture to the radius (48%), and the most common modes of injury were sports and falls from ≤ 1 m. A small year-to-year variation was reported during the five-year study period, but without any trends. CONCLUSION: Results show that paediatric distal forearm fractures are very common throughout childhood in both sexes, with almost 2% of males aged 13 years sustaining a forearm fracture each year. Cite this article: Bone Jt Open 2022;3(6):448-454.

Downregulating carnitine palmitoyl transferase 1 affects disease progression in the SOD1 G93A mouse model of ALS.

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease characterized by death of motor neurons. The etiology and pathogenesis remains elusive despite decades of intensive research. Herein, we report that dysregulated metabolism plays a central role in the SOD1 G93A mouse model mimicking ALS. Specifically, we report that the activity of carnitine palmitoyl transferase 1 (CPT1) lipid metabolism is associated with disease progression. Downregulation of CPT1 activity by pharmacological and genetic methods results in amelioration of disease symptoms, inflammation, oxidative stress and mitochondrial function, whereas upregulation by high-fat diet or corticosterone results in a more aggressive disease progression. Finally, we show that downregulating CPT1 shifts the gut microbiota communities towards a protective phenotype in SOD1 G93A mice. These findings reveal that metabolism, and specifically CPT1 lipid metabolism plays a central role in the SOD1 G93A mouse model and shows that CPT1 might be a therapeutic target in ALS.