Objective To determine the total blood loss and hidden blood loss associated with surgery for lumbar spinal stenosis and to identify risk factors for blood loss. Methods From September 2002 to July 2006, the cl inical data from 138 patients with lumbar spinal stenosis undergoing initial operation were analysed prospectively. There were 44 males and 94 females, aging 56-78 years (mean 66.7 years). A simple posterior lumbar spinal decompression was used in 26 cases;posterior spinal canal decompression, interbody distraction Cage, and bone graft between transverse process was used in 54 cases; pedicle screw fixation, posterior decompression and bone graft between transverse process was used in 32 cases; posterior decompression, pedicle screw fixation, interbody Cage, and graft between transverse process was used in 26 cases . Before operation, 23 patients took aspirin, and after operation 15 patients had gastrointestinal bleeding. Intraoperative blood loss was calculated by the aspirator and observed blood loss intraoperation. The whole estimated blood loss was calculated according to the level of hemoglobin, blood volume and blood transfusion at the time of admission and after 3 and 4 days of operation. Results The blood loss intraoperation was (485.51 ± 143.75) mL. The estimated blood loss was (1 218.60 ± 306.86) mL, which was significantly higher than the intraoperational blood loss (P lt; 0.001). There was significant difference between the estimated blood loss and observed blood loss during surgeries (P lt; 0.001). There were significant differences in the estimated blood loss and observed blood loss during surgery between patients treated with aspirin and without aspirin (P lt; 0.001), between patients with gastrointestinal bleeding and whiout gastrointestinal bleeding (P lt; 0.001). Conclusion The total blood loss after surgery for lumbar spinal stenosis is much greater than that of observed intra-operation. The type of surgery, treatment with aspirin and gastrointestinal bleeding or ulceration can all independently increase blood loss.
Usher syndrome (USH) is an autosomal recessive hereditary disease, characterized as retinitis pigmentosa and deafness. According to the severity of hearing loss, presence or absence of vestibular dysfunction, Usher syndrome is divided into 3 clinical subtypes: USH1, USH2 and USH3. Due to the genetically heterogeneous, it is important and valuable to find out the gene mutations in USH patients, which will be helpful to prenatal diagnosis, early intervention and gene therapy. Till now, the following 13 USH-related chromosomal loci were reported in the literature: USH1B, USH1C, USH1D (CDH23 gene), USH1F (PCDH15 gene), USH1G (SANS gene), USH1E, USH1H, USH1J and USH1K, USH2A, USH2C, USH2D and USH3 (CLRN1 gene). Ten out of all 13 loci have been located and identified. But more mechanisms should be further investigated, such as the relationship between the locus of gene mutations and clinical symptoms, how the modified protein structures and functions trigger clinical symptoms.
ObjectiveTo analyze the associated risk factors of hidden blood loss in the internal fixation of intertrochanteric fracture. MethodsA retrospective analysis was made on the clinical data of 317 cases of intertrochanteric fractures which were treated by internal fixation between January 1993 and December 2008. There were 154 males and 163 females with an average disease duration of 4.58 days (range, 7 hours to 33 days); the age was (69.86±15.42) years; the average height was 1.64 m (range, 1.50-1.84 m);and the average weight was 62.26 kg (range, 39-85 kg). Of them, intramedullary fixation was used in 203 patients and extramedullary fixation in 114 patients. The operation time was (61.99±18.25) minutes. The red blood cell transfusion was given to 84 patients, and the transfusion amount was 200-1 000 mL. The drainage volume was 0-750 mL (mean, 61.85 mL). Hidden blood loss was calculated through change of hematocrit level before and after operation. The multiple linear regression was performed to analyse the risk factors of hidden blood loss. ResultsThe total blood loss was (918.60±204.44) mL, the hidden blood loss was (797.77±192.58) mL, and intraoperative visible blood loss was (257.32±271.24) mL. Single factor analysis showed hidden blood loss was significantly higher in variables as follows:gender, age, injury cause, fracture type, American anesthesiologists grading, anesthesia mode, hypertension, diabetes, disease duration, operation time, intraoperative transfusion of red blood cells, and fixation type. Multiple linear regression showed age, fracture type, anesthesia mode, and fixation type were significant risk factors. ConclusionThe risk factors of hidden blood loss are advanced age (>60 years), unstable fracture, general anesthesia, and imtramedullary fixation. Especially in elder patients with unstable fracture treated by intramedullary fixation under general anesthesia, hidden blood loss is more significant.
ObjectiveTo observe the gene mutations and clinical phenotypes in patients with Usher syndrome type 2 (USH2) and retinitis pigmentosa (RP).Methods From August 2018 to January 2019, 4 patients and 11 normal family members from 3 families of USH2 and RP who visited Henan Eye Hospital were enrolled in the study. Detailed medical history was obtained and visual acuity, fundus color photography, OCT, visual field, full field ERG examination were performed. Among the three families, pedigree 1 was diagnosed with USH2, pedigree 2 and pedigree 3 were diagnosed with RP. The peripheral venous blood of patients and their family members were collected, and the whole genomic DNA was extracted. Targeted capture next generation sequencing analysis was performed on these members, and Sanger sequencing and family co-segregation were verified.ResultsIn the family F1, the proband had symptoms of RP and sensorineural deafness. Sequencing revealed two heterozygous frameshift variants: c.13877-13880 del AGAC (p. Q4626P) in exon 64 and c.798 del T (p. F266L) in exon 5 of USH2A. Both patients of family 2 and 3 showed RP signs without deafness. Two heterozygous variants c.15178T＞C (p. S5060 P) in exon 70 and c.6986C＞A (p. P2329H) in exon 37, and a pathogenic heterozygous variant c.5836C＞T (p. R1946X) in exon 29 of USH2A were identified in family F2. A heterozygous missense variant c.14951C＞T (p. P4984L) in exon 68 and a variant c.11156G＞A (p. R3719H) in exon 57 of USH2A were found in family F3. The results of conservation analysis showed that the corresponding amino acid sites of USH2A p.Q4626P, p.F266L, p.S5060P, p.P2329H and p.P4984L were highly conserved in many species. Among these 7 pathogenic variants detected, M1-M4 and M6 were novel.ConclusionsMutation USH2A gene are the main cause of USH2 and non-syndromic RP. Different variants affect protein translation and synthesis, consequently causing different clinical phenotypes.
Objective To compare the effects of rivaroxaban and enoxaparin on hidden blood loss after total hip arthroplasty (THA). Methods A retrospective analysis was made on the clinical data of 76 patients (93 hips) with avascular necrosis of the femoral head who underwent primary THA between June 2009 and January 2012. After operation, 10 mg rivaroxaban was used at 6-10 hours for 14 days in 44 cases (54 hips) (rivaroxaban group) and 4 000 U enoxaparin at 12 hours for 14 days in 32 cases (39 hips) (enoxaparin group). There was no significant difference in age, gender, weight, height, disease duration, grade of avascular necrosis of the femoral head, and lesion hips between 2 groups (P gt; 0.05). The total blood loss, dominant blood loss, hidden blood loss, and percentage of hidden blood loss were calculated according to the formula. The bleeding events were recorded within 35 days after operation. Results The total blood loss was (1 509.56 ± 325.23) mL; the dominant blood loss was (928.09 ± 210.50) mL; the hidden blood loss was (581.47 ± 215.01) mL; and the percentage of hidden blood loss was 37.88% ± 10.42% in the rivaroxaban group. The total blood loss was (1 521.38 ± 516.49) mL; the dominant blood loss was (917.50 ± 378.73) mL, the hidden blood loss was (603.88 ± 377.15) mL, and the percentage of hidden blood loss was 38.18% ± 18.33% in the enoxaparin group. There was no significant difference in the above indicators between 2 groups (P gt; 0.05). The incidence of bleeding event was 9.1% (4/44) in the rivaroxaban group and was 3.1% (1/32) in the enoxaparin group, showing no significant difference (χ2=1.073, P=0.390). Conclusion There is no significant difference in the risk of hidden blood loss and incidence of bleeding event for primary THA between the rivaroxaban and the enoxaparin use.