Home phototherapy for hyperbilirubinemia in term neonates-an unblinded multicentre randomized controlled trial.

The aim of this study was to assess whether home phototherapy was feasible and safe in a cohort of otherwise healthy term-born neonates who fulfilled the criteria for in-hospital phototherapy. This was a randomized controlled trial in which term newborns with a total serum bilirubin of 18-24 mg/dL (300-400 µmol) were randomized to either home phototherapy or conventional in-hospital phototherapy. The primary outcome measurements were safety and efficacy, length of stay and the number of failed treatments. The secondary outcomes were the number of blood samples and weight gain during treatment. One hundred forty-seven patients were recruited, 69 patients randomized to conventional phototherapy and 78 to home phototherapy. The results showed that no patients needed blood exchange and only 4% of the patients allocated to home phototherapy were admitted to the hospital. The duration of phototherapy, length of stay, amount of blood tests and weight change showed no statically significant differences.Conclusion: Home phototherapy could be a safe alternative to inpatient phototherapy for otherwise healthy newborns with hyperbilirubinemia if daily checkups and 24/7 telephone support can be provided. The parents should be informed to contact the hospital immediately if they fail to perform the treatment at home.Trial registration: Clinicaltrials.gov NCT03536078 What is Known: • Phototherapy in the hospital is a safe and effective treatment without major side effects. • Fibre optic equipment has made the choice of home phototherapy possible. What is New: • This is the first randomized controlled trial comparing home phototherapy with hospital phototherapy. • Results indicate that home phototherapy could be considered as a safe and feasible alternative when performed according to instructions given, to hospital treatment for otherwise healthy term newborns.

Outcome after hip arthroscopy for femoroacetabular impingement in 289 patients with minimum 2-year follow-up.

Femoroacetabular impingement (FAI) is a common cause of hip pain and dysfunction. The purpose of this study was to report outcome 2 years after the arthroscopic treatment of FAI using validated outcome measurements. Two hundred and eighty-nine patients (males = 190, females = 99) with a mean age of 37 years underwent arthroscopic surgery for FAI. Patients were included consecutively in a hip arthroscopy registry. The cohort was evaluated using online web-based validated health-related patient-reported outcomes measurements, including the iHOT-12, HAGOS, EQ-5D, HSAS for physical activity level, VAS for overall hip function and overall satisfaction. The mean follow-up time was 25.4 months. Pre-operative scores compared with those obtained at follow-up revealed statistically and clinically significant improvements (P < 0.05) for all measured outcomes; iHOT-12 (43 vs 66), VAS for global hip function (50 vs 71), HSAS (2.9 vs 3.6), EQ-5D index (0.58 vs 0.75), EQ-VAS (67 vs 75) and HAGOS different subscales (56 vs 76, 51 vs 69, 60 vs 78, 40 vs 65, 29 vs 57, 33 vs 58). At the 2-year follow-up, 236 patients (82%) reported they were satisfied with the outcome of surgery. We conclude that arthroscopic treatment for FAI resulted in statistically and clinically significant improvements in outcome parameters.

Serum level of cartilage oligomeric matrix protein is lower in children with idiopathic scoliosis than in non-scoliotic controls.

PURPOSE: The etiology of idiopathic scoliosis remains unknown, but growth is a risk factor for progression. Growth pattern differs in children with and without scoliosis. Cartilage oligomeric matrix protein (COMP) may be associated with scoliosis and growth. We, therefore, studied COMP in children with and without idiopathic scoliosis. METHODS: We included 105 children, with mean age 14.4 years (range 10-16), under observation or treatment for idiopathic scoliosis, and 103 children from an age-matched population-based cohort. COMP was measured in serum at the time of inclusion. Growth velocity was estimated from repeated height measurements. T tests, analysis of covariance or linear regression were used for statistical comparisons. RESULTS: COMP was mean (SD) 11 (5) units/liter (U/L) in children with scoliosis and 13 (5) U/L in the control cohort (p = 0.005, adjusted for sex and sampling time of the day). When patients and controls were analyzed together, high COMP was correlated with high growth velocity (ß = 0.19, p = 0.003). When patients and controls were analyzed separately, COMP was correlated with growth velocity in children with scoliosis (ß = 0.27, p = 0.007), but not in children without scoliosis (ß = 0.02, p = 0.83) (all analyses adjusted for age, sex and sampling time). Low COMP was significantly correlated with large curve size in children with scoliosis (ß = -0.29, p = 0.003), but not after adjustment for age, sex and sampling time (ß = -0.16; p = 0.14). CONCLUSION: COMP was lower in children with idiopathic scoliosis than in a control cohort. In children with scoliosis, high COMP was modestly correlated with high growth velocity, but not with curve severity.

Neonatal pneumothorax: symptoms, signs and timing of onset in the post-surfactant era.

AIM: The primary objective was to describe the incidence, symptoms, clinical signs, and time of onset of neonatal pneumothorax in Örebro County during 2011-2017. Secondary objectives were to describe risk factors, diagnostic procedures, treatments, and mortality and to compare preterm with term/post-term neonates. MATERIALS AND METHODS: This retrospective population-based descriptive study included all neonates born in Örebro County during 2011-2017 and admitted to the neonatal intensive care unit at Örebro University Hospital at age <28 days with an x-ray verified diagnosis of "Pneumothorax originating in the perinatal period" in their medical record. RESULTS: Seventy-five neonates matched the inclusion criteria. The incidence of neonatal pneumothorax in Örebro County during the study period was 3.1 (95% CI: 2.5-3.8) per 1000 live births. All neonates were <48 h at debut of respiratory symptoms and the most common symptom was tachypnea. Twelve (16%) received invasive treatment. The mortality rate was 2 (3%), none due to pneumothorax. CONCLUSION: The incidence of 3.1 per 1000 live births was relatively high, but the frequency of invasive treatment and mortality was low, indicating a high proportion of mild pneumothoraces. The lack of patients aged >48 h indicates that most neonatal pneumothoraces now occur very early in life.

Evaluation of a commercial multiplex PCR test (SeptiFast) in the etiological diagnosis of community-onset bloodstream infections.

The commercial polymerase chain reaction (PCR) test, SeptiFast, is designed to identify the DNA of individual bacterial and fungal pathogens in whole blood. We aimed to evaluate the usefulness of the test for the detection of community-onset bloodstream infections. We prospectively included adult patients who were subjected to blood culture (BC) at an infectious diseases department. For the evaluation, one BC/PCR set (two BC bottles and one PCR tube) per patient was used. When several sets were obtained and analyzed, the first set with any positive result was evaluated. Among 1,093 consecutively included patients, BC was positive in 138 and PCR was positive in 107. Fifty positive PCR results were supported by BC in the same BC/PCR set, ten were supported by other cultures, and, additionally, ten were supported by the clinical presentation. Compared with BC, PCR showed specificities and negative predictive values of >97% for all detectable pathogens. The following sensitivities and positive predictive values (PPVs) were noted: Staphylococcus aureus, 67% and 43%; Streptococcus pneumoniae, 12% and 67%; other Streptococcus species, 43% and 77%; Escherichia coli, 53% and 56%; and Klebsiella species, 43% and 23%. If support from other cultures and the clinical presentation were included in the reference standard, the PPVs for the detection of these bacteria were 57%, 100%, 92%, 75%, and 69%, respectively. Although the specificities were high, the low sensitivities and suboptimal PPVs noted in the present study discourage routine use of the test in its present form for the detection of community-onset bloodstream infections.

Rapid typing of neonatal Staphylococcus epidermidis isolates using polymerase chain reaction for repeat regions in surface protein genes.

Staphylococcus epidermidis is a significant pathogen in neonatal sepsis and other nosocomial infections. For further investigations of the colonisation patterns and invasive pathways, typing methods that are applicable on large populations of bacterial isolates are warranted. In the present study, a genotyping method based on polymerase chain reaction (PCR) for the repeat regions of four genes (sdrG, sdrF, aap and sesE) that encode for bacterial surface proteins was developed and applied to a sample of well-characterised neonatal blood isolates of S. epidermidis (n = 49). The PCR products were visualised on agarose gel (sdrG, sdrF and sesE) or by fragment analysis (aap). The discriminatory index (D-index) for genotyping of the different genes was compared to genotyping by pulsed-field gel electrophoresis (PFGE). The highest D-index for the PCR-based typing methods was found for the combination of sdrF, sdrG and aap (D-index 0.94), whereas the optimal two-gene combination (sdrF and aap) resulted in a D-index of 0.92. We conclude that the described method can be used for the genotyping of large populations of S. epidermidis isolates with a sufficient discriminatory capacity, and we suggest that the combination of sdrF and aap is the most suitable to use.

Soluble thrombomodulin activity and soluble thrombomodulin antigen in plasma.

Endothelial cell membrane-bound thrombomodulin (TM) plays a critical role as a cofactor in the protein C pathway, important in regulating coagulation as well as inflammation. Heterogeneous soluble TM fragments circulate in the plasma and are found at increased levels in various diseases such as cardiovascular disease and diabetes, and in ischemic and/or inflammatory endothelial injuries. The anticoagulant function of these soluble fragments has not been measured in healthy individuals or in patients. Using an immobilized monoclonal antibody against TM and a microtiter plate format, an assay was designed to capture the soluble TM fragments in plasma and measure their cofactor activity in the thrombin-mediated activation of protein C. In addition, soluble TM antigen levels were measured by enzyme-linked immunosorbent assay. Both assays were used to investigate a group of healthy blood donors. TM fragments released into plasma were shown to retain significant cofactor activity, and reference intervals for healthy men and women were established. Furthermore, a statistically significant correlation was observed between soluble TM antigen levels and soluble TM cofactor activity. This notwithstanding, soluble TM activity only accounted for a minor part of all variation in soluble TM antigen levels (R2 = 22% in men and R2 = 16% in women).

Tumor necrosis factors alpha and beta can stimulate bone resorption in cultured mouse calvariae by a prostaglandin-independent mechanism.

Human recombinant tumor necrosis factors alpha and beta (TNF-alpha and TNF-beta), at and above 1 ng/ml (approximately equal to 70 pM), caused a dose- and time-dependent enhancement of 45Ca release from neonatal mouse calvarial bones in vitro. In addition, TNF-alpha and TNF-beta (3-100 ng/ml) caused a dose-dependent stimulation of prostaglandin E2 (PGE2) formation in the calvarial bones. TNF-alpha also enhanced the biosynthesis of PGI2, as assessed by analysis of the stable breakdown product 6-keto-PGF1 alpha. The stimulatory actions of TNF-alpha and TNF-beta on PGE2 formation was maximal at 12 h. Indomethacin, flurbiprofen, and meclofenamic acid, three structurally unrelated nonsteroidal antiinflammatory drugs, abolished PGE2 biosynthesis induced by TNF-alpha and TNF-beta (100 ng/ml). The 45Ca release stimulated by TNF-alpha and TNF-beta (100 ng/ml), however, was only slightly reduced by indomethacin, flurbiprofen, and meclofenamic acid. The partial inhibitory effect of indomethacin on 45Ca release was seen over a wide range of TNF-alpha concentrations, without affecting the concentration producing half-maximal stimulatory response. TNF-alpha and TNF-beta (100 ng/ml) stimulated bone matrix breakdown, as assessed by analysis of the release of 3H from bone prelabeled with [3H]proline. Also, the stimulatory effect of TNF-alpha and TNF-beta on bone matrix degradation was partially reduced by indomethacin. Hydrocortisone (1 microM) and dexamethasone (0.1 microM) abolished TNF-alpha- and TNF-beta-induced production of PGE2. In contrast to the cyclooxygenase inhibitors, the corticosteroids did not affect the stimulatory action by the cytokines on 45Ca release.(ABSTRACT TRUNCATED AT 250 WORDS)

Thrombomodulin gene defects in families with thromboembolic disease--a report on four families.

It has been suggested that an impaired thrombomodulin (TM) function could constitute an abnormality leading to thromboembolic disease (TED). The TM gene from 51 unrelated American patients with TED and 100 American blood donors was screened for mutations. Four heterozygous point mutations in the TM gene were detected. The mutations are distributed throughout the TM gene and predict amino acid changes 1) Pro483 to Leu, 2) Gly61 to Ala, 3) Asp468 to Tyr (earlier described) and 4) a silent mutation not predicting any amino acid change at Glu163. Family studies reveal that the occurrence of the different TM mutations is associated with a history of TED, but there are indications of multiple risk factors and no perfect co-segregation of the TM defects and TED. Among the controls. three individuals carried heterozygous TM variants predicting either a Pro477-Ser mutation (two cases) or an Asp468-Tyr mutation. Our results thus demonstrate that a previously undocumented abnormality in the protein C anticoagulant pathway, a defect in the TM gene, to a certain extent co-segregates with familial thrombophilia. Further studies are needed to prove the causality of these TM mutations.

A novel thrombomodulin gene mutation in a patient suffering from sagittal sinus thrombosis.

Thrombomodulin is an endothelial cell membrane glycoprotein that promotes protein C activation. It has been clearly demonstrated that the anticoagulant functions of the protein C system are important in the prevention of thromboembolic disease. Patients with protein C or protein S deficiency and/or resistance to activated protein C (APC resistance) are at higher risk for developing thromboembolic disease. The first mutation in the thrombomodulin gene was discovered in an American patient suffering from pulmonary embolism at the age of 45 (Ohlin and Marlar 1995). Here we report a case of sagittal sinus thrombosis in a 42-year-old Swedish woman. She was found to carry a heterozygous point mutation changing G127 to A, predicting an Ala25 to a Thr change in the mature thrombomodulin protein. This mutation was also found in her 16-year-old daughter, who so far has not suffered from any thrombotic events. The patient had no other detectable prothrombotic genetic defects associated with the coagulation system. This case supports the hypothesis of an association between mutations in the thrombomodulin gene and venous thrombosis.

Thrombomodulin gene variations and thromboembolic disease.

Thrombomodulin (TM) is the endothelial cell cofactor for protein C activation. Since deficiencies of other protein C system proteins are known to cause thrombotic disease, then defects in the gene coding for TM could be responsible for inherited thrombophilia. We have searched for mutations in the TM gene among healthy controls as well as patients with thrombophilia and identified eight patients heterozygous for TM mutations that are distributed throughout the TM gene. We have shown that the respective TM mutation co-segregates with thromboembolic disease (TED) in four families. Moreover, we have demonstrated that the C allele in a common C/T dimorphism in the TM gene is significantly more frequent among survivors of premature myocardial infarction (MI) than in matched controls. We suggest that TM defects should be added to the list of risk factors in TED, and after further evaluation possibly be included in a routine laboratory evaluation of thrombophilia.

A common thrombomodulin amino acid dimorphism is associated with myocardial infarction.

Endothelial dysfunction and haemostatic imbalance are believed to be important aetiological factors in the development of acute coronary syndromes. Thrombomodulin (TM) is an integral membrane protein crucial for normal endothelial function and activation of the protein C anticoagulant pathway. We have investigated the importance of a common C/T dimorphism in the TM gene (nucleotide 1418) for development of premature myocardial infarction (MI). The C/T dimorphism predicts an Ala455 to Val replacement in the sixth EGF-like domain of TM. The dimorphism was investigated in 97 MI survivors and 159 healthy controls. The C allele was significantly more frequent among patients than controls (p = 0.035). The allele frequency for the C allele was 0.82 in the patients and 0.72 in the control group. The plasma concentration of TM was investigated among healthy controls but was not related to the C/T dimorphism. In conclusion, the association of the C allele with premature MI, suggests that the TM gene and the C/T dimorphism may be aetiological factors involved in the pathogenesis of MI. Possibly, the Ala455 to Val replacement may affect the function of the TM molecule and the activation of the protein C anticoagulant pathway.

Effect of intravenous nitroglycerin on lipid peroxidation after thrombolytic therapy for acute myocardial infarction.

Free oxygen radicals are produced after coronary artery occlusion and reperfusion. Polyunsaturated fatty acids are oxidized by free radicals to lipid peroxides. Measurements of plasma malondialdehyde (MDA) formed by the breakdown of lipid peroxides are often used as markers of lipid peroxidation. The effect of intravenous nitroglycerin on plasma MDA levels was studied in 43 patients who received thrombolytic therapy for acute myocardial infarction. Plasma MDA levels in patients were elevated on admission to the hospital compared with healthy controls, and normalized within 48 hours. A greater increase in plasma MDA concentrations after thrombolysis was found in patients with noninvasive signs of reperfusion than in patients judged to have a persistent occlusion. In the 23 patients receiving immediate intravenous nitroglycerin infusion, plasma MDA levels did not change from baseline to 90 minutes (0.92+/-0.22 and 0.92+/-0.23 micromol/L, p=0.99), whereas a significant increase was found in the 20 control patients who did not receive nitroglycerin (from 0.83+/-0.22 to 1.01+/-0.30 micromol/L, p=0.0004) (p=0.036 for the difference between groups). Successful reperfusion after thrombolytic therapy entails increased lipid peroxidation. Intravenous nitroglycerin reduces lipid peroxidation during myocardial ischemia and reperfusion.

Biocompatibility of polyoxymethylene (Delrin) in bone.

The bone tissue reaction to bulk polyoxymethylene (Delrin) was studied in eight adult albino rabbits followed for up to 5 months after insertion of implants into the tibial metaphyses. Each animal received two implants, one of pure Delrin, the other a 'mosaic' plug with alternating areas of commercially pure titanium and Delrin. At the passage through the cortex, a direct bone-Delrin contact was seen in more than half of the cases, but the contact was usually limited in extent. At the same time, in virtually all sections, a foreign-body reaction with macrophages and giant cells was prominent. It was concluded that bulk Delrin has inferior biocompatibility to titanium, and the advisability of using Delrin as a biomaterial for bone anchorage is questionable.

Spatial facilitation of motor evoked responses in monitoring during spinal surgery.

During spinal cord monitoring, motor responses in the tibialis anterior muscles were recorded on transcranial electrical stimulation of the motor cortex. In order to facilitate the responses, the cortical stimulus was preceded by a train of stimuli to the foot sole within the receptive field of the withdrawal reflex of the tibialis anterior muscle. This cutaneous input provides a spatial facilitation of the cortically elicited response. When the stimulus interval was 50-100 ms, large and reliable responses were seen in most cases.

Soluble thrombomodulin antigen in plasma is increased in patients with acute myocardial infarction treated with thrombolytic therapy.

Thrombomodulin (TM) is an integral endothelial cell membrane protein that functions as a cofactor for thrombin mediated activation of protein C. The anticoagulant functions of the protein C system are important in contributing to a hemostatic balance and prevention of thromboembolic disease. It has been suggested that impaired TM cofactor function could also constitute a prothrombotic abnormality leading to thromboembolic diseases. TM exists not only on the surface of endothelial cells but also as soluble fragment(s) circulating in plasma. The concept of a thrombotic occlusion as the critical event in acute myocardial infarction (AMI) forms the rationale for thrombolytic therapy. After successful reperfusion, patients remain at substantial risk for recurrent infarctions due to rethrombosis. The balance between procoagulant and anticoagulant mechanisms in the postthrombolytic phase have not been studied in detail. We have studied whether the plasma levels of soluble TM are influenced by thrombolytic therapy with streptokinase in patients suffering from AMI. Soluble TM concentrations increased significantly by 24 to 48 h after thrombolytic treatment, simultaneously with an increase in C-reactive protein (CRP, a marker of the inflammatory component of the cell damage) and in thio-barbituric acid reactive substances (TBARS, an indirect marker of lipid peroxidation).

Catabolism of prothrombin-chylomicron complexes in vivo in the rat.

The metabolism in vivo in the rat of 125I-prothrombin-chylomicron complexes was compared to that of free 125I-prothrombin injected in saline or together with chyle chylomicrons. The group that obtained 125I-prothrombin-chylomicron complexes exhibited a faster initial decrease of plasma 125I-prothrombin, a higher radioactivity in the liver and more trichloroacetic acid soluble 125I in plasma than in the other groups that did not differ. In the group injected with 125I-prothrombin-chylomicron complexes, 4% was in the HDL, 0.7% LDL, and 0.8% in VLDL 2 hours after injection. The data thus indicate that although most of the 125I-prothrombin is released during the metabolism of the prothrombin-chylomicron complexes, some is rapidly degraded and some is transferred to plasma lipoproteins and remains circulating for a considerable time period. The observations demonstrate that binding to chylomicrons influences the catabolism of prothrombin in vivo. Since chylomicrons did not influence the clearance of simultaneously injected free 125I-prothrombin, the prothrombin binding to chylomicrons or chylomicron remnants in vivo may, however, be too slow to influence the prothrombin catabolism under normal conditions.

Binding of prothrombin to chyle chylomicrons: effects of temperature and calcium ions, and role of surface phospholipids.

The ability of chyle chylomicrons to bind prothrombin has been studied. Rat chyle chylomicrons were incubated with human 125I-prothrombin and binding was examined by separating the chylomicrons from free 125-I-prothrombin by density-gradient ultracentrifugation, and by gel filtration on Sepharose CL-2B. A significant binding of prothrombin to chyle chylomicrons occurred. The complex formation was calcium dependent, and decreased markedly when the temperature was lowered from 37 degrees C to 20 degrees C and when PH was raised above 8. The time course for the binding at 37 degrees C in presence of 2 mmol/L CaCl2 exhibited an initial lag phase at about 10 minutes. Thereafter most of the binding occurred within 30 minutes. Bound prothrombin could not be removed from chyle chylomicrons by treatment with EDTA, suggesting that this binding is not a simple Ca2+ dependent association between prothrombin and chyle chylomicrons. Inclusion of 1% purified human serum albumin caused a 50% decrease in binding, half of which was reversed by increasing the Ca2+ ion concentration. Addition of pancreatic phospholipase A2 (PLA2) in doses sufficient to hydrolyze more than 95% of the phosphatidylethanolamine (PE) and 37% of the phosphatidylcholine (PC) decreased the binding by 50%. Doses of PLA2 that hydrolyze more than 95% of the phosphatidylethanolamine (PE) and 37% of the phosphatidylcholine (PC) decreased the binding by 50%. Doses of PLA2 that hydrolyzed 60-80% of (PE and 4-10% of the PC decreased the binding by only 7-15%. It is suggested that the binding of prothrombin to chyle chylomicrons is in part mediated by negatively charged phospholipids of the chylomicron surface, although a specific role of the PE could not be demonstrated.

Migration of acetabular components, inserted with and without cement, in one-stage bilateral hip arthroplasty. A controlled, randomized study using roentgenstereophotogrammetric analysis.

Twenty-one patients who had primary osteoarthrosis were managed with a bilateral total hip arthroplasty with insertion of a Charnley femoral component. In each patient, one hip was randomly allocated to have a Harris-Galante acetabular component inserted without cement, and the contralateral hip was treated with an all-polyethylene Charnley acetabular component fixed with cement. The clinical result was satisfactory in all patients. All forty-two hips were followed, with respect to migration of the acetabular component, with use of roentgenstereophotogrammetric analysis for a median of twenty-seven months (range, twenty-three to forty-nine months). Each patient served as his or her own control. Maximum migration in any direction was 1.7 and 2.1 millimeters, and maximum rotation was 2.2 and 2.0 degrees for the Harris-Galante and Charnley acetabular components, respectively. There was no significant difference in migration between the two designs of acetabular components (p = 0.98, p = 0.75, and p = 0.06 for the transverse, longitudinal, and sagittal axes, respectively). However, the Harris-Galante acetabular components rotated significantly more than the Charnley acetabular components around two of the three axes (p = 0.008, p = 0.08, and p = 0.03 for the transverse, longitudinal, and sagittal axes, respectively). The Charnley hip implant has been used clinically for a long time, with successful results. Comparison of new designs of implants with the Charnley prosthesis is therefore important. Roentgenstereophotogrammetric analysis provides a potential for detection of problems with fixation at an early stage rather than after long-term follow-up. No major difference in terms of skeletal fixation was found between the two designs of components after short to medium-term follow-up.

Complications after transpedicular stabilization of the spine. A survivorship analysis of 163 cases.

OBJECTIVES: The authors studied complications of transpedicular stabilization methods. SUMMARY OF BACKGROUND DATA: One hundred and sixty-three consecutive transpedicular stabilization procedures were performed between January 1987 and December 1991. The indications for stabilization were trauma (33 cases), metastatic spinal disorder (30 cases), spinal stenosis (33 cases), spondylolisthesis (27 cases), ankylosing spondylitis (6 cases), low back pain (22 cases), and miscellaneous (12 cases). METHODS: Patients records and the entire series of radiographs for each case were scrutinized by independent observers. All per- and postoperative complications, including implant loosening and fatigue, were recorded. Clinical and radiographic survivorship analyses of the implants were performed. RESULTS: Early complications were unusual and none were associated with permanent morbidity. The probability of not having the implant removed in the first postoperative year was 85%. There was a 40% risk of radiographic failure, defined as loosening or implant fatigue, at 6 months. The outcome was more favorable in cases in which anterior vertebral interbody fusion was also performed. CONCLUSIONS: Transpedicular fixation is a safe procedure with a low incidence of serious per- and early postoperative complications. The mechanical durability of transpedicular fixators used alone is a cause for concern.