There have been multiple approaches described for internal fixation of acetabular fractures. We discuss the results of acetabular fractures treated in our institution via a Stoppa intrapelvic approach. Between July 1997 to October 2002, the senior author surgically treated 14 acetabular fractures using this approach. Indications for utilizing this approach include displaced anterior column fractures, transverse fractures, T shaped fractures, both column fractures and anterior column or wall fractures associated with a posterior hemi transverse component. The fractures were classified according to Letournel and Judet. There were 10 males, 4 females with a mean age of 34 years (20–57 years). Patients were followed up for an average of 26 months (8–60 months). All fractures went on to union at an average of 12 weeks. There was one superficial wound infection, which was successfully treated with antibiotics. No patients suffered loss of fixation. There were no nerve or visceral injury in our series. Clinical results evaluated were based on the Harris Hip Score (out of 100). Our results show 13 patients had good to excellent results (Score 80–100), whereas one patient had a fair result. The Stoppa intrapelvic approach offers improved reduction and fixation techniques with a decrease in complications associated with extensile approaches.
Aseptic loosening of implants following hip arthroplasty is a cause of significant patient morbidity. We genotyped 99 revision hip arthroplasty patients and 116 primary hip arthroplasty patients for the C282Y and the H63D mutations, which cause Haemochromatosis. Haemochromatosis is an inherited condition leading to excessive iron absorption and deposition in the body. All patients at the time of their primary hip arthroplasty were diagnosed as having osteoarthritis. We identified 9 of the 99 revision arthroplasty patients as being homozygous for the C282Y mutation. The time to revision in this group was significantly lower (p<
0.005) when compared to the remaining 90 patients in the group (mean 8.7 years vs 14.8 years). Analysis of variables such as patient age and sex and also type of prosthesis, place of surgery and operating surgeon had no confounding influence. We hypothesise that undiagnosed iron overload in the patients homozygous for the C282Y mutation is likely to cause premature failure of their primary hip arthroplasty.
We have compared the rates of infection and resistance in an animal model of an orthopaedic procedure which was contaminated with a low-dose inoculum of
Previous reports have indicated that elderly patients suffer more operative complications than younger patients undergoing total hip arthroplasty (THR) We reviewed 46 consecutive patients over 85 years of age at the time of THR. All patients were at least 3 years post-op at the time of review. Pre and post operative D’Aubigne-Postel Hip Scores were assigned. Length of stay, transfusion rates, intra-operative blood loss and patient satisfaction were also noted. Statistical comparisons were mode with a control group of patients, average age 66.3 years. The average age at the time of operation was 86.6 (range 85–92) years. The average follow up was 52.8 (range 38–86) months. The average hospital stay was 21.1 (range 12–40, median 18) days. Pre-operative D’Aubigne-Postel Score averaged 8.4 (range 1–14) points, post-operative D’Aubigne-Postel Score averaged 13.1 (range 9–18) points. Subjective satisfaction was high. There were no operative complications and no dislocations during the follow up period. There were no deaths within one year of surgery. Four of the 45 patients died during the 3 year follow up period. When compared to the control group, patients over the age of 85 years had an increased intra-operative blood loss, p<
0.001, they also had an increased blood transfusion at rate, p=0.0005. Patients over the age of 85 remained in hospital longer, p=0.0002. Comparing D’Aubigne-Postel Score, patients over the age of 85 years benefited as much as the control group, p=0.0001. We conclude that THR is the over 85 years old patients is a safe procedure and yields good functional results.
Osteoarthritis of the hip exhibits progressive degeneration of articular cartilage frequently resulting in total hip arthroplasty (THA). Expression of cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL6) is increased in the synovium and articular cartilage of these patients. Furthermore, these cytokines have been shown to have a negative regulatory effect on chondrocyte proliferation and articular cartilage metabolism. We investigated the frequency of a G/C polymorphism at position −174 of the promoter region of the IL-6 gene and a G/A polymorphism at position −308 of the TNF alpha gene, both of which cause increased expression of these cytokines. We observed that the G variant of the IL6 gene was significantly higher in patients who had undergone revision THA compared to controls (P=0.05). It was also elevated in primary THA patients compared to controls. The G/A polymorphism in TNF alpha was not significantly associated with THA; however, this may reflect the lower incidence of this polymorphism in the population. These results suggest that an alteration in cytokine expression produced by the IL6 −174G/C mutation may have a role in the aetiology of osteoarthritis and the outcome of total hip arthroplasty.
Injury to the infrapatellar branch of the saphenous nerve has been reported as a complication of arthroscopic examination and surgery of the knee. This can result in altered sensation on the anterolateral aspect of the knee, reflex sympathetic dystrophy and, occasionally, severe deafferentation pain. The aim of this cadaveric study was to delineate the course of the infrapatellar branch as it passes across the anterior aspect of the knee and identify potential safe areas for blind puncture at arthroscopy. The risk of damage to the nerve branch from the various open incisions used for orthopaedic surgery of the knee is also discussed. The distribution of the infrapatellar branch was studied in both lower limbers of eleven cadavers (22 specimens). Two patterns of nerve distribution could be described in relation to its path across the proximal margin of the tibia. In 28% of examined cadavers, the infrapatellar branch of the saphenous nerve traverses the patellar tendon and runs laterally without ever crossing over the tibia. In the remaining 72% the infrapatellar branch crossed the proximal margin of the tibia prior to crossing the patellar tendon. Using the interior pole of the patella as a landmark, our results indicated that blind puncture is safe within an approximate wedge-shaped area ranging from 10mm inferior and 30mm medial to the inferior pole up to a level 10mm superior and 50mm medial to the inferior pole of the patella. The incidence of injury to this nerve can be reduced by clarifying the distribution of the infrapatellar nerve branch in relation to palpable landmarks.
Matsen in 1975 described Compartment Syndrome (CS) as a condition in which the circulation and function of tissues within a closed space are compromised by increased pressure within that space. Raised intra-compartmental pressures result in progressive venous obstruction, capillary stagnation and microvascular hypoxia. N-acetyl cysteine (NAC) is an anti-oxidant used clinically to reduce liver injury following paracetamol overdose. NAC has been shown previously to reduce lung injury following exposure to endotoxin. Our aim was to evaluate the efficacy of n-acetyl cysteine in the prevention of CS induced acute muscle injury. Sprague-Dawley rats (n=6/group) were randomised into Control, CS and CS pre-treated with N-Acetyl Cysteine (0.5g/kg i.p. 1 hr prior to induction). Cremasteric muscle was isolated on its neuro-vascular pedicle and CS injury was induced by placing the muscle in a specially designed pressure chamber. Arterial blood pressure was measured via a cannula placed in the carotid artery. To induce compartment syndrome chamber pressure was maintained at diastolic-10 mm Hg. After three hours pressure was released stimulating surgical fasciotomy. One hour after decompression muscle function was assessed by electrical field stimulation: peak twitch (PTV) and maximum tetanus (MTV) values were recorded. Tissue oedema was assessed by wet to dry ratio (WDR). Compartment Syndrome (CS) resulted in a significant decrease in muscle function (PTV, MTV). CS also resulted in a significant increase in tissue oedema (WDR). Pre-Treatment with N-Acetyl Cysteine attenuated CS injury as assessed by these parameters. These data show that administration of the anti-oxidant N-Acetyl Cysteine results in significant attenuation of the muscle injury and oedema caused by Compartment Syndrome. This work was supported by a grant from the Cappagh Trust.
Acute respiratory distress syndrome is a long established complication and continuing cause of significant morbidity and mortality in the multiply injured patient. Systemic inflammatory response syndrome (SIRS) is classically associated with acute pulmonary dysfunction. A variety of insults including trauma, sepsis, hypoxia, ischaemia reperfusion, can trigger systemic inflammatory response and acute lung injury. In models of sepsis, endotoxaemia and ischaemia-reperfusion, acute lung injury is characterised by widespread endothelial-neutrophil interaction and neutrophil activation. Another associated finding in these models of injury, is evidence of induced diaphragm muscle dysfunction, by electrophysiological testing of muscle strips post injury. An established model of incremental increasing skeletal trauma was employed. Adult male sprague dawley rats (mean weight 476grams, 370–520g) were randomised to control, single hindlimb fracture, bilateral hindlimb fracture and bilateral hind limb fracture + 20% haemorrhage. Indices of acute lung injury studied 2 hours post injury were bronchalveolar lavage, cell counts, and protein assays. Pulmonary tissue myeloperoxidase activity was assayed as an indicator of neutrophil activation and pulmonary wet/dry weights were measured as a marker of pulmonary oedema. Diaphragmatic electrophysiological testing was also performed 2 hours post injury. Freshly harvested diaphragmatic muscle strips had peak evoked muscle twitches measured, the maximal tetanic twitch and muscle strip fatigue times were also assessed. Statistical analysis was performed by means of analysis of variance (ANOVA).
Following ischaemia-reperfusion (I-R) tissues undergo a neutrophil mediated oxidant injury. Vitamin C is a water-soluble endogenous anti-oxidant, which has been shown in previous studies to abrogate neutrophil mediated endothelial injury. Our aim was to evaluate Vitamin C supplementation in the prevention of I-R induced acute muscle injury. Sprague-Dawley rats (n-6/group) were randomised into control, I-R and I-R pretreated with Vitamin C (3.3g over 5 days). Cremasteric muscle was isolated on its neuro-vascular pedicle and I-R injury induced by clamping the pedicle for 3 hours, the tissue was subsequently reperfused for 60 minutes. Following reperfusion muscle function was assessed by electrical field stimulation: peak twitch (PTV), maximum tetanus (MTV) and fatigability values were recorded. Tissue neutrophil infiltration was assessed by tissue myeloperoxidase (MPO) activity and tissue oedema by wet:dry ratio (WDR). Ischaemia-reperfusion (I-R) resulted in a significant decrease in muscle function (PTV<
MTV) there was no difference in fatigability values between groups. I-R also resulted in a significant increase in neutrophil infiltration (MPO) and tissue oedema (WDR). Pre-treatment with Vitamin C attenuated I-R injury as assessed by these parameters. This data suggests that oral Vitamin C reduce I-R induced acute muscle injury, possibly by attenuating neutrophil mediated tissue injury.
Ischaemia-reperfusion injury (IRI) is caused by endothelial and subendothelial damage by neutrophil-derived oxidants. Vitamin C is an antioxidant which attenuates endothelial injury after IRI. Our aim was to evaluate the effect of oral vitamin C in the prevention of IRI in skeletal muscle. We used a model of cross-clamping (3 hours) and reperfusion (1 hour) of the cremaster muscle in rats. Muscle function was assessed electrophysiologically by electrical field stimulation. Infiltration by neutrophils was determined by the activity of tissue myeloperoxidase (MPO) and tissue oedema by the wet-to-dry ratio. Neutrophil respiratory burst activity was measured in control animals and groups pretreated with vitamin C. IRI significantly decreased muscle function and increased muscle neutrophil MPO activity and muscle oedema. Pretreatment with vitamin C preserved muscle function and reduced tissue oedema and neutrophil infiltration. Neutrophil respiratory burst activity was reduced in the group treated with vitamin C compared with the control group. We conclude that pretreatment with oral vitamin C protects against acute muscle IRI, possibly by attenuating neutrophil respiratory burst activity.
Recent reports have suggested an association between Perthes’ disease and an underlying thrombophilic or hypofibrinolytic tendency. In Northern Ireland there is a high incidence of Perthes’ disease (11.7 per 100 000 or 1 in 607 children) in a stable paediatric population. We reviewed 139 children with Perthes’ disease and compared them with a control group of 220 aged- and gender-matched healthy primary schoolchildren with similar racial and ethnic backgrounds. There were no significant deficiencies of antithrombotic factors protein C, protein S, antithrombin III or resistance to activated protein C. A total of 53 (38.1%) of the children with Perthes’ disease had a prolonged activated partial thromboplastin time (>
38) compared with 13 (5.9%) of the control group (p <
0.001). Our findings have shown that using standard assays, thrombophilia secondary to antithrombotic factor deficiency or resistance to activated protein does not appear to be an aetiological factor for Perthes’ disease. The cause of the prolonged activated partial thromboplastin time, usually associated with a clotting factor deficiency, is under further investigation.
Compression foot pumps are widely used for the prevention of postoperative venous thrombosis. We tested the efficiency of the pump in ten healthy subjects; the velocity of venous blood flow in the common femoral vein was measured in the horizontal, Trendelenberg (foot-up) and reverse-Trendelenberg (foot-down) positions. Application of the foot pump produced an increase in the venous velocity in all subjects. The mean increase in the horizontal position was 27.2% and in the Trendelenberg position 15.4%. In the reverse-Trendelenberg position, the foot pump produced a mean increase of 102.8%. The efficiency of the compression foot pump in increasing venous return is improved by adopting the reverse-Trendelenberg position. This may increase its thromboprophylactic effect.
We have reviewed 59 patients with injury to the spinal cord to assess the predictive value of the sparing of sensation to pin prick in determining motor recovery in segments which initially had MRC grade-0 power. There were 35 tetraplegics (18 complete, 17 incomplete) and 24 paraplegics (19 complete, 5 incomplete), and the mean follow-up was 29.6 months. A total of 114 motor segments initially had grade-0 power but sparing of sensation to pin prick in the corresponding dermatome. Of these, 97 (85%) had return of functional power (≥ grade 3) at follow-up. There were 479 motor segments with grade-0 power but no sparing of sensation to pin prick and of these only six (1.3%) had return of functional power. Both of the above associations were statistically significant (chi-squared test, p <
0.0001). After injury to the spinal cord, the preservation of sensation to pin prick in a motor segment with grade-0 power indicated an 85% chance of motor recovery to at least grade 3.