Deficits in muscle strength are not seen following recovery from augmented primary repair of anterior cruciate ligament tears.

OBJECTIVES: Anterior cruciate ligament (ACL) repair for proximal tears, where the ligament is re-attached and augmented with suture tape, can negate the need for graft harvest, thereby maintaining native anatomy. Autograft harvest has been associated with persistent deficits in lower limb muscle strength after recovery from ACL reconstruction. The aim of this study is to compare lower limb muscle strength following ACL repair and reconstruction. METHODS: Nineteen ACL repair patients augmented with suture tape and nineteen ipsilateral semitendinosus-gracilis autograft ACL reconstruction patients (both mean 4 years postoperatively) were recruited, along with twenty healthy volunteers. Patient-reported outcome measures (PROMs) were obtained using the Knee Injury and Osteoarthritis Outcome Score (KOOS), Lysholm, and Tegner scores. Maximal isometric quadriceps and hamstring strength at 90° knee flexion were measured using a fixed Myometer after a warm-up and three maximal-effort contractions. RESULTS: Mean hamstring strength of the reconstructed legs was lower than that of healthy volunteers by 0.29 Nm/kg. The hamstring strength ratio of the operated side to the uninjured side was greater in the repair (95% â€‹± â€‹13) than in the reconstruction (81% â€‹± â€‹18) group. There were no statistically significant differences between sides for quadriceps peak torque or for hamstrings in the volunteer or repair group. PROMs scores for the reconstruction group were significantly lower than volunteers across all domains and lower than repair for KOOS activities of daily living and Lysholm scores. CONCLUSION: Hamstring weakness seen following ACL reconstruction is not evident following ACL repair with suture tape augmentation. Strength asymmetry could contribute to re-injury risk and influence functional performance, while altered loads affect knee biomechanics and may lead to osteoarthritis progression. The absence of these deficits in the repair group demonstrates a potential benefit of this technique when used in appropriate patients. LEVEL OF EVIDENCE: II.

Comparable rates of secondary surgery between anterior cruciate ligament repair with suture tape augmentation and anterior cruciate ligament reconstruction.

PURPOSE: The aim of this study was to determine the frequency of secondary surgery following anterior cruciate ligament (ACL) repair with suture tape augmentation in comparison to conventional hamstring ACL reconstruction. We hypothesised that there would be no differences between the groups. METHODS: This was a retrospective comparison study of patients undergoing ACL surgery between September 2011 and April 2018. Two hundred and 73 patients underwent ACL reconstruction using hamstring autograft. During the same timeframe, 137 patients with an acute proximal ACL rupture underwent ACL repair with suture tape augmentation. One patient was lost to follow-up in the ACL reconstruction group leaving 272 patients (99.6%) for the final analysis. In the ACL repair group, three patients were lost to follow-up leaving 134 patents (97.8%) for the final analysis. Secondary surgery was identified by contacting the patients by email/telephone and reviewing patient notes at the time of this analysis. RESULTS: Re-rupture occurred in 32 patients (11.8%) in the ACL reconstruction group compared to 22 patients (16.4%) in the ACL repair group (p = 0.194). Contralateral ACL rupture occurred in four patients (1.5%) in the ACL reconstruction group compared to three patients (2.2%) in the ACL repair group (p = 0.224). In the ACL reconstruction group, nine patients (3.3%) required secondary meniscal surgery whilst five patients (3.7%) required meniscal surgery in the ACL repair group (p = 0.830). Seven other operations were performed in the ACL reconstruction group (2.6%) compared to three other operations in the ACL repair group (2.2%) (p = 0.374). The overall number of patients undergoing secondary surgery in the ACL reconstruction group was 52 (19.1%) in comparison to 30 (22.4%) in the ACL repair group (p = 0.114). CONCLUSION: ACL repair with suture tape augmentation for acute proximal ruptures demonstrated comparable rates of secondary surgery with hamstring ACL reconstruction.

Anterior cruciate ligament repair with internal brace augmentation: A systematic review.

BACKGROUND: Primary repair of anterior cruciate ligament (ACL) ruptures has re-emerged as a treatment option for proximal tears, with internal brace augmentation often utilised. The aim of this study is to provide an overview of the current evidence presenting outcomes of ACL repair with internal bracing to assess the safety and efficacy of this technique. METHODS: All studies reporting outcomes of arthroscopic primary repair of proximal ACL tears, augmented with internal bracing from 2014-2021 were included. Primary outcome was failure rate and secondary outcomes were subjective patient reported outcome measures (PROMs) and objective assessment of anteroposterior knee laxity. RESULTS: Nine studies were included, consisting of 347 patients, mean age 32.5 years, mean minimum follow up 2 years. There were 36 failures (10.4%, CI 7.4% - 14.1%). PROMs reporting was variable across studies. KOOS, Lysholm and IKDC scores were most frequently used with mean scores > 87%. The mean Tegner and Marx scores at follow-up were 6.1 and 7.8 respectively. The mean side to side difference measured for anteroposterior knee laxity was 1.2mm. CONCLUSIONS: This systematic review with meta-analysis shows that ACL repair with internal bracing is a safe technique for treatment of proximal ruptures, with a failure rate of 10.4%. Subjective scores and clinical laxity testing also revealed satisfactory results. This suggests that ACL repair with internal bracing should be considered as an alternative to ACL reconstruction for acute proximal tears, with the potential benefits of retained native tissue and proprioception, as well as negating the need for graft harvest.

Altered kynurenine metabolism correlates with infarct volume in stroke.

Inflammation and oxidative stress are involved in brain damage following stroke, and tryptophan oxidation along the kynurenine pathway contributes to the modulation of oxidative stress partly via the glutamate receptor agonist quinolinic acid and antagonist kynurenic acid, and via redox-active compounds such as 3-hydroxyanthranilic acid. We have confirmed that following a stroke, patients show early elevations of plasma neopterin, S100B and peroxidation markers, the latter two correlating with infarct volume assessed from computed tomography (CT) scans, and being consistent with a rapid inflammatory response. We now report that the kynurenine pathway of tryptophan metabolism was also activated, with an increased kynurenine : tryptophan ratio, but with a highly significant decrease in the ratio of 3-hydroxyanthranilic acid : anthranilic acid, which was strongly correlated with infarct volume. Levels of kynurenic acid were significantly raised in patients who died within 21 days compared with those who survived. The results suggest that increased tryptophan catabolism is initiated before or immediately after a stroke, and is related to the inflammatory response and oxidative stress, with a major change in 3-hydroxyanthranilic acid levels. Together with previous evidence that inhibiting the kynurenine pathway reduces brain damage in animal models of stroke and cerebral inflammation, and that increased kynurenine metabolism directly promotes oxidative stress, it is proposed that oxidative tryptophan metabolism may contribute to the oxidative stress and brain damage following stroke. Some form of anti-inflammatory intervention between the rise of S100B and the activation of microglia, including inhibition of the kynurenine pathway, may be valuable in modifying patient morbidity and mortality.

Tryptophan, adenosine, neurodegeneration and neuroprotection.

This review summarises the potential contributions of two groups of compounds to cerebral dysfunction and damage in metabolic disease. The kynurenines are oxidised metabolites of tryptophan, the kynurenine pathway being the major route for tryptophan catabolism in most tissues. The pathway includes quinolinic acid -- an agonist at N-methyl-D-aspartate (NMDA) receptors, kynurenic acid -- an antagonist at glutamate and nicotinic receptors, and other redox active compounds that are able to generate free radicals under many physiological and pathological conditions. The pathway is activated in immune-competent cells, including glia in the central nervous system, and may contribute substantially to delayed neuronal damage following an infarct or metabolic insult. Adenosine is an ubiquitous purine that can protect neurons by suppressing excitatory neurotransmitter release, reducing calcium fluxes and inhibiting NMDA receptors. The extent of brain injury is critically dependent on the balance between the two opposing forces of kynurenines and purines.

Purine metabolism and clinical status of patients with rheumatoid arthritis treated with dipyridamole.

The anti-inflammatory activities of methotrexate and sulphasalazine may be mediated by increases in endogenous adenosine levels. Since the vascular protective drug dipyridamole inhibits the uptake and metabolism of adenosine we have now tested this compound in patients with rheumatoid arthritis to assess its effects on their symptoms. Forty patients (aged 18-75 years) received dipyridamole 400 mg/day or placebo. The levels of adenosine and its major metabolites were determined by high performance liquid chromatography (HPLC) in blood samples taken at baseline and at monthly intervals during treatment for 6 months. After three months of treatment there was a significant reduction in the modified Health Assessment Questionnaire (mHAQ) score, but these effects were not maintained, and dipyridamole did not modify disease severity scores or the levels of adenosine and its metabolites. We conclude that the symptoms of rheumatoid arthritis were not modified by treatment with dipyridamole.

Blood 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and melatonin levels in patients with either Huntington's disease or chronic brain injury.

Following a study of oxidative tryptophan metabolism to kynurenines, we have now analysed the blood of patients with either Huntington's disease or traumatic brain injury for levels of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and melatonin. There were no differences in the baseline levels of these compounds between patients and healthy controls. Tryptophan depletion did not reduce 5-HT levels in either the controls or in the patients with Huntington's disease, but it increased 5-HT levels in patients with brain injury and lowered 5-HIAA in the control and Huntington's disease groups. An oral tryptophan load did not modify 5-HT levels in the patients but increased 5-HT in control subjects. The tryptophan load restored 5-HIAA to baseline levels in controls and patients with brain injury, but not in those with Huntington's disease, in whom 5-HIAA remained significantly depressed. Melatonin levels increased on tryptophan loading in all subjects, with levels in patients with brain injury increasing significantly more than in controls. Baseline levels of neopterin and lipid peroxidation products were higher in patients than in controls. It is concluded that both groups of patients exhibit abnormalities in tryptophan metabolism, which may be related to increased inflammatory status and oxidative stress. Interactions between the kynurenine, 5-HT and melatonin pathways should be considered when interpreting changes of tryptophan metabolism.

Tryptophan metabolism and oxidative stress in patients with chronic brain injury.

The kynurenine pathway generates the excitotoxic N-methyl-d-aspartate receptor agonist, quinolinic acid and the glutamate antagonist, kynurenic acid, as well as free-radical generators. We investigated the status of the pathway following severe brain injury sustained at least 1 year previously in 15 patients compared with controls. At baseline, patients with brain injury showed increased levels of neopterin, erythrocyte sedimentation rate, C-reactive protein and peroxidation products in the blood compared with controls, indicating persistent inflammation and oxidative stress. At baseline and following tryptophan depletion, more tryptophan was converted to kynurenine in patients than controls, but less kynurenine was converted into the neuroprotectant, kynurenic acid. This suggests that neuroprotection by kynurenic acid may be inadequate in brain-damaged patients even many years after injury. On tryptophan loading, patients metabolized more kynurenine into kynurenic acid than controls, a process which may be neuroprotective. In addition, lower levels of 3-hydroxykynurenine and 3-hydroxyanthranilic acid in patients after tryptophan loading should be protective since these compounds generate free radicals. The results suggest that for brain-damaged patients, increased activation of the kynurenine pathway, oxidative stress and raised levels of inflammation continue many years after the original insult, possibly contributing to the continuing cerebral dysfunction in these patients.

Tryptophan metabolism and oxidative stress in patients with Huntington's disease.

Abnormalities in the kynurenine pathway may play a role in Huntington's disease (HD). In this study, tryptophan depletion and loading were used to investigate changes in blood kynurenine pathway metabolites, as well as markers of inflammation and oxidative stress in HD patients and healthy controls. Results showed that the kynurenine : tryptophan ratio was greater in HD than controls in the baseline state and after tryptophan depletion, indicating increased indoleamine dioxygenase activity in HD. Evidence for persistent inflammation in HD was provided by elevated baseline levels of C-reactive protein, neopterin and lipid peroxidation products compared with controls. The kynurenate : kynurenine ratio suggested lower kynurenine aminotransferase activity in patients and the higher levels of kynurenine in patients at baseline, after depletion and loading, do not result in any differences in kynurenic acid levels, providing no supportive evidence for a compensatory neuroprotective role for kynurenic acid. Quinolinic acid showed wide variations in blood levels. The lipid peroxidation data indicate a high level of oxidative stress in HD patients many years after disease onset. Levels of the free radical generators 3-hydroxykynurenine and 3-hydroxyanthranilic acid were decreased in HD patients, and hence did not appear to contribute to the oxidative stress. It is concluded that patients with HD exhibit abnormal handling of tryptophan metabolism and increased oxidative stress, and that these factors could contribute to ongoing brain dysfunction.

Tryptophan loading induces oxidative stress.

In previous studies tryptophan loads have been administered to human subjects in order to raise central levels of 5-hydroxytryptamine (5HT) and assess the effects of 5HT on behaviour and mood. However, tryptophan is metabolised primarily along the oxidative kynurenine pathway. In this study a 6 g oral tryptophan load was administered to 15 healthy volunteers and the levels of kynurenines and lipid peroxidation products (indicative of oxidative stress) were measured. The results demonstrate that tryptophan loading produces a highly significant increase in lipid peroxidation products in parallel with increased kynurenines. The oxidative stress may result from the generation of quinolinic acid, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid, all of which are known to have the ability to generate free radicals. The results may have implications for the use of tryptophan loading in psychiatric practice, and for the chronic use of diets high in tryptophan.

Venepuncture: the medicolegal hazards.

Venepuncture is commonly regarded as a trivial procedure allocated to the most junior medical staff. The result of this policy is that junior doctors are required to perform a minimally invasive procedure on consenting patients without any structured venepuncture training or assessment. Consequently, inexperienced doctors may perform multiple and sometimes unnecessary, venepunctures, which could damage essential venous access, eg, in the diabetic or renal patient. We review the medicolegal position and suggest that structured venepuncture training is essential and argue that unskilled treatment may be regarded by the Courts as demonstrating the mens rea of assault in the form of recklessness.

How drivers sit in cars.

This paper presents results from a study to measure the separation of the driver's head and shoulder to various internal features of the car. Drivers were filmed whilst driving in general traffic flow, hence were unaware that they were involved in a study. The results show that certain sub-groups of the driver population are likely to be more at risk for certain impact types. Small females are considerably closer to the steering wheel than the rest of the population, and therefore prone to head strikes in frontal impacts. Large males are likely to interact with the cant rail and B-pillar in side impacts.

Consent in medicine and sport.

Last year's football World Cup serves to highlight the confusion now surrounding the classical aim of both sport and sports medicine, namely a healthy mind in a healthy body. The recent focus on violent injuries and the exponential increase in medical litigation suggests that this relationship is not so clearly defined. One cornerstone of this traditional relationship is the concept of informed consent. We review the legal position of consent in sport, especially soccer, which still awaits clarification and draw clear parallels with surgical consent.

Benefits realised from a blood transfusion policy for elective joint arthroplasty.

Transfusion practice and blood ordering policy for major joint replacement was studied during 1989-93. Existing practice requiring automatic preoperative cross-match was prospectively audited. A blood ordering policy rationalising transfusion practice, using the group and screen technique, was then introduced. This resulted in a decrease in the total number of units cross-matched and increased the transfusion fraction significantly. The percentage of blood returned to the blood bank decreased by 46% for knees and 41% for hip arthroplasty. After the introduction of low molecular weight heparin (LMWH) as routine deep vein thrombosis (DVT) prophylaxis for all major total joint arthroplasties, the total transfusion requirement did not increase. In fact, the average number of units transfused per case after its introduction was marginally less at 1.3 units per hip, and 0.9 units per knee.

The limitations of current seatbelts in Europe--some population considerations.

Seatbelts are most likely to function as they were designed if the car occupants' survival space remains uncompromised during an impact. Crashed cars with negligible passenger compartment intrusion were used to study seatbelt effectiveness in that situation. Belted front seat occupants were investigated together with their front impacted vehicles. Current model seatbelts were seen to prevent many more forward contacts than those seen in a similar study 15 years ago. In the earlier study, head contacts occurred to 65% of drivers whereas the current sample contained 24%. The present study also found that thigh or knee contacts were common occurrences for drivers and front seat passengers, as were thoracic injuries caused by loads from the belt itself and neck injuries caused by deceleration. The results emphasize how real people, unlike crash test dummies, have varied characteristics that influence seatbelt performance.

Vertebral column injuries and lap-shoulder belts.

OBJECTIVE: To present cases of vertebral column fractures or fracture dislocations that occur to restrained front seat occupants where there is no evidence of body contact with interior car components based on both medical records and car inspection. MATERIALS AND METHODS: Reviewed were car crash injury cases investigated at the University of Michigan Transportation Research Institute and at the University of Birmingham (England) as well as the National Accident Severity Study files of the National Highway Traffic Safety Administration. Medical records and car inspections in the cases presented did not indicate any evidence of body contact with interior car structures. MAIN RESULTS: Vertebral fractures or fracture dislocations sustained by front seat occupants who were wearing lap-shoulder belts are rare, as evidenced by the relatively few cases identified in the literature and in the crash injury files reviewed. CONCLUSIONS: Infrequently, in frontal crashes, vertebral fractures or fracture dislocations can occur to lap-shoulder belted front seat car occupants without head or torso impacts with interior car structures. Cervical spine injuries are due to neck flexion over the shoulder portion of the restraint. Thoracolumbar fractures can occur in the frontal crash even at low crash velocity.

Chest and abdominal injuries caused by seat belt loading.

Injuries will inevitably occur when restraining loads are exerted on a car occupant by a seat belt during a crash. This study investigated the nature, frequency, and severity of such injuries to the chest and abdomen. Vehicle, occupant, and injury details were obtained from accidents occurring in the Midlands of England. The sample was chosen with emphasis on fatal and serious injuries while also representing slight injuries as rated by the British government scheme. All causes of injuries to 3,276 front-seat restrained occupants were considered. 29.6% had a minor (Abbreviated Injury Scale [AIS] 1) injury caused by seat belt loading, more than from any other cause. The study went on to focus on 1,025 occupants sustaining injuries caused solely by seat belt loading. Of those, 19.4% sustained chest/abdominal injuries rated at Maximum AIS > or = 2 with sternum fractures predominating, and 4.5% were rated at Maximum AIS > or = 3. Occupants were not excluded if they had injuries at other body regions enabling the frequency and severity of head injuries to be considered also. The role played by impact type, speed change at impact, seat belt usage problems, and some aspects of occupant characteristics were investigated. While females were at much greater risk of serious injury (AIS > or = 3) when aged > or = 70 years, the effects of aging were more obvious in the cases with chest injuries rated at AIS 2. Serious chest injuries were predominantly a function of higher speed changes at impact. Occupant height and weight were shown to influence injury outcome, and the study concluded that work is required to further define occupants most at risk. Comparisons were made with two studies into other types of injury at other body regions, and injuries rated AIS > or = 2 caused by seat belt loading were seen to be relatively unlikely. It must also be stressed that casualties sustained seat belt injuries would most likely have received more severe injuries had a seat belt not been worn.

A review of cervical fractures and fracture-dislocations without head impacts sustained by restrained occupants.

Crash injury reduction via lap-shoulder belt use has been well documented. Like any other interior car component, lap-shoulder belts may be related to injury in certain crashes. Relatively unknown is the fact that cervical fractures or fracture-dislocations to restrained front seat occupants occur where no head contact was evidenced by both medical records and car inspection. A review of the available literature on car crash injuries revealed more than 100 such cases. A review of the National Accident Severity Study (NASS) 80-88 file was also conducted, revealing more examples. Case capsule descriptions from the authors' files are also detailed along with examples of such injuries in infants and children in child restraints. However, cervical fractures or fracture dislocations are rare, as evidenced by the relatively few cases identified in the literature, in the author's files, and by an analysis of NASS 80-90 data that revealed a cervical spine injury frequency of only .4% at the AIS-3 level (Huelke, Morris, and Mackay 1992).

Restrained occupants on the nonstruck side in lateral collisions.

Of injury-producing collisions with high seat belt use, some 25% to 30% are lateral collisions. This paper describes some of the characteristics of those collisions as they relate to the front-seat occupant sitting on the side opposite to the impact. The data came from a stratified sample of in-depth crash investigations conducted in the Birmingham region in the period 1983 to 1989 involving current model cars. Crash severity was assessed using the Vehicle Deformation Index (VDI) of the Collision Deformation Classification (CDC) ratings and velocity change. Injury severity was assessed using AIS 85 for each body region. 193 cases of restrained occupants in nonstruck side collisions were examined. Of those occupants with head injuries of AIS < or = 2, 35% came out of the shoulder section of the seat belt. Of abdominal injuries of AIS < or = 2, 72% came from the seat belt itself. Interaction between front seat occupants was not a frequent cause of injury to the nonstruck side occupant. Some aspects of seat belt geometry might be changed so that the trajectory and loading of the nonstruck side occupant are improved.