Damage Control techniques involve primary external fracture fixation to reduce the ‘second hit’ of surgery. This study used a large animal (ovine) trauma model to compare pathophysiological responses of primary external femoral fixation and intramedullary stabilisation.

Under terminal anaesthesia bilateral femoral fractures and hypovolaemia were produced using a pneumatic ram. 24 sheep were randomised into 4 groups and monitored for 24 hours. Group 1 – Control; Group 2 – Trauma only; Group 3 – Trauma and external fixation; Group 4 – Trauma and reamed intramedullary stabilisation. Outcome measures: pulmonary embolic load (transoesophageal echocardiography); plasma coagulation markers; bronchoalveolar lavage differential cell counts (neutrophils, lymphocytes and macrophages).

Total embolic load was significantly higher (p<0.001) in the intramedullary fixation group (median score 42 versus 20). All trauma groups had a significant increase (p < 0.05) in prothrombin time with a fall in antithrombin III and fibrinogen levels. No significant differences occurred between trauma groups with any coagulation or alveolar lavage marker.

Intramedullary femoral fracture fixation produced a relatively higher pulmonary embolic load. However, the initial fracture fixation method did not affect any of the changes seen in the measured coagulation or inflammatory markers during the first 24 hours of injury.

Background: Transcranial Doppler Ultrasound has been used to detect cerebral micremboli following long bone fractures and intramedullary stabilization. However the clinical effects in terms of cognitive function remain unclear. We aim to measure the cerebral embolic load and to clarify clinical cognitive function following lower limb long bone fractures stabilised by reamed intramedullary fixation.

Methods: 27 femoral and tibial diaphyseal fractures (median age 36 years) were cognitively assessed 3 days following surgery and compared to the normal age and intelligence matched population. A wide range of cognitive tests assessed: global cognitive function; verbal fluency and speed; immediate and delayed memory recall; attention and mental processing speeds. 20 patients had intra-operative transcranial Doppler ultrasound monitoring of the middle cerebral artery for embolic signals. In addition a marker of neuronal injury (S-100B protein) was measured pre-operatively and at 0, 24 and 48 hours following surgery. One sample Wilcoxon signed rank test compared median (percentile) cognitive scores for the fracture patient cohort to a value of 50 representing the normal population.

Results: A significant deterioration in immediate memory recall of unstructured material was noted following surgery. Using established criteria, 4 patients had detectable cerebral emboli with a median count of 3 (range 2–9). Scatter plot graphs indicated no correlation between cerebral embolic events and clinical cognitive dysfunction. S-100B protein levels increased from a pre-operative median (interquartile range) of 0.20 (0.23) to a peak immediately following surgery of 0.51 (0.97) with no correlation to clinical cognitive dysfunction

Conclusions: A small number of cerebral embolic events occur during intramedullary fracture stabilisation but with no direct correlation made to cognitive dysfunction on detailed testing. Recent concerns over the specificity of S100B protein due to extracerebral tissue release appear to be confirmed.

Significance: Clarify cognitive function following intramedullary fracture stabilisation and correlate with cerebral (systemic) embolic load.

The stress response to trauma is the summation of the physiological response to the injury (the ‘first hit’) and by the response to any on-going physiological disturbance or subsequent trauma surgery (the ‘second hit’).

Our animal model was developed in order to allow the study of each of these components of the stress response to major trauma. High-energy, comminuted fracture of the long bones and severe soft-tissue injuries in this model resulted in a significant tropotropic (depressor) cardiovascular response, transcardiac embolism of medullary contents and activation of the coagulation system. Subsequent stabilisation of the fractures using intramedullary nails did not significantly exacerbate any of these responses.

Study Purpose To assess clinical cognitive function and measure cerebral embolic load following primary cemented hip arthroplasty.

Methods 34 primary cemented hip arthroplasty patients (mean age 69.9 (SD 11.0)0 and no history of cerebrovascular disease, underwent cognitive assessment before and after (day 4) surgery. Testing included: Verbal fluency and speed (Control Oral Word Association Test); Working memory to assess immediate and delayed recall (Weschler Memory Scale III); Attention and mental processing speeds (Colour Trails 1& 2). A one sample Wilcoxon signed rank test compared median differences before and after surgery. A sub-group of 20 patients had intra-operative transcranial Doppler ultrasound monitoring of the middle cerebral artery for embolic signals. A marker of neuronal injury (S-100B protein) was measured pre-operatively and at 0, 24 and 48 hours following surgery.

Results A significant difference was noted in Colour Trails tests 1& 2 following hip arthroplasty with P values (C.I.) of 0.002 (−21, −4) and 0.023 (−15.5, −1.0) respectively.

Using established emboli criteria 10 (50%) patients had true cerebral emboli with a range from 1 to 550 signals (median 2.5 interquartile range (IQ) 2 to 12.5). S-100B levels increased from a pre-operative median (IQ) of 0.15 microg/L (0.12 to 0.20) to a peak immediately following surgery of 1.88(1.36 to 4.24) returning to 0.26(0.18 to 0.37) by 48 hours (normal range: 0.03–0.15). Plotted scatter charts indicated no correlation between embolic load and cognitive dysfunction or with S-100B levels following surgery.

Conclusion Cognitive testing indicates deterioration in early measured attention, visual searching and mental processing speed shortly following hip arthroplasty. No direct correlation was found between cognitive dysfunction and cerebral embolic load.

Background: Long bone fractures and intramedullary stabilisation can result in the extravasation of fat and marrow emboli into the venous circulation. The effects of these emboli can become systemic causing neurological features.

Aim: To establish the cerebral microembolic load following femoral and tibial diaphyseal fractures treated by intramedullary fixation and to specify any neurological impairment with the application of a series of cognitive tests and a serum marker of neuronal injury.

Methods: 20 femoral and tibial fractures treated with intramedullary fixation had intra-operative transcranial doppler ultrasound monitoring of the middle cerebral artery with emboli detection software set to established guidelines. Cognitive testing (day 3), following surgery with an I.Q. assessment (PFSIQ) allowing comparison with age specific normative data. This included: verbal fluency and speed (COWAT – Control Oral Word Association Test); working memory with assessment of immediate and delayed recall; mini-mental state examination; executive function, attention and mental processing speeds (Colour Trails 1& 2). Beta S-100 levels measured pre-operatively, 0, 24 and 48 hours following surgery as a marker of neuronal injury.

Statistical Analysis: One sample Wilcoxon signed rank test to compare median of the cognitive scores with age matched normative data. Multiple regression analysis used to correlate embolic load with cognitive function.

Results: Mean age (SD) for the group is 32 (5.8). Mean PFSIQ of 52.8%, SD 21.4 [median 59.5, IQ range 28.3, 71.3]. No significant difference detected in cognitive testing compared with normative data. Cerebral microemboli detected in 17 of 20 patients with a count median (range) of 6 (0, 29). The mean pre-operative beta S-100 level was 0.36 micro g/l (normal range 0–0.15). This increased to a peak mean of 0.88 micro g/l immediately following surgery with a poor correlation to cerebral embolic load.

Discussion: Detailed clinical testing indicates no significant deterioration in cognitive function following intramedullary stabilisation of these fractures. A variable cerebral micro-embolic load was seen but with no detectable clinical effect. No direct correlation was found between the elevated levels of Beta S-100 seen following surgery and cerebral embolic load. This appears to correlate with previous concerns in the literature regarding the specificity and sensitivity of this established marker of neuronal injury.

Introduction Damage Control orthopaedic techniques have been proposed in the seriously injured with primary external fixation of long bone fractures, reducing the ‘second hit’ of surgery. We have developed a large animal (ovine) model for the study of major trauma.

Aim To clarify the sequence of pulmonary and systemic physiological responses over a 24-hour period following injury, comparing the effects of primary external femoral fixation to intramedullary stabilisation to better quantify the ‘second hit’ of these surgical techniques.

Methods Under terminal anaesthesia bilateral femoral diaphyseal fractures were produced using a mechanical pneumatic actuator (ram). Hypovolaemic shock was maintained for 4 hours before fluid resuscitation and surgical stabilisation.

24 sheep were randomised into 4 groups and monitored for 24 hours following injury:

Group 1 – Control Group (effects of general anaesthesia only)

Group 2 – Control Group for Trauma (injury but no long bone stabilisation)

Group 3 – Damage control group (Injury and external fixation)

Group 4 – Early total care (Injury and reamed intra-medullary stabilisation)

Outcome measures: Embolic load (Mayo score) using transoesophageal echocardiography; serum markers of coagulation (prothrombin time, activated partial thromboplastin time and fibrinogen levels) and inflammation (interleukin 6). Bronchoalveolar lavage to assess total cell count and cell differential to quantify the proportion of neutrophils present.

Results A sustained embolic shower was detected with each femoral fracture (mean Mayo score of 5 and 5.5 respectively). Intramedullary reaming and nailing produced further embolic events with a mean score of 2.5 and 1.5 respectively. Mean prothrombin time increased from a pre-fracture mean of 12 in each group to 18.8 (group 1) 20.7 (group 2); 24.8 (group 3); 31.1 (group 4). Alveolar lavage samples taken at 0, 4 and 24 hours following injury indicated a progressive neutrophilia developing in each group with a count pre-fracture of 4.3 increasing to 55.75 (group 1); 40 (group2); 49 (group3) and 31.7 (group 4) by 24 hours following injury.

Discussion The effects of damage control techniques in this model appear to be a reduced stimulation of the extrinsic coagulation system. An additional embolic hit was detected secondary to intramedullary reaming and nail insertion. Localised lung inflammation seems to develop in all groups with no significant differences seen due to treatment.

We measured the changes during operation in seven markers of coagulation in a prospective series of 84 patients with fractures of the tibia or femur who were undergoing reamed intramedullary nailing. All patients were also continually monitored using transoesophageal echocardiography to assess marrow embolism. In a subset of 40 patients, intraoperative cardiopulmonary function was monitored, using pulmonary and systemic arterial catheterisation.

The procedure produced a significant increase in prothrombin time, activated partial thromboplastin time, the level of prothrombin fragments F₁₊₂ and D-dimers, and a decrease in the fibrinogen level, suggesting activation of both the coagulation and fibrinolytic pathways. There was evidence of both platelet hyper-reactivity and depletion, as estimated by an increase in β-thromboglobulin levels and a decrease in the platelet count. In the patients who had invasive monitoring there was an incremental increase in mean pulmonary arterial pressure, with the changes being greatest during insertion of the guide-wire and reaming.

The change in markers of coagulation, pulmonary artery pressure and arterial oxygen partial pressures correlated with the intraoperative embolic response. Greater changes in these parameters were observed during stabilisation of pathological fractures and in those patients in whom surgery had been delayed for more than 48 hours.

Seven patients with pathological fractures developed more severe hypoxic episodes during reaming, which were associated with significantly greater arterial hypoxaemia, a fall in the right ventricular ejection fraction and an increase in the mean pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure and the pulmonary vascular resistance index. These changes suggested that the patients had transient intraoperative right heart strain.

Eight patients developed significant postoperative respiratory compromise. They all had severe intraoperative embolic responses and, in the three who had invasive monitoring, there was a significantly greater increase in pulmonary artery pressure and alveolar-arterial oxygen gradient, and a fall in the ratio of arterial partial pressure of oxygen to the inspired oxygen concentration. Operative delay, intraoperative paradoxical embolisation and the scores for the severity of the coagulative and embolic responses were predictive of the development of postoperative respiratory complications on univariate logistic regression analysis. On multivariate analysis, however, only the embolic and coagulative scores were significant independent predictors of respiratory complications.

We report a prospective study of the incidence of fractures in the adult population of Edinburgh, related to age and gender. Over a two-year period, 15 293 adults, 7428 males and 7865 females, sustained a fracture, and 5208 (34.0%) required admission.

Between 15 and 49 years of age, males were 2.9 times more likely to sustain a fracture than females (95% CI 2.7 to 3.1). Over the age of 60 years, females were 2.3 times more likely to sustain a fracture than males (95% CI 2.1 to 2.4). There were three main peaks of fracture distribution: the first was in young adult males, the second was in elderly patients of both genders, mainly in metaphyseal bone such as the proximal femur, although diaphyseal fractures also showed an increase in incidence. The third increase in the incidence of fractures, especially of the wrist, was seen to start at 40 years of age in women.

Our study has also shown that ‘osteoporotic’ fractures became evident in women earlier than expected, and that they were not entirely a postmenopausal phenomenon.

We performed a prospective, randomised study on 50 patients with Tscherne C1 tibial diaphyseal fractures comparing treatment with reamed and unreamed intramedullary nails. Our results show that reamed nailing is associated with a significantly lower time to union and a reduced requirement for a further operation. Unreamed nailing should not be used in the treatment of the common Tscherne C1 tibial fracture.

We reviewed 25 patients with tibial diaphyseal fractures which had been complicated by an acute compartment syndrome. Thirteen had undergone continuous monitoring of the compartment pressure and the other 12 had not.

The average delay from injury to fasciotomy in the monitored group was 16 hours and in the non-monitored group 32 hours (p < 0.05). Of the 12 surviving patients in the monitored group, none had any sequelae of acute compartment syndrome at final review at an average of 10.5 months. Of the 11 surviving patients in the non-monitored group, ten had definite sequelae with muscle weakness and contractures (p < 0.01). There was also a significant delay in tibial union in the non-monitored group (p < 0.05).

We recommend that, when equipment is available, all patients with tibial fractures should have continuous compartment monitoring to minimise the incidence of acute compartment syndrome.

We reviewed the results of the treatment of 30 tibial fractures with minor to severe bone loss in 29 patients by early soft-tissue and bony debridement followed by primary locked intramedullary nailing. Subsequent definitive closure was obtained within the first 48 hours usually with a soft-tissue flap, and followed by bone-grafting procedures which were delayed for six to eight weeks after the primary surgery. The time to fracture union and the eventual functional outcome were related to the severity and extent of bone loss. Twenty-nine fractures were soundly united at a mean of 53.4 weeks, with delayed amputation in only one patient. Poor functional outcome and the occurrence of complications were usually due to a departure from the standard protocol for primary management. We conclude that the protocol produces satisfactory results in the management of these difficult fractures, and that intramedullary nailing offers considerable practical advantages over other methods of primary bone stabilisation.

We randomised 24 patients before they had a cemented hemiarthroplasty for hip fracture to receive either thorough or minimal saline lavage of the femoral canal. We then determined the effect in each group on the thromboembolic and cardiopulmonary responses to the pressurised insertion of cement, using transoesophageal echocardiography to show the echogenic embolic response. We found a statistically significant reduction in both the duration of the response and the number of large emboli in patients who had had thorough lavage as compared with the control group with minimal lavage. There was also less disturbance of pulmonary function, as assessed by the change in end-tidal CO2 levels and oxygen saturation, in patients who had thorough lavage. Three patients had a significant fall in blood pressure during cement insertion; all had only minimal lavage. We consider that thorough lavage should be an essential part of the preparation of the proximal femur before cement insertion.

We performed transoesophageal echocardiography in 111 operations (110 patients) which included medullary reaming for fresh fractures of the femur and tibia, pathological lesions of the femur, and hemiarthroplasty of the hip. Embolic events of varying intensity were seen in 97 procedures and measured pulmonary responses correlated with the severity of embolic phenomena. Twenty-four out of the 25 severe embolic responses occurred while reaming pathological lesions or during cemented hemiarthroplasty of the hip and, overall, pathological lesions produced the most severe responses. Paradoxical embolisation occurred in four patients, all with pathological lesions of the femur (21%); two died. In 12 patients large coagulative masses became trapped in the heart. Extensive pulmonary thromboembolism with reamed bone and immature clot was found at post-mortem in two patients; there was severe systemic embolisation of fat and marrow in one who had a patent foramen ovale and widespread mild systemic fat embolisation in the other without associated foraminal defect. Sequential analysis of blood from the right atrium in five patients showed considerable activation of clotting cascades during reaming.

Exchange nailing for failure of union after primary intramedullary nailing of the tibia is widely used but the indications and effectiveness have not been reported in detail. We have reviewed 33 cases of uninfected nonunion of the tibia treated by exchange nailing. This technique was successful without open bone grafting in all closed fractures and in open fractures of Gustilo types I, II and IIIa. The requirement for open bone grafting was reduced in type-IIIb fractures, but exchange nailing failed in type-IIIb fractures with significant bone loss. For these we recommend early open bone grafting. The most common complication was wound infection, seen more often than after primary nailing. We discuss our protocol for the use and timing of exchange nailing of all grades and types of tibial fracture.

We performed transoesophageal echocardiography on 20 patients with femoral neck fractures randomly treated with an uncemented Austin-Moore or cemented Hastings hemiarthroplasty. Cemented arthroplasty caused greater and more prolonged embolic cascades than did uncemented arthroplasty. Some emboli were more than 3 cm in length. In some patients the cascades were associated with pulmonary hypertension, diminished oxygen tension and saturation, and the presence of fat and marrow in aspirates from the right atrium.

We performed transoesophageal echocardiography on 24 patients during reamed intramedullary nailing of 17 tibial and seven femoral fractures. In 14 patients there was only minimal evidence of emboli passing through the heart, but in six copious showers of small emboli (< 10 mm maximum dimension) were observed. In four other patients, there were also multiple large emboli (> 10 mm maximum dimension). Three of these patients developed fat embolism syndrome postoperatively and one died. Earlier nailing was associated with smaller quantities of emboli.

In two hospitals, 115 consecutive open femoral shaft fractures were treated by meticulous wound excision and early locked (97) or unlocked (18) intramedullary nailing. All the fractures united; union was delayed in four, three of which required bone grafting. The average range of knee flexion at follow-up was 134 degrees (60 to 148). Five patients had a final range of less than 120 degrees, but three of these improved after manipulation under general anaesthesia. Three patients developed staphylococcal infections and required further surgical treatment. All eventually healed.

We report the use of Grosse-Kempf reamed intramedullary nailing in the treatment of 41 Gustilo type II and III open tibial fractures. The union times and infection rates were similar to those previously reported for similar fractures treated by external skeletal fixation, but the incidence of malunion was less and fewer required bone grafting. The role of exchange nailing is discussed and a treatment protocol is presented for the management of delayed union and nonunion.