Non-severe burn injury causes sustained platelet hyperreactivity.

Individuals who present to a hospital for treatment of a burn of any magnitude are more frequently hospitalised for ischemic heart disease, even decades after injury. Blood platelets are key mediators of cardiovascular disease. To investigate platelet involvement in post-burn cardiovascular risk, platelet reactivity was assessed in patients at 2- and 6-weeks after non-severe (TBSA < 20%) burn injury, and in a murine model 30 days after 8% TBSA full-thickness burn injury. Platelets were stimulated with canonical agonists and function reported by GPIIb/IIIa PAC1-binding site, CD62P expression, and formation of monocyte-platelet aggregates. In vivo thrombosis in a modified Folts model of vascular injury was assessed. Burn survivors had elevated frequencies of circulating monocyte-platelet aggregates, and platelets were hyperreactive, primarily to collagen stimulation. Burn plasma did not cause hyper-reactivity when incubated with control platelets. Platelets from burn injured mice also demonstrated increased response to collagen peptides but did not show any change in thrombosis following vascular injury. This study demonstrates the persistence of a small but significant platelet hyperreactivity following burn injury. Although our data does not suggest this heightened platelet sensitivity modulates thrombosis following vascular injury, the contribution of sub-clinical platelet hyperreactivity to accelerating atherogenesis merits further investigation.

A quantitative assessment of facial protection systems in elective hip arthroplasty.

We aimed to assess the risk to surgeons of blood splatter during total hip arthroplasty. Hoods from personal protection systems used in 34 consecutive total hip replacements were collected and the area of blood splatter was measured and compared to goggles and visors. Thirty one primary THA's (13 cemented, 4 hybrid, 14 uncemented) and 3 revisions (1 hybrid, 2 uncemented) were collected. Splashes were detected on all of the masks with a mean of 034% cover. Splatter was greatest for the operating surgeon, followed by the first assistant, though the difference was not statistically significant. Operating personnel were at greater risk of contamination during uncemented arthroplasty (p < 0.0001; 95% CI). On average 50.60% and 45.40% of blood cover was outside the area protected by goggles and visors respectively. There was a significant difference between the Personal Protection Systems (PPS) and goggles (p = 0.0231; 95% CI) as well as between the PPS and visors (p = 0.0293; 95% CI).

Long term cardiovascular impacts after burn and non-burn trauma: A comparative population-based study.

OBJECTIVE: To compare post-injury cardiovascular disease (CVD) hospital admissions experienced by burn patients with non-burn trauma patients and people with no record of injury, adjusting for socio-demographic, health and injury factors. METHODS: Linked hospital and death data were analysed for a cohort of burn patients (n=30,997) hospitalised in Western Australia during the period 1980-2012 and age and gender frequency matched comparison cohorts (non-burn trauma: n=28,647; non-injured: n=123,399). The number and length of hospital stay for CVD admissions were used as outcome measures. Multivariate negative binomial regression was used to derive adjusted incidence rate ratios (IRR) and 95% confidence intervals (95%CI). Multivariate Cox regression models and hazard ratios (HR) were used to examine first time post-injury CVD admissions. RESULTS: The burn cohort had a higher rate of CVD (combined) admissions (IRR, 95%CI: 1.16: 1.08-1.24) and spent longer in hospital (IRR, 95%CI: 1.37, 1.13-1.66) than the non-burn trauma cohort. Both the burn cohort (IRR, 95%CI: 1.50, 1.40-1.60) and the non-burn trauma cohort (IRR, 95%CI: 1.29, 1.21-1.37) had higher adjusted rates of post-injury CVD admissions compared with the non-injured cohort. The burn cohort (HR, 95%CI: 2.27, 1.70-3.02) and non-burn trauma cohort (HR, 95%CI: 2.19, 1.66-2.87) experienced significantly elevated first time CVD admissions during the first 6 months after injury, decreasing in magnitude from 6 months to 5 years after injury (HR, 95%CI: burn vs. non-injured; 1.31, 1.16-1.48; non-burn trauma vs. non-injured; 1.16, 1.03-1.31); no significant difference in incident admission rates was found beyond 5 years (HR, 95%CI: burn vs. non-injured; 0.99, 0.92-1.07; non-burn trauma vs. non-injured; 1.00, 0.93-1.07). CONCLUSIONS: Burn and non-burn trauma patients experience elevated rates of post-injury CVD admissions for a prolonged period after the initial injury and are particularly at increased risk of incident CVD admissions during the first 5-years after the injury event. Detailed clinical data are required to help understand the underlying pathogenic pathways triggered by burn and non-burn trauma. This study identified treatment needs for injury patients, burn and non-burn, for a prolonged period after discharge.

The impact of non-severe burn injury on cardiac function and long-term cardiovascular pathology.

Severe burn injury significantly affects cardiovascular function for up to 3 years. However, whether this leads to long-term pathology is unknown. The impact of non-severe burn injury, which accounts for over 80% of admissions in developed countries, has not been investigated. Using a rodent model of non-severe burn injury with subsequent echocardiography we showed significantly increased left ventricular end systolic diameter (LVESD) and ventricular wall thickness at up to 3 months post-injury. Use of propranolol abrogated the changes in cardiac measures observed. Subsequently we investigated changes in a patient cohort with non-severe injury. Echocardiography measured at baseline and at 3 months post-injury showed increased LVESD at 3 months and significantly decreased posterior wall diameter. Finally, 32 years of Western Australian hospital records were used to investigate the incidence of cardiovascular disease admissions after burn injury. People who had experienced a burn had increased hospital admissions and length of stay for cardiovascular diseases when compared to a matched uninjured cohort. This study presents animal, patient and population data that strongly suggest non-severe burn injury has significant effects on cardiovascular function and long-term morbidity in some burn patients. Identification of patients at risk will promote better intervention and outcomes for burn patients.

Increased admissions for diabetes mellitus after burn.

BACKGROUND: Currently, limited long-term data on hyperglycaemia and insulin sensitivity in burn patients are available and the data that do exist are primarily related to paediatric severe burns. The aim of this study was to assess if burn is associated with increased post-burn admissions for diabetes mellitus. METHODS: A population-based longitudinal study using linked hospital morbidity and death data from Western Australia was undertaken of all persons hospitalized for a first burn (n=30,997) in 1980-2012 and a frequency matched non-injury comparison cohort, randomly selected from Western Australia's birth registrations and electoral roll (n=123,399). Crude admission rates and summed length of stay for diabetes mellitus were calculated. Negative binomial and Cox proportional hazards regression modelling were used to generate incidence rate ratios (IRR) and hazard ratios (HR), respectively. RESULTS: After adjustment for socio-demographic factors and pre-existing health status, the burn cohort had 2.21 times (95% Confidence Interval (CI): 1.36-1.56) as many admissions and almost three times the number of days in hospital with a diabetes mellitus diagnosis (IRR, 95% CI: 2.94, 2.12-4.09) than the uninjured cohort. Admission rates were significantly elevated for those burned during childhood (<18 years, IRR, 95% CI: 2.65, 1.41-4.97) and adulthood (≥18 years, IRR, 95% CI: 2.12, 1.76-2.55). Incident admissions were significantly elevated in the burn cohort during the first 5 years post-burn when compared with the uninjured (HR, 95% CI: 1.96, 1.46-2.64); no significant difference was found beyond 5 years post-burn (HR, 95% CI: 1.08, 0.82-1.41). CONCLUSIONS: Findings of increased hospital admission rates and prolonged length of hospital stay for diabetes mellitus in the burn cohort provide evidence that burns have longer term effects on blood glucose and insulin regulation after wound healing. The first five years after burn discharge appears to be a critical period with significantly elevated incident admissions for diabetes mellitus during this time. Results would suggest prolonged clinical management after discharge and or wound healing to minimise post-burn admissions for diabetes mellitus is required.

Non-severe burn injury leads to depletion of bone volume that can be ameliorated by inhibiting TNF-α.

Bone loss after severe burn injury is well established, and is thought to be a consequence of the severe hyper-metabolic response as well as changes in cytokine and glucocorticoid levels that decrease bone synthesis and increase rate of loss. However, 90% of presentations are for non-severe burns which do not elicit this response. Little is known about whether these non-severe injuries may also affect bone tissue, and whether other mechanisms may be involved. To investigate whether bone loss occurs after a non-severe burn injury we used a mouse model of an approximately 8% total body surface area (TBSA) full-thickness burn and micro-CT. We also assessed whether blocking TNF-α after a burn injury by administration of an antibody could modulate the impacts of the burn on bone tissue. There was a significant loss of trabecular bone volume of (3.27% compared to 5.27%, p=0.0051) after non-severe burn injury. Trabecular number was significantly decreased (0.57/mm after injury compared to 1.02/mm controls, p=0.0051) and spacing increased after burn injury (0.40 compared to 0.28, p=0.0083). Anti-TNF-α antibodies significantly improved trabecular bone volume (8.53%, p=0.0034) and number after burn injury (1.28/mm, p=0.0034). There was no significant change observed in cortical bone after burn injury or administration of anti-TNF-α antibodies. These findings show that non-severe burn injury can lead to changes in bone metabolism. Monitoring bone density in patients with non-severe injuries and interventions to limit the impacts of the inflammatory storm may benefit patient recovery and outcomes.