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Management of rib fractures constitutes a major part of the trauma workload of any unit. Rib fractures result in disrupted chest wall mechanics and ventilatory insufficiency. The ability of a lung injury scoring system to predict the degree of respiratory dysfunction after rib fractures was evaluated. 37 patients with rib fractures admitted to the South Birmingham Trauma Unit were studied prospectively. Injury Severity Score (ISS), Lung Injury Score (LIS) and number of rib fractures sustained were recorded on admission. The patients were followed up to assess whether mechanical ventilation was required, and if so, its duration was recorded. The relationship between the ISS and LIS, duration of ventilation and LIS and number of rib fractures and LIS were analyzed by means of linear regression and confidence intervals. LIS had a strong positive correlation with ISS (R = 0.62). There was a positive correlation between LIS and number of rib fractures (R = 0.40). LIS also showed a strong correlation with the duration of mechanical ventilation required (R = 0.50). Calculating LIS may be useful in assessing ventilatory dysfunction following rib fractures.

Myosin heavy chain (MHC) is a structurally bound contractile protein of the thick filaments. The magnitude of myoskeletal injury may be estimated by serial determinations of these contractile proteins released into the circulation as a consequence of loss of cell membrane integrity. The polymorphism of MHC is believed to be responsible, at least in part, for the variable contraction velocity of muscles. It was the aim of the present study to confirm the utility of MHC for the assessment of skeletal muscle damage within 24 hr of injury in patients with myoskeletal injuries. Plasma MHC fragments was measured in 25 patients with muscle injuries. Samples were obtained immediately on hospital admission (A1) and 24 hr after admission (A2). These were compared with 15 noninjured controls. In addition, creatine kinase (CK), myoglobin and cardiac troponin I (cTnI) were measured in order to confirm the extent of the injury and to exclude protein released from the heart. Radioimmunoassay, enzyme immunoassay, and one-step immunoenzymometric assay (IEMA) techniques were used for measurements of plasma MHC fragments, CK plus myoglobin and cTnI, respectively. Mean (SD) uU/l of MHC was (94.1±116.1) p=NS and (673.3±1943) p

To determine whether concentrations of the N-terminal peptide of pro-atrial natriuretic peptide (proANP) and of alpha atrial natriuretic peptide 1–28 (aANP) releases are affected by myoskeletal injuries, samples from 24 patients with muscle injuries were therefore collected within 48 h of injury. The mean age of patients was 65; range: 17–90 years. These were compared with 18 non-injured subjects with a mean age of 40; range: 17–80 years. A specific enzyme immunoassay (EIA) method suitable for the determination of proANP and aANP was used. aANP required plasma extraction and no extraction was needed for proANP determination. ProANP level was significantly higher in patients on admission and this level was maintained 24 h after admission (p

Calcitonin gene-related peptide [CGRP] — a powerful vasodilator, is a 37 amino acid peptide that is find primarily in the central and peripheral nervous system. It affects the regulation of local blood flow, smooth muscle tone and glandular secretion. It is an endocrine regulator and in the lungs it also exerts a bronchoconstricting effect. CGRP has a proliferative effect on human endothelial cells. Therefore, it is important for the formation of new vessels, example, in ischemia, inflammations, and in the healing of wounds. Plasma levels of CGRP are increase in patients with chronic cardiac failure and sepsis, indicating that CGRP may be another important peptide in chronic illness. We have therefore measured the release of this peptide and another sensory peptide [Substance P (SP)]; a vasoconstrictor peptide [Endothelin (ET)]; and a perivascular peptide [Neuropeptide Y (NPY)], within 24 hours of injury, in the plasma of patients with soft tissue injury. Neuropeptides were measure by enzyme immunoassay technique. Median:(lowerquartile-upperquartile) in pmol/L CGRP level was elevated in patients [50.37 : (12.4–110.9)] compared to controls [13.9 : (10.9–36.96)] p < 0.05; Endothelin and NPY did not vary much between groups p = NS; ET: patients [8.7 : (1.7–87.1), controls 8.8 : (1.7–32.9)]; NPY: Patients [11.7 : (10.5–14.99), controls 11 : (10.3–12.8)]. SP was increase in patients [302.3 : (79.9–707.3)], than controls [5.6 : (3.2–36.6)] p < 0.05. Furthermore, Elastase (a decisive marker for inflammation and infectious complications), was measure (ng/L), and found to be slightly higher in patients (102:25.5–223), than controls (91.8:45.9–127). In summary, plasma levels of sensory peptides increased significantly, in patients with soft tissue injury, in contrast to vasocostrictor peptides that remained unchanged. These sensory peptides may yet be another group of neuromodulators playing a significant role in immune, pain, inflammatory and wound healing in soft tissue injury patients.

In this study, the distributions of calcitonin gene-related peptide, neuropeptide Y, and α-atrial natriuretic peptide 1–28 immunoreactivity, were investigated within different regions of the guinea pig heart by utilising two different methods of tissue fixation for the immunocytochemistry. The results were compared with data obtained through radioimmunoassays. We observed similar concentrations and distributions of α-atrial natriuretic peptide in the right atrium, with results of radioimmunoassay and immunocytochemistry, but there were no myocytes containing α-atrial natriuretic peptide in the left atrium or ventricles with immunocytochemistry as opposed to radioimmunoassay. The immunoreaction obtained for neuropeptide Y was more intense in the right ventricle than left. Calcitonin gene-related peptide nerve fibres were about twice as abundant in the left atrium than in the right.

Summary The detrimental effect of stress on the immune response increases with age, though the mechanisms responsible are not fully understood. The physiological response to stress is regulated in part by the adrenocortical system. Adrenal hormones dehydroepiandrosterone sulphate (DHEAS) and cortisol have opposing effects on the innate immune system, DHEAS enhances while cortisol suppresses immunity and the molar ratio of cortisol to DHEAS increases with age. We found that elderly hip fracture patients produced a robust neutrophilia after injury, but circulating neutrophils showed an impaired antibacterial response. We therefore proposed that adrenocortical hormones mediate the heightened immunosuppression seen in the elderly after injury. We examined neutrophil function and adrenocortical hormone levels in elderly (> 65 years) hip fracture patients and age-matched healthy controls. Thirteen out of 35 elderly patients acquired infections following hip fracture. Neutrophil superoxide production was lower in elderly hip fracture patients compared with controls ( P < 0.005) and lower in patients who acquired infection following injury compared with those who did not ( P < 0.05). Serum cortisol:DHEAS ratio was higher in elderly hip fracture patients (0.56 ± 0.38) compared with either age-matched controls (0.36 ± ± ± 0.21; P < 0.05) or young fracture patients (0.087 ± ± ± 0.033; P < 0.0001). Moreover, cortisol: DHEAS was increased in elderly patients who succumbed to infection compared with those who did not (0.803 ± 0.42 vs. 0.467 ± 0.28; P < 0.02). In vitro cortisol significantly decreased neutrophil superoxide generation ( P < 0.05) and this was prevented by coincubation with DHEAS. We propose that increased cortisol:DHEAS ratios may contribute to reduced immunity following physical stress in the elderly.

Previous work has demonstrated an age-related decline in neutrophil function, including a decline in phagocytic capacity, with age in healthy individuals. This decline in function may contribute to increased susceptibility to bacterial infections in the elderly population. The present study has investigated the effects of age on susceptibility to infection and neutrophil function in elderly humans following mild trauma. Specifically, we have measured neutrophil function in 44 patients, all of whom had no significant co-morbidity, were over 65 years old (mean age 82.5 years) and had sustained a fractured neck of femur. We obtained neutrophils and examined the process of microbial engulfment by phagocytosis and the bactericidal mechanism of superoxide production. In the 5-week period after trauma, almost half of the elderly trauma patients succumbed to bacterial or fungal infection, with a predominance of chest and urinary tract infections. When examining neutrophil function, a decline in superoxide production was observed in neutrophils from the elderly trauma group at the time of hip fracture when compared with those from healthy elderly controls, and this was maintained 5 weeks after trauma. This was accompanied by an age-related reduction in phagocytic function during this period. We propose that trauma and an age-related decline in neutrophil function combine to decrease the immune response to bacteria in the elderly.

The skeletal isoform of troponin-I (sTnI) is a myofibrillar protein highly specific for myoskeletal injury. We used an indirect immunoenzymometric assay method with high analytical sensitivity to measure sTnI in patients with soft-tissue injury and in orthopedic patients. We assessed 20 soft-tissue injury patients and 16 orthopedic patients for sTnI, cardiac troponin-I (cTnI), creatine kinase (CK), myoglobin, and elastase within 24 h of injury, in comparison with 17 control subjects. The mean (SD) ng/ml value for sTnI was higher in orthopedic patients (15.25 ± 2.4) and in soft-tissue injury patients (10.41 ± 1.8) than that in controls (2.5 ± 0.9) P < 0.001, P < 0.05 respectively. Cardiac TnI was not detectable in any subjects (below the assay detectable limit of 0.3 ng/ml). CK was significantly higher in orthopedic patients than in controls (P < 0.005) and myoglobin and elastase were not significantly changed in patients samples. The assay appeared to be suitable as a supplementary tool of reliability and relevance, for the study, identification, and diagnosis of skeletal muscle specific injuries in humans.

Myosin heavy chain fragments (MHC) levels are observed to be higher in myoskeletal injuries after surgery. MHC could be a helpful supplementary tool in the study of myoskeletal injuries.Serum levels of myosin heavy chain fragments (MHC) were assessed in orthopedic patients before operation (OBO) and after operative (OAO) repairs and in the early phase of soft tissue injury (STI) using a radioimmunoassay involving monoclonal antibodies to the human beta-type MHC.Mean (SD) microU/L of MHC in comparison with the control subjects (75.3 +/- 47.1) was higher in OAO (305.8 +/- 38.1) p0.0001, and no significant changes in MHC were found in STI (67 +/- 77.5). Myoglobin was notably higher in OBO (81.9 +/- 95.0) compared to STI (43.9 +/- 55.9) or controls p0.05, but there was no further change in the protein after surgery. The mean proportional raised level of myoglobin in OBO wastwofold, and MHC increased by 27%. Neither myoglobin nor MHC increased in the plasma of the STI within 24 h of injury.These data suggest that the release of MHC could be a helpful supplementary tool in the study of tissue damage in humans.

Atrial natriuretic peptide (ANP) plays a part in the regulation of volume homeostasis and possibly, in the pathophysiology of water and electrolyte disorder. Patients with serious burn injuries risk huge body fluids losses, which are compensated for by perfusion. Blood volume and the renin and aldosterone system are also disturbed. This study measured plasma ANP and vasoactive intestinal polypeptide (VIP) in patients with >20% total burned surface area (TBSA), at admission and 24 h post-admission. Eleven patients (mean age 46.5 years, 8 males) with a mean TBSA of 34.5% were sampled. Standard treatment was given. Eleven closely age-matched volunteers were used as controls. A specific ELISA method suitable for the measurement of ANP and VIP was used. ANP was higher (p

Most investigators have reported high levels of endothelin (ET)-1 in patients with thermal injury. We attempted to examine the hypothesis that ET-1 levels increase in patients with severe burn injury.Plasma from 28 adult subjects, 14 of whom had thermal injuries with a median (range) percentage of total burn surface area of 22% (20%-76%), was assessed for ET-1 and tumor necrosis factor (TNF) alpha. Samples from closely age-matched patients were obtained on admission (day 1) and 24 hours postinjury (day 2). Samples were obtained before blood transfusion or surgical treatment occurred. Enzyme immunoassay techniques suitable for the measurements of the cytokines were used.Median (range) of TNF-alpha was higher in patients (day 1, 10.0 ng/L [1.2-35.0 ng/L]; day 2, 12.0 ng/L [0.4-39.0 ng/L]) than controls (0. 8 ng/L [0.3-3.2 ng/L]) (P.005) while ET-1 levels remained significantly unchanged in patients (mean [SD], day 1, 183.0 [42.2] ng/L; day 2, 204.7 [41.7] ng/L) compared with controls (170.0 [59.8] ng/L) (P.05).We observed no significantly raised levels of ET-1 in patients with thermal injury within 24 hours after burn injury. We found no significant correlation between the plasma levels of TNF-alpha and ET-1. Endothelin-1 levels did not seem to reflect severity of illness. The actual evaluation of ET-1 release in patients with thermal injury could enhance the pathophysiological study of human thermal injury.

Using autoradiography, I studied the effect of diaphyseal injuries on the DNA synthesis of growth plate cells in Swiss Albino rats and found that mitotic activity of germinal and proliferation zone cells of the growth plate and periosteal callus increased 24 hours after the fracture and peaked at 48 hours. The mitotic activity continued until the eighteenth day with gradual decline from the second day onwards. It appears as if the growth plate cells are stimulated by the same mitogenic activator as the periosteal cells. I therefore postulate that the overgrowth of long bones after fractures is due to local mitogenic stimulating factor(s), and is not due to an increased blood supply to the epiphyses, as is presently widely claimed.