Rodeo related large animal injury: is protective head-gear warranted?

To compare rodeo associated large animal injuries to large animal associated trauma from other aetiologies in order to determine whether mandatory protective head-gear during rodeo is warranted. Retrospective analysis related to injury involving large animal admissions between 1 January 1990 and 31 December 1995. The setting is at the University of New Mexico Health Science Center, a level 1 trauma centre. All patients admitted with Injury Severity Scores of 1 or higher following large animal associated injuries. There were 140 admissions for which mechanism of injury was known. Thirty-nine occurred during rodeo competition and 101 occurred during other activities. Bovine associated activities were the aetiology in 34 (87%) of rodeo related injuries while equine related activities were the aetiology in 97 (96%) of non-rodeo related injuries (P<0.001). Rodeo related injuries involved the head and neck in five patients (13%) compared to 42 patients (42%) in non-rodeo activities (P=0.001). Mean Regional Injury Severity Score head and neck was 0.4 for injured rodeo riders and 1.5 for injured non-rodeo riders (P<0.001). Mean admission Glascow Coma Scale was 14.9 for rodeo-injured patients and 13.3 for non-rodeo-injured patients (P<0.001). Total ISS was significantly lower for rodeo injured patients (9.1 vs. 11.7, P=0.03). No rodeo injured patient died as a result of head injury. Mechanism of injury, ISS head, GCS, total ISS, and outcome differ between rodeo and non-rodeo injuries. While routine helmet use during non-rodeo events appears justified, mandatory use of helmets in rodeo events is unwarranted. Orthotics to protect the chest and abdomen are more likely to reduce morbidity and mortality for rodeo participants.

CT imaging of intrathoracic lymph nodes in dogs with bronchoscopically administered iodinated nanoparticles.

RATIONALE AND OBJECTIVES: The purpose of the study was to determine if airway instillation of iodinated nanoparticles results in contrast material enhancement of tracheobronchial lymph nodes in dogs. MATERIALS AND METHODS: Eight dogs underwent intrabronchial instillation of iodinated nanoparticles; six dogs received 900 mg each, and two dogs received 450 mg each. Spiral computed tomography (CT) was then performed 2-34 days later. RESULTS: CT scans obtained 2 days after instillation showed the presence of contrast material within the lung parenchyma but no nodal enhancement. Scans obtained 6-34 days after instillation showed enhancement of the right, left, and middle tracheobronchial lymph nodes (analogous to the mediastinal nodes in humans). Mean nodal attenuation on CT images was 117 HU +/- 43, and the mean nodal volume was 129 mm3 +/- 113. Histologic specimens of the nodes showed macrophage hyperplasia. CONCLUSION: Iodinated nanoparticles instilled into small airways are transported to the tracheobronchial lymph nodes, where they result in contrast enhancement.

A new view of pulmonary edema and acute respiratory distress syndrome.

The old division of lung edema into two categories--cardiogenic (hydrostatic) and noncardiogenic (increased permeability)--is no longer adequate. For instance, it fails to distinguish between the capillary leak caused by acute respiratory distress syndrome from that caused by interleukin-2 treatment. Further, it fails to account for the capillary leak ('stress-failure') that may accompany edema. A modern view of edema must recognize the natural barriers to the formation and spread of edema. These barriers are the capillary endothelium and the alveolar epithelium. Varying degrees of damage to them can account for the varying radiographic and clinical manifestations of lung edema. Thus, interleukin-2 administration causes increased endothelial permeability without causing alveolar epithelial damage. The result is lung edema that is largely confined to the interstitium, causing little hypoxia and clearing rapidly. However, acute respiratory distress syndrome, which is characterized by extensive alveolar damage, causes air-space consolidation, severe hypoxia, and slow resolution. Thus, a reasonable classification of lung edema requires at least four categories: 1) hydrostatic edema; 2) acute respiratory distress syndrome (permeability edema caused by diffuse alveolar damage); 3) permeability edema without alveolar damage; and (4) mixed hydrostatic and permeability edema. The authors emphasize the importance of the barriers provided by the capillary endothelium and the alveolar epithelium in determining the clinical and radiographic manifestations of edema. In general, when the alveolar epithelium is intact, the radiographic manifestations are those of interstitial (not air-space) edema; this radiographic pattern predicts a mild clinical course and prompt resolution.

Distinguishing hantavirus pulmonary syndrome from acute respiratory distress syndrome by chest radiography: are there different radiographic manifestations of increased alveolar permeability?

Hantavirus infection may cause diffuse air space disease, termed hantavirus pulmonary syndrome (HPS). The authors sought to determine if chest radiographs could differentiate HPS from typical acute respiratory distress syndrome (ARDS). The authors identified patients with either HPS (n = 11) or acute ARDS (n = 32) and selected the earliest chest radiograph showing diffuse airspace disease, and a chest radiograph taken 24 to 48 hours previously. Thoracic and general radiologists first viewed the chest radiograph showing diffuse air space disease, and ranked the likelihood that each case represented HPS versus ARDS. Afterward, readers viewed earlier chest radiographs and rescored each case. Receiver operating characteristic (ROC) curves from both scoring sessions were generated. The mean areas under the ROC curves for the entire group was 0.83 +/- 0.12 initially, and improved to 0.87 +/- 0.09 (p < 0.05) after viewing prior chest radiographs. Receiver operating characteristic curves of thoracic radiologists described greater areas than those of general radiologists both before and after viewing prior chest radiographs; 0.95 +/- 0.01 versus 0.78 +/- 0.08 (p < 0.05) and 96 +/- 0.02 versus 0.80 +/- 0.05 (p < 0.05). The mean sensitivity and specificity of chest radiograph interpretation for HPS was 86 +/- 13% and 74 +/- 11%, respectively. Chest radiographs can differentiate HPS from ARDS. Accuracy is improved by the use of serial radiographs and more highly trained readers. The chest radiograph findings may represent differences in the extent of alveolar epithelial damage seen in HPS and ARDS.

Head, face, and neck trauma from large animal injury in New Mexico.

BACKGROUND: Head, face, and neck injuries (HFNI) occur during animal-related trauma. We compared patients with HFNI and without HFNI after animal-related injuries to determine the significance of these injuries. METHODS: Retrospective review of admissions for animal injuries between January 1, 1990, and December 31, 1995, by age, gender, mechanism, animal, Glasgow Coma Scale (GCS) score, Injury Severity Score (ISS), Abbreviated Injury Severity score for head and neck (AIS Head/Neck), AIS score for face (AIS Face), intensive care unit stay, hospitalization length, morbidity, and mortality. RESULTS: There were 153 admissions: 61 HFNI and 92 no HFNI. Significant differences occurred in gender, animal, activity, GCS, and ISS. HFNI had higher AIS Head/Neck, AIS Face, and mortality. HFNI were from horses in 87% and occurred during recreation in 89%; 39% of patients with HFNI were 18 years or younger. CONCLUSION: HFNI occur in females and young people and produce lower GCS score, higher ISS, higher AIS Head/Neck, higher AIS Face, and higher mortality. Most occur during recreational horseback riding. Protective headgear should be mandated.

Hantavirus pulmonary syndrome: radiographic findings in 16 patients.

PURPOSE: To characterize chest radiographic features of Hantavirus pulmonary syndrome. MATERIALS AND METHODS: Initial and follow-up chest radiographs from 16 patients with confirmed Hantavirus pulmonary syndrome were reviewed for radiographic findings of either cardiogenic pulmonary edema or pulmonary edema due to increased permeability of the alveolar capillary membranes. RESULTS: Findings indicative of interstitial edema were present more frequently (14 [88%] of 16 patients) than is typically seen in adult respiratory distress syndrome (5%). Alveolar flooding subsequently developed in 11 (69%) of 16 patients and was not the peripheral pattern usually seen in the acute phase of adult respiratory distress syndrome. Overall mortality was 43%. Lung specimens obtained at autopsy showed a pattern of endothelial leak with minimal epithelial injury. CONCLUSION: The lung disease caused by Hantavirus in these patients may explain the findings of interstitial edema and central alveolar filling atypical of adult respiratory distress syndrome. Recognition of the radiographic pattern will be important in identifying this apparently widespread cause of increased permeability pulmonary edema.

The course of nosocomial oropharyngeal colonization in patients recovering from acute respiratory failure.

We sought to determine the duration of nosocomially acquired Gram-negative bacilli (GNB) oropharyngeal colonization following hospitalization for acute respiratory failure (ARF). We selected 24 inpatients recovering from ARF who had positive oropharyngeal cultures for GNB. Follow-up cultures were obtained at the time of hospital discharge, and 2 and 4 weeks afterwards. The prevalence of GNB colonization in these patients was 14/21 (67 percent) at the time of hospital discharge and 14/23 (60 percent) 2 weeks afterwards. Both rates were greater than the control population's 7/30 (23 percent, p < 0.02 and < 0.05, respectively). Four weeks after hospital discharge, the prevalence of colonization had fallen to 7/19 (37 percent) which was not significantly different from that of controls. Five of 24 subjects were rehospitalized during the follow-up period. Pneumonia was diagnosed in only two of the five and both proved to be due to pathogens other than GNB. We conclude that the prevalence of GNB oropharyngeal colonization following ARF approaches control levels within four weeks of hospital discharge. We speculate that a post-ARF patient's risk for GNB pneumonia similarly declines.

Tissue release of adenosine triphosphate degradation products during shock in dogs.

Clinical monitoring of cellular metabolism during shock, based largely on traditional metabolic indicators, remains unsatisfactory. The purpose of this study was to compare venous oxygen tension and blood lactate gradients with blood gradients of purine nucleotide degradation products which are derived from tissue ATP catabolism during hypovolemic shock. Sixteen dogs were instrumented to sample arterial and venous blood. Measurements of arteriovenous lactate and PNDP gradients during spontaneous respiration were examined at four tissue sites: gut, kidney, hindlimb, and diaphragm. Hypovolemic shock (mean arterial blood pressure 35 to 40 mm Hg) was induced and maintained for one hour. The above parameters were remeasured at 30 and 60 minutes after induction of shock. Hypoxanthine gradients were greater than that of other PNDP, and so were used as the primary indicator of tissue ATP metabolism. In the hindlimb, the mean AV gradients for hypoxanthine (1 +/- 1 microM) were not significantly greater than baseline, while the lactate gradient (700 +/- 300 microM) rose markedly. In contrast, across the kidney there was a significantly greater AV hypoxanthine gradient (16 +/- 3 microM, p less than 0.002) but no lactate gradient (-400 +/- 200 microM). Both the hypoxanthine and lactate AV gradients were significantly elevated across the diaphragm and gut. Venous PO2 values less than 35 mm Hg predicted an increased hypoxanthine gradient across the kidney, but not across the hindlimb. We conclude that the metabolic response to hypovolemic shock as assessed by PNDP gradients, lactate gradients, and venous PO2 differs among tissues. Although resting muscle such as the hindlimb may be an important source of blood lactate, the viscera and working skeletal muscle (the diaphragm) are major contributors to circulating PNDP.

Plasma hypoxanthine and exercise.

During exercise, ATP is converted to ADP and AMP to supply energy for muscular contraction. It is then regenerated via various pathways of intermediary metabolism. However, with high levels of exercise, net ATP degradation in muscle occurs. In exercise and other clinical situations, adenine nucleotide degradation leads to an accumulation of degradative purine products including hypoxanthine. In an effort to monitor events of energy metabolism, we examined plasma hypoxanthine levels at various exercise intensities. Peak plasma hypoxanthine levels after maximal exercise (18.9 +/- 2.6 microM, mean +/- SEM) were significantly greater than resting levels (1.1 +/- 0.1 microM; p less than 0.001). Hypoxanthine levels after steady state exercise at 52, 76, and 97% of ventilatory threshold did not exceed resting levels. However, plasma hypoxanthine rose significantly after exercise at 124% of ventilatory threshold (6.3 +/- 1.0 microM; p less than 0.01) and at 152% of ventilatory threshold (17.0 +/- 3.6 microM; p less than 0.001). Exercise at subventilatory threshold intensity (74% of ventilatory threshold) for a prolonged time period, such that total work equaled that performed at 152% of ventilatory threshold, did not elevate hypoxanthine levels (0.46 +/- 0.1 microM) above resting values. We conclude that elevation of plasma hypoxanthine levels occur during exercise at intensities that exceed the ventilatory threshold and indicate that net adenine nucleotide degradation has occurred.

Purine efflux after cardiac ischemia: relevance to allopurinol cardioprotection.

Allopurinol is thought to protect hearts against damage due to hypoxia or ischemia by inhibiting xanthine oxidase and oxygen radical generation. We subjected isolated rabbit hearts, equilibrated by perfusion at 37 degrees C, to 1 h of global ischemia at 27 or 37 degrees C with or without brief pretreatment with 100 microM allopurinol. The total absence of xanthine or uric acid in the coronary effluent following ischemia, the presence of hypoxanthine (25 +/- 4 microM peak concentration), and the failure of allopurinol to alter purine washout profiles or postischemic cardiac function suggest that rabbit myocardium lacks xanthine oxidase or dehydrogenase. Data obtained with a similar rat heart preparation showed appreciable formation of xanthine (12 +/- 2 microM peak) and uric acid (10 +/- 3 microM). Allopurinol pretreatment inhibited xanthine and uric acid formation and significantly improved key indicators of postischemic left ventricular function. We conclude that there is species dependency in the myocardial activity of xanthine oxidase or dehydrogenase, that when present it can be inhibited by acute allopurinol pretreatment, and that xanthine oxidase activity and its ability to generate oxygen radicals are not universal contributors to cardiac ischemic damage.

Absence of xanthine oxidase or xanthine dehydrogenase in the rabbit myocardium.

We directly measured the activity of the enzymes xanthine oxidase and xanthine dehydrogenase in rabbit and rat hearts, using a sensitive radiochemical assay. Neither xanthine oxidase activity nor xanthine dehydrogenase activity was detected in the rabbit heart. In the rat heart, xanthine oxidase activity was 9.1 +/- 0.5 mIU per gram wet weight and xanthine dehydrogenase activity was 53.0 +/- 1.9 mIU per gram wet weight. These results argue against the involvement of the xanthine oxidase/xanthine dehydrogenase system as a mechanism of tissue injury in the rabbit heart, and suggest that the ability of allopurinol to protect the rabbit heart against hypoxic or ischemic damage must be due to a mechanism other than inhibition of these enzymes.

C3a and adult respiratory distress syndrome after massive transfusion.

We compared the degree of complement activation in 15 patients receiving massive blood transfusions and 21 patients with the septic syndrome and examined its association with other risk factors for adult respiratory distress syndrome (ARDS). Patients with massive transfusion (n = 8) as their only risk factor for ARDS had lower C3a levels (250 +/- 80 ng/ml) and a lower incidence of ARDS (0%) than patients with massive transfusion plus other risk factors (n = 7; C3a, 600 +/- 120 ng/ml; ARDS, 55%) or patients with the septic syndrome (n = 21; C3a, 540 +/- 80 ng/ml; ARDS, 19%). In our patients, the degree of complement activation appeared to reflect the presence of complicating clinical conditions.

Oxidant activity in expired breath of patients with adult respiratory distress syndrome.

Hydrogen peroxide levels were measured in the breath condensate of 43 patients receiving mechanical ventilation. In 16 patients the mean breath condensate peroxide level was 1.68 +/- 0.35 mumol/l on the day they met diagnostic criteria for adult respiratory distress syndrome (ARDS). The peak breath condensate peroxide level in the 27 patients in whom ARDS did not develop was significantly lower (0.34 +/- 0.08 mumol/l). Plasma lysozyme, a measure of in-vivo neutrophil turnover, was significantly higher in ARDS than in non-ARDS patients (9.2 +/- 2.2 U/ml v 3.4 +/- 1.1 U/ml). These findings support the hypothesis that neutrophil activation and oxidant production are involved in the pathogenesis of ARDS.