Responses to trauma: fifty years of ebb and flow.
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Biomedical subjects
Publications and source records attributed to H B Stoner.
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1. Total heat loss and its components have been studied in cool (20 degrees C) and warm (30 degrees C) environments in 30 healthy children and 21 children who had been burned (10-17% body surface area) 0.5-29 h previously. 2. In healthy naked children at 20 degrees C, the partition of total heat loss was: radiation, 64%; convection, 32%; evaporation, 4%. On transfer to the warm, total heat loss was reduced by approximately 50%, with disproportionate reductions in the contributions from radiation and convection being offset, to some extent, by an increase in evaporative heat loss. 3. In patients during the first 5.5h after injury, the magnitude and pattern of heat loss at 20 degrees C and 30 degrees C were similar to those in control subjects and were unaffected by bandaging. 4. Ten to twenty-nine hours after injury, when the patients were bandaged and body temperature and heat content were significantly higher than in control subjects, radiant and convective heat losses were increased, but as evaporative heat loss tended to be reduced; total heat loss in the warm was unchanged. However, at this time at 20 degrees C, total heat loss was reduced compared with healthy children at the same ambient temperature. 5. The findings of unchanged or reduced total heat loss and reduced evaporative heat loss in injured patients are interpreted as inappropriate responses to an increased body temperature and heat content in children after burn injury.
Relationships between skin temperature (Tsk) and perfusion have been studied to provide a basis for the use of Tsk in the non-invasive assessment of limb circulation in peripheral vascular disease. Raising the ambient temperature (Ta) from 20 to 30 degrees C increased the perfusion of the glabrous skin of the hands and feet without changing that of the skin of the forearm or calf. On a fractional basis the response in the hand and foot was the same. Tsk was higher in the arms than the legs and in the proximal than distal parts of the limbs. A fall in Tsk was often seen when Ta rose from 20 to 25 degrees C and was attributed to counter-current cooling. Subsequently Tsk rose even in regions where there was no increase in skin perfusion. Tsk can only be related to its perfusion in the fingers, palm and toes. Forearm Tsk was related to the perfusion of the digits. This relationship implies a link with the arterial inflow to the limb which determines the size of its thermal core. Heat conduction from the core seemed important for the skin of areas like the forearm and calf where the constant, low perfusion limited the amount of heat which could be transported to it directly by the blood. The importance of conduction was supported by studies, at Ta 20 degrees C, on subjects during calf muscle exercise and on patients with arterio-venous fistulae. Here an increase in the arterial inflow to the limb was associated with a rise in Tsk of the forearm/calf unrelated to the perfusion of its skin.
In order to forecast the healing of a Burgess type below-knee amputation the skin temperature of the leg has been studied before operation in 39 instances using infra-red thermography in a 26 degrees C environment. Healing bore no relation to the mean skin temperature of the calf or that of the skin at the site of the anterior incision. However, when the skin temperature at the site of the incision for the long posterior flap was greater than 30.4 degrees C or when the ratio of the temperatures at the posterior and anterior incision sites (P/A) was greater than 0.98 healing was significantly more likely to occur. It is proposed that the temperatures at these sites should be used to assess the prospect of such an amputation healing.
1. Changes in body heat content in five normal adults, in 30 healthy children and in 24 children who had suffered burn injury 1-5 h previously, have been studied in cool (20 degrees C) and warm (30 degrees C) environments. 2. On moving from a cool to a warm environment, the heat content rose in both normal adults and healthy children, but the increase was significantly larger in the children. 3. Much larger changes occurred in the burned children in whom the heat content rose to a new plateau within about 8 h of the accident. 4. The changes after burn injury were unrelated to the bandaging of the burn and were little affected by the environmental temperature.
When samples were taken within 2 hr of accidental injury, plasma cortisol levels increased with injury severity score (ISS) in patients with minor and moderate injuries (ISS, 1-12) but decreased at higher ISS. Radioimmunoassay of adrenocorticotrophin (ACTH) showed very variable plasma concentrations at all ISS ranges. Like cortisol, ACTH increased with ISS up to a score of about 13, but it thereafter plateaued, and in patients with severe injuries plasma cortisol fell in relation to ACTH as well as in absolute terms. This suggested that although ACTH secretion was generally far from maximal the relatively low cortisol concentrations in the most severely injured were at least partly due to a poor response of the adrenal cortex to ACTH. In patients who presented late (more than 2 hr after injury) plasma cortisol levels were more variable and more strongly related to ACTH than at shorter times after injury. The variability of cortisol also increased with age. Patients with severe head injuries had cortisol and ACTH concentrations similar to those without head injuries but with a similar ISS from injuries in other parts of the body.
There are conflicting reports on plasma insulin concentrations in the acutely injured. Plasma insulin and glucose concentrations have been measured in 504 patients within 8 h of injury, and related to the severity of injury as assessed by the injury severity score (ISS). As in previous surveys of injured patients, an extremely wide range of insulin concentrations was found (2-141 mU/l). Most of the variability occurred at lower severities of injury. In very severely injured patients (ISS greater than or equal to 30), insulin concentrations were uniformly suppressed (less than 20 mU/l), especially in relation to the hyperglycaemia in these patients. Two small subgroups, patients dying within 3 h of injury and known psychiatric patients on psycho-active drugs, differed from the general pattern in displaying elevated insulin concentrations despite very severe injuries. The results bear out the idea that insulin secretion is usually acutely suppressed by adrenaline after severe injury; after less severe injuries, however, the response is much less uniform.
John Hunter suggested that the body's responses to injury were defensive and had survival value. Now, many years later, we are still uncertain about this. Although our appreciation of the endocrine and metabolic responses to injury, both physical and bacterial, has increased enormously our knowledge of these events, particularly at a molecular level, is still very incomplete. Patterns have been identified, however, in the sphere of energy metabolism, and this provides a basis for interpreting at least some of the biochemical responses to injury. The views developed support the idea that the responses are defensive--initially against the impact of the injury and then to meet the demands of the new "organ" which the wounds or septic focus seem to have added to the body. A reason for wanting to interpret these responses is to improve patient care. Current interpretations at least help to clarify our view of what is happening in the injured or septic patient and sometimes indicate lines of treatment. Nevertheless, many serious problems, particularly changes in protein metabolism, remain to be solved before we can advise on the metabolic care of patients at all stages from accident to recovery.
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The effect of trauma on human thermoregulation has been studied using a behavioural test and the vascular response to cold exposure. It was confirmed, in controls, that a pleasurable temperature for the hand (Thand) depended on core temperature (Tc) to which it was negatively related. Shortly after moderately severe fractures in a leg this relationship was lost and in the patients the slope of this regression line was not significantly different from zero and they usually chose a Thand towards the upper end of the normal range irrespective of Tc. This effect was not imitated in controls by removing 500 ml blood but Thand was increased by occluding the circulation to one leg. Naloxone did not alter Thand in controls but when given in a suitable dose it reduced the rise in Thand during a short period of limb ischaemia. Immersing one hand and forearm in water at 17 degrees C reduced the blood flow through the contralateral forearm and hand. The reduction in flow was positively related to the initial rate of flow in both controls and injured but the slope of the regression line was significantly less after injury. It is concluded that thermoregulation is affected by trauma in man.
Plasma catecholamine (adrenaline, noradrenaline and dopamine) concentrations have been measured in 48 patients within 6 hours of the onset of symptoms of an acute myocardial infarction. The concentrations of all three catecholamines were elevated, and there were positive correlations between plasma noradrenaline concentrations and the severity of infarct as assessed by the coronary prognostic index and serum LDH levels. Plasma glucose, free fatty acid, lactate and cortisol levels were elevated while insulin levels were reduced. The site of infarction did not influence the pattern of hormonal and metabolic responses although heart rate was significantly lower in the inferior than in the anterior infarct group. Seven patients went into ventricular fibrillation shortly (less than 1.8 h) after blood sampling. Plasma catecholamine concentrations were markedly elevated in these patients with levels similar to those previously reported after cardiac arrest.
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Plasma catecholamine concentrations in cardiac arrest (ventricular fibrillation and asystole) are significantly higher than after myocardial infarction. The levels reached are well above those normally required to stimulate cardiac activity. Possible reasons for the failure of the myocardium to respond to the catecholamines are discussed and the rationale for giving more catecholamines is questioned.
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Plasma catecholamine concentrations in 40 patients shortly after accidental injury rose progressively with increasing severity of injury. Norepinephrine and epinephrine concentrations were unrelated other than by a common rise with severity; dopamine was closely related norepinephrine and not independently related to injury severity. Plasma glucose concentrations rose after injury; however, this was related only to the plasma epinephrine concentration and not independently to injury severity. Plasma lactate concentrations, in contrast, showed components related both to severity of injury and independently to norepinephrine and epinephrine concentrations. Plasma insulin concentrations were uniformly low, especially with respect to the hyperglycemia, in patients with high plasma epinephrine concentrations. Plasma concentrations of free fatty acids and of cortisol were unrelated to plasma catecholamine concentrations, as were pulse rate and blood pressure. These relationships confirm the expected role of the sympathoadrenal system in the metabolic changes following injury in man.
Changes in gaseous exchange, plasma substrates and hormones and excretion of nitrogen were followed in 13 non-septic male patients, all of whom had sustained at least 1 fracture of a long bone. Results were compared with normal subjects given glucose to produce a range of substrate and hormone concentrations. Over the 3 weeks following injury, oxidation of fat decreased from high levels whilst oxidation of carbohydrate rose. This reflected to some extent changes in availability of substrate, but early after injury oxidation of fat was higher than expected for the concentration of free fatty acids in plasma and later oxidation of carbohydrate was increased relative to concentrations of glucose and insulin. Concentrations of insulin in plasma were high for the prevailing concentrations of glucose, and peak urinary excretion of nitrogen coincided with maximum levels of insulin. It was concluded that in the injured patient there are changes at the level of utilization and oxidation of plasma substrates as well as in their availability, and that there is marked unresponsiveness of protein metabolism to the normal anabolic effect of insulin.