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Does pyrexia improve outcome?
- Richard G Fiddian-Green (5 April 2003)
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maintaining perioperative normothermia
- john r. may (6 April 2003)
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Maintaining perioperative normothermia--prevention is better (and easier) than cure
- Mark D Stoneham (7 April 2003)
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Addressing perioperative normothermia
- Alexander J Parry-Jones (9 April 2003)
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theory and practice are different things
- christopher m harpper (10 April 2003)
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Perioperative normothermai should be the norm
- Malcolm G Booth, David Anderson, Geraldine Gallagher and John Kinsella (11 April 2003)
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Normothermia is not always the goal
- Michael A Cooper (12 April 2003)
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Forced air-warming devices require risk assessments before use
- Richard P Cooke, Mandy Catchpole (30 April 2003)
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another reason for maintaining perioperative normothermia?
- Carolyn J Stamper (30 April 2003)
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Avoiding hyperthermia
- C Mark Hearn, K Chandradeva (3 May 2003)
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Temperature - the forgotten vital sign
- Jason J Smith (3 July 2003)
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Richard G Fiddian-Green, None None
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Mitochondria have two actions of fundamental physiologic importance, maintaining acid-base balance (1,2)and body temperature (3). Respiratory and renal buffering, shivering and vasoconsiction, and peripheral vasodilatation and sweating are fine-tuning mechanisms. Acid-base balance and temperature homeostasis are essential for normal enzyme function for enzymatic activity is very sensitive to abnormal changes in pH and temperature. The rate at which biochemical reactions proceed is, however, primarily dependent upon the availability of chemical energy released by ATP hydrolysis and the potential energy stored in the electochemical gradients it maintains. An impairment of mitchondrial oxidative phosphorylation will, for example, inhibit the ability to secrete acid in response to pentagastrin (4) and cause organ dysfunctions and failures (5,6). Infections are an important cause of an impairment of ATP resynthesis by oxidative phosphorylation the fall in tissue pH that accompanies an impairment being most likely to be caused by hypovolaemia and/or the uncoupling oxidative phosphorylation. The likelihood of developing organ dysfunctions and failures appears to increase as the degree and duration of tissue acidosis increase regardless of the cause of the tissue acidosis. Infections also cause an increase in local and often global body temperature. A fall in tissue temperature, which has an adverse effect upon outcome (7), decreases the rate of enzymatic reactions and the demand for energy from ATP hydrolysis. A rise in temperature, however, increases the rate of enzymatic reactions and might also increase the fluidity of all membranes (3). In so doing it is said to decrease the amount of energy needed to drive biochemical reactions. Might, therefore, the rise in temperature induced by infections be a host defense mechanism for improving outcome? Certainly the failure to show a pyrexial response to severe infections is known to be associated with a poor prognosis. During exercise the local temperature and permeability of mitochondrial membranes in skeletal muscle are said to increase (3). One would presume that the rise in temperature is directly related to the rate of ATP turnover, heat being a product of ATP hydrolysis and in the normal course of events some thirty percent of oxygen being consumed by metabolic processes other than ATP restnthesis by oxidative phosphoryation. In which case the increase in mitochondrial membrane permeability in skeletal muscles during exercise might be the result rather than a cause of the rise in temperature. Exercise might alternatively, or additionally, cause the rise in temperature seen in exercise by uncoupling oxidative phosphorylation. A fall in pH, rise in ionised calcium and the release of free radicals are all said to be able to increase mitochondrial membrane permeability and thereby uncouple oxidative phosphorylation. The degree of fall in tissue pH is a measure of the degree of unreversed ATP hydrolysis present in the anaerobiosis that develops with severe exercise. It is accompanied by porportional rise in ionised calcium concentrations. Free radicals may be generated in these circumstances by the conversion of xanthine dehydrogenase to xanthine oxidase(8). Severe infections may increase mitochondrial permeability and thereby uncouple oxidative phosphorylation by the same and/or other means. Severe infections are a potent cause of a tissue acidosis and accompanying rise in ionised calcium concentrations. The cytokines released by infections may also generate free radical release either directly or indirectly by promoting the conversion of xanthine dehydrogenase to xanthine oxidase. As mentioned above free radicals may also increase mitochondrial membrane permeability. Changing the mitochondrial membrane permeability, or the degree of openess of the permeability transition pores, must be a very dynamic process. Judging from a febrile patient's temperature chart significant changes in mitochondrial membrane permeability must occur within minutes. Interestingly the gastric intramucosal pH in a patient with a severe infection or indeed any other critical illness will often show the same degree of variablilty. In healthy volunteers, on the other hand, both the gastric body temperature and the intramucosal pH are remarkably constant. The variability in pH and temperature seen during the course of a serious infection must be a reflection of the battles being fought in the war between the adverse effects of the invading organsisms and the host reponses. Other than variations in oxygen delivery and consumption, these might include variations in the concentrations of cytokines, hormones and/or neurotransmitters released. Thyroxine, for example, is known to opens the permeability transition pore (3). Steroids might close the permeability transition pore for they prevent lysosomal disruption. Another important variable might be the size of the adenine nucleotide pool, depletion of ATP pools taking one hundred days to be reversed by de novo synthesis even in patients whose metabolism has been fully restored. A reduction in the magnitude of the ATP pools can be expected to have a negative effect upon endocrine and neurotransmitter turnover rates and pool sizes. Together these may be responsible for the "pooped-out syndrome" complicating major surgery and other serious illnesses (4). Given this pathophysiologic scenario might increasing the core temperature to abnormally elevated levels improve outcome in patients by decreasing the amount of metabolic energy needed to maintain organ function and cellular integrity? Certainly increasing body temperature is known to have a beneficial effect upon schizophrenia, hypothetically the product of a cerebral enegy deficit (5). The same therapeutic benefit may evidently be obtaned by increasing membrane fluidity with a diet that includes omega 3 fatty acid supplements. Might increasing the openess of the permeability transition pore with thyroxine in these circumstancs have a similar therapeutic effect in schizophrenia? Should these therapeutic options be evaluated prospectively it would be important not to do increase mitochondrial permeability so much that it uncouples oxidative phosphorylation to the degree that causes cellular apoptosis or even necrosis. Knowing the tissue pH at all times might enable such eventualities to be avoided. 1. Fiddian-Green RG. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br J Anaesth. 1995 May;74(5):591-606. Review. 2. Fiddian-Green RG. Monitoring of tissue pH: the critical measurement. Chest. 1999 Dec;116(6):1839-41. 3. Hochachka PA, Somero GW. Biochemical adaptation. Oxford University Press, New York, NY, 2002. 4. The pooped-out syndrome, ATP stores and hypothyroidism Richard G Fiddian-Green bmj.com/cgi/eletters/326/7384/295#30166, 4 Mar 2003 5. Madness, hyperhomocysteinemia, metabolic rate and body temperature Richard G Fiddian-Green bmj.com/cgi/eletters/325/7378/1433#28469,<br>6 Jan 2003 6. Higgins D, Mythen MG, Webb AR. Low intramucosal pH is associated with failure to acidify the gastric lumen in response to pentagastrin. Intensive Care Med. 1994;20(2):105-8. 7. Maintaining perioperative normothermia Christopher Mark Harper, Thomas McNicholas, and S Gowrie-Mohan BMJ 2003; 326: 721-722 8."Lactic acidosis": the common denominator? Richard G Fiddian-Green bmj.com/cgi/eletters/325/7374/1202#28322, 2 Jan 2003 Competing interests: None declared |
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john r. may, consultant anaesthetist raigmore hospital nhs trust iv2 3uj
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dear sir i found this article interesting insofar that the subject was deemed topical enough to merit an editorial in your journal. whilst not wishing to detract from the advice given, the importance of maintaining normothermia may appear to be a little "old hat" to anaesthetists and operating department practitioners who have been implementing the findings of the papers quoted for a few years now. Competing interests: None declared |
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Mark D Stoneham, Consultant Anaesthetist John Radcliffe Hospital, Oxford, OX3 9DU
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EDITOR Harper et al's editorial is timely and relevant to modern anaesthetic practice (1). However, it does not emphasize enough the importance of prevention of heat loss from the outset rather than the treatment of the subsequent hypothermia. Forced air warming blankets and the use of warmed irrigation and intravenous fluids are important methods of warming patients but do not by themselves prevent the development of perioperative hypothermia. Body temperature falls rapidly by up 1 degree C following anaesthetic induction due to redistribution of cold blood from periphery to core as a result of the obligatory vasodilatation accompanying general anaesthesia (2). This fall in core temperature may be avoided by active warming pre-induction (3,4). For patients undergoing major surgery, body temperature may fall further in the anaesthetic room whilst arterial and central venous catheters, epidural and urinary catheters are inserted. These procedures are commonly performed in the anaesthetic room after induction of general anaesthesia before the introduction of active warming measures. The combination of these factors can mean that the patient's temperature has fallen below 35 degrees C before surgery has even started (5). The maximum rate of core temperature increase using forced air warmers depends on several factors including: the percentage of body surface which is covered, obesity and body cavity rather than body surface surgery. It is rarely above 0.5 degrees C per hour. Thus it may take several hours for core temperature to return to normal. Attention should be paid to methods of preventing heat loss from the outset. 1. Harper CM. McNicholas T, Gowrie-Mohan S. Maintaining perioperative normothermia. BMJ 2003;326:721-2. 2. Sessler, D. I. Consequences and treatment of peri-operative hypothermia. Anesthesiology Clinics of North America 1994;12:425-456. 3. Bock, M., Muller, J., Bach, A., Bohrer, H., Martin, E., and Motsch, J. Effects of preinduction and intraoperative warming during major laparotomy. British Journal of Anaesthesia 1998;80:159-163. 4. Just, B., Trevien, V., Delva, E., and Lienhart, A. Prevention of intraoperative hypothermia by preoperative skin- surface warming. Anesthesiology 1993;79:214-218. 5. Stoneham MD, Howell S, Neill F. Heat loss during induction of anaesthesia for elective aortic surgery. Anaesthesia. 2000;55:79-82 Competing interests: None declared |
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Alexander J Parry-Jones, Locum Consultant in Intensive Care. UCL Hospitals, Mortimer Street, London W1T 3AAon
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I was interested to read the excellent editorial by Harper et al.1 in drawing attention to the importance of maintaining normothermia in the perioperative period. The difficulty lies not in understanding that maintenance of Bernard's 'milieu interieur' as far as possible during surgery is likely to reduce morbidity, mortality and shorten hospital stay but in changing existing practices to achieve this. The dinosaurs may not have understood the importance of keeping warm but we can. The challenge to all involved in perioperative care lies in achieving normothermia and not in reading the results of the randomised control trial that the authors advocate to further prove its importance. Maintaining normothermia in an individual can be surprisingly difficult and implementing changes to maintain normothermia in all will be harder still. 1 Harper C, McNicholas T, Gowrie-Mohan S. Maintaining perioperative normothermia. A simple, safe, and effective way of reducing complications of surgery. BMJ 2003; 326:721-722 Competing interests: None declared |
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christopher m harpper, research fellow middlesex hospital, W1T 3AA
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I would like to thank Dr May for his interest in our editorial. He points out that this is all old hat to anaesthetists. As far as the theoretical side goes he is probably correct. However, as a number of audits that we have carried out go to show, not only are patients still getting cold, but they are still getting cold unneccessarily through the underutilisation of current technology. Dr Stoneham quite rightly points out that prevention is better than cure. We are currently setting up a trial to see if we can reduce the incidence of mild hypothermia in our institution even further by 'pre-warming' our patients. Competing interests: author of article |
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Malcolm G Booth, consultant Anaesthetist Glasgow Royal Infirmary, Glasgow G4 0SF, David Anderson, Geraldine Gallagher and John Kinsella
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We were surprised to read an editorial in the Journal extolling the virtues of perioperative normothermia (1). The detrimental effects of hypothermia are well known and are, from the anaesthetists' perspective, old news. It is accepted on the basis of the several papers quoted that perioperative hypothermia puts the patient at risk of wound infection, blood transfusion, cardiac events, prolonged recovery and hospitalisation (2,3,4,5). This is already widely disseminated in the anaesthetic literature (6). The potential cost savings from preventing perioperative hypothermia are probably underestimated by Harper and colleagues. Reducing hospital length of stay has a major financial impact. Uneventful hypothermia with its associated extra two days of hospital stay costs approximately £800 (assuming a daily cost of £400 per day in a surgical ward). A perioperative wound infection will, therefore, cost a minimum of £2800 extra per patient. Forced air warmers cost about £2000 each. The drapes cost, depending on local contracts £10-20 each. Kurz's study that demonstrated lower wound infection rates in the normothermic patient had an NNT of 8. Therefore preventing one wound infection will cost £2000 in nonrecurring capital expenditure and, perhaps, £160 in disposable items. Thus, even if the full list price is paid the cost of maintaining normothermia is easily recovered. Preventing perioperative hypothermia should be the standard of practice and is achievable (7). In 1998, following the introduction of forced air warmers and effective fluid warmers an audit in our institution demonstrated that perioperative hypothermia following elective surgery lasting more than 90 minutes had been eliminated (8,9). As we have previously stated, the Declaration of Helsinki states that the importance of the objective of research should outweigh the inherent risk to the subject (10). Therefore to intentionally allow patients to become hypothermic would put them at risk of the well-documented side effects without any apparent prospect of benefit. Consequently a randomised-controlled trial as proposed by Harper would be currently unnecessary and unethical. References 1. Harper CM, McNicholas T and Gowrie-Mohan S. Maintaining perioperative normothermia. BMJ 2003; 326:721-22. 2. Kurz A, Sessler DI and Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. The New England Journal of Medicine 1996; 334: 1209-15. 3. Lenhardt R, Marker E, Goll C, Tschernich H, Kurz A, Sessler DI, Nrzt E and Lackner F. Mild intraoperative hypothermia prolongs postanesthetic recovery. Anesthesiology 1997; 87: 1318-23. 4. Schmied H, Kurz A, Sessler DI, Kozek S, reiter. Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty. Lancet 1996; 347: 289-92. 5. Frank SM, Fleisher LA, Breslow MJ, Higgins MS, Olson KF, Kelly S, Beattie C. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. Journal of the American Medical Association 1997; 277: 1127-34. 6. Gallagher G and Booth MG. Critical appraisal of the anaesthetic literature: prevention of perioperative hypothermia. Royal College of Anaesthetists, 2002; Bulletin 14: 687-89. 7. NHS in Scotland, Quality Improvement Scotland. Draft Anaesthesia Clinical Standards, October 2002;p44. 8. Gallagher G, Thomson A, McLintock T and Booth MG Prevention of post-operative hypothermia. British Journal of Anaesthesiology 1999, 82 supplement 1 A2. 9. Gallagher G, McLintoch T and Booth MG. Closing the audit loop – prevention of perioperative hypothermia, audit and reaudit of perioperative hypothermia. European Journal of Anaesthesia 2003 (in press). 10. Booth MG, Gallagher G and Kinsella J. Randomizing patients to permit the development of perioperative hypothermia is inappropriate (letter). European Journal of Anaesthesiology 2002; 19: 687. Competing interests: None declared |
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Michael A Cooper, Clinical Fellow Cardiothoracic AW1M 8PHnaesthesia The Heart Hospital, Westmoreland street, London
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I read with interest the editorial by Harper, McNicholas and Gowrie- Mohan. Anaesthetists have advocated aggressive temperature management for many years. Clinical evidence now seems to support the logical assumption that the enzymatic cascades and cellular reactions underpinning acute physiology function optimally at 37 oC. The authors do not comment on site of temperature monitoring. To manage temperature in the perioperative phase an appropriate site of measurement, and modality of measurement, must be chosen. In cardiac surgery central temperature is estimated from thermistor monitored naso-pharyngeal temperature. This, however, is known to underestimate cerebral temperature by about one degree Celsius. Rewarming post hypothermic (32o C) surgery is therefore to 35 or 36o C in an attempt to limit central hyperthermia and possible attenuation of any neural injury. Postoperatively, peripheral temperature and the central-peripheral gradient can give extra information to help the clinician in an assessment of cardiac output and vascular tone. Thermovigilance is clearly part of perioperative care. Unit policies may improve this and the managers who resist the cost of the required disposables should note the trust wide benefits from morbidity reduction that the authors describe. However, temperature flux can also provide valuable clinical information and situations do exist where normothermia is not the goal. Competing interests: None declared |
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Richard P Cooke, Infection Control Doctor Dept of Microbiology & Infection prevention & Control, Eastbourne District General Hospital BN21 2UD, Mandy Catchpole
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EDITOR- There are a wide range of medical devices that can be used for the maintenance of perioperative normothermia. These include warming lamps, circulating warm-air devices, rooms with thermal regulation capability, airway humidifiers and fluid-warming devices.1 As mentioned in the editorial by Harper et al,2 forced air-warming devices are a popular choice and widely used. However, their design features vary between manufacturers and there are few published evaluations to compare their performance. This is of concern since forced air-warming systems have the potential for both harm and good. This has been highlighted in two short reports which studied the risk of cross-infection associated with these devices.3,4 Aviden et al grew potentially pathogenic organisms directly from the airstream of two types of warming systems.3 However, they concluded that the risk of hospital-acquired infection was low provided that microbial filters were changed as specified by the relevant manufacturer and the detachable hoses were decontaminated regularly. In a study involving an ultra-clean ventilation system for orthopaedic surgery, Tumia et al noted that the use of warm air convection heaters produced a small increase in the number of colony forming units in the ultra-clean air but the levels were unlikely to be clinically significant.4 The risk of cross-infection from external contamination of these devices is unknown. Before procuring a forced-air-warming device, a risk assessment should be undertaken.5 The potential for harm to the patient is low provided manufacturer’s instructions are followed and staff are suitably trained. Their use in ultra-clean theatres however does need to be evaluated further. Improper use can have serious consequences. Traumatic thermal injuries (including third degree burns) have been reported due to a failure to properly attach the blanket to the hose. Similarly, a new warming blanket must be used for each patient. The temptation to simply place the hose under a sheet or blanket should be avoided at all costs. Richard PD Cooke Mandy Catchpole Eastbourne District General Hospital, Eastbourne, BN21 2UD
1 Hackel A, Badguell JM, Binding RR et al. Guidelines for the pediatric perioperative anesthesia environment. American Academey of Pediatrics. Section on Anesthesiology. Pediatrics 1999; 103: 512-515. 2 Harper CM, McNicholes T, Gowrie-Mohen S. Maintaining perioperative normothermia. BMJ 2003; 326: 721-722. 3 Aviden MS, Jones N, Ing R, Khoosel M, Lundgren C, Morrell DF. Convection warmers – not just hot air. Anaesthesia 1997; 1073-1076. 4 Tumia N, Ashcroft GP. Convection warmers – a possible source of contamination in laminar airflow operating theatres? J Hosp Infect 2002; 52: 171-174 5 Baker N, King D, Smith EG. Infection control hazards of intraoperative forced air warming. J Hosp Infect 2002; 51: 153-154. Competing interests: None declared |
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Carolyn J Stamper, SpR Anaesthetics Southport DGH, PR8 6NJ
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Harper et al collect and present evidence that maintaining a core temperature at or above 36 degrees celsius during surgery 'can be beneficial for the patient and cost effective'. Specified end points which are thought to be improved are; rates of wound infection, cardiac events, blood loss, and length of stay in recovery and in hospital. It is possible that an addition to this list is oxygen desaturation in the immediate post -operative period. During the past few months I have audited the need and use of supplemental oxygen in patients recovering from anaesthesia, whether general or regional. This was a prospective look at 114 patients who underwent all manner of predominantly elective procedures in a district general hospital. For the purposes of the study significant desaturation was taken as a fall in oxygen saturation to below 95% as recorded in the theatre recovery area. Five out of the eight patients (62.5%) in whom this happened had temperatures below 36.0 degrees celsius when measured at the tympanic membrane in recovery. In contrast, amongst the patients who did not desaturate only 35.1% had a temperature below this level. There will be many variables influencing post-operative desaturation, as with all the end points brought to our attention by Harper et al, not just patient temperature. However, while the influence of perioperative temperature on desaturation could be a good area for some research it is likely to provide more weight to the suggestion that 'maintaining perioperative normothermia' is 'a simple, safe, and effective way of reducing complications of surgery.' Competing interests: None declared |
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C Mark Hearn, Anaesthetic SHO Queen Mary's Hospital, Sidcup KENT DA14 6LT, K Chandradeva
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EDITOR - We read with interest the timely editorial by Harper et al (1). We agree with the importance of maintaining normothermia, but feel an important point has been overlooked, namely the potential complications of active patient warming. It is clear that direct thermal injury is a possibility, particularly with warm air blankets. A less obvious complication is that of hyperthermia. Smith et al (2) had an incidence of hyperthermia (core temperature greater than 37 degrees C) requiring cessation of convective warming in 33% of their patients receiving convective and fluid warming. We feel that if active patient warming is to be used then continuous core temperature monitoring should be obligatory to avoid accidental hyperthermia. Thus any business plan must also include provision for temperature monitoring, although it is very likely that there will still be a strong economic as well as clinical argument for active patient warming. 1. Harper CM. McNicholas T, Gowrie-Mohan S. Maintaining perioperative normothermia. BMJ 2003;326:721-2. 2. Smith CE, Desai R, Glorioso V, Cooper A, Pinchak AC, Hagen KF. Preventing hypothermia: convective and intravenous fluid warming versus convective warming alone. J Clin Anesth Aug 1998;10(5):380-5. Competing interests: None declared |
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Jason J Smith, SHO in Plastic Surgery The Royal Hospital Haslar
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The points made by Harper et al. are well founded in historical evidence. The aim of maintaining core temperature is now well accepted and appropriate practices are generally adopted in providing health care. A wide variety of interventions are used such as warmed fluids, minimising exposure and warm air blankets. Whilst these actions are readily utilised to control temperature the regular measurement and recording of the physiological parameter they affect is not. To illustrate, an audit of accident and emergency admissions to the resuscitation room showed only 7% of patients had a temperature measured and documented. A simple series of re-emphasising the importance of monitoring a physiological parameter that was purposefully being influenced dramatically improoved performance. It is important not only to impress the necessity of maintaining normothermia, but also to re-emphasise the basic principle of monitoring the physiological parameter you are trying to influence. Competing interests: None declared |
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