NDT Advance Access originally published online on December 20, 2005
Nephrology Dialysis Transplantation 2006 21(5):1450-1451; doi:10.1093/ndt/gfi322
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Haemodialysis and thermoregulation
Email: Jkoo{at}groupwise.azm.nlSir,
We read with great interest the editorial comment of Drs Passlick-Deetjen and Bedenbender-Stoll [1]. This editorial rightly stresses the importance of thermal factors in the pathogenesis and prevention of intra-dialytic hypotension (IDH). Thermal factors are primarily responsible for the inappropriate cutaneous vasodilation observed during dialysis with standard dialysate temperatures (37–37.5°C) and are the explanation for differences in the haemodynamic response between haemodialysis on the one hand and isolated ultrafiltration and haemo(dia)filtration on the other hand [2–4].
However, we would like to comment on two issues addressed in this review. The first concerns the pathophysiology of the increase in core temperature during haemodialysis, which even occurs if no energy is added from the extracorporeal circuit to the patient (so-called thermoneutral treatments). The authors state that this phenomenon is primarily due to initial cutaneous vasoconstriction caused by ultrafiltration, which prevents the dissipation of heat from the body (Gotch hypothesis). This hypothesis appeared to be confirmed by the significant relation between the ultrafiltration rate and the energy removal needed to prevent the increase in core temperature during so-called isothermic dialysis [5]. However, in collaboration with the group of Nathan Levin, we performed a falsification study of this hypothesis and found no differences in core temperature changes between thermoneutral dialysis treatments either with or without ultrafiltration. Moreover, no differences in extracorporeal energy flow rate were observed between isothermic treatments respectively performed with and without ultrafiltration [6]. In addition, no study yet demonstrated initial vasoconstriction followed by vasodilation during haemodialysis. In contrast, cutaneous vasodilation is already observed shortly after the start of dialysis [7]. Therefore, although we were not able to elucidate the primary responsible factors for the increase in core temperature during dialysis in this study, the Gotch hypothesis clearly did not pass the falsification process.
Our second comment concerns the use of cool (temperature) dialysis. The reader of the editorial might feel somewhat discouraged to lower dialysate temperatures because cool dialysis may lead to shivering. However, as the authors rightly indicate, numerous earlier studies have consistently shown the benefits of cool dialysis in the prevention of IDH.
Certainly, prescription of isothermic treatments controlled by the blood temperature feedback module (BTM) is not only appealing from a theoretical point of view, but was also found to be efficacious for the prevention of IDH in the randomized crossover trial by Maggiore et al. [8]. However, a practical drawback for the use of BTM-controlled dialysis is that this feature is only available on dialysis modules of a single manufacturer, whereas dialysate temperature can be easily adjusted on every dialysis module. Also, a feeling of coldness is not entirely prevented by isothermic dialysis sessions (5% of sessions) [8], which might be theoretically explained by an increase in the temperature setpoint during dialysis.
In our dialysis centre, we have the practice of gradually reducing dialysate temperature from 36.5°C to a minimum of 35.5°C, depending on the haemodynamic response and subjective feelings of comfort in our patients. By this approach, together with strict volume control, aided by the use of vena cava echography, and adjustment of dialysis time if necessary, the incidence of IDH in our centre is well below 5%. Treatments are well tolerated by the patients without shivering.
Thus, we believe that in patients prone for IDH, a gradual lowering of dialysate temperature, which should be individualized according to the haemodynamic response and side effects in the patient, would appear a rational alternative when BTM-controlled modules are not available.
Conflict of interest statement. None declared.
Department of Internal Medicine University Hospital Maastricht, The Netherlands
References
- Passlick-Deetjen J, Bedenbender-Stoll E. Why thermosensing? A primer on thermoregulation. Nephrol Dial Transplant 2005; 20: 1784–1789
[Free Full Text] - Pizzarelli F, Sisca S, Zoccali C et al. Blood temperature and cardiovascular stability in hemofiltration. Int J Artif Organs 1983; 6: 37–41[Web of Science][Medline]
- van der Sande FM, Kooman JP, Konings CJ, Leunissen KM. Thermal effects and blood pressure response during postdilution hemodiafiltration and hemodialysis: the effect of amount of replacement fluid and dialysate temperature. J Am Soc Nephrol 2001; 12: 1916–1920
[Abstract/Free Full Text] - van der Sande FM, Gladziwa U, Kooman JP, Böcker G, Leunissen KML. Energy transfer is the single most important factor for the difference in vascular response between isolated ultrafiltration and hemodialysis. J Am Soc Nephrol 2000; 11: 1512–1517
[Abstract/Free Full Text] - Rosales LM, Schneditz D, Morris AT, Rahmati S, Levin NW. Isothermic hemodialysis and ultrafiltration. Am J Kidney Dis 2000; 36: 353–361[Web of Science][Medline]
- van der Sande FM, Rosales LM, Brener Z et al. Effect of Ultrafiltration on thermal variables, skin temperature, skin blood flow, and energy expenditure during ultrapure hemodialysis. J Am Soc Nephrol 2005; 16: 1824–1831
[Abstract/Free Full Text] - Kooman JP, Gladziwa U, Böcker G, van Bortel LMAB, van Hooff JP, Leunissen KML. Role of the venous system in hemodynamics during ultrafiltration and bicarbonate dialysis. Kidney Int 1992; 42: 718–726[Medline]
- Maggiore Q, Pizzarelli F, Santoro A et al. Study group of thermal balance and vascular stability. The effects of control of thermal balance on vascular stability in hemodialysis patients: results of the European randomized clinical trial. Am J Kidney Dis 2002; 40: 280–290[CrossRef][Web of Science][Medline]
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