Clinical paperDecreased fluid volume to reduce organ damage: A new approach to burn shock resuscitation? A preliminary study☆
Introduction
Resuscitation from burn shock is a formidable challenge for intensive care specialists. The extensive capillary damage which follows thermal injury is responsible for massive plasma extravasation into burned tissues with consequent hypovolaemia and shock.1, 2, 3 Too vigorous resuscitative efforts may lead to severe protein depletion with further oedema accumulation into both burned and unburned tissues. In the past decades several formulae have been developed for optimal fluid resuscitation of burn patients, the most popular being the Parkland Formula.4 This time-honoured approach allows for sufficient vital organ perfusion, while avoiding excessive oedema formation.
Although adequate resuscitation has long been recognised as the single most important therapeutic intervention of burn critical care, the routine use of invasive haemodynamic monitoring has never been recommended as guide for fluid volume replacement by fear of infections. Nowadays, the adequacy of resuscitative efforts is still assessed by a combination of both traditional and semi-invasive variables, the insertion of a pulmonary artery catheter being restricted to patients with refractory shock or limited cardiopulmonary reserve.5 In recent years, the introduction of trans-pulmonary indicator dilution technique at the bedside has made the use of invasive haemodynamic monitoring in burned patients easier.6, 7, 8 Its reduced invasiveness as compared with pulmonary artery catheterisation9 and the possibility of direct cardiac preload estimation10 also allowed for a haemodynamic-oriented approach to burn shock resuscitation.6 Since 2000, we routinely use both intrathoracic blood volume (ITBV) and cardiac output measurement as earlier and more sensitive indicators of critical hypovolaemia than vital signs, hourly urine output and central venous pressure. The trans-pulmonary indicator dilution technique enabled us to appreciate that the Parkland Formula did not allow for the early (<24 h) correction of intravascular volume deficit as complete ITBV normalisation could only be achieved after the first 48 h post-burn. Additionally, a condition of fluid unresponsiveness was present throughout the first 12-h period, any increase of the administered fluids only accelerating post-burn oedema accumulation. In a recent study, the rate of intravascular volume replacement was found to be independent from the amount of crystalloid infused as the administration of supranormal volumes failed into the early (24 h) achievement of normal preload and DO2 values.8 We therefore speculated that the adoption of a reduced rather than aggressive approach was preferable as the potential existed for decreased oedema formation, provided that resuscitation was not delayed. Since 2004, we therefore reduced the volume given as low as possible by titrating the infusion rate to a minimum ITBV value that allowed for sufficient vital organ perfusion, while at the same time avoiding any resuscitation delay. This approach was referred to as permissive hypovolaemia. We also hypothesised that if the deliberate reduction of resuscitation volume could allow for decreased extravasation of fluids, then less multiple-organ dysfunction might be anticipated as consequence of reduced oedema formation. Therefore, the present study evaluates the effectiveness of permissive hypovolaemia in reducing multiple-organ dysfunction as compared with the Parkland Formula.
Section snippets
The study was performed in accordance with guidelines laid down by the hospital ethics committee
Two cohorts of patients were compared. Twelve patients resuscitated with permissive hypovolaemia and admitted to our eight general ICU beds from January 2004 to December 2005 were matched with 12 patients receiving the Parkland Formula in the two preceding years. Patients were enrolled only if they were equipped with the PiCCO© system (Pulsion Medical System, Munich, Germany) thus allowing for both ITBV and cardiac output measurements. Other admission criteria were age >14 years, burn size ≥20%
Results
Table 1 lists both demographics and main burn characteristics for the patient cohorts. By design, mean age (P = 0.31), total burn surface area (P = 0.90) and full-thickness burn depth (P = 0.78) were similar between groups.
Discussion
The main study result is that resuscitation volume can be safely reduced below the Parkland estimate, provided that reduction of administered fluids is guided by close haemodynamic monitoring. Additionally, we provide the first objective evidence that post-burn oedema is detrimental to organ function and that such a deleterious effect is proportional to the amount of extravasated fluids. Permissive hypovolaemia allowed for 3.2 ± 0.75 ml/kg/% burn of total resuscitation volume against an
Conclusions
Permissive hypovolaemia seems to be effective in reducing both organ and system dysfunction as induced by oedema accumulation. This haemodynamic-oriented resuscitative approach allows for a better refinement of fluids volume administration during the very early post-burn period thus minimising unnecessary fluids overload.
Conflict of interest statement
The authors state that no financial or personal conflict of interest exists with regard to the present study.
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Fluid Resuscitation and Cardiovascular Support in Acute Burn Care
2024, Clinics in Plastic SurgeryRisk factors and the associated limit values for abnormal elevation of extravascular lung water in severely burned adults
2019, BurnsCitation Excerpt :Previous studies have shown that fluid resuscitation guided by PiCCO monitoring typically results in over-resuscitation, leading to exacerbation of burn edema and compartment syndromes in burn patients [15,34]. By contrast, permissive hypovolemia protocols and a below-normal ITBVI as resuscitation targets have been proven to be safe [12,35]. Our findings concurred with this notion and, more importantly suggested an ITBVI goal to help maintain a normal EVLWI and thereby reduce the risk of early pulmonary edema during the fluid reabsorption stage.
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A Spanish translated version of the summary of this article appears as Appendix in the final online version at 10.1016/j.resuscitation.2006.07.010.