Introduction

There are many ways to resuscitate a major burn injury. This chapter will cover the three most widely used methods. First, there will be a short recapitulation of the pathophysiology and the general physiological principles involved. Then the ‘Parkland’, the ‘Hypertonic lactated saline’, and finally the ‘Muir and Barclay’ formulae will be described. The monitoring and assessment of a successful resuscitation for each formula will be explained in a pragmatic fashion. It is hoped that this will enable the reader to perform a successful resuscitation, no matter which path is chosen.

Pathophysiology

Both local and systemic alterations to physiology occur after a thermal injury. The greater the injury, the more marked the alterations. Immediately, post-burn haemodynamic stability is reflected by a normal blood pressure, a slight tachycardia, and an increased respiratory rate. Within several hours the cardiac output will fall, the severity of the fall being dependent on the size of the burn. There will be a compensatory increase in peripheral resistance to maintain a normal blood pressure. The initial depression of cardiac output will occur before any significant hypovolaemia. Isotonic fluid is sequestered into the burn wound and also into nonburned tissue. Hypovolaemic shock would soon occur if the intravascular volume was not repleted. Cardiac output slowly returns to near normal levels within 24 hours in all but the largest burns.

Fewer than 3% of all acute burns die from hypovolaemic shock and acute renal failure. These ‘resuscitation failures’ generally occur in burns exceeding 90% body surface area. Patients with pre-existing cardiac or renal disease may have an uneventful resuscitation when adequate intravenous fluids are administered promptly.