Abstract

The care of the patient with major burns in the ICU is a complex and challenging task. They differ from the other critical care patient groups in several ways. One of the major challenges faced is confronting their hypermetabolic state and temperature management [1]. It is widely known that major burn injury is associated with the most profound of hypermetabolic responses to a pathological state. Hyperthermia that is non-infectious is a feature of the systemic inflammatory response to this. In burns intensive care, the disproportionate increase in metabolic rate to small rises in core temperature can have significant impact on resuscitation and prognosis. The pathophysiology of the hyperthermic response in major burn injury is poorly understood. It could be secondary to an infective etiology or a metabolic response to the systemic inflammation. Irrespective of the reason, sustained hyperthermia above 40°C can culminate in cellular injury and death [2]. The hypermetabolic response starts within the first 5 days of the major burn and can last for a year after the injury. Because of the ongoing systemic inflammatory stimulation, patients with major burns often have pyrexia and their thermoregulatory system reset at a higher baseline temperature around 38.5°C [3]. While therapeutic cooling is widely used in neuro intensive care in the management of hyperthermic brain-injured patients and in patients after out-of-hospital cardiac arrests, there is very scarce literature available on the management of hyperthermia in burns intensive care. We, in this article, would like to share our experience of using the intravascular temperature management system (IVTM) Thermoguard XP® in our unit to manage refractory hyperthermia in patients with major burns. We report the responses of two major burns patients to core intravascular thermoregulation during periods of severe hyperthermia (>40°C). Case 1 A 24-year-old male had sustained 80% mixed depth, total body surface area (TBSA) flame burns following a road traffic accident. He had no significant past medical history. Initial resuscitation including endotracheal intubation and fluid resuscitation was instituted in the nearby district general hospital and was transferred over to our burns ICU without much delay. On admission to the ICU, detailed assessment of the burn injuries revealed second-degree and third-degree burns involving the trunk, abdomen, back, upper and lower extremities. Initial temperature recorded was 34°C. He responded to external warming, which included nursing in a warm environment, use of warm air blanket and warm fluids. The patient underwent extensive escharatomies on the day of admission as a part of his initial resuscitation. He developed multiorgan failure requiring high inotropic support, renal replacement therapy and high FiO2. He developed hyperpyrexia (temperature >42°C) on day 11 post burn. Relevant microbiology investigations had demonstrated no obvious focus of ongoing infection. The hyperpyrexia was resistant to conventional active cooling (bladder/gastric lavage, hemofiltration, external cooling with cooling blanket). The hyperpyrexia was associated with marked tachycardia (heart rate >150 beats/minute) with increasing oxygen demands and hypotension with escalating inotropic support. Forced core thermoregulation was commenced due to instability attributed to high core temperature. The Thermogard XP® was inserted in the femoral vein, the target temperature was set at 37°C. Within 2 hours of initiating the IVTM, the core body temperature dropped by 3°c down to 39°C. It took a further 3 hours to stabilise at the target temperature of 37°C. The IVTM system was used for a period of 6 days. The objective measurements of pulse rate, blood pressure, respiratory rate and urine output were seen to improve in the presence of a normothermic state (Figure ​(Figure1).1). After a protracted and convoluted stay in the ICU, the patient was discharged to a ward after 38 days. Open in a separate window Figure 1 Response in vital parameters in the first 20 hours after initiating IVTM: case 1.

Highlights

  • A1 Update on therapeutic temperature management Gregor Broessner1*, Marlene Fischer1, Gerrit Schubert2, Bernhard Metzler3, Erich Schmutzhard1 1Department of Neurology, Medical University, Innsbruck, Austria; 2Department of Neurosurgery, Medical University, Innsbruck, Austria; 3Department of Cardiology, Medical University, Innsbruck, Austria Critical Care 2012, 16(Suppl 2):A1It is a pleasure to announce the 2nd Innsbruck Hypothermia Symposium

  • Mild therapeutic hypothermia after cardiac arrest has become standard in post-resuscitation care in many hospitals as it is recommended by current guidelines

  • Some authors report that both b1-adrenoceptors and aadrenoceptors increase their sensitivity to catecholamines during hypothermia [18,20,21,22] as b1-adrenoceptor activity was potentiated by low temperature, and they claim the existence of hypothermia-induced supersensitivity and increased agonist activity for b1-adrenoceptors

Read more

Summary

Introduction

A1 Update on therapeutic temperature management Gregor Broessner1*, Marlene Fischer, Gerrit Schubert, Bernhard Metzler, Erich Schmutzhard1 1Department of Neurology, Medical University, Innsbruck, Austria; 2Department of Neurosurgery, Medical University, Innsbruck, Austria; 3Department of Cardiology, Medical University, Innsbruck, Austria Critical Care 2012, 16(Suppl 2):A1It is a pleasure to announce the 2nd Innsbruck Hypothermia Symposium. It could be shown that hypothermia may lead to increased rate of infections, hypotension, shivering, disturbances in blood clotting, rewarming injuries and significant changes in pharmacokinetics and pharmacodynamics possibly limiting outcome effects of the treated patients [4,5,6,7,8]. Aggressive treatment of fever in the ICU without risk elevation through the side effects of therapeutic hypothermia led to the concept of controlled prophylactic normothermia This concept is based upon strict control of body core temperature with a target of 36.5°C beginning as early as possible with the goal of complete fever prevention. All planned measures to reduce reperfusion damage before revascularization should preferably be applied in a very short time

Objectives
Findings
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call