Case report: severe heat stroke with multiple organ dysfunction – a novel intravascular treatment approach

Corresponding author: Gregor Broessner 0 Assistant Professor, Department of Neurology, Neurological Intensive Care Unit, Medical University , Innsbruck , Austria 1 Resident, Department of Neurology, Neurological Intensive Care Unit, Medical University , Innsbruck , Austria 2 Professor and Chairman, Department of Neurology, Neurological Intensive Care Unit, Medical University , Innsbruck , Austria Introduction We report the case of a patient who developed a severe post-exertional heat stroke with consecutive multiple organ dysfunction resistant to conventional antipyretic treatment, necessitating the use of a novel endovascular device to combat hyperthermia and maintain normothermia. Methods A 38-year-old male suffering from severe heat stroke with predominant signs and symptoms of encephalopathy requiring acute admission to an intensive care unit, was admitted to a ten-bed neurological intensive care unit of a tertiary care hospital. The patient developed consecutive multiple organ dysfunction with rhabdomyolysis, and hepatic and respiratory failure. Temperature elevation was resistant to conventional treatment measures. Aggressive intensive care treatment included forced diuresis and endovascular cooling to combat hyperthermia and maintain normothermia. - Introduction Heat stroke is a life-threatening disease characterized by hyperpyrexia (elevated core body temperature exceeding 40C) and predominant central nervous system dysfunction resulting in delirium, convulsion or coma [1]. In many clinical and pathogenetic aspects, heat stroke resembles sepsis, requiring aggressive intensive care treatments, and there is growing evidence that endotoxemia and cytokines may be implicated in its pathogenesis [1-3]. We report a case of severe heat stroke with secondary multiple organ dysfunction being successfully treated with an intravascular cooling device. Case report A 38-year-old male underwent a hiking tour on a hot, humid day in late July 2003. At the end of this exhausting trip he complained of dizziness, finally falling into an 'apathic' state. On the arrival of the emergency physician, the patient suffered from a generalized epileptic seizure. Subsequently, the comatose patient (Glasgow Coma Scale 6 (E 1, V 1, M 4)) developed respiratory insufficiency and cardiovascular failure (blood pressure 60/20 mmHg, heart rate 166/min). He was immediately intubated (using fentanyl (0.3 mg), etomidate (40 mg) and midazolam (20 mg)) and transported to our neurological intensive care unit (NICU). BUN = blood urea nitrogen; CK = creatine kinase; IL = interleukin; NICU = neurological intensive care unit; NSAIDs = non-steroidal anti-inflammatory drugs; R = receptor; TNF = tumor necrosis factor. Course of core body temperature in a patient with heat stroke. The red line denotes the core body temperature while using 'conventional' temperature control methods. The blue line denotes the core body temperature while using an endovascular (CoolGard) cooling treatment. Blue arrows denote the start of CoolGard treatment. Red arrows denote attempts to terminate the active cooling procedure. On admission, the patient was deeply sedated and under analgesia, but still suffering from hypotension requiring immediate use of catecholamines (norepinephrine). The patient had normal weight (body mass index = 24) and no significant previous medical history. The initial cerebral computed tomography (CT) scan in combination with CT angiography did not reveal any pathologies and, to exclude an infectious origin for the central nervous system dysfunction, a lumbar puncture was carried out yielding normal cerebrospinal fluid. An initial extensive laboratory work up revealed impaired liver function (glutamic-oxaloacetic transaminase 312U/l (normal range: 10 to 50 U/l), glutamic-pyruvic transaminase 244 U/l (normal range: 10 to 50 U/l), gamma-glutamylcyclotransferase 94 U/l (normal range: 10 to 66 U/l) and a prothrombin time of 60% (normal range: 70 to 130%). Serum creatinine levels as well as blood urea nitrogen (BUN) were elevated (creatinine 2.6 mg/100 ml (normal range: 0.8 to 1.3 mg/100 ml) and BUN 30 mg/100 ml (normal range: 5 to 25 mg/100 ml)) indicating the beginning of renal failure. This situation was further complicated by rhabdomyolysis with elevation of myoglobin and creatine kinase (CK) (myoglobin peak level 33.124 g/l (day 2), normal range: 0 to 116 g/l) and CK peak level 102.4 U/l (day 4), normal range: 38 to 174 U/l. At the time of admission, core body temperature measured by urinary bladder probe (Foley catheter; Kendall Curity, Mansfield, MA, USA), was 40.8C. During the first 20 h of treatment, conventional temperature control methods including highdose non-steroidal anti-inflammatory drugs (NSAIDs) (acetylsalicylic acid 1000 mg and paracetamol 2000 mg) and opioids (pethidine 100 mg), as well as external cooling devices such as cooling blankets (Blanketrol II, Cincinnati Sub-Zero, Cincinnati, OH, USA) and Bair Hugger (Arizant Healthcare Inc, Eden Prairie, MN, USA), which were applied for 8 h, did not lead to any significant decrease in core body temperature (Figure 1). Because of subsequent deterioration of the patient's condition and insufficient conventional temperature control, an aggressive treatment approach with a novel intravascular cooling system (CoolGard 3000 and Cool Line, Alsius, Irvine, CA, USA) was begun. The heat-exchange catheter (Cool Line) was placed into the left superior vena cava and cooled saline was infused through a closed loop system into two heat-exchange balloons located near the distal end of the catheter. The temperature of the saline solution was adjusted automatically by the CoolGard 3000, which is an external temperature control unit, according to feedback to the external pump/refrigerant device from a microthermister attached to a Foley bladder catheter. Target temperature was set at 37C for the first 25 h of intravascular treatment and subsequently at 37.5C. Target temperature was reached within 7 h at a maximum cooling rate of 0.6C/h and 'cooling' was prolonged at this level. Multiple organ dysfunction and secondary rhabdomyolysis led to increased levels of myoglobin and CK (myoglobin peak level 33.124 g/l (day 2), CK peak level 102.4 U/l (day 4)). To prevent imminent renal failure, forced diuresis was initiated and continued for 40 h using high-dose furosemide and fluids, resulting in an urinary excretion rate of more than 400 ml/h, leading to a fluid turnover of up to 24,000 ml/24 h. With this aggressive measure, we suceeded in avoiding the use of extracorporal hemofiltration and the renal parameters returned to normal values within 3 days. Core body temperature was maintained at about 37C and subsequently maintained at 37.5C ( 0.2C) with the use of the intravascular catheter over the next 5 days (Figure 1). Several attempts to stop the active cooling within this period (Figure 1) led to an immediate steep increase of core body temperature, which (...truncated)