Aggressive Rewarming Research Articles

Special Traumatized Populations: Accidental Hypothermia in Children.

Physicians caring for children in trauma settings must consider and treat hypothermia as a cause for morbidity and mortality. Knowledge of treatment of accidental hypothermia with and without an asphyxial event is paramount. Clinicians need to identify hypothermia immediately and be aware of the overall management utilizing aggressive rewarming and cardiopulmonary resuscitation to help improve the survival of these critically ill children. This section reviews the epidemiology, clinical effects, and management options for accidental hypothermia in children.

Severe Accidental Hypothermia in A Trauma Patient in A Tropical City

Introduction: Severe accidental hypothermia in trauma patients is rarely encountered in tropical areas. However, unnoticed hypothermia may lead to deleterious consequences and even sudden death.Case report: We report the case of a middle-aged patient who sustained hemorrhagic shock secondary to a traffic accidentinduced severe intraabdominal injury, followed by prolonged exposure to a cold and wet environment. Thereafter, the patient was sedated and paralyzed and was administered large infusion volumes of fluid and blood components. In the emergency department, profound hypothermia could not be detected using an infrared forehead thermometer. Subsequently, the patient had a sudden cardiac arrest during the emergency surgery.Conclusion: This case report highlights that even in a tropical city, fatal severe hypothermia may occur in severe trauma patients. Therefore, to avoid accidental hypothermia, emergency physicians and trauma surgeons should use invasive temperature monitoring, and aggressive rewarming should be performed for correcting hypothermia in severe trauma patients

A recommended early goal-directed management guideline for the prevention of hypothermia-related transfusion, morbidity, and mortality in severely injured trauma patients.

Hypothermia is present in up to two-thirds of patients with severe injury, although it is often disregarded during the initial resuscitation. Studies have revealed that hypothermia is associated with mortality in a large percentage of trauma cases when the patient’s temperature is below 32 °C. Risk factors include the severity of injury, wet clothing, low transport unit temperature, use of anesthesia, and prolonged surgery. Fortunately, associated coagulation disorders have been shown to completely resolve with aggressive warming. Selected passive and active warming techniques can be applied in damage control resuscitation. While treatment guidelines exist for acidosis and bleeding, there is no evidence-based approach to managing hypothermia in trauma patients. We synthesized a goal-directed algorithm for warming the severely injured patient that can be directly incorporated into current Advanced Trauma Life Support guidelines. This involves the early use of warming blankets and removal of wet clothing in the prehospital phase followed by aggressive rewarming on arrival at the hospital if the patient’s injuries require damage control therapy. Future research in hypothermia management should concentrate on applying this treatment algorithm and should evaluate its influence on patient outcomes. This treatment strategy may help to reduce blood loss and improve morbidity and mortality in this population of patients.

Clinical experience with an active intravascular rewarming technique for near-severe hypothermia associated with traumatic injury.

Hypothermia and acidosis are secondary causes of trauma-related coagulopathy. Here we report the case of a 72-year-old patient with severe trauma who suffered near-severe hypothermia despite the initiation of standard warming measures and was successfully managed with active intravascular rewarming. The patient was involved in a road traffic accident and was transported to a hospital. He was diagnosed with massive right-sided hemothorax, blunt aortic injury, burst fractures of the eighth and ninth thoracic vertebrae, and open fracture of the right tibia. He was referred to our hospital, where emergency surgery was performed to control bleeding from the right hemothorax. During surgery, the patient demonstrated progressive heat loss despite standard rewarming measures, and his temperature decreased to 32.4°C. Severe acidosis was also observed. A Cool Line® catheter was inserted into the right femoral vein and lodged in the inferior vena cava, and an intravascular balloon catheter system was utilized for aggressive rewarming. The automated target core temperature was set at 37°C, and the maximum flow rate was used. His core temperature reached 36.0°C after 125 min of intravascular rewarming. The severe acidosis was also resolved. The main active bleeding site was not identified, and coagulation hemostasis as well as rewarming enabled us to control bleeding from the vertebral bodies, lung parenchyma, and pleura. The total volume of intraoperative bleeding was 5,150 mL, and 20 units of red cell concentrate and 16 units of fresh frozen plasma were transfused. After surgery, he was transferred to the intensive care unit under endotracheal intubation and mechanical ventilation. His hemodynamic condition stabilized after surgery. The rewarming catheter was removed on day 2 of admission, and no bleeding, infection, or thrombosis associated with catheter placement was observed. Extubation was performed on day 40, and his subsequent clinical course was uneventful. He recovered well following rehabilitation and was discharged on day 46. These findings suggest that active intravascular rewarming should be considered as an aggressive, additional rewarming technique in patients with near-severe hypothermia associated with traumatic injury.

Rewarming strategy and neuromonitoring are significant details in neurological outcome after surgical repair of type A aortic dissection

We with great interest read the article by Haldenwang et al. [1] on the evaluation of the risk factors for transient neurological dysfunction and adverse outcome after repair of acute type A dissection. We recognize the importance of their aim to assess preand intraoperative factors that can cause neurological impairment. We do, however, have a few comments and suggestions for more proper clinical management in such complex cases. One form of transient neurological deficit (TND) was defined by Haldenwang et al. as persistent loss of cognitive function without changes on computed tomography or complete resolution before discharge, which is, in our opinion, closer to the definition of permanent neurological damage. Morphological changes that cause persistent cognitive loss can be detected with more sensitive methods such as MR, but functional changes may regress or disappear before discharge because of brain plasticity [2]. Therefore, the evaluation of cognitive function requires the application of specific functional tests [3]. Axillary cannulation is technically difficult, but is associated with less local and systemic complications. In the case of emergency, an alternative, but safer approach often has to be used [4]. Haldenwang et al. did not specify what type of cannulation modality was used in patients with poor mental status prior to surgery (n = 36), which was found to be a significant predictor of adverse outcome and TND. Although the authors found a statistically significant correlation between femoral cannulation and stroke incidence, analysis of cannulation modality in this subset of patients with poor mental status may cast a different light on the stipulated correlation. Selective cerebral perfusion (SCP) is a widely accepted strategy for cerebral protection during aortic surgery. However, certain technical difficulties can occur during SCP. Therefore, the use of an additional method for neuromonitoring is required. Near-infrared spectroscopy and transcranial Doppler are safe and non-invasive methods that can detect the occurrence of embolization and significant decrease in regional cerebral saturation and blood flow, events that are associated with worse neurological outcome. That information could help the surgical team to act in a timely manner to prevent a neurological deficit [5]. An aggressive rewarming rate after HCA can cause brain hyperthermia. A rapid rewarming rate and large temperature variations during that process may cause imbalance between metabolic needs and inadequate cerebral perfusion as a result of impaired autoregulation of cerebral blood flow. Mismatch between cerebral oxygen supply–demand causes markedly decreased oxygen saturation in the jugular bulb, which receives most of the venous blood from the brain. It is known that oxygen desaturation in the jugular bulb is a risk factor for neurocognitive dysfunction. Also, hyperthermia >37°C 24 h after a surgical procedure is associated with poorer neurocognitive outcome after 6 weeks [6]. It is noteworthy that the authors did not specify the value of oxygen saturation in the jugular bulb, rewarming rate, target rewarming temperature or temperature maintenance in the intraoperative and postoperative periods. In conclusion, we believe that a proper rewarming strategy and additional neuromonitoring methods could increase the efficacy of routine cerebral protection during surgery. We congratulate the authors on their useful and clinically applicable research.

Endovascular Catheter as a Rewarming Method for Accidental Hypothermia

The human body functions within a very narrow range of optimal core body temperature. Mechanisms are in place that enable it to thermoregulate despite large fluctuations in external temperature. Going beyond the normal physiologic range is poorly tolerated. Profound hypothermia is a devastating condition that warrants prompt recognition and management. This is a case of an 89-year-old man who was admitted for altered mental status. On arrival, the patient was found to be bradycardic, hypotensive, and hypothermic at 28.8°C. Warmed saline and vasopressors were started; an Icy catheter connected to a Zoll Coolgard was placed in the vena cava via the femoral vein and the patient was rewarmed at a rate of 1°C without complications. He was later transferred out of the coronary care unit hemodynamically stable. Although there are no clinical practice guidelines in place, severe hypothermia has been traditionally managed with invasive and aggressive rewarming techniques; endovascular catheters as an alternative for rapid and controlled rewarming may be a worthy and safe alternative to these more invasive procedures.

Cardiopulmonary bypass in malignant hyperthermia susceptible patients: A systematic review of published cases

Malignant hyperthermia susceptibility is an important risk factor during general anesthesia. Affected patients have an asymptomatic but potentially lethal hypermetabolic reaction after contact with volatile anesthetics or succinylcholine. Classic symptoms include hemodynamic instability, combined with acidosis, rigor, and hyperthermia. During cardiopulmonary bypass, these signs may be obscured, delaying correct diagnosis and lifesaving treatment. Malignant hyperthermia-susceptible individuals are more sensitive to heat and stress, so rewarming and catecholamine administration may trigger an episode, necessitating prophylactic measures. This systematic review identified typical malignant hyperthermia symptoms during cardiopulmonary bypass and investigated other factors in cardiac surgery that might trigger an episode in susceptible individuals. Approaches used to treat and prevent malignant hyperthermia during cardiopulmonary bypass were systematically analyzed. We conducted a systematic search for reports about malignant hyperthermia and cardiopulmonary bypass. Search terms included malignant hyperthermia and cardiopulmonary bypass, extracorporeal circulation, or cardiac surgery. We found 24 case reports and case series including details of 26 patients. In 14 cases, malignant hyperthermia crises during or shortly after cardiopulmonary bypass were described. Fourteen reports discussed prevention of an episode. Early symptoms of a malignant hyperthermia episode include excessive carbon dioxide production and metabolic acidosis. Massively increased creatine kinase levels are a strong indicator of a malignant hyperthermia reaction. Rewarming is associated with development of clinical signs of malignant hyperthermia. In potentially susceptible patients, apart from avoiding classic trigger substances, aggressive rewarming should not be applied. Hemodynamic instability in conjunction with the described symptoms should result in a diagnostic algorithm.

Akzidentelle Hypothermie beim Polytrauma

Hypothermia, defined as a body core temperature below 35 °C, could be divided into an endogeneous, therapeutic and accidental hypothermia. At admission in the emergency room multiple trauma patients show a hypothermic core temperature in up to 66 %. A core temperature below 34 °C seems to be critical in these patients as this temperature limit has been demonstrated to be associated with an increased risk for post-traumatic complications and a decreased survival. In polytraumatised patients with a core temperature below 32 °C a mortality rate of 100 % has been described. The main pathophysiological effects of hypothermia concern the haemo-dynamic, coagulatory and immune systems. Mild hypothermia (35-32 °C) leads to a vasoconstriction, tachycardia and increased cardiac output. After an increasing arrhythmia and bradycardia severe hypothermia (< 32 °C) finally results in a cardiac arrest. Hypothermia-induced coagulopathy comprises a dysfunction of the cellular and plasmatic coagulation with an increased blood loss. Due to the attenuation of the post-traumatic, pro-inflammatory immune response and enhancement of anti-inflammatory reactions, hypothermia counteracts an overwhelming systemic inflammation, concomitantly resulting in an increased susceptibility for infectious complications. Because of the negative effects of the -accidental hypothermia, effective rewarming is essential for adequate bleeding control and successful resuscitation. As aggressive rewarming (> 0.5 °C / h) has been reported to be associated with an increased mortality during the further course, this procedure should only be applied in hypothermic multiple trauma patients with haemorrhagic shock. Accidental hypothermia represents a serious problem in multiple trauma patients due to its frequency and negative pathophysiological effects. Therefore, early and effective re-warm-ing is essential in the treatment of hypothermic trauma patients. Possible protective effects of a therapeutic hypothermia in the treatment of trauma patients after initial resuscitation and operative bleeding control have to be clarified in further experimental and clinical studies.

Case Report of Valproate-Induced Hypothermia in a Patient With Schizoaffective Disorder

Case Report of Valproate-Induced Hypothermia in a Patient With Schizoaffective Disorder

Bedeutung der Hypothermie in der Traumatologie

Accidental hypothermia is a common complication in severely injured patients. Risk factors include environmental exposure of the patient at the accident site or in the clinic, infusion of cold fluids, hemorrhagic shock and anesthetics which influence thermoregulation. In contrast to animal studies, human studies and clinical experiences have identified accidental hypothermia of the severely injured patient to be associated with increased complication and mortality rates. As a consequence, hypothermia together with acidosis and coagulopathy, have been coined the lethal triad in severely injured patients. On a cellular level hypothermia reduces cellular activity and metabolism resulting in reduced oxygen consumption, which is therapeutically used in patients following cardiac arrest. However, the activity of important enzymes, such as those of the coagulation pathway, is simultaneously down regulated. Hypothermia-induced coagulopathy, which is refractory to substitution of coagulation factors, is a major complication of hypothermia in traumatized patients. Therefore, hypothermic trauma patients with hemodynamic instability require aggressive rewarming.

Optimal Perfusion During Cardiopulmonary Bypass: An Evidence-Based Approach

In this review, we summarize the best available evidence to guide the conduct of adult cardiopulmonary bypass (CPB) to achieve "optimal" perfusion. At the present time, there is considerable controversy relating to appropriate management of physiologic variables during CPB. Low-risk patients tolerate mean arterial blood pressures of 50-60 mm Hg without apparent complications, although limited data suggest that higher-risk patients may benefit from mean arterial blood pressures >70 mm Hg. The optimal hematocrit on CPB has not been defined, with large data-based investigations demonstrating that both severe hemodilution and transfusion of packed red blood cells increase the risk of adverse postoperative outcomes. Oxygen delivery is determined by the pump flow rate and the arterial oxygen content and organ injury may be prevented during more severe hemodilutional anemia by increasing pump flow rates. Furthermore, the optimal temperature during CPB likely varies with physiologic goals, and recent data suggest that aggressive rewarming practices may contribute to neurologic injury. The design of components of the CPB circuit may also influence tissue perfusion and outcomes. Although there are theoretical advantages to centrifugal blood pumps over roller pumps, it has been difficult to demonstrate that the use of centrifugal pumps improves clinical outcomes. Heparin coating of the CPB circuit may attenuate inflammatory and coagulation pathways, but has not been clearly demonstrated to reduce major morbidity and mortality. Similarly, no distinct clinical benefits have been observed when open venous reservoirs have been compared to closed systems. In conclusion, there are currently limited data upon which to confidently make strong recommendations regarding how to conduct optimal CPB. There is a critical need for randomized trials assessing clinically significant outcomes, particularly in high-risk patients.

Less invasive quick replacement of the proximal arch with aggressive rapid rewarming for type A acute aortic dissection

We describe a newly modified technique, which we term "less invasive quick replacement" (LIQR) for type A acute aortic dissection (AAD). After cooling to a rectal temperature of 28 degrees C without any cerebral perfusion, circulating blood in the cardiopulmonary bypass (CPB) circuit was warmed up to 40 degrees C during open distal anastomosis. As soon as the distal anastomosis was completed, rapid rewarming was initiated by perfusing blood at 40 degrees C. The average CPB and total operative times were 71.8 +/- 9.6 and 130.6 +/- 7.7 min, respectively. The shortest operative time was 101 min from skin incision to skin closure. All patients were weaned off the ventilator within 12 h of surgery. The postoperative hospital stay was 9.3 +/- 1.2 days. There was no incidence of cerebral damage or hospital mortality. Our initial results showed LIQR to be safe and effective.

Postoperative Hypothermia and Blood Loss After the Neonatal Arterial Switch Procedure

Numerous studies have demonstrated that mild hypothermia helps reduce hypoxic/ischemic brain injury that may occur during neonatal cardiac procedures. However, traditional intensive care practices emphasize aggressive rewarming, and the risk of excessive bleeding that may be related to hypothermia. An analysis was conducted of prospectively collected temperature and blood loss data on 47 neonates (30 boys, 17 girls) with transposition of the great arteries who underwent an arterial switch operation at median age 6 days (range, 2 to 23 days) and a mean weight of 3.6 +/- 0.6 kg. Blood loss was compared between 26 patients with mean temperatures below 35.5 degrees C for first 6 hours after operation (mild hypothermia group) and 21 patients at 35.5 degrees C or higher (normothermia group). Repeated-measures analysis of variance and regression modeling were used to evaluate the association between temperature and blood loss and to detect outliers. Total postoperative blood loss was 31 +/- 28 mL in the first 6 hours and 61 +/- 37 mL at 24 hours (range, 15 to 238 mL). Postoperative blood loss between two groups at 6 or 24 hours did not differ significantly. After two outliers were removed, no significant relationship remained between body temperature at 6 hours and cumulative blood loss at 24 hours. Mild postoperative hypothermia does not increase blood loss in neonates after the arterial switch operation. Lack of a difference between the two groups is not likely due to the study being underpowered. We recommend avoidance of aggressive rewarming, which might exacerbate potential neurologic injury.

Rapid rewarming after mild hypothermia accentuates the inflammatory response after acute volume controlled haemorrhage in spontaneously breathing rats

Accidental hypothermia is a common companion of trauma/haemorrhage, and several clinical studies have identified reduced body temperature as an independent risk predisposing to increased morbidity and mortality. Accordingly, the majority of trauma care guidelines prescribe early and aggressive rewarming of hypothermic patients. Enzyme reactions are generally downregulated at temperatures below 37 °C, including most of those responsible for the inflammatory response. The rationale for adhering to these recommendations uncritically may therefore be questioned. In a rat model of mild hypothermia and haemorrhagic shock we wanted to compare the influence of rapid rewarming with persistently reduced temperature on the synthesis of early inflammatory mediators and organ function. Thirty-four male albino Sprague–Dawley rats were studied. Withdrawal of 2.5 ml blood/100 g body weight was performed over 10 min, with simultaneous reduction of body temperature to 32.5–33.5 °C. Seventy-five minutes after initiation of bleeding, two-thirds of the shed blood was retransfused. One group ( n=17) was rewarmed to normothermia, the other ( n=17) was kept hypothermic. The study was terminated after an observation period of 2 h. At the end of the study the rewarmed animals had a significantly lower mean arterial pressure, higher heart rate, higher synthesis of reactive oxygen species from peritoneal phagocytes, increased circulating levels of nitric oxide, and higher values of the organ markers aspartate aminotransferase and urea. The pro-inflammatory cytokines TNF-α and IL-6, the anti-inflammatory cytokine IL-10, the organ markers alanine aminotransferase, α-glutathione S-transferase and creatinine, as well as organ injury scores were equal in both groups. Three rewarmed rats died prematurely, versus one hypothermic animal. In conclusion, the results suggest that during the early stages after haemorrhagic shock, rapid rewarming from mild hypothermia may have unfavourable effects both on basic haemodynamic variables, and on the internal inflammatory environment of cells and tissues.

Hypothermia is a marker for adequacy of resuscitation in severe truncal injury

Hypothermia after massive resuscitation is known to lead to coagulopathy, myocardial depression, and a depressed immune response. Attempts at prevention or correction of hypothermia in the perioperative period frequently fail in spite of utilizing aggressive rewarming modalities. We hypothesized that the response to rewarming is directly correlated to control of bleeding and adequacy of resuscitation.

Hypothermie majeure accidentelle

Two cases of severe accidental hypothermia (core temperature below 25 °C) are reported. Both occurred in an urban area during the same winter period. Both patients had the same age and similar clinical symptoms. In the first patient, the EEG, the echocardiography and the blood gases were in favour of a good tolerance of hypothermia, which led to choice a non aggressive rewarming method. The latter included the rewarming of inhaled gas mixture as well as i.v. fluids and gastro-intestinal lavage fluid. The outcome was uneventful. In the second patient, the visceral and biological consequences were more important (pH : 6.80, blood glucose concentration : 1.48 mmol · L −1, major coagulation disorders). Therefore a rapid rewarming via a cardiopulmonary bypass was preferred. The patient died from a prolonged shock with disseminated intravascular coagulation. The use of cardiopulmonary bypass which is essential in case of cardiac arrest rhythm, is controversial in case of severe hypothermia with a still beating heart.

Current Concepts in the Pathophysiology and Management of Near-Drowning

Approximately 6,500 people drown in the United States each year. Nearly 50,000 of the estimated 500,000 annual near-drowning victims seek medical attention. Near-drowning is most common among children, young adults, blacks, males, and in the southern states. Risk factors for near-drowning include ethanol use, drugs, seizures, boating accidents, water sports, inadequate supervision of children, and voluntary hyperventilation. Alcohol use alone is associated with 37 to 47% of these cases. Although anoxia and hypothermia produce the major pathological changes associated with the morbidity of near-drowning, hypothermia may paradoxically exert a protective effect in some cases and is associated with most of the spectacular long term survivals. There is almost no difference in the clinical presentation of freshwater and saltwater near-drowning. Both situations often involve hypothermia, anoxic injury due to cardiac arrest, and the frequent progression to the adult respiratory distress syndrome. Basic principles of management include the immediate institution of cardiopulmonary resuscitation; aggressive rewarming, preferably with cardiopulmonary bypass; continuation of cardiopulmonary resuscitation at least until the patient has been effectively rewarmed; and appropriate supportive care if the patient develops the adult respiratory distress syndrome. Cerebral salvage techniques have not been proved to be beneficial in these patients.

Prevention of body temperature reduction (afterdrop) following hypothermic perfusion

This study investigated the possibility of preventing the postoperative reduction in body temperature (afterdrop) which followed a period of hypothermic cardiopulmonary bypass. In addition to warming all the infused fluids and inspired gases, the patients also had active warming by way of a system of hot water mattresses and limb jackets. In the eight male patients randomly allocated to the active treatment there were no significant changes on the central (aural) temperature in the five hours following the end of perfusion. The eight male control patients showed significant ( p&lt;0.05) falls in central temperature from 36.5 (0.3)°C at the end of bypass to 35.3 (0.2)°C and 35.0 (0.2)°C at one and two hours postperfusion. In addition, the mean skin temperatures were always significantly higher in the active warming group during the study period. This maintenance of a stable body temperature was reflected in the carbon dioxide production, which showed no significant changes in the actively warmed group. In the control group the carbon dioxide production was reduced from the preoperative value of 189 (26)ml/min (mean (SEM)) to 155 (9.2)ml/min ( p&lt;0.05) at two hours postperfusion. These data show that afterdrop following perfusion can be prevented by an aggressive rewarming policy and suggest that this may have beneficial effects in producing a metabolically and physiologically more stable patient.

Cardiac Arrest in Hypothermia-Reply

In Reply.— We agree with Dr White that sinus bradycardia in patients with core temperatures of less than 26 °C can be associated with a grave prognosis, since such patients are at high risk of having ventricular fibrillation develop. We included sinus bradycardia in our discussion to warn physicians to avoid therapeutic measures (intubation, overventilation, excessive bicarbonate replacement, and pacing wire placment) that might precipitate this hemodynamically less favorable rhythm. As discussed by Wickstrom et al, 1 monkey experiments suggest that any physical stimulus can trigger the onset of ventricular fibrillation in the cold heart. Hypothermic patients should be handled gently. Rewarming, of course, must be instituted. External rewarming has been associated with conversion to fibrillation. 2,3 In view of the high risk of this arrhythmia in patients with bradycardia and core temperatures below 26 °C, perhaps aggressive core rewarming by peritoneal dialysis should be instituted in hope of preventing