Intravascular Cooling Device in Neurologic Intensive Care
Intravascular Cooling Device in Neurologic Intensive Care
Objective: To determine the safety and efficacy of a novel intravascular cooling device (Cool Line catheter with Cool Gard system) to control body temperature (temperature goal <37°C) in neurologic intensive care patients.
Design: A prospective, uncontrolled pilot study in 51 consecutive neurologic intensive care patients.
Setting: A neurologic intensive care unit at a tertiary care university hospital.
Participants: Patients were 51 neurologic intensive care patients with an intracranial disease requiring a central venous catheter due to the primary (intracranial) disease. We excluded patients under the age of 19 yrs and those with active cardiac arrhythmia, full sepsis syndrome, bleeding diathesis and infection, or bleeding at the site of the intended catheter insertion. Male to female ratio was 31:20, and the median age was 55 yrs (range, 24-85 yrs). Forty-four of 51 patients (86.3%) had an initial Glasgow Coma Scale score of 3, three patients had a Glasgow Coma Scale score of 9, one patient presented with an initial Glasgow Coma Scale score of 11, two patients had an initial Glasgow Coma Scale score of 13, and one patient had an initial Glasgow Coma Scale score of 15. The mean initial tissue injury severity score was 45.1 and the median initial tissue injury severity score 45.0 (range, 19-70).
Interventions: Patients were enrolled prospectively in a consecutive way. Within 12 hrs after admission, the intravascular cooling device (Cool Line catheter) was placed, the temperature probe was located within the bladder (by Foley catheter), and the Cool Gard cooling device was initiated. This Cool Gard system circulates temperature-controlled sterile saline through two small balloons mounted on the distal end of the Cool Line catheter. The patient's blood is gently cooled as it is passed over the balloons. The Cool Gard system has been set with a target temperature of 36.5°C. The primary purpose and end point of this study was to evaluate the cooling capacity of this intravascular cooling device. Efficacy is expressed by the calculation formula of fever burden, which is defined as the fever time product (°C hours) under the fever curve.
Measurements and Main Results: The cooling device was in operation for a mean of 152.4 hrs. The ease of insertion was judged as easy in 42 of 51 patients; in a single patient, the catheter was malpositioned within the jugular vein, requiring early removal. The rate of infectious and noninfectious complications (nosocomial pneumonia, bacteremia, catheter-related ventriculitis, pulmonary embolism, etc.) was comparable to the rate usually observed in our neurologic intensive care patients with such severe intracranial diseases. The total fever burden within the entire study period of (on average) 152.4 hrs was 4.0°C hrs/patient, being equivalent to 0.6°C hrs/patient and day. Thirty of 51 patients showed an elevation of the body temperature (>37.9°C) within 24 hrs after termination of the cooling study. One awake patient (subarachnoid hemorrhage, Glasgow Coma Scale score 15) experienced mild to moderate shivering throughout the entire period of 7 days. The mortality rate was 23.5%.
Conclusion: This novel intravascular cooling device (Cool Line catheter and Cool Gard cooling device) was highly efficacious in prophylactically controlling the body temperature of neurologic intensive care patients with very severe intracranial disease (median Glasgow Coma Scale score, 3-15). Morbidity and mortality rates were consistent with the ranges reported in the literature for such neurologic intensive patients.
Fever, defined as body temperature >37.9°C, is common in critically ill neurologic and neurosurgical patients, especially those with a prolonged length of stay in the neurologic intensive care unit (NICU) or with intracranial disease. In recent years, a large body of evidence has been accumulated showing that such a temperature elevation clearly worsens the degree of neuronal injury in both animals and humans. In ischemic stroke, the association between hyperthermia and early neurologic deterioration is known to increase morbidity and mortality rates. The deleterious effect of hyperthermia has also been shown in patients with subarachnoid hemorrhage, intracranial hemorrhage, and traumatic brain injury as well as diffuse cerebral hypoxia after cardiopulmonary resuscitation. This finding has been corroborated by many animal studies. In particular, in primary or secondary ischemia models, intraischemic brain temperature elevation to 39°C has been shown to enhance neuropathological alterations in vulnerable brain regions. Importantly, even structures not affected or not primarily affected by ischemia may be damaged by hyperthermia. The neuroprotective effect of reducing even mild spontaneous postischemic hyperthermia is paralleled by the reduced efficacy of otherwise neuroprotective drugs in case of even mild hyperthermia. Even when delayed by 24 hrs after the acute insult, a moderate hyperthermia still worsens the pathologic and neurobehavioral outcome. Up-regulation of neurotransmitters, release of free oxygen radicals, aggravation of blood-brain barrier disruption, increase of potentially damaging ischemic depolarizations in the focal ischemic penumbra, enhanced inhibition of protein kinases, and deterioration of cytoskeletal proteolysis are all mechanisms incriminated in worsening neuronal damage in case of hyperthermia.
In the severely injured brain, the brain temperature might be even disproportionately elevated, exceeding the usually found brain-core body temperature gradient. All these aspects have led to the introduction of therapeutic mild to moderate short-term hypothermia in patients with both traumatic brain injury and stroke (ischemia as well as subarachnoid hemorrhage).
Decades ago, the concept of induced hypothermia was abandoned due to uncontrolled and uncontrollable complications. However, several smaller studies recently have shown that moderate hypothermia in traumatic brain injury might confer a neuroprotective effect. In contrast, a very recent study in 392 patients with severe traumatic brain injury clearly showed that complications outweigh the potential benefit of moderate hypothermia, and the authors concluded that treatment with hypothermia with the body temperature reaching 33°C within 8 hrs after injury does not improve outcomes in patients with severe brain injury.
These two contradictory facts, namely a) the detrimental effect of hyperthermia leading to additional neuronal damage and b) the lack of efficacy of induced mild hypothermia in patients with severe brain injury, have led to the concept of induced prophylactic normothermia in critically ill neurologic patients. Technically, body temperature may be contained by medical treatment and/or application of cooling blankets. Both methods, however, do not always enable best possible control of body temperature.
Here we present a preliminary study on efficacy and safety of a newly developed intravascular cooling device that was employed in 51 consecutive neurologic critical care patients in a prophylactic way, that is, within 12 hrs after admission to the NICU of the University Hospital Innsbruck, Austria, irrespective of the type of disease and the admission body temperature.
Objective: To determine the safety and efficacy of a novel intravascular cooling device (Cool Line catheter with Cool Gard system) to control body temperature (temperature goal <37°C) in neurologic intensive care patients.
Design: A prospective, uncontrolled pilot study in 51 consecutive neurologic intensive care patients.
Setting: A neurologic intensive care unit at a tertiary care university hospital.
Participants: Patients were 51 neurologic intensive care patients with an intracranial disease requiring a central venous catheter due to the primary (intracranial) disease. We excluded patients under the age of 19 yrs and those with active cardiac arrhythmia, full sepsis syndrome, bleeding diathesis and infection, or bleeding at the site of the intended catheter insertion. Male to female ratio was 31:20, and the median age was 55 yrs (range, 24-85 yrs). Forty-four of 51 patients (86.3%) had an initial Glasgow Coma Scale score of 3, three patients had a Glasgow Coma Scale score of 9, one patient presented with an initial Glasgow Coma Scale score of 11, two patients had an initial Glasgow Coma Scale score of 13, and one patient had an initial Glasgow Coma Scale score of 15. The mean initial tissue injury severity score was 45.1 and the median initial tissue injury severity score 45.0 (range, 19-70).
Interventions: Patients were enrolled prospectively in a consecutive way. Within 12 hrs after admission, the intravascular cooling device (Cool Line catheter) was placed, the temperature probe was located within the bladder (by Foley catheter), and the Cool Gard cooling device was initiated. This Cool Gard system circulates temperature-controlled sterile saline through two small balloons mounted on the distal end of the Cool Line catheter. The patient's blood is gently cooled as it is passed over the balloons. The Cool Gard system has been set with a target temperature of 36.5°C. The primary purpose and end point of this study was to evaluate the cooling capacity of this intravascular cooling device. Efficacy is expressed by the calculation formula of fever burden, which is defined as the fever time product (°C hours) under the fever curve.
Measurements and Main Results: The cooling device was in operation for a mean of 152.4 hrs. The ease of insertion was judged as easy in 42 of 51 patients; in a single patient, the catheter was malpositioned within the jugular vein, requiring early removal. The rate of infectious and noninfectious complications (nosocomial pneumonia, bacteremia, catheter-related ventriculitis, pulmonary embolism, etc.) was comparable to the rate usually observed in our neurologic intensive care patients with such severe intracranial diseases. The total fever burden within the entire study period of (on average) 152.4 hrs was 4.0°C hrs/patient, being equivalent to 0.6°C hrs/patient and day. Thirty of 51 patients showed an elevation of the body temperature (>37.9°C) within 24 hrs after termination of the cooling study. One awake patient (subarachnoid hemorrhage, Glasgow Coma Scale score 15) experienced mild to moderate shivering throughout the entire period of 7 days. The mortality rate was 23.5%.
Conclusion: This novel intravascular cooling device (Cool Line catheter and Cool Gard cooling device) was highly efficacious in prophylactically controlling the body temperature of neurologic intensive care patients with very severe intracranial disease (median Glasgow Coma Scale score, 3-15). Morbidity and mortality rates were consistent with the ranges reported in the literature for such neurologic intensive patients.
Fever, defined as body temperature >37.9°C, is common in critically ill neurologic and neurosurgical patients, especially those with a prolonged length of stay in the neurologic intensive care unit (NICU) or with intracranial disease. In recent years, a large body of evidence has been accumulated showing that such a temperature elevation clearly worsens the degree of neuronal injury in both animals and humans. In ischemic stroke, the association between hyperthermia and early neurologic deterioration is known to increase morbidity and mortality rates. The deleterious effect of hyperthermia has also been shown in patients with subarachnoid hemorrhage, intracranial hemorrhage, and traumatic brain injury as well as diffuse cerebral hypoxia after cardiopulmonary resuscitation. This finding has been corroborated by many animal studies. In particular, in primary or secondary ischemia models, intraischemic brain temperature elevation to 39°C has been shown to enhance neuropathological alterations in vulnerable brain regions. Importantly, even structures not affected or not primarily affected by ischemia may be damaged by hyperthermia. The neuroprotective effect of reducing even mild spontaneous postischemic hyperthermia is paralleled by the reduced efficacy of otherwise neuroprotective drugs in case of even mild hyperthermia. Even when delayed by 24 hrs after the acute insult, a moderate hyperthermia still worsens the pathologic and neurobehavioral outcome. Up-regulation of neurotransmitters, release of free oxygen radicals, aggravation of blood-brain barrier disruption, increase of potentially damaging ischemic depolarizations in the focal ischemic penumbra, enhanced inhibition of protein kinases, and deterioration of cytoskeletal proteolysis are all mechanisms incriminated in worsening neuronal damage in case of hyperthermia.
In the severely injured brain, the brain temperature might be even disproportionately elevated, exceeding the usually found brain-core body temperature gradient. All these aspects have led to the introduction of therapeutic mild to moderate short-term hypothermia in patients with both traumatic brain injury and stroke (ischemia as well as subarachnoid hemorrhage).
Decades ago, the concept of induced hypothermia was abandoned due to uncontrolled and uncontrollable complications. However, several smaller studies recently have shown that moderate hypothermia in traumatic brain injury might confer a neuroprotective effect. In contrast, a very recent study in 392 patients with severe traumatic brain injury clearly showed that complications outweigh the potential benefit of moderate hypothermia, and the authors concluded that treatment with hypothermia with the body temperature reaching 33°C within 8 hrs after injury does not improve outcomes in patients with severe brain injury.
These two contradictory facts, namely a) the detrimental effect of hyperthermia leading to additional neuronal damage and b) the lack of efficacy of induced mild hypothermia in patients with severe brain injury, have led to the concept of induced prophylactic normothermia in critically ill neurologic patients. Technically, body temperature may be contained by medical treatment and/or application of cooling blankets. Both methods, however, do not always enable best possible control of body temperature.
Here we present a preliminary study on efficacy and safety of a newly developed intravascular cooling device that was employed in 51 consecutive neurologic critical care patients in a prophylactic way, that is, within 12 hrs after admission to the NICU of the University Hospital Innsbruck, Austria, irrespective of the type of disease and the admission body temperature.
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