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Hyperthermia After Cardiac Arrest Is Associated With an Unfavorable Neurologic Outcome
Andrea Zeiner, MD;
Michael Holzer, MD;
Fritz Sterz, MD;
Waltraud Schörkhuber, MD;
Philip Eisenburger, MD;
Christof Havel, MD;
Andreas Kliegel, MD;
Anton N. Laggner, MD
Arch Intern Med. 2001;161:2007-2012.
ABSTRACT
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Background Moderate elevation of brain temperature, when present during or after
ischemia, may markedly worsen the resulting injury.
Objective To evaluate the impact of body temperature on neurologic outcome after
successful cardiopulmonary resuscitation.
Methods In patients who experienced a witnessed cardiac arrest of presumed cardiac
cause, the temperature was recorded on admission to the emergency department
and after 2, 4, 6, 12, 18, 24, 36, and 48 hours. The lowest temperature within
4 hours and the highest temperature during the first 48 hours after restoration
of spontaneous circulation were recorded and correlated to the best-achieved
cerebral performance categories' score within 6 months.
Results Over 43 months, of 698 patients, 151 were included. The median age was
60 years (interquartile range, 53-69 years); the estimated median no-flow
duration was 5 minutes (interquartile range, 0-10 minutes), and the estimated
median low-flow duration was 14.5 minutes (interquartile range, 3-25 minutes).
Forty-two patients (28%) underwent bystander-administered basic life support.
Within 6 months, 74 patients (49%) had a favorable functional neurologic recovery,
and a total of 86 patients (57%) survived until 6 months after the event.
The temperature on admission showed no statistically significant difference
(P = .39). Patients with a favorable neurologic recovery
showed a higher lowest temperature within 4 hours (35.8°C [35.0°C-36.1°C]
vs 35.2°C [34.5°C-35.7°C]; P = .002)
and a lower highest temperature during the first 48 hours after restoration
of spontaneous circulation (37.7°C [36.9°C-38.6°C] vs 38.3°C
[37.8°C-38.9°C]; P<.001) (data are given
as the median [interquartile range]). For each degree Celsius higher than
37°C, the risk of an unfavorable neurologic recovery increases, with an
odds ratio of 2.26 (95% confidence interval, 1.24-4.12).
Conclusion Hyperthermia is a potential factor for an unfavorable functional neurologic
recovery after successful cardiopulmonary resuscitation.
INTRODUCTION
WITHIN recent years, strikingly consistent and persuasive evidence has
shown that moderate hyperthermia, when present during or after a period of
brain ischemia or trauma, markedly exacerbates the degree of resulting neural
injury. In laboratory animals, the outcomes of focal and global cerebral ischemia
are profoundly affected by alterations in body temperature.1-2
Experimental mammalian models provide evidence that even mild hyperthermia
up to 2°C above normal significantly increases ischemic neuronal injury.3
Terent and Andersson4 found in patients
with cerebrovascular ischemic attacks and stroke that fever (temperature  38°C)
was significantly associated with poor survival. There have been few investigations5-6 on the influence of the natural body
temperature course on neurologic outcome immediately after successful cardiopulmonary
resuscitation.
This study determines the influence of hyperthermia within 48 hours
and the impact of the natural body temperature course after cardiac arrest
and successful restoration of spontaneous circulation on neurologic performance
within 6 months after cardiopulmonary resuscitation.
PATIENTS AND METHODS
PATIENTS
Patients for this study were selected from the population served by
the department of emergency medicine of a general hospital, a tertiary care
university hospital. The following procedures were in accordance with the
ethical standards of the responsible committee on human experimentation and
with the Declaration of Helsinki of 1975, as revised in 1983.
The study period ranged from June 1, 1992, through December 31, 1995.
Patients older than 18 years who experienced a witnessed cardiac arrest of
presumed cardiac cause with subsequent cardiopulmonary resuscitation and return
of spontaneous circulation were included in the study. Patients whose cardiopulmonary
arrest was associated with trauma, hypothermia, drowning, drug overdose, primary
respiratory arrest, and primary neurologic or metabolic reasons were excluded
from the study. Patients with pulmonary infiltrates, either a clinical or
a radiological suggestion of pneumonia, or a C-reactive protein (CRP) level
higher than 1.5 mg/dL on admission to the emergency department were excluded;
patients with known infection and patients receiving antibiotic therapy were
also excluded. Furthermore, we excluded patients whose functional neurologic
status could not be assessed, ie, if they died before the withdrawal of sedation
and analgesia.
Cardiopulmonary arrest was defined as the absence
of spontaneous respiration and a palpable pulse. Return
of spontaneous circulation was defined as electrical activity on the
electrocardiogram and a palpable pulse for at least 10 minutes. Treatment
in the field and in the hospital was according to the American Heart Association's
guidelines for basic and advanced cardiac life support and postresuscitation
care.7 In the hospital, all patients received
standard intensive care treatment, such as controlled mechanical ventilation
and sedation and analgesia with midazolam hydrochloride, 0.2 mg/kg per hour,
and fentanyl citrate, 0.004 mg/kg per hour, for at least 24 hours. Other treatment,
such as fluids, vasopressors, fibrinolysis, anticoagulants, and antipyretics,
and the initiation and selection of the antibiotic strategy were left to the
discretion of the attending physician. No mechanical or external means to
reduce the temperature were used.
STUDY DESIGN AND DATA COLLECTION
Data were collected prospectively, as an observational study according
to the Utstein style, the recommended guidelines for uniform reporting of
data on arrival of patients after out-of-hospital cardiac arrest.8 Attention has been focused on the periods from collapse
(eg, cardiac arrest) until basic and/or advanced life support and from the
beginning of life support until the return of spontaneous circulation; the
first monitored rhythm in the electrocardiogram; and the recorded history
for the individual patients, especially regarding the cause of cardiac arrest.
The interval from collapse to first basic and/or advanced life support was
defined as no-flow duration, and the interval from
the beginning of life support until the return of spontaneous circulation
was defined as low-flow duration.
For practical reasons, the temperature immediately after admission was
monitored with infrared tympanic thermometry (Ototemp LighTouch; Exergen Corporation,
Watertown, Mass); within 30 minutes and during the observation period, it
was monitored in the pulmonary artery (Edwards Swan-Ganz VIP catheter; Baxter
Healthcare Corporation, Santa Ana, Calif). Information about the method of
calibration of temperature probes, the range of linearity of measurement,
and the repeatability, reproducibility, and coefficient of variation of each
apparatus used to monitor the temperature has been provided elsewhere.9 The temperature was measured on admission to the emergency
department and after 2, 4, 6, 12, 18, 24, 36, and 48 hours. The CRP and fibrinogen
levels and the white blood cell count were analyzed on admission and after
12, 24, 36, and 48 hours. Chest x-ray films were reviewed for pulmonary infiltrates
every 24 hours (on admission and after 24 and 48 hours).
To define the temperature course and to compare groups, we defined the
following variables: the lowest measured temperature within the first 4 hours
after return of spontaneous circulation and the highest temperature observed
during the first 48 hours after return of spontaneous circulation. The threshold
temperature between normothermia and hyperthermia was considered to be 37°C.10-11 To account for a possible time effect
of elevated body temperature, the area under the temperature curve higher
than 37°C was divided by the time when the temperature was elevated.
OUTCOME MEASURES
Cerebral function was assessed prospectively on arrival and at regular
intervals for 6 months after the return of spontaneous circulation. Functional
neurologic recovery was expressed in cerebral performance categories (CPCs),12 which are based on the Glasgow overall performance
categories.13 The performance categories are
defined as follows: CPC 1, conscious and alert with
normal function or only slight disability; CPC 2,
conscious and alert with moderate disability; CPC 3,
conscious with severe disability; CPC 4, comatose
or in a persistent vegetative state; and CPC 5, brain
death. The best-achieved CPC score within 6 months was used for calculation.
A CPC score of 1 or 2 represents favorable functional neurologic recovery,
and a CPC score of 3, 4, or 5 reflects unfavorable functional neurologic recovery.
STATISTICAL ANALYSIS
According to the Utstein style, data are expressed as the median and
the interquartile range (IQR).8 Percentages
were determined for dichotomous variables. For the comparison of continuous
variables, the Mann-Whitney test was used. The  2 test was
used for the comparison of dichotomous variables. A logistic regression analysis
was performed to test for independent predictors of unfavorable neurologic
recovery. For this age, sex and known predictors of neurologic outcome were
included into the model. The required 2-tailed significance level for all
tests was set at .05. All data were computed with Microsoft Excel 97 for Windows
(Redmond, Wash) and Statistical Product and Service Solutions for Windows,
version 8.0 (SPSS Inc, Chicago, Ill).
RESULTS
Within the 43-month study period, 698 patients were admitted to the
emergency department after having a cardiac arrest. Of these patients, 151
fulfilled the inclusion criteria and were enrolled into the study. The median
age was 60 years (IQR, 53-69 years), and 108 patients (72%) were men. In 118
patients (78%), cardiac arrest occurred outside of the hospital. In all patients,
the estimated median no-flow duration was 5 minutes (IQR, 0-10 minutes) and
the median low-flow duration was 14.5 minutes (IQR, 3-25 minutes). Forty-two
patients (28%) underwent bystander-administered basic life support; the median
no-flow duration in these patients was 1 minute (IQR, 0-2 minutes). The median
arterial lactate concentration on admission was 8.7 mmol/L (IQR, 6.0-11.7
mmol/L), and the median pH on admission was 7.30 (IQR, 7.21-7.37). Within
6 months, 74 patients (49%) had a favorable functional neurologic recovery,
and a total of 86 patients (57%) survived until 6 months after the event.
The no-flow and low-flow durations, the time from cardiac arrest until
restoration of spontaneous circulation, and the cumulative epinephrine dose
were significantly lower in patients with a favorable neurologic recovery
(Table 1). No significant differences
were found comparing the rate of bystander-administered basic life support
(Table 1) or the initial electrocardiographic
results between groups (Table 2).
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Table 1. Cardiac Arrest and Resuscitation Characteristics in Patients
With Good and Unfavorable Functional Neurologic Recovery After a Witnessed
Cardiac Arrest*
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Table 2. Demographic Characteristics and Mortality in Patients With
Good and Unfavorable Functional Neurologic Recovery After a Witnessed Cardiac
Arrest*
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The lactate level on admission was significantly lower and pH values
on admission were significantly better (Table 1) in patients with a favorable outcome. At 24 hours, lactate
levels were lower in patients with a favorable outcome, but this was not statistically
significant. The pH value was in normal ranges in both groups.
The temperature on admission was lower in patients with an unfavorable
functional neurologic recovery, but without statistical difference (Table 3 and Figure 1). Within 4 hours after restoration of spontaneous circulation,
the temperature in patients with a good functional recovery showed a trend
of elevation, while the temperature in patients with a bad functional recovery
showed a trend toward a slight decrease. Comparing the lowest temperature
within the first 4 hours after restoration of spontaneous circulation, patients
with a good functional neurologic recovery had significantly higher values
(Table 3). During the following
period, the temperature increased in both groups, reaching a significantly
lower maximum temperature in patients with a favorable neurologic recovery
(Table 3 and Figure 1). Patients with a good functional neurologic recovery showed
a continuum starting at 12 hours after restoration of spontaneous circulation
until 36 hours after restoration of spontaneous circulation, with a following
downward trend of the temperature curve, in contrast to patients with a bad
functional neurologic recovery, who had the continuum until 48 hours after
restoration of spontaneous circulation (Figure
1). Comparing the weighted mean temperature (the area under the
temperature curve higher than 37°C when divided by the time the temperature
was elevated), patients with a favorable neurologic recovery had significantly
lower values than did patients with an unfavorable neurologic recovery (Table 3).
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Table 3. Body Temperature in Patients With Good and Unfavorable Functional
Neurologic Recovery After a Witnessed Cardiac Arrest
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Temperature curves within 48 hours after successful cardiopulmonary
resuscitation. Data are expressed as the median.
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C-reactive protein and fibrinogen levels were lower in the group with
a favorable outcome; however, a statistically significant difference was found
at 24 hours after restoration of spontaneous circulation only for the CRP
level (Table 4). The course of
CRP showed a maximum 36 hours after restoration of spontaneous circulation,
with a following decrease, more pronounced in the group with a favorable outcome.
The white blood cell count showed no trend at all during the observation period.
Signs of pneumonia in the chest x-ray film were found in 11 (7.3%) of the
patients after 24 hours (P = .83) and in 12 (7.9%)
of the patients after 48 hours (P = .65), without
a statistically significant difference between groups. After 24 and after
48 hours, significantly fewer patients with a favorable neurologic recovery
received antibiotic treatment (33 patients [37%] compared with 39 patients
[63%] [P = .006] and 36 patients [40%] compared with
40 patients [65%] [P = .009], respectively). Within
the first 48 hours after successful cardiopulmonary resuscitation, no patient
received antipyretics.
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Table 4. Markers of Infection in Patients With Good and Unfavorable
Functional Neurologic Recovery After a Witnessed Cardiac Arrest
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Variables showing a significant difference between groups in a univariate
analysis were included into a logistic regression model (age, male sex, no-flow
duration, low-flow duration, out-of-hospital cardiac arrest, pH level on admission,
lactate level on admission, and highest temperature observed during the first
48 hours after return of spontaneous circulation). The number of countershocks
and the cumulative epinephrine dose (measured in milligrams) were not included,
to keep the number of cases for calculation high in the model. The logistic
regression model showed that fever going over the threshold temperature of
37°C was a strong independent predictor for an unfavorable functional
neurologic recovery (Table 5).
For each degree Celsius higher than 37°C, the association with an unfavorable
neurologic recovery increases, with an odds ratio of 2.26 (95% confidence
interval, 1.24-4.12).
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Table 5. Multivariate Logistic Regression Analysis Relating Known Influencing
Factors and Temperature to Neurologic Recovery*
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COMMENT
This investigation of the influence of body temperature on functional
neurologic recovery showed that hyperthermia (a temperature higher than the
threshold value of 37°C) was associated with an unfavorable functional
neurologic recovery after cardiopulmonary resuscitation of persons who experienced
cardiac arrest with a presumed cardiac cause. Each degree Celsius higher than
37°C showed an increased association with the risk of severe disability,
coma, or a persistent vegetative state (CPC 3-4), with an odds ratio of 2.26.
One cause of hyperthermia after cardiopulmonary resuscitation might
be infection. Global ischemia during and after cardiac arrest leads to gut
ischemia, which makes translocation of bacteria or toxins possible.14 Another reason for infection could be pulmonary aspiration
due to the comatose state.15-16
Gaussorgues17 and Gueugniaud18
and colleagues showed that 39% of patients had 2 or more blood cultures that
were positive for infection within 12 hours after cardiopulmonary resuscitation.
No data were available on the underlying causes of fever, but the higher
risk of poor neurologic recovery suggested that high temperature was an independent
component of poor prognosis. In patients who experience stroke, the most frequent
cause of fever is infection, but hyperthermia is occasionally an expression
of cell necrosis or of changes in thermoregulatory mechanisms that occur when
lesions are located in the anterior region of the hypothalamus.19-20
In agreement with studies21-22
of patients who experienced stroke, we found that patients with a higher temperature
had a worse prognosis for neurologic recovery.
However, the aim of our study was not to focus on causes of infection
after cardiopulmonary resuscitation but to correlate hyperthermia to neurologic
recovery. We did not focus on the data of bacterial screening (blood culture
or Uricult results or the presence of tracheal fluid), as results mainly come
late and are of less help in the empirical start of antibiotic therapy; we
only compared markers of infection (white blood cell count, fibrinogen level,
and CRP level) and suggested pneumonia and/or signs of pneumonia on the chest
x-ray film within patient groups (those with a favorable and an unfavorable
neurologic recovery), and found no statistically significant differences for
all of these variables.
On the other hand, there was a statistically significant difference
in the application of antibiotic drugs 24 and 48 hours after cardiac arrest
and successful cardiopulmonary resuscitation. Patients with an unfavorable
neurologic recovery had a significantly higher rate of antibiotic treatment.
As antibiotic treatment within the first 48 hours after successful cardiopulmonary
resuscitation was started because of fever, elevated markers of infection,
and signs of pneumonia in the chest x-ray film, the main reason for this significant
difference seems to be the higher temperature in patients with an unfavorable
neurologic recovery.
Takino and Okada5 showed that patients
with an unfavorable functional neurologic recovery (prolonged coma and brain
death) more often had initial hypothermia (temperature <35°C), but
the number of cases is few and most patients experienced prolonged coma or
brain death. In our study, we found that patients with an unfavorable functional
neurologic recovery showed a decrease of temperature within the first 4 hours
after restoration of spontaneous circulation; compared with patients with
a good functional neurologic recovery, they had significantly lower temperatures.
Patients with an unfavorable functional neurologic recovery had a significantly
higher highest temperature observed and weighted mean temperature (the area
under the temperature curve higher than 37°C when divided by the time
the temperature was elevated) within 48 hours after restoration of spontaneous
circulation. This temperature course might be due to impaired temperature
control after cardiac arrest and successful cardiopulmonary resuscitation
and might correlate with the amount of postischemic central nervous system
damage. The usual temperature homeostasis showed an initial decrease and fever
thereafter in patients with an unfavorable neurologic outcome. This study
does not establish that temperature elevation worsened outcome, and it may
be that enhanced initial brain damage indeed elevated the temperature.
From animal studies, we know by which mechanisms hyperthermia may influence
the ischemic brain and can worsen cerebral ischemia. The cellular mechanism
seems rather nonspecific but tends to collectively involve key items rendering
neurons resistant to ischemic damage. The release of neurotransmitters in
global ischemia is accentuated by hyperthermia and diminished by hypothermia.
In an animal study23 of prosencephalon ischemia
in rats, hyperthermic rats showed a significant increase of ganglionic glutamate
levels and a trend toward higher levels thereafter compared with normothermic
rats. An additional mechanism is the production of cortical oxygen radical
in the recirculation period, which showed no elevation in moderate hypothermic
ischemia, a 2- to 3-fold elevation in the normothermic period, and a 4- to
5-fold elevation in hyperthermic ischemia.24-25
In addition, hyperthermia influences the brain metabolism by adenosine triphosphate
depletion and by less complete recovery of adenosine triphosphate levels and
by adenylate energy changes in cortical and subcortical regions.26
These changes in adenosine triphosphate metabolism in combination with metabolic
insults are highly correlated with the release of endogenous glutamate and
aspartate.27
Furthermore, hyperthermia markedly enhances calpain activation and spectrin
proteolysis in cortical pyramidal neurons soon after the onset of reperfusion,
which became marked by 4 and 24 hours, in association with morphological evidence
of irreversible neuronal injury.28
Various methods of temperature measurement are available (eg, the brain
temperature may be measured via a ventricular catheter, a tympanic probe,
a vesical probe, or a Swan-Ganz catheter). The brain temperature may be dissociated
from the systemic temperature by 0.2°C to 0.1°C, although differences
are usually small.29 Measurement of tympanic
temperature has the advantage of being noninvasive, fast, and easily applicable
and, therefore, has been used routinely. Swan-Ganz catheter measurements were
taken if there was an indication for invasive hemodynamic monitoring.
In conclusion, hyperthermia during recovery after primary successful
cardiopulmonary resuscitation worsens ischemic damage. Although the cause
and effect of elevated temperature on survival are not proved, it seems prudent
to rigorously control temperature in such patients. An elevated temperature
should be aggressively treated and should not exceed normal values for a long
time. This is especially true in view of the fact that mild resuscitative
hypothermia, used for resuscitation in patients who experience cardiac arrest,
seems to mitigate neurologic damage.30
AUTHOR INFORMATION
Accepted for publication December 4, 2000.
Corresponding author and reprints: Fritz Sterz, MD, Universitätsklinik
für Notfallmedizin, Währingergürtel 18-20/6/D, 1090 Vienna,
Austria (e-mail: Fritz.Sterz{at}AKH-Wien.ac.at).
From the University Clinic of Emergency Medicine, Medical School, University
of Vienna, Vienna, Austria.
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