(Stroke. 1995;26:543-549.)
© 1995 American Heart Association, Inc.
Articles |
Early Determination of Neurological Outcome After Prehospital Cardiopulmonary Resuscitation
From the Departments of Neurology (K.B., G.L., L.S.), Internal Medicine (P.L., F.D.), Anesthesiology and Intensive Care Medicine (A.S.), and Magnetic Resonance (S.F., F.A), University Hospital Innsbruck; and the Department of Statistics, University Innsbruck (C.T.) (Austria).
Correspondence to Dr Klaus Berek, Universitätsklinik für Neurologie, Anichstraße 35, A-6020 Innsbruck, Austria.
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Abstract |
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Background and Purpose Although there are various methods of determining neurological prognosis after cardiopulmonary resuscitation, the final outcome of patients often remains unclear for quite a long time.
Methods We investigated 30 consecutively admitted patients who had been successfully resuscitated by the team of the local mobile intensive care unit after cardiac arrest. Determinations of the period of anoxia and of the cardiopulmonary resuscitation time, clinical investigation, echocardiography, electroencephalography, evoked potentials, magnetic resonance imaging, and magnetic resonance spectroscopy were performed.
Results Demonstration of brain lactate in proton magnetic resonance spectroscopy (P<.01) and absent N20 waves in short-latency somatosensory evoked potentials (P<.01) proved to be significant in terms of a poor prognosis. Correlations between both duration of anoxia and cardiopulmonary resuscitation time and neurological outcome could be shown as well (both P<.05).
Conclusions Proton magnetic resonance spectroscopy and short-latency evoked potentials are of great benefit in the prognostic evaluation after cardiopulmonary resuscitation.
Key Words: cardiopulmonary resuscitation • evoked potentials • prognosis • spectroscopy, nuclear magnetic resonance
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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As a consequence of the growing frequency of cardiopulmonary resuscitation (CPR) in the last three decades, the number of patients with severe neurological deficits has increased. Several studies have demonstrated the prognostic importance of clinical neurological signs,1 2 3 laboratory parameters such as blood glucose level,4 5 lactate concentration in serum6 7 and cerebrospinal fluid,1 8 electroencephalography (EEG),1 and evoked potentials (EP)9 after circulatory arrest. The Glasgow Coma Scale (GCS)10 and various neurological signs such as pupillary light reflex, vestibulo-ocular reflex, corneal reflex, spontaneous breathing, purposeful reaction to pain,1 2 11 12 and coma duration12 13 14 have been used as clinical predictors of outcome. However, the reliance on individual clinical signs or single laboratory investigations can be potentially misleading, which may be a problem for decision making in intensive care medicine.12
In 1988 localized and water-suppressed proton magnetic resonance spectroscopy (MRS) became available for the examination of patients, and several investigators found that metabolic abnormalities can be detected early after ischemia.15 16 17 18 19 20 21 22 23 24 These changes included rise in lactate and decrease in N-acetylaspartate (NAA). Since lactate1 6 7 8 is a factor of known predictive value after cardiac resuscitation, we hypothesized that intracerebral lactate as determined by localized proton MRS might be helpful in establishing prognosis after cerebral hypoxia. We therefore performed magnetic resonance imaging (MRI) and proton MRS together with various clinical and electrophysiological investigations to evaluate further criteria for early determination of neurological outcome after prehospital resuscitation in patients with cardiac arrest.
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Subjects and Methods |
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We studied 30 consecutive patients (7 women, 23 men) older than the age of 14 years (mean age, 61.4 years; range, 18 to 86 years; median, 63 years) who had been admitted to the intensive care unit (ICU) in Innsbruck after successful out-of-hospital CPR. Only patients who had been resuscitated by the team of the local mobile ICU were included in our study. In 28 patients cardiac arrest had occurred because of coronary heart disease, 1 patient had carbon monoxide intoxication, and in 1 a high-voltage current accident led to cardiorespiratory arrest. Ventricular fibrillation was found initially in 21 patients and asystolia in 9. Exclusion criteria were known preexisting diseases of the central nervous system, traumatic brain injuries, intoxication, age younger than 14 years, and incomplete exact data regarding the period of anoxia and CPR time.
According to the Utstein style,25 cardiac arrest was defined as cessation of cardiac mechanical activity, confirmed by the absence of a detectable pulse, unresponsiveness, and apnea. Duration of anoxia was defined as the interval between collapse and the beginning of CPR; time of CPR was defined as the interval between the beginning of CPR and the return of spontaneous circulation. These intervals were inferred from the automatically recorded emergency call protocol and the protocol of the mobile ICU, respectively. Coma rating with the GCS and the Innsbruck Coma Scale (ICS)26 was done initially by the mobile ICU team and then every 3 hours during the first 24 hours after admission and twice daily until patients left the ICU; a final neurological examination was performed 4 weeks after admission. For estimation of cerebral outcome we used the Glasgow-Pittsburgh Cerebral Performance Scale (GPCPS)27 and classified the outcome of our patients as favorable (categories 1 and 2) or unfavorable (categories 3, 4, and 5).
After successful CPR, the treatment on the ICU was fairly uniform. All patients were ventilated artificially to normalize arterial blood gases. If necessary, midazolam and fentanyl were used for sedation and analgesia, respectively. As soon as possible, controlled ventilation was changed to simultaneous intermittent mandatory ventilation, or continuous positive airway pressure was used to support spontaneous breathing. Only in those patients in whom MRI revealed evidence of diffuse brain swelling was controlled hyperventilation performed after MRI. In the majority of our patients coronary heart disease had led to cardiac arrest. They were treated with acetylsalicylic acid 250 mg IV on the first day, followed by an oral dose of acetylsalicylic acid 100 mg daily, heparin intravenously (to increase partial thromboplastin time twofold to threefold), and nitroglycerin infusions (2 to 4 mg/h). If necessary, ß-blockers and antiarrhythmic drugs were used. Mild forms of heart failure were treated with loop diuretics. If systolic blood pressure was greater than 100 mm Hg, angiotensin-converting enzyme inhibitors were used. In cases of advanced heart failure catecholamines such as dopamine and dobutamine were used, and in treatment-refractory cases norepinephrine or the phosphodiesterase-blocking agent amrinone was administered. Patients with cardiac arrest due to other causes did not receive intravenous heparin, acetylsalicylic acid, and nitroglycerin infusions.
Within the first 24 hours after admission, EEG, short-latency somatosensory evoked potentials (SSEP), brain stem auditory evoked potentials (BAEP), motor evoked potentials (MEP) (Medelec Sensor ER 94a/ST 10, Medelec Limited), and echocardiography (Sonotron Ving Med, CFM 750) were performed.
Two-dimensional transthoracic and/or transesophageal echocardiography was used for measuring left ventricular ejection fraction (LVEF) according to the Simpson rule.28 29
While EEG was only controlled on days 3 and 7 in case of any abnormality at the initial examination, SSEP, BAEP, and MEP were repeated in every patient on days 3 and 7.
SSEP were elicited by bipolar stimulation of the median nerve at the
wrist. Electric unipolar square waves with a duration of 0.2
millisecond were delivered at a rate of 5 Hz with an intensity of 10%
above motor threshold. Recordings were obtained with silver/silver
chloride disk electrodes (diameter, 9 mm) placed over Erb's
point30 using the contralateral side as reference and over
the seventh cervical vertebra referred to the midfrontal reference
(Fz) or to a noncephalic reference and over the hand area
of the contralateral sensory cortex (2 cm posterior to C3/C4 according
to the 10-20 System) recorded with Fz as reference.
Impedance was kept below 2 k
. Three series of 512 responses were
averaged during a period of 50 milliseconds and amplified 10 000 or
25 000 times (Erb's point), 25 000 times (cervical), and 50 000 or
100 000 times (cortical). The low filter was set at 10 Hz and the high
filter at 3000 Hz.30 N20, N13, and the central conduction
time (CCT) were measured for each trial. An amplitude ratio (AR)
between the positive peak at 25 milliseconds (P25) and N20 as well as
the peak at 13 milliseconds (N13) and the subsequent positive peak was
calculated for each side. For practical reasons the SSEP patterns were
classified into three types. Type 1 consisted of a clearly recognizable
contralateral N20 wave, giving rise to a normal CCT on both sides and a
normal AR (N20/N13 at least 0.5). SSEP with bilaterally discernible N20
waves but delayed CCT or a reduced AR (at least on one side) were
designated type 2. Recordings without a recognizable N20 wave on at
least one side were classified as type 3.
MEP and BAEP were recorded in the classic way.30 The results were divided into three categories, similar to those for SSEP.
All MRI and MRS examinations were performed on a 1.5-T scanner (Magnetom, Siemens) equipped with a 10-mT/m gradient system with the use of nonferromagnetic ventilation devices, transdermal monitoring of blood oxygenation, end-expiratory CO2 measurements in ventilated patients, blood pressure measurements, and electrocardiographic monitoring. The MRI/MRS examination was scheduled to be performed within 48 hours of admission. This was achieved in all except five patients, whose examinations had to be postponed until the following 48-hour period because of initial circulatory instability.
For the examination of the brain we used a sagittal relaxation time 1 (T1)–weighted spin-echo sequence (repetition time [TR], 550 milliseconds; echo time [TE], 15 milliseconds) and a transverse and a coronal long TR (2800 milliseconds)/triple TE (20, 60, 120 milliseconds) sequence. MRI readings were done by two independent investigators.
Then a 30x30x30-mm (27-mL) volume of interest was selected from the relaxation time 2 (T2)–weighted images within an area of the hemispheric white matter that did not exhibit signal abnormalities, and localized proton spectra were obtained by means of a stimulated echo sequence as described previously.17 24 For adequate ratios of signal to noise, 384 stimulated echoes were accumulated, which resulted in a 9-minute acquisition time for the localized spectrum. The TR of the stimulated echo sequence was set to 1500 milliseconds, which has been shown to represent a clinically useful compromise between T1 saturation and overall examination time. We chose a TE of 270 milliseconds to resolve the J-coupled methyl protons of lactate at 1.3 ppm in phase and to avoid the possibility that short T2 compounds, such as fatty acids, would hamper the detection of lactate. The spectral peaks were assigned to choline at 3.2 ppm, creatine and phosphocreatine at 3 ppm, NAA at 2 ppm, and lactate at 1.3 ppm according to previous investigations.17 24 The spectra were filtered in the time domain with a 1- to 2-Hz line-broadening Gauss filter and corrected for eddy current influences with the use of a localized water spectrum without water suppression. Then the spectra were phase-corrected and displayed without further baseline correction.
Treatment and management of our patients were not influenced by the results of the additional investigations. The relation between clinical, electrophysiological, and imaging methods and the course of the disease were analyzed, and early signs of prognostic importance were evaluated.
Statistical Analysis
Initial assessment of metric data regarding normal distribution
showed that they were normally distributed, and therefore an ANOVA was
performed to test whether the difference between the means of each
group was statistically significant. To test the difference between two
groups concerning an ordinal variable, a Mann-Whitney U test
was calculated. Nominal variables were tested with a
2 test or Fisher's exact test. By a two-tailed
analysis, a level of P<.05 or P<.01 was
considered statistically significant.
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Results |
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Thirteen of the 30 resuscitated patients survived and were discharged from the ICU after a mean of 16.2 days. At the final clinical neurological examination 4 weeks after admission, 6 of them (46.2%) presented with a good cerebral performance (consciousness, alertness, and the ability to work and lead a normal life [GPCPS category 1]).27 In 5 patients (38.5%) moderate cerebral disability was found (GPCPS category 2): 2 of them suffered from a slight hemiparesis, 1 patient developed generalized seizures, and 2 patients exhibited memory deficits and mental changes. One patient survived with severe cerebral disability (GPCPS category 3), suffering from cortical blindness, hemiplegia, seizures, and severe memory disturbance. One patient presented with persistent vegetative state (apallic syndrome).31
Seventeen patients did not survive. Twelve of them (70.6%) died of cardiac causes such as reinfarction (3 patients) and pump failure (9 patients) leading to therapy-resistant cardiogenic shock. In all these patients LVEF was below 35%, whereas in the remaining patients (29.4%), who died of cerebral causes, LVEF was at least 40%.
Age did not predict outcome reliably in our patients; mean age did not differ significantly in the survivor and nonsurvivor groups (nonsurvivors, 62.9 years; survivors, 59.4 years). The prognostic value of coma rating was also low.
The most important determinant of hypoxic trauma was time of anoxia. Results of an ANOVA indicated a significant difference between those patients with favorable and unfavorable outcomes (mean, 4.1 minutes versus 8.0 minutes, respectively; P=.0143; df=29). There was also a significant difference between patients who died of cardiac and cerebral causes (mean, 7.5 minutes versus 11.6 minutes, respectively; P<.001). The overall mean time of anoxia was 6.56 minutes. CPR time was significantly longer in patients with an unfavorable outcome than in those with a favorable outcome (mean, 34.53 minutes versus 17.72 minutes, respectively; P=.0241). The overall mean CPR time was 28.37 minutes.
A simple visual rating scale was used for EEG classification.1 32 Different prognostic values could be determined in patients who had normal EEGs with reactive dominant alpha rhythm and only rare theta waves, high scores on the ICS, and LVEF greater than 40% on the one hand and in patients with EEG patterns such as "alpha coma," burst suppression, and isoelectric tracing, low or unmeasurable ICS scores, and reduced LVEF on the other hand. In the majority of patients the EEG was diffusely abnormal.
MRI and MRS were performed in 21 of our patients. Death in the first 24 hours (n=4), cardiac instability (n=3), metal implant (n=1), and refusal of investigation (n=1) made the investigation impossible in the remainder.
MRI showed signal abnormalities on T2-weighted images in 18 patients. In 11 patients these changes could be partially attributed to the acute hypoxic event. Two patients had border zone infarctions between the middle cerebral artery and the posterior cerebral artery. Acute ischemic changes in the territory of the posterior cerebral artery were observed in 3 patients; these involved the calcarine cortex in 1 patient and the cerebellar hemispheres in 2 patients. These 3 patients also had increased signal intensity of the hippocampus, parahippocampal gyrus, and basal ganglia, which could be seen in 2 other patients as well. Three patients showed diffuse cerebral edema in the acute stage. In 10 patients periventricular white matter lesions did not change their signal behavior or their size on sequential examinations and were therefore attributed to preexisting white matter changes related to vascular risk factors.33 Seven patients had signs of cortical and subcortical atrophy as well.
Proton spectra revealed a decrease in NAA and an increase in lactate
compared with normal volunteers. Since decreases in NAA may be
explained by the considerably higher mean age of our study population
compared with previous examinations of volunteers,17 34 we
did not include NAA as a parameter in this study, and no attempts were
made to quantify the NAA changes. Elevated cerebral lactate resonances
were found in 10 patients. Because none of our patients had been
hyperventilated at the time of the MRI investigation, the influence of
actual carbon dioxide levels on brain lactate, which has been described
earlier,35 36 can be excluded. Previous investigations
with our scanner that used an identical examination protocol have shown
that physiological cerebral levels of lactate are beyond the
sensitivity of our technique.17 34 Therefore, only the
differentiation between absent and detectable lactate resonances was
used for statistical analysis. No quantification of individual
lactate levels was attempted. The demonstration of lactate positivity
was highly significant with regard to the outcome of our patients
(2=6.89659; df=1;
P=.00864). Eight of the 10 lactate-positive patients died (3
of cardiac and 5 of cerebral causes). Two lactate-positive patients
survived, both of whom suffered from severe neurological defects; one
developed persistent vegetative state (Table
).
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Among all electrophysiological investigations (SSEP, BAEP, and MEP on
days 1, 3, and 7), SSEP on the third day after admission, performed in
25 patients, served as the most significant parameter
(P<.01, Mann-Whitney U test). Clearly
recognizable N20 waves together with normal CCT and AR (N20/N13)
greater than 0.5 (type 1) were detected in all but 1 of the survivors
(91.7%), whereas no recognizable N20 wave on at least one side (type
3) was found in 4 of the 5 patients with cerebral death (80%) (Table
,
Fig 1).
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Discussion |
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Hypoxic coma after cardiac arrest is a common problem with great ethical, economic, social, and legal consequences. Various investigations concerning neurological outcome have been performed, but a considerable degree of uncertainty remains.12 The aim of our study was to evaluate further prognostic criteria after out-of-hospital cardiac arrest. In addition to clinical investigations (GCS, ICS) and the recording of duration of anoxia and CPR, we used a wide range of investigations including LVEF, EEG, EP, MRI, and MRS. This combination of easily obtainable practical parameters with investigations of high technical value on the one hand and of cardiological and neurological investigations on the other hand is the outstanding feature of our study. Heart and brain are a functional unit, and only combined examinations can be the future standard for prognostic evaluation after cardiac arrest. At this early stage the number of patients is too small for multiple logistic regression analysis, which would be beneficial for investigations with many variables.
To estimate the prognostic value of the various investigations, it is
important to find an objective parameter of cardiac function. For this
purpose we used transthoracic and transesophageal echocardiography for
measuring LVEF. Our data indicate that a good prognosis can be
predicted with a very high probability in those patients whose LVEF is
greater than 40% and who have lactate-negative MRS and type 1 SSEP,
whereas in patients with poor cardiac condition and low LVEF both
favorable and unfavorable results of MRS and SSEP can be seen. As shown
in the Table, 36.4% of the lactate-negative patients died (of cardiac
causes, with pump failure as the predominant factor); in all of them
LVEF was less than 35%. SSEP on day 3 varied from type 1 to type 3 in
patients who died of cardiac causes (Table, Fig 1); in patients who
died despite a better cardiac performance with an EF greater than 35%,
SSEP type 3 in 4 patients and type 2 in 1 patient could be demonstrated
(Table, Fig 1). It is quite understandable that in patients who suffer
from severe coronary heart disease leading to ventricular fibrillation,
additional cerebral damage can be induced by hypoxia, prolonged
hypotension, and reduced cerebral perfusion. Nevertheless, cardiac
function remains the main problem of such patients. This is confirmed
by our observation that even in patients with hypoxia-induced apallic
syndrome, the prognosis is not necessarily poor in all cases provided
that cardiac function is normal.37 However, there is
another group of patients who develop ventricular fibrillation or
asystolia, eg, after ischemia of the conduction system of the heart,
although their cardiac muscle function is more or less in the normal
range. Depending on the period of anoxia, they may develop severe
brain damage with prolonged CCT or even missing N20 waves on SSEP and
lactate positivity on MRS as a consequence of anaerobic glycolysis.
These patients usually recover from the cardiac point of view; however,
their prognosis is poor, and they die of cerebral causes or develop
severe neurological deficits. In this group of patients MRS and SSEP
play an important role in early prognostic assessment. In our study
group, all patients who died of cerebral causes were lactate positive
on MRS, and in none of them could SSEP type 1 be demonstrated (Table,
Fig 1).
SSEP were the most significant electrophysiological parameter
regardless of whether the test was performed on day 1 or 3, with a
maximum of significance on day 3. Interestingly, SSEP type 2 also may
be suggestive of a poor outcome, particularly if it is found on day 3
(Table, Fig 1), whereas type 1 is usually followed by good neurological
recovery. In contrast to Madl et al,9 we did not perform
long-latency SSEP, which are influenced by sedation and also by
technical artifacts in the ICU.
Many of the imaging abnormalities could be attributed to preexisting changes of the periventricular white matter of the hemispheres. Such changes have been observed in the elderly population without neurological deficits and in correlation with vascular risk factors.33 We noted evidence of acute cerebral lesions solely due to hypoxia in only three of our patients. These consisted of diffuse brain edema in two patients and ischemia of the visual cortex in one patient, whereas changes in the so-called vulnerable areas, such as border zone infarctions and lesions in the hippocampus, parahippocampal gyrus, and basal ganglia,38 were nearly always combined with periventricular white matter lesions and cortical or subcortical atrophy, respectively. Because of the inconstant pattern of the described pathological changes, valid statistical evaluation of the outcome after CPR was not possible.
Lactate in cerebrospinal fluid has been reported to provide information
regarding the extent of brain damage caused by cardiac
arrest.1 8 Because there are contradictory reports about
the development of elevated intracranial pressure after cardiac
arrest,39 40 the dangers of spinal tap cannot be ruled out
in patients suffering from anoxic coma. MRS, however,
represents a new, noninvasive method to obtain information
regarding intracellular lactate concentration in the brain. Elevation
of cerebral lactate after hypoxia is induced by anaerobic glycolysis,
cellular necrosis, and hypoperfusion, with resulting disturbances of
lactate removal.41 Additionally, the migration of
macrophages with anaerobic energy metabolism contributes to cerebral
lactate elevation.42 The aim of our study was the
detection of lactate as a result of general hypoxia. Therefore, the
volume of interest for MRS was targeted to those regions of the
supratentorial white matter that appeared normal on
T2-weighted images. The parameter setting with a long TE of
270 milliseconds was chosen to avoid contributions of other moieties
such as free fatty acids, mobile lipids, and cytosolic proteins to the
lactate resonance.17 24 The MRS protocol used in this
study has been shown to be insensitive to physiological concentrations
of cerebral lactate.17 34 Therefore, any detectable
lactate on the spectra was considered abnormal. Since little is known
about the time course of cerebral lactate elevations and the actual
contribution of anaerobic glycolysis in different cell populations, we
did not attempt to quantify individual lactate concentrations.
Consequently, the statistical evaluation is based on the variables
lactate positivity and lactate negativity. Of the 10 patients with
elevated lactate levels, 8 died and 2 are severely disabled. In
contrast, the lactate-negative patients recovered well from a
neurological point of view or died of cardiac causes (Table).
The duration of anoxia and CPR time can be used as prognostic
parameters as well, but one must be aware that they are the cause
rather than the effect of hypoxic trauma. Our data demonstrate that the
duration of anoxia and CPR time influence the final outcome of patients
with sudden cardiac arrest. Furthermore, a correlation between long
duration of hypoxia with consecutive anaerobic glycolysis and lactate
positivity on MRS was found (Figs 2 and 3), but it is important to note that the
overall mean times of anoxia and CPR were not as significant as the
mean times calculated separately for the groups with favorable and
unfavorable outcomes (Table).
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In addition to the neurological investigation, ICS and GCS were also used for clinical evaluation. The use of ICS is well established in traumatic brain injuries,26 but it has also proved to be useful in other diseases such as subarachnoid hemorrhage.43 The prognostic value of coma rating was rather low in this study. This can be explained by the study design, which included only comatose patients after cardiac arrest. Comparing patients with traumatic brain injuries or subarachnoid hemorrhage, we find that their scores on the ICS reflect the cerebral situation much better26 43 because cerebral perfusion is still present; therefore, reduced scores on the ICS are caused by direct mechanical damage of the brain. In hypoxic patients the duration of oxygen deprivation is the most important factor with regard to outcome. At the moment of cardiac arrest, with sudden cessation of cerebral perfusion, no reaction to any stimulus can be elicited, whereas at the moment of reperfusion reactions to stimuli return, provided that the period of anoxia has not been too long. Consequently, it is to be expected that the maximal score on the ICS was 3 or less than 3 in all of our patients initially. During their stay on the ICU most of the surviving patients recovered quickly in terms of their cerebral performance, reaching high scores on the ICS even on the first or second day, whereas in most of the nonsurvivors, who had to be ventilated artificially, a definite neurological evaluation was not possible.
In conclusion, our study demonstrates that in addition to methods described earlier,1 2 9 10 12 14 SSEP and MRS show great promise as tools for prognostic evaluation after cardiac arrest. Both SSEP and MRS offer great advantages compared with clinical evaluation: they are objective parameters and are not influenced by sedating drugs or any other medical treatment. Although based on completely different technical principles, the prognostic value of both methods is nearly equivalent. Nevertheless, there are some practical disadvantages of MRS, namely, cost and availability as well as mandatory anesthesiological and intensive care monitoring. In contrast, short-latency SSEP are technically easy to perform, can be performed without problems in the ICU, and are inexpensive. However, at the present time our findings do not yet justify general limitation of treatment in cases of lactate positivity on MRS and SSEP type 3 on the third day after cardiac arrest. At present every case has to be considered separately, but if our results can be substantiated by further trials, decision making regarding ICU treatment might be influenced in the future. Even MRS may become cost-effective if it helps to reduce the huge financial burden of intensive care medicine in cases with very poor prognoses.
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Acknowledgments |
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We are most grateful to Professor F. Gerstenbrand for supporting our investigation in every phase with his longstanding experience and advice. We thank Maria Hoch and Drs R. LoPresti, M. Jeschow, and G. Grubwieser for their technical assistance.
Received July 18, 1994; revision received January 19, 1995; accepted January 22, 1995.
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