In this study we performed invasive hemodynamic monitoring in patients suffering from acute SCI using the thermodilution-based PiCCO™ system. To our knowledge, this is the first study that provides advanced hemodynamic monitoring of patients with SCI that are not treated with vasopressors and in which data is not biased by septic or cardiogenic shock.
Few studies have examined advanced hemodynamic parameters in patients with acute SCI. In 1993 Levi et al used hemodynamic monitoring via Swan-Ganz catheter in 50 patients with SCI to maintain a hemodynamic profile with adequate cardiac output . Similarly, Vale et al. maintained mean arterial blood pressure above 85 mmHg in 77 patients with acute SCI also using a Swan-Ganz catheter to monitor the hemodynamic status . Both prospective studies aimed to show that maintaining a certain hemodynamic profile improved neurological outcome of patients with acute SCI and ultimately lead to the recommendation to keep the MAP > 85mmHg for the first 7 days after acute SCI. However, data was collected only within the first week after injury and most measurements were obtained under the influence of vasopressors. Furthermore, the MAP goal as well as the period of time for that goal were selected arbitrarily. Another study used impedance cardiography to assess the hemodynamic profiles in 9 patients with neurogenic shock after acute SCI, but only one measurement was obtained from each patient on admission and use of vasopressors was not reported . In 2019 Squair et al monitored MAP and central spinal fluid pressure during the first week after injury and suggested that spinal cord perfusion pressure rather than MAP was an indicator of neurologic outcome . As in previous studies the measurements were taken within the first week postinjury and vasopressors were used to maintain the MAP goals.
By contrast, our data consists of hemodynamic measurements performed largely without the use of vasopressors. Factors that could affect the cardiocirculatory system other than the SCI such as infections, sepsis or pre-existing heart disease led to exclusion of patients. Hence, our study provides a mostly unbiased hemodynamic profiling of patients with acute SCI.
SVRI was reduced significantly compared to the resistance considered normal in non-SCI patients whether patients required vasopressor therapy or not. Since the SVRI is calculated from MAP, CVP and CI, the reduced vascular resistance can be attributed to a change in one of these values. A consistently high CVP, a high-normal CI and a standard MAP were shown both with catecholamine therapy and without pharmacological vasoconstriction. Our data therefore suggests that in acute SCI cardiac output is increased to compensate for the loss of the afterload (SVRI). The increase in cardiac output could be explained by an increase in preload. CVP is used as a marker for preload in the formula for SVRI mentioned above. Since the venous pressure can be influenced by many factors and is not recommended on its own for neither volume status nor fluid responsiveness , we included the GEDVI as a preload marker. In accordance with the CVP, GEDVI lies at the upper margin of the reference range. This supports the theory, that the cardiac output is increased by an augmented preload. In addition to a reduced SVRI independent of vasopressor use, the mixed model analysis shows a negative correlation between MAP, SVRI as well as GEDVI and norepinephrine treatment. CI, SI and CVP were not affected by vasopressor use. As a standard practice in the ICU of the university hospital Bergmannsheil Bochum an MAP of 70mmHg is tolerated in patients with SCI if there are no signs of reduced organ perfusion i.e., serum lactate, oliguria, dizziness. Therefore, whenever the MAP dropped below 70mmHg norepinephrine was used to achieve an MAP of 70mmHg. Hence, the mean MAP under vasopressor therapy (73,69mmHg) was lower than without norepinephrine treatment (83,97mmHg) (Table 4). Since the calculation of the SVRI relies on the MAP a negative correlation for the peripheral resistance due to the MAP goal was to be expected. Whenever vasopressor support was indicated, the loss of peripheral resistance could not be compensated for by an increase in preload and consecutively by an increase of the cardiac index. As a result, the GEDVI was also lower under norepinephrine treatment. Due to this compensation mechanism, a sufficient perfusion seems to be maintained even with reduced peripheral resistance. From a cardiocirculatory point of view, it can be assumed that a lower resistance can be tolerated and thus an adjustment of the reference value is to be considered as long as the patient does not show signs of reduced organ perfusion.
In clinical practice, the aforementioned evidence has led to relatively high MAP goals in patients with SCI. However, the resulting use of vasopressors and consecutive need for invasive monitoring leads to delays in patient mobilization and longer hospitalization .
Our data suggests that adjustment of the target values for MAP and SVRI could be justified and lead to a more focused application as well as reduced dosage of vasopressors. We acknowledge that this study did not assess the neurological outcome of patients and therefore cannot say whether a more restrictive use of vasopressors for blood pressure management might lead to a worse neurological outcome. However, to our knowledge, there is no evidence that “high normal” blood pressure (MAP 85mmHg) leads to a better neurological outcome than normotension. Rather, based on the experience in severe cerebral trauma, the spinal perfusion pressure seems to be responsible for a difference in outcome. Therefore, a general recommendation of a “high normal” MAP goal in light of the aforementioned negative effects of vasopressor use should be critically questioned.
Furthermore, use of thermodilution-based PiCCO™ system could serve as a safe and easy-to-use means of hemodynamic monitoring in acute SCI. However, the use of the thermodilution based measurements is limited to the ICU and only reserved for those patients who need invasive blood pressure monitoring or regular blood gas analysis as part of the intensive care treatment. The indication to maintain or remove a central catheter in the ICU setting especially in the case of invasive blood pressure monitoring using vasopressors must be questioned daily. In the author’s view, a continuous surveillance of the blood pressure in patients with SCI is a key aspect in early mobilization as it allows for a quick an accurate adaptation of the vasopressor dosage if the blood pressure suddenly drops. In the author’s experience the arterial catheter itself does not delay early mobilization, rather the vasopressor therapy often hinders the physician to begin mobilization. Especially in Patients with acute SCI the blood pressure may vary greatly depending on the patients’ position. Therefore, in our view, invasive monitoring is mandatory in early mobilization.
As maintaining central catheters only for research purposes might escalate cures without any clinical need, we did not include a set period of time for measurements in our study protocol. Therefore, the duration of measurements varies greatly between patients (Table 1). Additionally, the start of measurements was delayed depending on the duration of the initial external treatment (Table 1). Since the university hospital Bergmannsheil Bochum is listed as a specialised centre for SCI, patients are admitted directly after trauma as well as transferred from various regions of Germany. Both adaptations to the study protocol renders our study less comparable to the studies mentioned earlier. However, in light of the main focus of our study i.e., hemodynamic profiles over a longer period of time, this adaptation was justified.
Some of the hemodynamic measurements were performed while patients were ventilated and/or sedated, which may have biased measurement. Furthermore, we did not differentiate between the neurological level/location of the SCI.
In addition, the number of patients enrolled in the study is very small. With the begin of the corona crisis the number of traumatic SCI cases dropped significantly and less patients than initially anticipated were included. This could reduce the statistical power of our findings.
Further studies that examine the hemodynamic profile after acute SCI with a greater patient collective are needed for a better understanding of the cardiocirculatory changes caused by SCI. Long-term follow-up and regular assessment of the neurological status of these patients could show whether a certain hemodynamic profile might yield a higher or lower chance of neurological improvement and complications.