Hemodynamic Parameters in Patients with Acute Cervical Cord Trauma

Abstract

The cardiovascular response of the patient with acute spinal cord injury (SCI) is known to be altered secondary to the cord injury. Our current protocol of managing the acute phase of patients with SCI includes invasive hemodynamic monitoring (with arterial line and Swan-Ganz catheter) and support with fluids and dopamine and/or dobutamine, titrated to maintain a hemodynamic profile with adequate cardiac output (to be determined by oxygen consumption and delivery) and a mean blood pressure of > 90 mm Hg. We feel that this protocol provides two benefits: 1) maintaining the mean blood pressure improves the morbidity of these patients by deterring ischemia and accompanying secondary insults; 2) aggressive monitoring and hemodynamic intervention help stabilize the hemodynamic status of these patients and make it possible to consider early surgery in selected cases. Our hypothesis is that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI. We analyzed the demographic, neurologic, and hemodynamic data of 50 consecutive patients during their first week postinjury. All had signs of myelopathy; 31 (62%) were considered clinically complete. Of the 50 patients, 9 (18%) died, 20 did not improve functionally, and 21 improved. The mean heart rate (82.1 +/- 13.3), blood pressure (94.4 +/- 9.4), pulmonary artery pressure (22 +/- 5) and wedge (12.7 +/- 3.4), cardiac index (4.5 +/- 0.9), systemic vascular resistance index (SVRI) (1637 +/- 399), pulmonary vascular resistance index (PVRI) (181 +/- 80), and oxygen transport (694 +/- 156) showed good response to the treatment. Because the measurements were obtained during treatment, they differ from the expected "classic sympathectomized" response, but they provide a database for further analysis of hemodynamic manipulation in SCI. An analysis of the hemodynamic parameters did not differentiate between complete and incomplete lesions or between patients with functional improvement. We determined, on the basis of the initial hemodynamic measurements, that no patient with a clinically complete motor deficit (Frankel Grade A+B) improved of the 10 who had measurements compatible with either: 1) PVRI < 100 with SVRI < 1200; or 2) PVRI < 115 with SVRI < 1300 or PVR/SVR ratio of < 0.08 when SVRI was < 1600. These patients could not have other measurements that showed low SVRI < 1350 with PVRI > 139. At odds with this unique group, 13 of 29 patients with the same clinical picture and without the above physiological criteria of severe hemodynamic deficit eventually improved (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

“…Acute spinal surgery, within the first 24 h following SCI, to alleviate mechanical shearing and compression forces is used to restrict primary damage to the cord, as well as secondary damage that can result from extended periods of compression [13]. In addition to spinal cord stabilization, arterial oxygenation and maintenance of mean arterial blood pressure between 85 and 90 mm Hg following acute SCI is vital in reducing secondary damage due to ischemia and hypoxia, and improving functional outcome [11,[14][15][16][17][18]. Hypothermia is also currently in clinical testing as a means of limiting secondary damage immediately following injury [19,20].…”

The effect of preexisting hypertension on early neurologic results of patients with an acute spinal cord injury

“…Similarly, Levi et al 26 reported on 50 patients with an acute SCI. The maps of all these patients was kept above 90 mm Hg, and 42% demonstrated clinical recovery.…”

“…Two studies have demonstrated improved neurologic function and a decrease in mortality in SCI patients who were kept relatively hypertensive. 26,27 Although no consensus has been established on the exact target blood pressure or treatment duration necessary, clinical protocols often aim to keep the mean arterial pressure (MAP) above 85 mm Hg or 90 mm Hg for between 5 and 7 days after injury. [26][27][28] Whereas a MAP of 85-90 mm Hg is an acceptable baseline number, this goal may need to be modified based on patient factors such as preexisting HTN.…”

“…26,27 Although no consensus has been established on the exact target blood pressure or treatment duration necessary, clinical protocols often aim to keep the mean arterial pressure (MAP) above 85 mm Hg or 90 mm Hg for between 5 and 7 days after injury. [26][27][28] Whereas a MAP of 85-90 mm Hg is an acceptable baseline number, this goal may need to be modified based on patient factors such as preexisting HTN. Chronic HTN has been shown to affect the autoregulation of blood flow to the brain, 29,30 and although strong scientific evidence establishing the same phenomenon in the spinal 1 cord is lacking, animal studies have demonstrated nearly identical autoregulation of blood flow in the brain and spinal cord.…”

Hyponatremia-induced transient visual disturbances in acute spinal cord injury

“…It has been suggested that maintenance of an MAP within normal range may play a neuroprotective role in the acute phase. 6 However, this can be done with other means that will not put the patient at risk of overhydration. Moreover, it was previously reported that the most significant predictor of hyponatremia in individuals with SCI is the level and the severity of the injury.…”