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)

From June, 1982, through June, 1985, 113 patients were evacuated to Rambam Maimonides Medical Center with penetrating craniocerebral injuries sustained in ongoing military hostilities in Lebanon. Two factors distinguished this group of patients from those presenting in earlier conflicts: 1) this was the first large series in which computerized tomography (CT) was routinely used to initially evaluate combat head injuries; and 2) in an effort to preserve maximum cerebral tissue, intracranial debridement was significantly less vigorous than that advocated during the Korean or Vietnam conflicts. No efforts were made to locate or remove in-driven bone or metal fragments visualized on CT unless they readily presented themselves on gentle irrigation. In fact, it was elected to treat a number of patients without intracranial hematomas nonoperatively. The acute outcome was quite similar to that reported in Vietnam series in respect to both complications and mortality. Of the 83 survivors, 46 were Israeli citizens and thus were available for follow-up review. These 46 patients were reevaluated in late 1988, a mean follow-up period of 5.9 years. None had died in the interim; 10 had developed chronic seizure disorders, and there was one case of delayed meningitis in a patient with no retained fragments. Repeat CT scans were performed on 43 patients; 22 (51%) were found to have retained intracranial bone fragments. No relationship existed between the presence of retained fragments and the development of either a seizure disorder or an infection of the central nervous system. These findings suggest that not only is it unnecessary to reoperate for retained bone fragments, but it may also be possible to temper the initial debridement in an effort to preserve additional cerebral tissue.

To clarify the ideal timing of anterior decompression and stabilization for all patients with cervical spine trauma as well as its efficacy for patients with complete deficits, we reviewed the records of 103 consecutive patients with cervical spine trauma (50 incomplete deficits, Group A; 53 complete deficits, Group B) who underwent this procedure during a 5-year period at the Shock Trauma Center. We subdivided each group according to time of surgery: early and delayed (&lt;24 and &gt;24 hours past injury, respectively). In Group A, 10 patients underwent early surgery and 40 patients underwent delayed surgery (range, 2 to 77 days past injury; mean, 13 days). One patient (2.5%) in the delayed group died. The following data refer to the early and delayed subgroups, respectively: average acute hospitalization, 20 and 22 days; patient motor score improvement (at discharge), 37.2 and 45.0%; functional grade improvement (at discharge), 5 (50.0%) and 9 (22.5%) patients. At 1-year follow-up, every patient who had had a deficit had progressed to a higher functional grade. In Group B, 35 patients underwent early surgery and 18 underwent delayed surgery (range, 2 to 45 days past injury; mean, 13 days). One patient (2.9%) in the early group died. The following data refer to the early and delayed subgroups, respectively: average acute hospitalization, 38.7 and 45.2 days (P &lt; 0.05); respiratory care (number of daily suction procedures), 6.0 and 9.86 (P &lt; 0.05); patient motor score improvement (at discharge), 3.9 and 4.5%; functional grade improvement (at discharge), 4 (11.4%) and 1 (5.6%) patients. At 1-year follow-up, 16 (45.7%) and 7 (38.9%) patients, respectively, had progressed to a higher functional grade (mean motor score improvement, 15.0 and 16.7%, respectively). Only 5 patients (14.3%) did not gain the function of at lease one more segment. Although our study demonstrated no statistically significant difference in outcome between early surgery and delayed surgery subgroups, we feel early anterior decompression and stabilization is appropriate for selected patients because this process has a comparable adverse sequelae rate to that of delayed surgery; it provides superior ease of patient care, it facilitates earlier transfer to rehabilitation (an important parameter in decreasing medical expenses), and it may benefit even patients with complete deficits diagnosed on the first day.

Fifty-two patients with acute traumatic bilateral locked facets were treated at one trauma center during a 3 1/2-year period (July, 1987, to December, 1990). The patients presented with complete motor quadriplegia (34 cases), incomplete myelopathy (13 cases), or intact long-tract function (five cases). The injuries occurred at C2-3 (one patient, with intact function), C4-5 (12 patients), C5-6 (16 patients), C6-7 (19 patients), and C7-T1 (four patients). Immediate traction (with increasing weight and serial x-ray studies) and/or induction of general anesthesia and muscle relaxation reduced the dislocation in 40 patients, but 12 needed prompt operative reduction as their injuries failed to reduce within 4 hours. Stabilization was indicated for all patients, but three did not undergo surgery: two elderly patients with complete injuries (one refused surgery and one died), and one patient with multiple injuries (fusion was achieved by halo-vest immobilization for 3 months). Of the 49 patients treated operatively, 23 (44.2%) underwent surgery on the day of injury and 26 on a delayed basis (mean 8.7 days postinjury). Surgical treatment included fusion of the posterior facet to a spinous process (44 cases), an anterior Caspar plate technique (three cases), and both procedures (two cases). Of these 49 patients, three (6.1%) with complete injuries died due to an adult respiratory distress syndrome. Improvement of cord function, judged by functional grade change, was observed at discharge in 15 patients (31.9%) and in 15 (71.4%) of the 21 patients with a 1-year follow-up period. Of the 34 patients with complete myelopathy on admission, three are ambulatory after 1 year, and 13 others have gained function in at least one nerve root. It is concluded that prompt reduction (nonoperative or surgical) and internal stabilization facilitate recovery even in neurologically compromised patients, and that early operative intervention is a wiser option than conservative management. This report also documents a higher incidence of this injury without deficit (five of the 52 cases) than reported in other series.

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)