The physiopathology of respiration in neurosurgical patients

1979 ◽  
Vol 50 (6) ◽  
pp. 699-714 ◽  
Author(s):  
Elizabeth A. M. Frost

✓ Regulation of respiration is summarized as to peripheral and central chemoreceptors, controllers of voluntary and automatic respiration, and stimulators (CO2, O2, and pH). The information that may be obtained from blood-gas analysis is reviewed and basic problems in acid-base imbalance described. Commonly employed respiratory patterns are discussed. Preoperative pulmonary assessment necessary in elective intracranial situations, spinal cord injuries, and pediatric neurosurgery is outlined. Some of the special problems of the patient with multiple trauma, including injury to the central nervous system are reviewed. Central and peripheral factors that cause respiratory difficulty in head-injured patients are tabulated, and an outline is given of diagnosis and therapy. There are many possible causes of intraoperative hypoxia and hypercarbia, and these complications with their prevention or treatment are examined. Criteria for extubation are established. Finally, postoperative pulmonary care in elective, emergency, and cord injury situations is discussed. The key to successful perioperative pulmonary care of the neurosurgical patient requires close cooperation between the neurosurgeon and anesthesiologist.

1984 ◽  
Vol 61 (5) ◽  
pp. 925-930 ◽  
Author(s):  
Ronald W. J. Ford ◽  
David N. Malm

✓ Hypocarbia, normocarbia, or hypercarbia was maintained for an 8-hour period beginning 30 minutes after acute threshold spinal cord injuries in cats. No statistically significant differences in neurological recovery or histologically assessed tissue preservation were found among the three groups of animals 6 weeks after injury. No animal recovered the ability to walk. It is concluded that maintenance of hypercarbia or hypocarbia during the early postinjury period is no more therapeutic than maintenance of normocarbia. Mortality rates and tissue preservation data suggest, however, that postinjury hypocarbia may be less damaging than hypercarbia.


1988 ◽  
Vol 69 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Joseph M. Piepmeier ◽  
N. Ross Jenkins

✓ Sixty-nine patients with traumatic spinal cord injuries were evaluated for changes in their functional neurological status at discharge from the hospital, and at 1 year, 3 years, and 5+ years following injury. The neurological examinations were used to classify patients' spinal cord injury according to the Frankel scale. This analysis revealed that the majority of improvement in neurological function occurred within the 1st year following injury; however, changes in the patients' status continued for many years. Follow-up examinations at an average of 3 years postinjury revealed that 23.3% of the patients continued to improve, whereas 7.1% had deteriorated compared to their status at 1 year. An examination at an average of 5+ years demonstrated further improvement in 12.5%, with 5.0% showing deterioration compared to the examinations at 3 years. These results demonstrate that, in patients with spinal trauma, significant changes in neurological function continue for many years.


1974 ◽  
Vol 40 (1) ◽  
pp. 3-33 ◽  
Author(s):  
Jewell L. Osterholm

✓ In this review of spinal cord injury research, the author has selected contributions which in his opinion best represent modern experimental concepts regarding the mechanism and management of spinal cord injuries. He has placed special emphasis on the controversial issues appropriate to a new, stimulating, and competitive area of research.


1990 ◽  
Vol 72 (6) ◽  
pp. 894-900 ◽  
Author(s):  
Thomas J. Zwimpfer ◽  
Mark Bernstein

✓ The hallmark of concussion injuries of the nervous system is the rapid and complete resolution of neurological deficits. Cerebral concussion has been well studied, both clinically and experimentally. In comparison, spinal cord concussion (SCC) is poorly understood. The clinical and radiological features of 19 SCC injuries in the general population are presented. Spinal cord injuries were classified as concussions if they met three criteria: 1) spinal trauma immediately preceded the onset of neurological deficits; 2) neurological deficits were consistent with spinal cord involvement at the level of injury; and 3) complete neurological recovery occurred within 72 hours after injury. Most cases involved young males, injured during athletics or due to falls. Concussion occurred at the two most unstable spinal regions, 16 involving the cervical spinal and three the thoracolumbar junction. Fifteen cases presented with combined sensorimotor deficits, while four exhibited only sensory disturbances. Many patients showed signs of recovery with the first few hours after injury and most had completely recovered within 24 hours. Only one case involved an unstable spinal injury. There was no evidence of ligamentous instability, spinal stenosis, or canal encroachment in the remaining 18 cases. Two patients, both children, suffered recurrent SCC injuries. No delayed deterioration or permanent cord injuries occurred. Spinal abnormalities that would predispose the spinal cord to a compressive injury were present in only one of the 19 cases. This suggests that, as opposed to direct cord compression, SCC may be the result of an indirect cord injury. Possible mechanisms are discussed.


1997 ◽  
Vol 87 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Fernando L. Vale ◽  
Jennifer Burns ◽  
Amie B. Jackson ◽  
Mark N. Hadley

✓ The optimal management of acute spinal cord injuries remains to be defined. The authors prospectively applied resuscitation principles of volume expansion and blood pressure maintenance to 77 patients who presented with acute neurological deficits as a result of spinal cord injuries occurring from C-1 through T-12 in an effort to maintain spinal cord blood flow and prevent secondary injury. According to the Intensive Care Unit protocol, all patients were managed by using Swan—Ganz and arterial blood pressure catheters and were treated with immobilization and fracture reduction as indicated. Intravenous fluids, colloid, and vasopressors were administered as necessary to maintain mean arterial blood pressure above 85 mm Hg. Surgery was performed for decompression and stabilization, and fusion in selected cases. Sixty-four patients have been followed at least 12 months postinjury by means of detailed neurological assessments and functional ability evaluations. Sixty percent of patients with complete cervical spinal cord injuries improved at least one Frankel or American Spinal Injury Association (ASIA) grade at the last follow-up review. Thirty percent regained the ability to walk and 20% had return of bladder function 1 year postinjury. Thirty-three percent of the patients with complete thoracic spinal cord injuries improved at least one Frankel or ASIA grade. Approximately 10% of the patients regained the ability to walk and had return of bladder function. As of the 12-month follow-up review, 92% of patients demonstrated clinical improvement after sustaining incomplete cervical spinal cord injuries compared to their initial neurological status. Ninety-two percent regained the ability to walk and 88% regained bladder function. Eighty-eight percent of patients with incomplete thoracic spinal cord injuries demonstrated significant improvements in neurological function 1 year postinjury. Eighty-eight percent were able to walk and 63% had return of bladder function. The authors conclude that the enhanced neurological outcome that was observed in patients after spinal cord injury in this study was in addition to, and/or distinct from, any potential benefit provided by surgery. Early and aggressive medical management (volume resuscitation and blood pressure augmentation) of patients with acute spinal cord injuries optimizes the potential for neurological recovery after sustaining trauma.


1988 ◽  
Vol 68 (5) ◽  
pp. 781-792 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator ◽  
R. Dean Linden

✓ Recent work has indicated that direct-current (DC) fields may promote recovery after acute spinal cord injury. In the present experiments, the therapeutic value of an applied DC field was studied in 40 rats with clip compression injuries of the cord at C7–T1. The rats were randomly allocated to one of four groups including 10 rats each: two groups received a 17-gm cord injury and two groups a 53-gm injury. One group at each injury severity received implantation of a treatment (14 µA) DC stimulator and the other group a control (0 µA) stimulator. Clinical neurological function was assessed weekly by the inclined-plane technique. At 8 weeks after injury, motor and somatosensory evoked potentials (MEP's and SSEP's) were recorded, and the axonal tracer horseradish peroxidase (HRP) was introduced into the cord at T-6. The total number of HRP-labeled cells was counted in every sixth coronal section through the brain stem and motor cortex. All outcome parameters were assessed blindly. In the 17-gm group, there were no significant differences in any outcome measure between control and treated rats. In contrast, in the 53-gm group, the inclined-plane scores, the amplitude of the MEP's, and the number of labeled cells in the red nucleus, raphé nuclei, and vestibular nuclei were greater in treated than in control rats. These data strongly indicate that an applied DC field can produce functional neurological and anatomical improvement in rats with acute spinal cord injuries.


1972 ◽  
Vol 36 (4) ◽  
pp. 379-385 ◽  
Author(s):  
Henry L. Heyl

✓ This report summarizes in one document the four federal programs devoted specifically to the care and study of spinal cord injuries. The accompanying editorial emphasizes the need for coordination between these agencies in the optimal use of specific capabilities and separate federal budgets, particularly in the planning for regional spinal cord injury centers.


1980 ◽  
Vol 53 (6) ◽  
pp. 756-764 ◽  
Author(s):  
Eugen J. Dolan ◽  
Ensor E. Transfeldt ◽  
Charles H. Tator ◽  
Edward H. Simmons ◽  
Kenneth F. Hughes

✓ Distraction is considered to be a factor in many spinal cord injuries. With a specially designed distraction apparatus and the 14C-antipyrine autoradiographic technique, the effect of distraction on spinal cord blood flow (SCBF) in cats was studied. Distraction was performed at L2–3 at a rate of 0.25 cm/10 min, and the spinal evoked response (SER) was monitored by stimulating the sciatic nerve and recording at T-13. The SCBF was assessed in five control animals, four animals in whom the SER was markedly altered by distraction, and five animals after the SER had been abolished and an additional 0.5 cm distraction applied. Control cats had gray- and white-matter flows of 44.5 ± 1.4 (SEM) and 10.5 ± 0.4 ml/100 gm/min, respectively. Distraction to the point of marked SER alteration caused a 50% loss of SCBF at and caudal to the distraction site. An additional 0.5 cm distraction produced total abolition of SCBF at the distraction site and for a considerable distance rostral and caudal to it. Thus, it is shown that spinal distraction causes cord ischemia similar to that seen with other types of spinal cord injury. In addition, distraction severe enough to cause loss of the SER has already produced severe cord ischemia.


1971 ◽  
Vol 35 (3) ◽  
pp. 277-286 ◽  
Author(s):  
David J. Fairholm ◽  
Ian M. Turnbull

✓ The pathology of spinal cord injury has been studied in 34 rabbits and 5 dogs with attention focused on the condition of the microvasculature during the evolution of neuronal and axonal degeneration and necrosis. The animals were killed and perfused arterially with colloidal barium from 10 min to 14 days after a controlled spinal injury. Microradiographs of the injured tissues were obtained and compared with corresponding histological sections. Microangiography at 7 to 14 days defines two zones in the injured spinal cord. Zone 1 is located in the posterocentral part of the cord. Capillaries in this region progressively lose their ability to conduct blood and perfusate over the first 4 hours. Degenerative changes in neurons are visible by 1 hour after injury. Necrosis of all elements including capillaries ensues. Zone 2 surrounds Zone 1. Microvascular patterns are normal in Zone 2 although neuronal and axonal degeneration is severe. Pericapillary hemorrhages which occur as early as 10 min after injury in Zone 1 and become progressively larger over the first 4 hours seldom are seen in Zone 2. The evidence indicates that at all times in the pathogenesis of spinal cord injury the microvasculature in Zone 2 is capable of perfusion. Degeneration of neural structures either precedes microvascular breakdown (Zone 1) or occurs in the absence of microvascular disruption (Zone 2). Recovery of damaged neurons and axons depends upon a preserved microcirculation.


1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.


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