Medical Management of Adult and Pediatric Spinal Cord Injury

Published on 27/03/2015 by admin

Filed under Neurosurgery

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1232 times

Chapter 70 Medical Management of Adult and Pediatric Spinal Cord Injury

The three primary goals of managing both adult and pediatric spinal cord injury (SCI) are to optimize neurologic outcome, provide for early mobilization, and facilitate rehabilitation. These goals are difficult to meet when medical complications supervene. Unfortunately, SCI patients are uniquely vulnerable to a variety of complications that, at a minimum, prolong hospitalization, increase costs, and delay entry into rehabilitation, and at the other extreme may impair neurologic recovery.

Fortunately, mortality after SCI is relatively low and continues to decline. However, morbidity, even in children, remains significant. Thus, attention to the medical management of SCI is essential, and the skills of a multidisciplinary team of spine surgeons, critical care specialists, and physiatrists are often required.

The American Association of Neurological Surgeons published guidelines in 2002 for the management of acute injuries of the cervical spine and spinal cord. This supplement includes medical management strategies for these challenging injuries.1

Pharmacologic Intervention

Administration of the steroid methylprednisolone within 8 hours of adult SCI has been shown from the National Acute Spinal Cord Injury Studies (NASCIS II and NASCIS III) to improve American Spinal Injury Association (ASIA) motor and sensory scores in patients.24 In response to SCI, the spinal cord swells, and methylprednisolone is administered to reduce inflammation in hope of preventing further nerve cell death. However, these NASCIS studies are controversial because they failed to address potentially important recovery-influencing details regarding surgical intervention and rehabilitative therapies.5,6 Furthermore, later analysis revealed that these studies did not demonstrate an improvement in patients’ primary outcome measures, which indicates that the improved recovery could be due to random events.58 Because these studies are not entirely credible, evidence is lacking to decisively recommend the use of methylprednisolone following acute SCI.

The studies, however, do demonstrate that it is inadvisable to use methylprednisolone more than 8 hours after SCI because it is associated with a slight decrease in neurologic recovery.4 Additionally, the NASCIS studies document conclusively that methylprednisolone has serious side effects, such as higher infection rates, respiratory complications, and gastrointestinal hemorrhage. Therefore, methylprednisolone has no benefit in a neurologically intact patient.

Trials with other neuroprotective agents such as the ganglioside GM1, gacyclidine, tirilazad, and naloxone have also failed to demonstrate conclusive effectiveness, and their use cannot be justifiably recommended due to their potential side effects.

Clinical trials involving a new nerve repair drug, BA210 (Cethrin), have been conducted to investigate its safety and effectiveness in restoring neurologic function following traumatic SCI. Cethrin is a recombinant protein that acts as a rho inhibitor to promote neuroregeneration and neuroprotection in the CNS. Rho proteins are involved in a key pathway that promotes apoptosis, and the inhibition of this pathway facilitates axon regeneration at the site of the injury. The clinical trials demonstrated that topical administration of 0.3, 1, 3, or 6 mg of Cethrin following surgical decompression is safe. Recently, a placebo controlled trial has been initiated in order to better assess the drug’s clinical efficacy.9

Pulmonary Considerations

The respiratory system is uniquely susceptible to SCI because primary neurologic dysfunction profoundly affects respiratory physiology directly, as well as indirectly. Cervical injury is more commonly associated with pulmonary complications, as 84% of all respiratory complications are the result of C1-4 injuries. However, more than 60% of patients with lower-level injuries develop pulmonary problems, so these may also occur from thoracic-level injuries.11 Pulmonary complications are the single most common cause of morbidity and mortality after pediatric SCI.

The muscles of respiration include the abdominal, intercostal, diaphragm, and cervical accessory muscles. The abdominal muscles are the primary muscles of active expiration and account for over 50% of expiratory capacity. Thus, thoracic SCI with abdominal muscle paralysis may lead to ineffective expiration, excessive end-tidal volumes, and, subsequently, a diminished lung capacity.12,13

To diagnose an abdominal injury in a patient with cervical SCI and hypotension, a Focused Assessment with Sonography for Trauma (FAST) abdominal ultrasound examination is recommended.14 FAST is a diagnostic tool used to screen for significant hemoperitoneum after blunt trauma.15 In the absence of or after a positive FAST examination, an abdominal CT scan is advisable to better define the nature of the injury. In a hemodynamically stable patient, a FAST examination is less reliable and the use of a CT scan is necessary to reduce the number of missed injuries.16

The intercostal muscles play an important role in stabilizing the chest wall during inspiration. Their paralysis results in a functionally flail chest, in which the chest wall collapses during inspiration and expands during expiration, resulting in an overall loss of tidal volume.

The diaphragm muscles account for approximately 50% to 60% of the inspiratory force generated. When the other muscles of respiration are nonfunctional, however, the diaphragm assumes 100% of the workload and may rapidly fatigue.17

Overall, generalized muscle weakness associated with midthoracic injury levels contributes to diminished contraction force for effective coughing and clearing of secretions. These muscle abnormalities, singly or in combination, may ultimately significantly decrease functional residual capacity, tidal volume, and inspiratory and expiratory volumes, while markedly increasing residual lung volumes.18 Nasotracheal suctioning is often insufficient to mobilize secretion, and consequently, expiratory aids such as mechanical insufflation-exsufflation or quad coughing are necessary.19,20

Remember that the vital capacity and the tidal volume of the quadriplegic patient are greater in the supine position than in the upright position. In the supine position, the weight of the abdominal contents helps in forcing the diaphragm rostrally, which leads to a decrease in residual volumes.21

Despite attention to these details, some patients may require intubation for respiratory support. The two primary indications are the inability to ventilate effectively (partial pressure of carbon dioxide >50 mm Hg) and the inability to oxygenate adequately (partial arterial oxygen pressure <80 mm Hg). It is critical to monitor these blood oxygen and carbon dioxide levels via pulse oximetry or arterial blood gas measurement early during SCI management.

Endotracheal intubation is often required before the location of an injury can be determined, so it is essential to keep the cervical spine as stationary as possible while securing the airway in case of a cervical-level injury. Succinylcholine is the recommended neuromuscular blocking agent to use during intubation, but only within the first 48 hours after injury due to the risk of hyperkalemia.22

Intubation with current endotracheal tubes can be safely maintained for several weeks, although there are some proponents of early tracheotomy. An early tracheotomy should be considered for any patient with high tetraplegia or one who is likely to remain ventilator dependent for an extended period of time, since the tracheotomy simplifies the ventilator weaning process. One review of tracheotomy in critically ill patients illustrated that early tracheotomy reduces the duration of both the stay in the ICU and time needed for mechanical ventilation.23 Although almost all surgery for acute SCI requires an endotracheal tube, one disadvantage of early tracheotomy is that it may interfere with anterior cervical surgery in those patients who require internal stabilization from such an approach.

Except for quadriplegics with injury at very high levels, most SCI patients can be weaned from ventilatory support during acute hospitalization. A limited number of studies have demonstrated that high tidal volume ventilation of 20 mL/kg or greater (except for patients with adult respiratory distress syndrome or acute lung injury) during rehabilitation reduces the time to ventilator weaning and improves the outcomes for atelectasis.24 The use of a progressive ventilator-free breathing T-piece protocol also reduces ventilator weaning time.25 Most patients can be successfully weaned when the vital capacity is greater than 1 L, maximal negative inspiratory force exceeds 30 cm H2O, and minute ventilation is less than 10 L.26

Despite attention to these details, atelectasis and ventilator-associated pneumonia are still common in the SCI population, and thus, constant vigilance is of utmost importance to diagnose and treat pneumonia rapidly. Preventative strategies that reduce the risk of ventilator-associated pneumonia include the maintenance of the patient in a semirecumbent position, the assessment of the patient’s readiness for accepted ventilator weaning protocols, and the use of an orotracheal route of intubation.2729 The use of prophylactic antibiotics is not encouraged, even in those patients who require prolonged intubation or tracheotomy. Routine use may increase the occurrence of antibiotic-resistant infection.12,30

Another potential pulmonary complication of SCI is sleep apnea. Automatic respiration is regulated by spinal cord tracts that lie in the rostral cervical spinal cord. If these pathways are significantly damaged, only voluntary respiration (which is dependent on consciousness) is possible, and breathing may cease during sleep. One should maintain a high index of suspicion of this syndrome in any patient with a high cervical SCI. An apnea monitor or pulse oximeter should be used on a continuous basis for 7 to 10 days after injury in such patients.

Hemodynamic Considerations

The transection of sympathetic pathways after SCI, with concomitant unopposed vagal activity or hyperactivity, accounts for the majority of cardiovascular complications associated with SCI.31 Monitoring with a Swan-Ganz catheter, however, has documented far-reaching hemodynamic derangements in these patients. The primary immediate concerns are generally bradycardia and neurogenic spinal shock. Although the majority of patients with cervical SCI have bradycardia, only rarely does this become of significant clinical concern to warrant treatment with atropine or use of a temporary transvenous cardiac pacer. Nevertheless, it is important to utilize electrocardiographic monitoring during the early phase after cervical SCI.32

In addition to electrocardiographic monitoring, it is necessary to monitor both the temperature and blood glucose level of an SCI patient. Temperature is a factor because the disruption of the autonomic nervous system can cause a loss of vasomotor control, which impairs the patient’s thermoregulation. Blood glucose levels are significant because insulin therapy may be needed to maintain normoglycemia in mechanically ventilated patients. A randomized study has shown that regulating blood glucose levels between 80 and 110 mg/dL reduced ICU mortality rates when compared with conventional treatments.33

The most important aspect of initial hemodynamic management is to prevent and treat hypotension, particularly in cases of high-level SCI where hypotension is most common. Treatment with early fluid resuscitation, while avoiding fluid overload, is employed to maintain tissue perfusion. Once intravascular volume is restored, vasopressors may be used to constrict the blood vessels to treat hypotension.34 Fluids and vasopressors are administered to maintain a mean arterial pressure of 85 mm Hg for up to 7 days, and the initial base deficit or lactate level may be useful when determining the need for ongoing fluid resuscitation.35,36 It is important to raise the blood pressure as soon as possible to improve neurologic recovery, especially in brain-injured patients with reduced cerebral perfusion.37 A number of experimental models suggest improved outcomes after spinal cord blood flow is maximized by paying careful attention to systemic resuscitation.38,39

Neurogenic shock results from inadequate circulating fluid or blood volume due to loss of vascular tone, pooling of blood in the periphery, and third spacing of fluids. Hypotension and systematic vascular resistance, which may be less than 50% of normal, along with an inconsistent heart rate response, are indications of neurogenic shock.40 However, other injuries should still be investigated as possible causes of hypotension. Neurogenic shock occurs secondary to sympathetic denervation and, when combined with unopposed vagal activity, results in diminished myocardial contractility and bradycardia.

Due to decreased systematic vascular resistance, fluid resuscitation alone may be insufficient to restore normal blood pressure, and pressor agents are frequently required to offset the loss of sympathetic tone and give chronotropic support to the heart. An ideal agent should include both α- and β-adrenergic agonists, such as dopamine, norepinephrine, or epinephrine. On occasion, however, these agents produce a paradoxical effect by decreasing cardiac output and by secondarily decreasing tissue perfusion. Vasopressors should also be chosen as to minimize the exacerbation of bradycardia.

Another manifestation of sympathetic denervation is orthostatic hypotension. Children seem particularly predisposed to this problem. Raising an SCI patient abruptly from the supine to the upright position may result in a significant drop in blood pressure because of an inability to regulate vascular tone. Thus, once the patient has medical and spinal stability, mobilization often requires gradual progressive elevation with elastic stockings, elastic wraps, and abdominal binders.

Deep Venous Thrombosis and Pulmonary Embolism

Deep venous thrombosis (DVT) is another common complication associated with acute SCI. Venous pooling secondary to decreased vascular resistance, combined with a lack of muscle contraction, are the primary factors in its occurrence. Because DVT may not be clinically overt, a high index of clinical suspicion is required, and these patients are best treated with aggressive preventive measures. DVT is dangerous because it can lead to a catastrophic pulmonary embolism (PE), which is fatal in approximately 4% of acutely hospitalized patients. Venous thromboembolism (VTE) has been reported in 6% of more than 16,000 admitted patients with SCI according to California hospital discharge data, and without prophylaxis it is likely to develop in at least 50%.41 VTE is infrequent in children, and PE has rarely been reported after pediatric SCI.

Early after SCI, it is beneficial to apply a mechanical compression device. Mechanical compression decreases the likelihood of blood clotting by increasing venous outflow and reducing venous stasis.42 Despite being relatively ineffective in high-risk patients, compression devices are very safe and should therefore be implemented in all patients with acute SCI.43

Anticoagulation with low-molecular-weight heparin (30 mg enoxaparin SC every 12 hours) or unfractionated heparin (5000 units every 8 hours) with intermittent pneumatic compression, administered once primary hemostasis is apparent is the mainstay of prophylaxis. Enoxoparin is the preferred low-molecular-weight heparin because the incidence of PE and major bleeding was infrequent in the Spinal Cord Injury Thromboprophylaxis Investigators enoxaparin study.44 Bleeding should be stabilized before anticoagulants are administered, and potential contraindications include intracranial bleeding, perispinal hematoma, and hemothorax.

The clinical diagnosis of DVT is difficult to establish, and therefore some surgeons advocate the routine use of venous Doppler ultrasonography. Such studies have a 90% accuracy rate in detecting significant venous thrombosis.

An increased vigilance for the possibility of PE should be maintained once DVT is established, because signs and symptoms may be absent or misleading. Fever is often the first manifestation, because SCI patients may not be able to perceive pleuritic pain or mount a tachycardic and tachypneic response to altered pulmonary perfusion. Because of the unreliability of chest radiography and ventilation-perfusion scans in diagnosing PE, pulmonary CT is most often necessary.

If anticoagulation is not possible because active bleeding is expected to continue for 72 hours, a vena cava filter should be considered. However, 26% to 36% of patients with permanent filters eventually developed DVT according to a long-term follow-up study.45,46 Additionally, a vena cava filter can be a complication for patients with a manually assisted coughing machine because the filter can dislodge when bronchial secretions are cleared.47,48 To avoid these filter-related complications, a change to pharmacologic prophylaxis is appropriate if the patient’s risk of bleeding decreases.

Gastrointestinal Considerations

Gastrointestinal concerns in the SCI patient vary from minimizing gastric and abdominal distension and stress ulcerations to providing nutrition and bowel retraining.

The simplest and most effective means of preventing most acute GI complications is by using nasogastric suction. Gastric atony and paralytic ileus may compromise respiratory function by further decreasing lung capacity or by leading to vomiting and aspiration.

The primary GI concerns for SCI patients are GI bleeding and stress ulceration, which usually occur within the first 4 weeks of injury. The risk of ulceration can be minimized by maintaining a gastric pH above 4. Ranitidine is a histamine H2-receptor antagonist (H2RA) that inhibits stomach acid production. It is administered for stress ulcer prophylaxis because it decreases the risk of GI bleeding without increasing the likelihood of ventilator-associated pneumonia or altering the gastric pH.49 Another option is the use of proton pump inhibitors (PPIs), which block the final common pathway in acid secretion as opposed to H2RAs, which only block one of three pathways. PPIs are as effective as H2RAs in preventing upper GI bleeding and more effective for maintaining a pH above 4 for critically ill patients requiring mechanical ventilation.50 Nevertheless, both options are safe ways to suppress acid levels and prevent stress-related mucosal disease.

More severe and life-threatening acute abdominal complications, such as splenic rupture or liver lacerations, or chronic complications, such as bowel obstruction or perforation or other similar conditions, may be obscured because of a lack of pain perception after SCI. Occasionally, vague pain may be appreciated secondary to autonomic visceral afferent branches that are conducted into the spinal cord via the splanchnic nerves. Also, if the SCI is not above the C5 level, referred pain secondary to diaphragmatic irritation may be felt in the shoulder region. Other signs of ongoing abdominal complications, such as temperature elevation, elevated white blood cell count, or associated ileus are not reliable signs for the identification of abdominal disease in these patients. Similarly, clinical examination may be misleading because localized abdominal tenderness, muscle guarding, and rigidity are likely to be absent, even though peritonitis may be present. Thus, it must be recognized that patients with SCI can develop such abdominal complications. The patient should be observed carefully for any indirect signs that may point to an ongoing acute abdominal problem.51

Because SCI patients are hypermetabolic and hypercatabolic acutely, enteral nutrition should be provided for the patient once swallowing is evaluated, resuscitation is complete, and there is no evidence of ongoing shock or hypoperfusion. Enteral feeding is advised because it has a lower incidence of infection and hyperglycemia than parenteral feeding methods.52,53 The patient’s caloric needs during rehabilitation are usually 45% to 90% of the calculated values and are lower for tetraplegics than for paraplegics.54 The need for caloric support decreases progressively as the SCI patient recovers.

Bowel retraining is a critical component of GI management and should be begun early after injury due to the patient’s loss of colonic motility and sacral reflexes. Appropriate procedures for a bowel program can be chosen based on the bulbocavernosus reflex. This reflex is an indicator of upper versus lower motor neuron bowel dysfunction. An effective daily bowel regimen can be implemented using oral medications, suppositories, and digital stimulation.55

Urologic Considerations

SCI patients often have the neurologic loss of the ability to void due to the sudden loss of autonomic control. Placement of an indwelling urinary catheter is recommended no later than in the emergency department when IV fluids are initiated in order to monitor urinary output during the early period of hypotension and third fluid spacing. However, the longer the need for an indwelling catheter, the greater the risk of urinary tract infection. Thus, the catheter may be removed once the patient is hemodynamically stable and strict monitoring of fluid status is no longer necessary. If the use of an indwelling urinary catheter is contraindicated, emergent suprapubic drainage will suffice.

Some situations require additional input from a urologist, such as if the patient suffered a urethral injury. For any pelvic fracture or penetrating injury near the urethra, instrumentation such as a urinary catheter should be avoided as it can exacerbate urethral injury. Also, priapism is common during the early period after SCI, but a urethral catheter may still be used, and usually no special treatment is required.

Depending on the level of the SCI, the bladder may be areflexic and flaccid or dyssynergic and spastic. With an areflexic bladder, voiding may be accomplished by using abdominal pressure—the Credé maneuver. However, if residual urine remains high, this maneuver should be supplemented by clean, intermittent catheterization.56 With a spastic bladder, spontaneous voiding is possible as long as the intravesicular pressure is not too high and there is no overriding sphincter spasticity. In this situation, at least in men, an external condom catheter is acceptable.57 If the pressure is too high or if the sphincter is spastic, pharmacologic intervention may be helpful. The bladder musculature may be relaxed with anticholinergics such as propantheline or smooth muscle relaxants such as oxybutynin.

Pediatric SCI regimens for bladder management depend on the age, gender, size, and weight of the child and the type of bladder. Fluid intake and output are crucial in establishing programs and schedules. In infants and toddlers, for whom the use of diapers is appropriate, one should ensure adequate emptying of the bladder. With school-aged children, diapers are no longer appropriate, and their continued use may be detrimental to the child’s self-esteem and self-image. Clean intermittent catheterization is an alternative and can be instituted at any age.

Psychological and Rehabilitation Issues

Not only does SCI create a physical disability but it is a severe psychological stress on both the patient and family members. Because this stress may not be readily appreciated initially, it is important to provide appropriate levels of psychiatric support and counseling within a few days of SCI. The patient’s mental health status should be regularly assessed, paying attention to depression, posttraumatic stress disorder, life stressors, and any suicidal ideations. It is constructive to foster effective coping strategies, promote healthy behaviors, acknowledge the patient’s suffering, and treat for any underlying causes for depression. For some patients who become rapidly depressed because of their physical limitations, the use of antidepressant medications may be appropriate. Any treatment refusal or requests for withdrawal from treatment are serious matters, and the patient’s decision-making capabilities should be evaluated under these circumstances.

Additionally, SCI rehabilitation aims to facilitate maximal neurologic recovery while helping the individual develop compensatory strategies for the neurologic loss. The involvement of a rehabilitation specialist, beginning early after injury, is beneficial for the treatment of an SCI patient. Protocols for physical therapy, occupational therapy, and speech and language pathology should be developed and initiated early to ensure the efficiency and effectiveness of the rehabilitation process.

References

1. Guidelines for the management of acute cervical and spinal cord injuries. Neurosurgery. 2002;50(3):S1.

2. Bracken M.B., Collins W.F., Freeman D.F., et al. Efficacy of methylprednisolone in acute spinal cord injury. JAMA. 1984;251(1):45-52.

3. Bracken M.B., Shepard M.J., Collins W.F., et al. A randomized, controlled trial of methyl prednisolone or naloxone in the treatment of acute spinal cord injury. Result of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322(20):1405-1411.

4. Bracken M.B., Shepard M.J., Holford T.R., et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. JAMA. 1997;277(20):1597-1604.

5. Hurlbert R.J. Methylprednisolone for acute spinal cord injury: an inappropriate standard of care. J Neurosurg. 2000;93(1):1-7.

6. Hurlbert R.J. Strategies of medical intervention in the management of acute spinal cord injury. Spine (Phila Pa 1976). 2006;31(11):S16-S21.

7. Coleman W.P., Benzel D., Cahill D.W., et al. A critical appraisal of the reporting of the National Acute Spinal Cord Injury Studies (II and III) of methylprednisolone in acute spinal cord injury. J Spinal Disord. 2000;13(3):185-199.

8. Short D.J., El Masry W.S., Jones P.W. High-dose methylprednisolone in the management of acute spinal cord injury: a systematic review from a clinical perspective. Spinal Cord. 2000;38(5):273-286.

9. Baptiste D., Tighe A., Fehlings M.G. Spinal cord injury and neural repair: focus on neuroregenerative approaches for spinal cord injury. Expert Opin Investig Drugs. 2009;18(5):663-673.

10. Tator C.H., Duncan E.G., Edmons V.E., et al. Neurological recovery, mortality, and length of stay after acute spinal cord injury associated with changes in management. Paraplegia. 1995;33:254-262.

11. Jackson A.B., Groomes T.E. Incidence of respiratory complications following spinal cord injury. Arch Phys Med Rehabil. 1994;75(3):270-275.

12. Kocan M.J. Pulmonary considerations in the critical care phase. Crit Care Clin North Am. 1990;2:369-374.

13. Ledsome J.R., Sharp J.M. Pulmonary function and acute cervical cord injury. Am Rev Respir Dis. 1981;124:41-44.

14. Scalea T.M., Rodriguez A., Chiu W.C., et al. Focused assessment with sonography for trauma (FAST): Results from an international consensus conference. J Trauma. 1999;46(3):466-472.

15. Farahmand N., Sirlin C.B., Brown M.A., et al. Hypotensive patients with blunt abdominal trauma: performance of screening US. Radiology. 2005;235(2):436-443.

16. Brown M.A., Casola G., Sirlin C.B., et al. Blunt abdominal trauma: screening use in 2,693 patients. Radiology. 2001;218(2):352-358.

17. Estenne M., DeTroyer A. Respiratory muscle involvement in tetraplegia. Tobin M., editor. Problems in respiratory care: the respiratory muscles. Philadelphia: JB Lippincott. 1990;vol 3:360-374.

18. Mansel J.K., Norman J.R. Respiratory complications in management of spinal cord injuries. Chest. 1990;97:1440-1452.

19. Bach J.R. Update and perspectives on noninvasive respiratory muscle aids. Part 2: The expiratory aids. Chest. 1994;105:1538-1544.

20. Garstang S.V., Kirshblum S.C., Wood K.E. Patient preference for in-exsufflation for secretion management with spinal cord injury. J Spinal Cord Med. 2000;23(2):80-85.

21. Estenne M., DeTroyer A. Mechanism of the postural dependence of vital capacity in tetraplegic subjects. Am Rev Respir Dis. 1987;135:367-371.

22. Gronert G.A., Theye R.A. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology. 1975;43(1):89-99.

23. Griffiths J., Barber V.S., Morgan L., Young J.D. Systematic review and meta-analysis of studies of the timing of tracheostomy in adult patients undergoing artificial ventilation. BMJ. 2005;330:1243.

24. Consortium for Spinal Cord Medicine. Respiratory management following spinal cord injury: a clinical practice guideline for health-care professionals. Washington, DC: Paralyzed Veterans of America; 2005.

25. Peterson W., Charlifue W., Gerhart A., Whiteneck G. Two methods of weaning persons with quadriplegia from mechanical ventilators. Paraplegia. 1994;32(2):98-103.

26. Weber R.K. Respiratory management of acute cervical cord injuries. In: Tator C.H., editor. Early management of acute spinal injury. Philadelphia: Lippincott-Raven; 1982:195-215.

27. Drakulovic M.B., Torres A., Bauer T.T., et al. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial. Lancet. 1999;354:1851-1858.

28. Dries D.J., McGonigal M.D., Malian M.S., et al. Protocol-driven ventilator weaning reduces use of mechanical ventilation, rate of early reintubation, and ventilator-associated pneumonia. J Trauma. 2004;56:943-951. discussion 951–952

29. Kress J.P., Pohlman A.S., O’Connor M.F., Hall J.B. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med. 2000;342:1471-1477.

30. Fishburn M.J., Marino R.J., DiTunno J.F. Atelectasis and pneumonia in acute spinal cord damaged patients: a retrospective study of 44 patients. Paraplegia. 1990;24:208-220.

31. Lehman K.G., Lane J.G., Piepmeir J.M. Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course, and severity. J Am Coll Cardiol. 1987;10:46-56.

32. Meincke F.W. Regulation of the cardiovascular system in patients with fresh injuries to the spinal cord. Paraplegia. 1971;9:109-112.

33. Van den Berghe G., Wouters P., Weekers F., et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;345:1359-1367.

34. Stevens S., Bhardwaj A., Kirsch J., Mirski M. Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol. 2003;15(3):215-229.

35. Levi L., Wolf A., Belzberg H. Hemodynamic parameters in patients with acute cervical cord trauma. Description, intervention, and prediction of outcome. Neurosurgery. 1993;33:1007-1016.

36. Vale F.L., Burns J., Jackson A.B., Hadley M.N. Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. J Neurosurg. 1997;87:239-246.

37. Chesnut R.M., Marshall S.B., Piek J., et al. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochir Suppl. 1993;59:121-125.

38. Ducker T.B., Salcman M., Perot P.L., et al. Experimental spinal cord trauma. I: Correlation of blood flow, tissue oxygen, and neurologic status in the dog. Surg Neurol. 1978;10:60-62.

39. Guha A., Tator C.H. Acute cardiovascular effects of experimental spinal cord injury. J Trauma. 1988;28:481-490.

40. Bilello J.F., Davis J.W., Cunningham M.A., et al. Cervical spinal cord injury and the need for cardiovascular intervention. Arch Surg. 2003;138:1127-1129.

41. Jones T., Ugalde V., Franks P., et al. Venous thromboembolism after spinal cord injury: incidence, time course, and associated risk factors in 16,240 adults and children. Arch Phys Med Rehabil. 2005;86:2240-2247.

42. Geerts W.H., Pineo G.F., Heit J.A., et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004;126:338S-400S.

43. Winemiller M.H., Stolp-Smith K.A., Silverstein M.D., Therneau T.M. Prevention of venous thromboembolism in patients with spinal cord injury: effects of sequential pneumatic compression and heparin. J Spinal Cord Med. 1999;22:182-191.

44. Spinal Cord Injury Thromboprophylaxis Investigators. Prevention of venous thromboembolism in the acute treatment phase after spinal cord injury: a randomized, multicenter trial comparing low-dose heparin plus intermittent pneumatic compression with enoxaparin. J Trauma. 2003;54:1116-1124.

45. Duperier T., Mosenthal A., Swan K.G., Kaul S. Acute complications associated with greenfield filter insertion in high-risk trauma patients. J Trauma. 2003;54:545-549.

46. Prepic Study Group. Eight-year follow-up of patients with permanent vena cava filters in the prevention of pulmonary embolism: the PREPIC (Prevention du Risque d’Embolie Pulmonaire par Interruption Cave) randomized study. Circulation. 2005;112:416-422.

47. Rogers F.B., Cipolle M.D., Velmahos G., et al. Practice management guidelines for the prevention of venous thromboembolism in trauma patients: the EAST practice management guidelines work group. J Trauma. 2002;53:142-164.

48. Wilson J.T., Rogers F.B., Wald S.L., et al. Prophylactic vena cava filter insertion in patients with traumatic spinal cord injury: preliminary results. Neurosurgery. 1994;35:234-239.

49. Cook D., Guyatt G., Marshall J., et al. A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Canadian Critical Care Trials Group. N Engl J Med. 1998;338(12):791-797.

50. Conrad S.A., Gabrielli A., Margolis B., et al. Randomized, double-blind comparison of immediate-release omeprazole oral suspension versus intravenous cimetidine for the prevention of upper gastrointestinal bleeding in critically ill patients. Crit Care Med. 2005;33(4):760-765.

51. Charney K.J., Juler G.I., Comarr A.E. General surgery problems in patients with spinal cord injuries. Arch Surg. 1975;110:1083-1088.

52. Gramlich L., Kichian K., Pinilla J., et al. Does enteral nutrition compared to parenteral nutrition result in better outcomes in critically ill adult patients? A systematic review of the literature. Nutrition. 2004;20(10):843-848.

53. Heyland D.K., Dhaliwal R., Drover J.W., et al. Canadian Critical Care Clinical Practice Guidelines Committee. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients. JPEN J Parenter Enteral Nutr. 2003;27(5):355-373.

54. Cox S.A., Weiss S.M., Posuniak E.A., et al. Energy expenditure after spinal cord injury: an evaluation of stable rehabilitating patients. J Trauma. 1985;25(5):419-423.

55. Spinal Cord Medicine Consortium. Clinical practice guidelines: neurogenic bowel management in adults with spinal cord injury. J Spinal Cord Med. 1998;21(3):248-293.

56. Barkin M., Dolfin D., Herschorn S., et al. The urologic care of the spinal cord injured patient. J Urol. 1983;129:335-339.

57. Herschorn S., Gerridzen R.G. The management of the nerogenic bladder. In: Bloch R.F., Basbaum M., editors. Management of spinal cord injuries. Baltimore: Williams & Wilkins, 1986.

58. Consortium for Spinal Cord Medicine. Pressure ulcer prevention and treatment following spinal cord injury: a clinical practice guideline for health-care professionals. Washington, DC: Paralyzed Veterans of America; 2000.