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Anesthesia for adults with chronic spinal cord injury

Anesthesia for adults with chronic spinal cord injury
Literature review current through: Aug 2023.
This topic last updated: Oct 20, 2022.

INTRODUCTION — Spinal cord injury (SCI) produces a wide variety of changes in systemic physiology that can lead to complications over time. Patients with chronic spinal cord dysfunction often require anesthesia for urologic, orthopedic, and plastic surgical procedures.

For the purpose of this discussion, chronic injury will be defined as the condition beyond several weeks after injury.

This topic discusses the anesthetic management of patients with chronic SCI. Anesthesia for patients with acute SCI and the chronic complications of patients with SCI are discussed separately. (See "Anesthesia for adults with acute spinal cord injury" and "Chronic complications of spinal cord injury and disease".)

PREOPERATIVE EVALUATION — A medical history and anesthesia-directed physical examination should be performed for all patients who undergo anesthesia. For these patients, we focus the evaluation on the diverse systemic complications that can occur with SCI and that can affect anesthetic management.

Chronic complications of SCI of particular concern for anesthesia are discussed here; other complications are discussed more fully separately. (See "Chronic complications of spinal cord injury and disease".)

Cardiovascular complications

Autonomic dysreflexia — Patients with high SCI are at risk for autonomic dysreflexia (AD) and may require deep general anesthesia or regional anesthesia, even without sensory function at the surgical site. (See 'Management of intraoperative autonomic dysreflexia' below.)

Occurring in 20 to 70 percent of patients with SCI above T6, AD is an exaggerated sympathetic response to a stimulus below the SCI level. AD is manifested by diffuse vasoconstriction below the level of SCI and hypertension producing headache, diaphoresis, brady- or tachycardia, and other symptoms. The noxious stimulus is most commonly a distended viscus, usually the bladder; however, constipation, pain from pressure sores, and other stimuli may be problematic in some patients. SCI lesions lower than T6 do not produce this complication. AD is discussed in more detail separately. (See "Chronic complications of spinal cord injury and disease", section on 'Autonomic dysreflexia'.)

A history of AD episodes should be sought preoperatively, including inciting events, treatment regimens, and prior surgical and anesthesia histories.

Coronary artery disease — Risk factors for coronary artery disease (CAD) are more prevalent in patients with chronic SCI, and the prevalence of CAD is 3 to 10 times higher in patients with SCI compared with the general population [1]. In addition, patients with high SCI may exhibit atypical chest pain or other symptoms as a result of cardiac ischemia. Therefore, SCI should lower the threshold to perform preoperative pharmacologic stress testing, especially before major surgery, and these patients should have appropriately aggressive individualized diagnostic workup.

Others — The autonomic dysfunction that results from SCI disrupts normal cardiovascular homeostasis, separate from AD. In patients with SCI above T6, baseline blood pressure (BP) is usually reduced, and baseline heart rate (HR) may be as low as 50 to 60 beats/minute (bpm) [1,2]. In addition, these patients are often hypovolemic, and approximately 50 percent are anemic [3].

A reduction in the dose of anesthetic agents and/or administration of vasoactive medication may be required to avoid hypotension [4]. Orthostatic hypotension may persist beyond the acute injury phase; these patients may not tolerate quick changes in position during surgery or the head-up position for preoxygenation prior to airway management.

Autonomic dysfunction also results in impaired thermoregulation. Patients are at risk for hypothermia, or for hyperthermia with the use of warming devices [5,6].

Pulmonary complications — Cervical and high thoracic SCI affect respiratory muscles. The likelihood of pulmonary complications depends on the level and completeness of SCI, with a greater risk in persons with higher and neurologically more complete SCI [7,8]. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Respiratory insufficiency'.)

Pulmonary issues of particular concern when patients require anesthesia include the following:

Pulmonary infection – Because of impaired cough and difficulty mobilizing lung secretions, patients with SCI are at increased risk for pneumonia.

Reduced lung volumes – Lung volumes for patients with chronic SCI may deteriorate over time. A survey study of men at least one year after SCI reported that increasing body mass index (BMI) and longer time since injury were associated with decreases in all measured lung volumes [9]. These patients may desaturate quickly with apnea during induction of anesthesia.

Assisted ventilation – Patients who retain adequate bulbar function after SCI may require a variety of assisted ventilation techniques, including noninvasive positive pressure ventilation (PPV), mechanical cough assist, glossopharyngeal breathing, and abdominal respirators. A plan for the perioperative management of these devices should be made in advance. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Cervical cord injury with intact bulbar function'.)

For patients with an intact phrenic nerve, either phrenic nerve pacing or percutaneous diaphragmatic pacing may allow independence from a ventilator [10]. Perioperative management of these devices should be coordinated with the clinician managing the device.

The specific methods of assisted ventilation must be considered when planning airway management, emergence from anesthesia, and postoperative care.

Musculoskeletal complications — Contractures are common after SCI and can complicate positioning for surgery. Muscle spasms are common after SCI and may be precipitated by cutaneous or proprioceptive stimuli.

General or regional anesthesia may be necessary to control spasms during surgery, even for patients with complete lack of sensation at the operative site. (See "Chronic complications of spinal cord injury and disease", section on 'Musculoskeletal complications' and 'Choice of anesthetic technique' below.)

Pressure ulcers — Skin breakdown and pressure ulceration can occur with relatively brief immobility, as might occur during operative procedures. Patients should be examined preoperatively for signs of existing or impending skin breakdown, with particular attention to bony prominences. Patients should be positioned and moved carefully, with adequate padding, avoiding shear forces, friction, and wet linens. (See "Chronic complications of spinal cord injury and disease", section on 'Pressure ulcers'.)

Chronic pain — A significant number of patients develop a chronic pain syndrome several months to years after SCI. On average, two-thirds of patients suffer chronic pain [11,12]. Treatment regimens may be complicated and may include opioids and other medications that affect the response to anesthetics and the plan for postoperative pain management. Management of pain syndromes in patients with chronic spinal cord injury is discussed separately. (See "Chronic complications of spinal cord injury and disease", section on 'Pain syndromes'.)  

Airway evaluation — Airway management in patients with chronic SCI may be more challenging for those who have undergone cervical fusion for spine stabilization. In particular, decreased range of neck motion may make direct laryngoscopy more difficult. Alternative devices for endotracheal intubation should be readily available. (See "Management of the difficult airway for general anesthesia in adults", section on 'Planning the airway management approach'.)

ANESTHESIA MANAGEMENT

Choice of anesthetic technique — The choice of anesthetic technique depends on the level of SCI, remaining sensory function, and the surgical procedure. Many patients with chronic SCI undergo anesthesia repeatedly; they often have a preference and know what has worked well in the past. In particular, both general and spinal anesthesia can effectively prevent autonomic dysreflexia (AD) in response to surgery.

General anesthesia may be preferable for patients who cannot tolerate lying flat, who have upper extremity muscle spasms, contractures that make positioning difficult, or high anxiety.

For patients at risk for, or with a history of, AD, or for those with lower extremity muscle spasms, either general or regional anesthesia may be used.

For patients without sensation at the surgical site and who are not at risk for AD (ie, SCI below T6 and no history of AD), monitored anesthesia care with or without sedation is an option.

For patients with incomplete sensory loss without risk for AD or spasms, local anesthesia or peripheral nerve block may be adequate for surgery.

Monitoring — In most cases, monitoring for anesthesia for patients with chronic SCI should be performed as it would be for patients without SCI, determined by the surgical procedure and other comorbidities.

Continuous intraarterial pressure monitoring may be appropriate for patients with a history of severe AD, allowing immediate response to hemodynamic changes, and the use of potent vasodilators.

Premedication — Patients with high SCI may be more sensitive to sedative medications than those without SCI. We do not routinely premedicate these patients with sedatives, and when we do, we titrate the dose to effect (eg, midazolam, 0.5-mg intravenous [IV] increments).

General anesthesia

Induction of anesthesia — Induction of anesthesia with IV medication is appropriate for most adults who require general anesthesia. Rarely, induction is performed with inhalation of a volatile anesthetic. Choice of induction agents relates to the plan for airway management, as well as other patient factors.

Induction agents — The choice of induction agent for general anesthesia is determined by factors other than the patient's SCI. (See "General anesthesia: Intravenous induction agents".)

However, patients with thoracic and cervical SCI are more sensitive to induction agents than non-injured patients and are at risk for hypotension with induction of anesthesia, which may be a result of direct effects of induction agents, hypovolemia [13], reduced muscle mass, and reduced sympathetic and baroreceptor activity [14]. We administer a fluid bolus prior to induction of anesthesia (500 to 1000 mL Ringer's lactate) and reduce the dose of induction agents. (See "General anesthesia: Intravenous induction agents", section on 'Dosing considerations'.)

We connect a vasopressor infusion to the IV line and often start a low dose (eg, phenylephrine 20 to 40 mcg/minute) prior to or with induction as prophylaxis for hypotension if the patient is not bradycardic, as phenylephrine usually causes reflex bradycardia. For bradycardic patients, we often administer ephedrine 5 to 15 mg or glycopyrrolate 0.2 to 0.4 mg IV with or without phenylephrine to prevent hypotension.

Neuromuscular blocking agents — We avoid succinylcholine in patients with SCI that has been present longer than 48 hours. Alternatives to succinylcholine include nondepolarizing neuromuscular blocking agents (NMBAs) or intubation with remifentanil. The choice of NMBA may be affected by neuromonitoring for spine surgery. (See "Rapid sequence induction and intubation (RSII) for anesthesia", section on 'Neuromuscular blocking agents (NMBAs)' and "Neuromonitoring in surgery and anesthesia", section on 'Neuromuscular blocking agents'.)

While succinylcholine causes a transient increase in serum potassium level of approximately 0.5 mEq/L in normal patients, it can cause life-threatening, severe hyperkalemia in patients with SCI after 48 to 72 hours postinjury [15]. Potassium levels of 11 to 13 mEq/L have been reported with succinylcholine in quadriplegic patients [16-19]. We avoid succinylcholine after 48 hours after SCI. (See "Neuromuscular blocking agents (NMBAs) for rapid sequence intubation in adults for emergency medicine and critical care", section on 'Contraindications and side effects'.)

Airway management — Patients who have undergone cervical spine stabilization surgery may have restricted range of motion of the neck and may be at risk for difficult airway management. The choice of airway management device should be made as it would be for non-injured patients.

If the patient has a tracheostomy, a cuffed tracheostomy device should be used, or the device should be replaced with a flexible cuffed endotracheal tube (ETT) inserted directly into the stoma. (See "Management of the difficult airway for general anesthesia in adults" and "Airway management for induction of general anesthesia".)

Maintenance of anesthesia — Choice of medications for maintenance of general anesthesia depends on patient factors and the planned procedure. (See "Maintenance of general anesthesia: Overview", section on 'Inhalation anesthetic agents and techniques'.)

Patients with chronic SCI may be more sensitive to the vasodilatory and myocardial depressant effects of both IV and inhalation anesthetics, a result of relative hypovolemia [13] and reduced sympathetic and baroreceptor responses [14]. A processed electroencephalogram (EEG) monitor to help guide the dose of anesthetic agents may be useful if the anesthetic concentration is significantly below the level typically considered safe to prevent awareness (eg, 0.7 to 0.8 minimum alveolar concentration [MAC]). (See "Accidental awareness during general anesthesia", section on 'End-tidal anesthetic concentration'.)

Emergence from anesthesia — After general anesthesia, NMBAs should be fully reversed, documented by a peripheral nerve stimulator. Importantly, neuromuscular monitoring should not be performed on a paralyzed limb. Facial nerve monitoring may be required for patients with high SCI and ulnar nerve paralysis (see "Monitoring neuromuscular blockade", section on 'Paralyzed limb'). Patients with high SCI should be fully awake with adequate tidal volumes before extubation. Patients with ventilatory compromise may require bilevel positive airway pressure ventilation (BIPAP) or continuous positive airway pressure (CPAP) to support ventilation until they are back to baseline function after anesthesia. Respiratory mechanics may be best in the supine or slightly-head-up position.

Regional anesthesia — Regional anesthesia is an alternative to general anesthesia for lower abdominal and extremity surgery. Peripheral nerve block may be appropriate for minor procedures on the upper or lower extremities, with the usual indications and contraindications. (See "Overview of peripheral nerve blocks".)

Spinal anesthesia may be used, especially for the urologic procedures that are commonly performed for patients with chronic SCI. Spinal anesthesia can effectively prevent autonomic dysfunction. The level of spinal block may be difficult to determine in patients with high spinal cord lesions, though in practice, a standard dose of spinal drug usually results in an acceptable block. (See "Spinal anesthesia: Technique", section on 'Choice of spinal drugs'.)

Hypotension from spinal anesthesia-induced sympathectomy does not seem to occur in these patients [20], perhaps because of their baseline low sympathetic tone.

Epidural anesthesia is less appropriate than spinal anesthesia for patients with SCI. With epidural anesthesia, sacral anesthesia may be unreliable, and patchy block is possible, especially when there are spinal deformities. There are reports of failure of epidural anesthesia to prevent AD [21]. Also, sensory deficits may complicate interpretation of the epidural test dose; total spinal has been reported in this setting.

Positioning for surgery — Positioning for patients with SCI requires meticulous attention to detail. These patients are at high risk for pressure injury of skin and bony prominences during even relatively brief procedures. Pressure points should be padded, as should all plastic connectors and other parts of IV tubing and monitoring devices. Positioning may be challenging for patients with contractures.

Hemodynamic management — The following section discusses general hemodynamic management for patients with chronic SCI. Management of intraoperative autonomic dysreflexia is discussed separately. (See 'Management of intraoperative autonomic dysreflexia' below.)

Goal blood pressure (BP) – We aim to maintain mean arterial pressure within 20 to 25 percent of baseline for patients with chronic SCI during anesthesia in order to maintain spinal cord and coronary perfusion. However, data to support specific BP goals for these patients are lacking.

The majority of neurologic recovery after SCI occurs within the first three to six months postinjury, but a small proportion of patients will have late recovery of function out to five years, particularly with incomplete SCI [22].

Patients with chronic SCI are at high risk for coronary artery disease, and may be asymptomatic. We maintain a high index of suspicion for cardiovascular disease.

Fluid management Patients with high thoracic or cervical spinal cord lesions may be hypovolemic and anemic, and may be unable to compensate for even modest blood loss with an increase in sympathetic activity. Preloading with volume prior to induction and diligent replacement of blood loss are important for maintaining adequate cardiac output. Their loss of baroreceptor activity also makes them more susceptible to hypotension with positive pressure ventilation (PPV).

Vasoactive medications – In addition to volume resuscitation, vasoactive medications are often required during anesthesia for patients with SCI. With injury above the cardioaccelerator sympathetic innervation (T1 to T4), vasopressors with inotropic and chronotropic properties in addition to vasoconstriction (ie, dopamine, norepinephrine, epinephrine) are often required to treat hypotension. With lower spinal injuries, peripheral sympathectomy and vasodilation often require treatment with a pure vasoconstrictor (eg, phenylephrine). (See "Use of vasopressors and inotropes".)

Vasodilators are usually required to treat episodes of autonomic dysreflexia.

Vagal tone – The increase in vagal tone that is common with acute SCI may persist and may increase the risk of bradycardia with airway manipulation and tracheal suctioning. Therefore, an adequate depth of anesthesia should be achieved prior to intubation or suctioning. We often pretreat with a vagolytic medication (eg, glycopyrrolate 0.2 to 0.4 mg IV) prior to endotracheal suctioning if the patient has a history of significant bradycardia with airway manipulation.

Management of intraoperative autonomic dysreflexia — AD may occur intraoperatively, despite what appears to be adequate anesthesia, and should be treated rapidly. Signs and symptoms of AD may include the following (table 1):

Sudden hypertension – Systolic BP can rapidly rise to >200 mmHg.

Dysrhythmias – Bradycardia, tachycardia, heart block, and sinus arrest are all possible.

Cutaneous changes – Typically, vasoconstriction occurs with blanching below the spinal lesion and with vasodilation, flushing, and sweating above the lesion.

Headache and nasal congestion Awake patients may complain of headache and nasal congestion.

Cardiovascular effects – With severe AD – especially in patients with cardiovascular comorbidities – myocardial ischemia, myocardial infarction, and acute left heart failure can occur.

Neurologic complications Intracranial hemorrhage and seizures are possible.

Treatment includes the following:

Remove inciting stimulus Surgery should be paused; if appropriate, relieve distention of hollow viscus (ie, the bladder should be emptied, endoscope removed).

Deepen anesthesia – For patients under general anesthesia, administer a bolus of propofol or deepen the inhalation agent.

Position head up – Tip the operating table head-up to take advantage of orthostatic BP drop.

Administer 100 percent oxygen Increase the fraction of inspired oxygen (FiO2) until AD is resolved.

Administer a vasodilator Administer a rapid-onset, short-acting vasodilator to avoid hypotension when AD resolves:

Nicardipine 0.2 to 0.5 mg IV bolus with nicardipine infusion (2.5 to 15 mg/hour), or

Nitroglycerin infusion (5 mcg/minute to 200 to 500 mcg/minute), or

For severe hypertension, nitroprusside infusion (0.2 to 10 mcg/kg/minute). The hypotensive effects of nitrates (ie, nitroglycerin and nitroprusside) may be exaggerated in patients who are using sildenafil for erectile dysfunction.

Longer acting vasodilators may be administered cautiously; hypotension may occur once the AD event resolves. Options include:

Hydralazine 5 mg IV every 10 minutes, titrated to effect, up to 20 mg total dose

or

Labetalol 5 mg every 5 minutes, titrated to effect, up to 50 mg total dose; beta blockers may exacerbate AD related bradycardia

Treat arrhythmias Treat arrhythmias as necessary with beta blockers, anticholinergics, and advanced cardiac life support (ACLS) medications.

Treat myocardial ischemia – Treat ST and T-wave changes on electrocardiogram (ECG) as necessary (eg, with nitroglycerin infusion).

Invasive monitoring – An arterial catheter should be placed for continuous BP monitoring if AD does not resolve quickly.

In most cases, rapid treatment, pause in surgery, and deepening anesthesia resolves the AD event quickly. However, severe complications such as intracranial hemorrhage, acute heart failure, and death can occur.

Temperature control — Patients with SCI are at risk for hypothermia during anesthesia and in a cold operating room (OR) or, less commonly, hyperthermia with overly aggressive warming measures. Temperature should be monitored during and after anesthesia. Warm air blankets and fluid warming should be used intraoperatively and may be continued into the recovery period. (See "Perioperative temperature management".)

POSTOPERATIVE CARE — Patients with chronic SCI may require extended recovery room stay to allow for blood pressure (BP), breathing and airway, and temperature stabilization, as well as control of postoperative pain. If ongoing vasodilator infusion is required, the patient should be transferred to the intensive care unit (ICU).

Autonomic dysreflexia may occur in the postoperative period, most often related to bladder distention. (See 'Management of intraoperative autonomic dysreflexia' above.)

The plan for postoperative pain control must be individualized and will be affected by the surgical procedure, the level of sensory impairment, and preoperative chronic use of opioids. In many cases, a multimodal approach to pain management will be appropriate. (See "Approach to the management of acute pain in adults".)

ANALGESIA FOR LABOR AND DELIVERY — Pregnant patients with high SCI are at risk for autonomic dysreflexia (AD) with distention or irritation of the cervix, vagina, bowel, or bladder during labor contractions. Women with SCI below T11 will be able to perceive labor pain, while those with lesions at T5 to T10 may have painless delivery. Symptoms of AD may be the only signs of labor for patients with high SCI. In addition to malignant hypertension with the risk of intracranial hemorrhage and hypertensive encephalopathy, AD during labor may lead to uteroplacental vasoconstriction and fetal hypoxia. (See "Neurologic disorders complicating pregnancy", section on 'Spinal cord injury'.)

These patients should have an antepartum consultation with an anesthesiologist to develop a plan for labor analgesia. Epidural analgesia should be established early or before labor and may be challenging because of contractures, spasms, or prior spine surgery. Continuous spinal, combined spinal-epidural (CSE), and epidural techniques have all been used successfully for parturients at risk for, or who have developed, AD. Patients with SCI above T6 require either general or regional anesthesia for cesarean delivery to prevent AD. Regional anesthesia should be continued in the postpartum period until hemodynamics are stable, as postpartum uterine contractions may elicit an AD response. (See "Neuraxial analgesia for labor and delivery (including instrumented delivery)" and "Anesthesia for cesarean delivery".)

Monitoring during labor and delivery for parturients with high SCI should include continual blood pressure (BP) and electrocardiographic (ECG) monitoring. There should be a low threshold to place an arterial catheter to monitor BP; the decision to use invasive BP monitoring must be individualized based on the degree of hemodynamic lability, the progress of labor, the patient's history of AD, and comorbidities.

If AD occurs during labor and delivery, treatment options include:

Optimizing epidural or intrathecal anesthesia

Head-up positioning to take advantage of orthostasis

Hydralazine (5 to 20 mg intravenously [IV], titrated to effect), or

Sublingual nitroglycerin (0.3 mg) or nitroglycerin infusion (5 mcg/minute to 200 to 500 mcg/minute), or

Nicardipine bolus (0.2 to 0.5 mg IV) or nicardipine infusion (2.5 to 15 mg/hour)

Nitroglycerin and nicardipine may decrease uterine tone and increase uterine hemorrhage [23]. Nitroprusside is relatively contraindicated since it may cause fetal cyanide intoxication. Magnesium has been used successfully in a case of AD during labor [24].

Severe uncontrolled hypertension with AD may be an indication for emergency cesarean delivery under general anesthesia. (See 'Management of intraoperative autonomic dysreflexia' above.)

SUMMARY AND RECOMMENDATIONS

Preoperative evaluation

Spinal cord injury (SCI) results in a wide variety of complications over time, many of which affect anesthetic management. (See 'Preoperative evaluation' above.)

Patients with SCI above approximately T6 are at risk for autonomic dysreflexia (AD), which consists of a potentially life-threatening, exaggerated sympathetic response to stimulus below the level of the spinal injury (table 1). Patients who are at risk for AD require anesthesia, even with complete loss of sensation at the surgical site, to prevent AD. (See 'Autonomic dysreflexia' above.)

Choice of anesthetic technique

Patients without sensation at the surgical site, with SCI below T6, and with no history of AD may require no anesthesia, or monitored anesthesia care. (See 'Choice of anesthetic technique' above.)

Patients who are at risk for AD require anesthesia, even with complete loss of sensation at the surgical site, to prevent AD. Either general anesthesia or regional anesthesia may be used for lower abdominal or lower extremity surgery for patients at risk for AD. (See 'Autonomic dysreflexia' above.)

Intraoperative management

Patients with high SCI are often hypovolemic and are more sensitive to the sedative and cardiodepressant effects of anesthetic induction agents. We administer an intravenous (IV) fluid bolus prior to induction and reduce the dose of induction agent. (See 'Induction of anesthesia' above.)

Succinylcholine can cause severe hyperkalemia after approximately three days after SCI. We avoid succinylcholine after 48 hours after injury. (See 'Neuromuscular blocking agents' above.)

Blood pressure (BP) should be managed carefully in patients with chronic SCI to maintain spinal cord and coronary perfusion. We aim for a mean arterial pressure within 20 to 25 percent of baseline. (See 'Hemodynamic management' above.)

Autonomic dysreflexia

Intraoperative AD may be a life-threatening emergency that requires immediate recognition and treatment (table 1). (See 'Management of intraoperative autonomic dysreflexia' above.)

Patients with SCI above T6 are at high risk for AD during labor and delivery. Epidural, combined spinal–epidural (CSE), or continuous spinal should be established early in labor for these patients. Patients with SCI above T6 need general anesthesia or neuraxial anesthesia for cesarean delivery to prevent AD. (See 'Analgesia for labor and delivery' above.)

  1. Myers J, Lee M, Kiratli J. Cardiovascular disease in spinal cord injury: an overview of prevalence, risk, evaluation, and management. Am J Phys Med Rehabil 2007; 86:142.
  2. McKinley WO, Gittler MS, Kirshblum SC, et al. Spinal cord injury medicine. 2. Medical complications after spinal cord injury: Identification and management. Arch Phys Med Rehabil 2002; 83:S58.
  3. Perkash A, Brown M. Anemia in patients with traumatic spinal cord injury. J Am Paraplegia Soc 1986; 9:10.
  4. Yoo K, Hwang J, Jeong S, et al. Anesthetic requirements and stress hormone responses in spinal cord-injured patients undergoing surgery below the level of injury. Anesth Analg 2006; 102:1223.
  5. Khan S, Plummer M, Martinez-Arizala A, Banovac K. Hypothermia in patients with chronic spinal cord injury. J Spinal Cord Med 2007; 30:27.
  6. Schmidt KD, Chan CW. Thermoregulation and fever in normal persons and in those with spinal cord injuries. Mayo Clin Proc 1992; 67:469.
  7. Jackson AB, Groomes TE. Incidence of respiratory complications following spinal cord injury. Arch Phys Med Rehabil 1994; 75:270.
  8. Cotton BA, Pryor JP, Chinwalla I, et al. Respiratory complications and mortality risk associated with thoracic spine injury. J Trauma 2005; 59:1400.
  9. Stepp EL, Brown R, Tun CG, et al. Determinants of lung volumes in chronic spinal cord injury. Arch Phys Med Rehabil 2008; 89:1499.
  10. Dalal K, DiMarco AF. Diaphragmatic pacing in spinal cord injury. Phys Med Rehabil Clin N Am 2014; 25:619.
  11. Burchiel KJ, Hsu FP. Pain and spasticity after spinal cord injury: mechanisms and treatment. Spine (Phila Pa 1976) 2001; 26:S146.
  12. Siddall PJ, Loeser JD. Pain following spinal cord injury. Spinal Cord 2001; 39:63.
  13. Houtman S, Oeseburg B, Hopman MT. Blood volume and hemoglobin after spinal cord injury. Am J Phys Med Rehabil 2000; 79:260.
  14. Yoo KY, Jeong CW, Kim SJ, et al. Cardiovascular and arousal responses to laryngoscopy and tracheal intubation in patients with complete spinal cord injury. Br J Anaesth 2009; 102:69.
  15. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology 2006; 104:158.
  16. Stone WA, Beach TP, Hamelberg W. Succinylcholine-induced hyperkalemia in dogs with transected sciatic nerves or spinal cords. Anesthesiology 1970; 32:515.
  17. Tobey RE. Paraplegia, succinylcholine and cardiac arrest. Anesthesiology 1970; 32:359.
  18. Carter JG, Sokoll MD, Gergis SD. Effect of spinal cord transection on neuromuscular function in the rat. Anesthesiology 1981; 55:542.
  19. John DA, Tobey RE, Homer LD, Rice CL. Onset of succinylcholine-induced hyperkalemia following denervation. Anesthesiology 1976; 45:294.
  20. Barker I, Alderson J, Lydon M, Franks CI. Cardiovascular effects of spinal subarachnoid anaesthesia. A study in patients with chronic spinal cord injuries. Anaesthesia 1985; 40:533.
  21. Schonwald G, Fish KJ, Perkash I. Cardiovascular complications during anesthesia in chronic spinal cord injured patients. Anesthesiology 1981; 55:550.
  22. Kirshblum S, Millis S, McKinley W, Tulsky D. Late neurologic recovery after traumatic spinal cord injury. Arch Phys Med Rehabil 2004; 85:1811.
  23. Vadhera RB, Pacheco LD, Hankins GD. Acute antihypertensive therapy in pregnancy-induced hypertension: is nicardipine the answer? Am J Perinatol 2009; 26:495.
  24. Maehama T, Izena H, Kanazawa K. Management of autonomic hyperreflexia with magnesium sulfate during labor in a woman with spinal cord injury. Am J Obstet Gynecol 2000; 183:492.
Topic 104423 Version 15.0

References

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