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I. General considerations

Spinal anatomy and physiology
Structure
1. The vertebral column consists of 33 superimposed vertebrae that are divided into 7 cervical (C), 12 thoracic (T), 5 lumbar (L), 5 sacral (fused), and 4 coccygeal (fused) bones. Each individual vertebra (Figure-1) is composed of a ventral vertebral body and a dorsal bony neural arch formed from a pedicle on either side of the vertebral body, both of which join with the lamina posteriorly to form the spinous process. The posterior vertebral body, pedicles, and lamina form the vertebral foramen. The neural laminar arches bear lateral transverse processes and superior and inferior articular facets.
2. The vertebral column is stabilized (from posterior to anterior) by the supraspinous, interspinal, ligamentum flavum, posterior longitudinal, and anterior longitudinal ligaments (Figure-1). The ligaments provide flexibility and limit excessive movement that could damage the spinal cord.
3. The spinal cord begins at the foramen magnum and terminates at the conus medullaris (L2 in adults). Below the termination of the spinal cord, the lumbar and sacral roots form the cauda equina. The spinal cord is surrounded by the meninges, layers of tissue including the dura mater and arachnoid membranes which have cerebrospinal fluid (CSF) between them. This provides additional protection for the spinal cord. The anterior portion of the cord gives rise to the motor nerves. Nerves that originate posteriorly are sensory in function.
Blood supply
1. Anterior spinal artery. A single vessel, formed from the union of the two anterior spinal branches of the vertebral arteries, descends down the entire length of the anterior portion of the spinal cord. This artery supplies perfusion to the anterior 75% of the cord including the anterior column and most of the lateral column.

 

Figure-1. A: View of a typical vertebra from above; B: Lateral view; C: Ligaments of the spine.

Posterior spinal arteries. Two vessels originating from the posterior inferior cerebellar arteries supply the posterior 25% of the cord including the entire posterior column and the balance of the lateral column.
Radicular arteries. These vessels originate from branches of the vertebral, deep cervical, intercostal, and lumbar arteries. They anastomose with the anterior and posterior spinal arteries. The artery of Adamkiewicz (arteria radicularis magna), the major radicular artery, is most commonly located in the lower thoracic or upper lumbar region and provides most of the blood supply to the lower cord.
Regulation of blood flow (Figure-2). Autoregulation maintains spinal cord blood flow (SCBF) by altering vascular resistance in response to changes in mean arterial pressure (MAP).
1. Normal autoregulation exists for a MAP between 50 and 150 mm Hg.
2. Failure of autoregulation at a MAP of <50 mm Hg leads to ischemia.
 

Figure -2. Illustration of effect of changes in Paco2, Pao2, and mean arterial pressure (MAP) on spinal cord blood flow (SCBF)

3. At a MAP of >150 mm Hg, the increased flow leads to tissue edema and disruption.
4. The autoregulatory range of individuals who have chronic hypertension is shifted to the right (higher range of MAP).
5. Alterations in the partial pressure of carbon dioxide (Paco2) and oxygen (Pao2) disrupt autoregulation in the spinal cord much as they do in the brain. Between 20 and 80 mm Hg, SCBF is linearly related to Paco2. SCBF is well maintained at varying degrees of oxygenation until Pao2 falls to 50 mm Hg; below this value, SCBF increases as oxygenation decreases further.

II. Spinal cord injury (SCI)

Introduction. In the United States, 11,000 new cases of SCI occur each year. The annual incidence of traumatic SCI is approximately 40 cases per million population, with an estimated prevalence approaching 250,000 cases. SCI in the United States remains more common in males than in females by a 4:1 ratio. Early mortality is around 50% with <10% of survivors experiencing neurologic improvement. Accordingly, the perioperative care of patients during the acute phase of injury is extremely important. Perioperative strategies that prevent further injury, limit the extension of the existing injury, or salvage even a few dermatomal levels can have a significant influence on morbidity, mortality, long-term disability, quality of life, and health care costs.
The distribution of SCI consists of incomplete tetraplegia, 29.5%; complete paraplegia, 27.9%; incomplete paraplegia, 21.3%; and complete tetraplegia, 18.5%. Common causes of SCI include motor vehicle accidents (40% to 56%), falls (15% to 20%), violence (5% to 20%), sports injuries (5% to 16%), and other causes (5% to 10%). Most injuries occur at the mid-cervical (C4-6, C5 most common) or thoracolumbar (T12) region and are often associated with concomitant injuries. Surgical treatment for SCI is aimed at immobilization, medical stabilization, spinal alignment, operative decompression, and spinal stabilization. The focus here is directed on the perioperative care of the patient who has acute SCI or is at risk for it. It also discusses specific issues pertaining to the intermediate or chronic phase of injury.
Pathogenic correlates of SCI
Primary SCI, caused by the mechanical forces of the trauma, results in direct neuronal disruption and destruction, petechial hemorrhages, and hematomyelia. Histologic changes consist of hemorrhage and protein extravasation into the central gray matter, which spread to the adjacent white matter. The traumatized areas then undergo cavitating necrosis and ultimately glial scar formation. Spinal cord edema is maximal at 3 days and can persist for 2 weeks. Rarely does physical transection of the spinal cord occur.
Secondary SCI is caused by the activation of biochemical, enzymatic, and microvascular processes in proportion to the severity of the initial lesion. Damage results from progressive hemorrhagic necrosis, loss of cellular membrane integrity, edema, inflammation, arachidonic acid release, lipid peroxidation, and loss of vascular autoregulation. These processes lead to vascular stasis, decreased blood flow, ischemia, and cell death.
Anatomical correlates of SCI. (Table-1) Flexion injuries cause anterior subluxation or fracture-dislocations of the vertebral bodies. Hyperextension is associated with transverse fractures of the vertebra, disruption of the anterior longitudinal ligaments, and posterior dislocations. Vertical compression produces burst fractures and ligamentous rupture. Rotational injuries result in fractures of the vertebral peduncles and facets. The designation of a SCI as stable or unstable considers the potential for furthering spinal injury or failure to heal properly if left untreated.

Table -1. Spinal injury, clinical finding, and indicated treatment

Spinal Injury Clinical Finding Treatment
Atlanto-occipital dislocation Usually unstable; commonly fatal Reduction, immobilization, fusion
Atlantoaxial injury
Isolated atlas fracture Usually stable/no neurologic injury Philadelphia collar
Isolated odontoid fracture Usually neurologically intact Immobilization
Displaced fracture C1-2 Commonly fatal or quadriplegic Immobilization and reduction
Posterior subluxation C1-2 Usually neurologically intact Immobilization
Axis pedicle fracture Can be neurologically intact Immobilization
Hyperflexion dislocation C3-T1 Any subluxation is unstable If neurologic deficit, decompression
Dislocated facets Neurologically variable Traction and surgery
Flexion-rotation injuries Neurologically variable Surgical reduction and fusion if anterior subluxation and jumped facet
Compression fractures C3-T1
Wedge compression/burst fractures Frequent neurologic damage Surgical decompression
Teardrop fractures (vertebra dislocated anteriorly with inferior vertebral fracture) Usually unstable Posterior fusion
Hyperextension injuries Geriatric patients with spondylosis producing central cord syndrome Immobilization; if significant spinal canal narrowing, decompression
Thoracic spine injuries Incomplete neurologic injury most common Realignment and stabilization
Thoracolumbar injuries Neurologic deficits complex Decompression and fusion
Lumbar injuries Incomplete neurologic injury Realignment and decompression
Penetrating injuries Neurologic deficit variable Decompression/foreign body removal


Clinical correlates of SCI. SCI can result in either complete (total loss of sensory and motor function distal to the injury) or incomplete (presence of any nonreflex function distal to the injury; Table-2) loss of neurologic function. Complete SCI has less than a 10% chance of total return of normal neurologic function. Incomplete SCI has a 59% to 75% chance of recovering lost function. Table-3 details the range of cardiac and respiratory dysfunction, depending on the site of acute SCI. Medical problems include these:
Cardiovascular
1. Spinal shock
2. Bradycardia
3. Myocardial contractility
4. Deep venous thrombosis
5. Hypothermia
Respiratory
1. Respiratory impairment
2. Poor cough
3. Viscous mucous
Gastrointestinal
1. Atony
2. Prone to aspiration
Genitourinary
1. Bladder distension
2. Infection
Electrolytes
1. Hypercalcemia
2. Hyperphosphatemia
3. Hyponatremia
4. Hyperkalemia

 

Table-2. Incomplete spinal cord injury syndromes

Syndrome Clinical Findings
Anterior cord syndrome Motor, sensory, temperature and pain lost; vibration/position intact
Central cord syndrome Motor impairment of upper more than lower extremities
Posterior cord syndrome Loss of fine, vibratory, and position sensation; preserved motor function
Brown-Sequard (hemicord) syndrome Ipsilateral paralysis, loss of proprioception, touch, and vibration; contralateral loss of pain and temperature
Conus medullaris syndrome Areflexic bladder, bowel, and lower extremities; sacral reflexes can be preserved; reduced rectal tone and perirectal sensation
Cauda equina syndrome Sensory loss with flaccid weakness; sacral reflexes abnormal or absent

The effect of SCI on the cardiovascular system depends on the level of injury (Table-3). For levels of SCI below T6, the major problem involves varying degrees of hypotension resulting from the functional sympathectomy. With complete SCI above T6, more significant cardiovascular abnormalities including bradycardia, hypotension, ventricular dysfunction, and dysrhythmias are encountered.
Spinal shock, seen most commonly with physiologic or anatomic transection of the spinal cord above C7, results from a total loss of impulses from higher centers as an immediate consequence of the injury.

 

Table-3. Level of spinal cord injury and pulmonary/cardiac function

Level of Spinal Cord Injury Pulmonary Function Ventilatory Function Cough Cardiovascular Function Sympathetic Function Cardiovascular Reserve
C1-2 0 0 Minimal Minimal
C3-4 0 0 Minimal Minimal
C5-6 + + Minimal Minimal
C7 + to ++ + to ++ Minimal +
High thoracic ++ ++ + to ++ ++
Low thoracic ++ to +++ ++ to +++ ++ to +++ ++ to +++
Lumbar +++ +++ +++ +++
Sacral +++ +++ +++ +++
Scale is 0 (no function) to +++ (normal).

1. Spinal shock is characterized by flaccid paralysis, loss of reflexes below the level of the lesion, paralytic ileus, and loss of visceral and somatic sensation, vascular tone, and the vasopressor reflex.
2. This syndrome of autonomic dysfunction and loss of sensory and motor function lasts from days to weeks and is prolonged by serious infection.
3. Neurogenic shock is manifest by hypotension, bradycardia, and hypothermia. The higher the spinal level of injury, the more severe the physiologic derangements. Shock occurs from the disruption of the sympathetic outflow from T1-L2, which results in unopposed vagal tone and vasodilatation with pooling of blood in the peripheral vascular beds. The most common cardiovascular abnormalities encountered after an acute cervical SCI and the associated incidence are listed in the following table.

 

Tabel-4. Cardiovascular derangement in neurogenic shock

Marked bradycardia (<45 beats/minute) 71%
Episodic hypotension 68%
Need for intravenous pressors 35%
Use of atropine or temporary transvenous pacemaker 29%
Primary cardiac arrest 16%

These cardiovascular derangements remain most problematic during the first 2 weeks after acute cervical SCI.
(1) Bradycardia, universal with acute complete cervical SCI, results from a functional sympathectomy with interruption of cardiac accelerator nerves (T1-4) and unopposed vagal innervation. Bradycardia usually resolves over a 2- to 6-week period. More profound degrees of bradycardia, as well as cardiac arrest, can occur during stimulation of the patient (e.g., turning the patient, performing tracheal suctioning). Familiarity with the factors precipitating bradycardia lead to the use of preventive interventions (sedation, anticholinergics, 100% oxygen before suctioning, and limiting the time allowed for suctioning). Although the bradycardia is effectively treated with atropine in most cases, a temporary pacemaker can be required.
(2) Hypotension, defined as a systolic blood pressure (BP) below 90 mm Hg or 30% below baseline, is seen in 60% to 80% of patients after acute cervical SCI. Early intervention to maintain the MAP at 85 mm Hg for the first 7 days after injury is recommended to preserve neurologic function while autoregulation is impaired. The heart rate is useful in differentiating between neurogenic shock, manifest by the triad of bradycardia, hypotension, and hypothermia, and hemorrhagic shock as the cause of tachycardia. Hypovolemia from coexisting hemorrhagic shock in patients who also have spinal shock is treated with prompt blood replacement and administration of isotonic crystalloid. The total volume of fluid administered is limited because pulmonary edema and cardiac decompensation can occur, especially in the setting of high SCI.
(a) If hypotension persists despite adequate fluid administration, vasopressor therapy should be instituted. The vasopressor should have beta-agonist properties (e.g., dopamine or dobutamine). Supplementation with an alpha-agonist such as phenylephrine could be necessary. However, care is indicated when choosing a more potent alpha-agonist, such as norepinephrine, which can substantially increase cardiac afterload, impair cardiac output, and precipitate frank left ventricular failure.
(b) Invasive central hemodynamic monitoring is recommended in high SCI as an aid in guiding the clinical management of hypotension. A pulmonary artery occlusion pressure of 14 to 18 mm Hg appears to optimize spinal cord perfusion. In patients who have suffered multiple trauma, hypotension and bradycardia secondary to neurogenic shock can conceal hemorrhagic shock. Operative intervention for spinal injury should be postponed until the patient's hemodynamic status has been optimized.
Disturbances of cardiac rhythm are commonly observed in SCI and include bradycardia, primary asystole, supraventricular dysrhythmias (atrial fibrillation, reentry supraventricular tachycardia), and ventricular dysrhythmias. An acute autonomic imbalance resulting from a disruption of sympathetic pathways in the cervical cord is causative. The arrhythmias usually resolve within 14 days of injury.
Left ventricular impairment has been noted in complete cervical SCI and is attributed to the functional sympathectomy with resulting autonomic imbalance.
Autonomic hyperreflexia occurs in 85% of patients who have spinal cord transections above T6. This clinical constellation is secondary to autonomic vascular reflexes, which usually begin to appear approximately 1 to 3 weeks after injury (when spinal shock has resolved).
1. Afferent impulses originating from cutaneous, proprioceptive, and visceral stimuli (bladder or bowel distention, childbirth, manipulations of the urinary tract, or surgical stimulation) are transmitted to the isolated spinal cord. They, in turn, elicit a massive sympathetic response from the adrenal medulla and sympathetic nervous system, which is no longer modulated by the normal inhibitory impulses from the brain stem and hypothalamus. Vasoconstriction occurs below the level of the spinal cord lesion. Reflex activity of carotid and aortic baroreceptors produces vasodilatation above the lesion, which is often accompanied by bradycardia, ventricular dysrhythmias, and even complete heart block.
2. Common signs and symptoms include hypertension, bradycardia, hyperreflexia, muscle rigidity and spasticity, diaphoresis, pallor, flushing above the lesion, and headache. Horner's syndrome, pupillary changes, anxiety, and nausea occur less frequently. Systolic pressures in excess of 260 mm Hg and diastolic pressures of 220 mm Hg have been reported.
3. Adverse sequelae include myocardial ischemia, intracranial hemorrhage, pulmonary edema, seizures, coma, and death.
4. Treatment involves cessation of the offending stimulus and a change to the upright position (pooling of blood in the lower extremities). Pharmacologic intervention includes direct-acting vasodilators (e.g., sodium nitroprusside), beta-blocking drugs (e.g., esmolol), combination alpha- and beta-blocking drugs (e.g., labetalol), calcium-channel blocking drugs, and ganglionic blocking drugs. Because the attacks are often paroxysmal, drugs of rapid onset and short duration are preferred.
Acute care of the patient after SCI. Preservation of spinal cord function involves maintaining oxygen delivery, stabilizing the spine, and decreasing spinal cord edema and the secondary biochemical processes that exacerbate the neurologic injury. The initial care of the patient after SCI can be considered in the following areas:
External splinting and immobilization. The spine is immobilized in the field by placing the patient on a spine board with sandbags on either side of the head to prevent rotation.
Medical management. Identification of associated injuries is crucial. These include the following:
1. Cervical Spine Injury
a. Head
b. Airway
c. Esophagus
2. Lumbar Spine Injury
a. Abdominal
b. Pelvic
3. Thoracic Spine Injury
a. Myocardial
b. Pulmonary
c. Ribs
d. Major vascular
Airway
(1) SCI presents several problems in airway management. Many maneuvers used for intubation can cause displacement and worsening of the injury, especially at the level of the cervical spine (C-spine). For this reason, all patients who have head trauma, multiple trauma, or decreased level of consciousness should be considered as having a spinal injury until proved otherwise radiographically (see Figure -3 for the algorithm for airway management for suspected C-spine injury).
(2) Patients who have a normal level of consciousness, an intact "gag reflex" and a patent airway can be managed conservatively with supplemental oxygen. However, these patients should be observed closely to detect progressive loss of ventilatory ability as a result of developing diaphragmatic or intercostal paralysis. Because profound reductions in forced vital capacity (FVC) and expiratory flow rates are observed immediately after injury, nearly all patients who have an acute cervical SCI require mechanical ventilation within 24 to 48 hours of hospital admission.
(3) The initial airway management of the C-spine injured patient includes consideration of the following issues:
(a) The urgency of airway intervention
(b) The presence of associated facial, neck, or soft tissue injuries

 

Figure-3. Airway management algorithm for the patient who has suspected C-spine injury.

(c) The presence of basilar skull fracture or midface fractures that contraindicate nasal intubation
(d) The status of the patient, whether awake or not
(e) The skill of the operator in using different airway techniques
(4) Direct laryngoscopy remains the method of choice for emergent airway control in patients who have confirmed or possible C-spine injuries. Mouth opening for laryngoscopy can be facilitated by removing the cervical collar, and neck movement can be minimized by manual in-line stabilization without axial traction. Manual in-line stabilization can in fact result in more movement of unstable structures lower in the neck. Manual in-line stabilization can sometimes make a difficult intubation more difficult. Cricoid pressure can be utilized to reduce the risk of pulmonary aspiration of gastric contents.
(5) Blind nasal intubation is commonly recommended for airway management. The benefit of this technique is minimal head movement. Potential disadvantages include an extended period of time to perform and trauma to the nasal passage. Nasotracheal intubation is contraindicated in the presence of a basilar skull fracture or extensive facial trauma.
(6) Fiberoptic intubation is appropriate in nonemergent situations in which the airway is free of blood and stomach contents. This technique can facilitate intubation of the larynx with the least amount of neck movement.
(7) In patients who have particularly difficult airways, a catheter passed through a needle inserted into the cricothyroid membrane ("retrograde intubation") and directed out the nose or mouth can also serve as a guide for intubation. Cricothyroidotomy is also an appropriate choice for an anatomically abnormal airway in an emergent situation.
(8) Flexion and extension of the neck during maintenance of the airway and intubation could lead to catastrophic exacerbation of the SCI. Therefore, in-line manual stabilization should be carefully utilized when traditional laryngoscopy proves necessary. This is accomplished by having an assistant hold the sides of the neck and the mastoid process, preventing any movement of the neck. The airway can be opened with a "jaw thrust" technique while the head is maintained in a neutral position without either flexion or extension.
(9) Because of gastric atony and paralytic ileus, SCI patients are considered to have "full stomachs" and are at increased risk for aspiration. Therefore, airway adjuncts such as the laryngeal mask, although helpful in maintaining oxygenation in a situation in which intubation has proven difficult, should not be relied on as a long-term solution. Cricoid pressure is administered with minimum force to avoid inadvertent further injury to the cord. As the application of cricoid pressure can cause neck displacement of up to 9 mm, the risk of causing or exacerbating C-spine injury should be weighed against the risk of pulmonary aspiration. Although excessive movement of the spine is to be avoided, hypoxia secondary to a failure to intubate worsens the prognosis even more so that intubation should be accomplished as expeditiously as possible.
(10) A brief neurologic examination after intubation reveals any further deterioration in the patient's neurologic condition related to manipulation of the airway or positioning in preparation for intubation.
Pulmonary system. SCI can have a profound effect on the respiratory system, depending on the level and degree of injury, because of paralysis of the abdominal, intercostal, diaphragmatic, and accessory muscles. Problems include respiratory failure, recurrent lobar atelectasis, hypoventilation, ventilation-perfusion mismatching, pulmonary edema (neurogenic, cardiogenic), bacterial pneumonia, aspiration pneumonitis, and coexisting blunt chest trauma.
(1) Respiratory failure is present in nearly all patients with SCI above C7. The resultant abnormality in respiratory mechanics leads to a reduction in lung volume (tidal volume, expiratory reserve volume, functional residual capacity), impairment of respiratory function (decreased FVC, forced expiratory volume in 1 second [FEV1], peak forces, peak flows), and retention of pulmonary secretions with progressive hypoxemia and CO2 retention. In addition, patients can have abdominal distention secondary to gastric atony, which further impairs pulmonary function. Even patients whose weakness does not extend above the abdominal muscles are at risk for abnormal respiratory function because of their inability to clear secretions.
(2) Patients require frequent assessment of respiratory function because significant declines in pulmonary reserve can occur before overt clinical signs of respiratory failure are seen. It is particularly important to perform serial measurements of vital capacity (VC) and negative inspiratory force. When the VC decreases to <50% of predicted, more frequent serial determinations of VC must be made (i.e., every 6 hours). When the VC decreases to <1 L, especially if the patient is dyspneic and hypoxemic, endotracheal intubation should be performed.
(3) The aim of mechanical ventilation in this scenario is to incorporate spontaneous patient effort into the respiratory dynamic so as to maintain diaphragmatic muscle mass. The combination of synchronized intermittent mandatory ventilation with pressure support will achieve this goal.
(a) Positive end-expiratory pressure is added, beginning with 5 cm H2O, to recruit collapsed alveoli and prevent further atelectasis. Choosing intermittent "sigh" breaths (e.g., 1 to 2 "sigh" breaths per minute at 10 mL/kg) can also enhance alveolar recruitment.
(b) Weaning from mechanical ventilation after cervical SCI is facilitated by the respiratory muscles' development of spasticity at approximately 3 weeks. Spasticity of the respiratory muscles stabilizes the chest wall sufficiently to improve lung volume and overall ventilatory ability. The VC doubles in volume within 5 weeks of injury in patients whose injuries are at the C4-5 level. Respiratory dynamics in the supine position improve owing to the more cephalad position of the diaphragm. This position is therefore used when weaning.
(4) Lobar atelectasis, common in SCI above C7, requires aggressive pulmonary therapy emphasizing the prevention, recognition, and treatment of secretion retention. Instituted at the time of hospitalization, this regimen includes frequent nasotracheal suctioning, frequent repositioning or rotational beds (i.e., continuous lateral rotation to 45), chest percussion, bronchodilator therapy, deep breathing exercises, incentive spirometry, and assisted coughing. Even with the most aggressive pulmonary care and management, retained secretions result in repeated lobar collapse during the first 2 weeks of hospitalization. Therapeutic bronchoscopy is frequently required during this period.
(5) Pulmonary edema is observed in patients who have acute SCI. Neurogenic causes include intracranial hypertension with high cervical cord injury and increases in extravascular lung water secondary to autonomic dysfunction with sympathetic discharge at the time of injury. Cardiogenic pulmonary edema could also occur because of reduced myocardial inotropy and overzealous fluid administration.
Meticulous fluid management guided by central monitoring is essential in limiting pulmonary complications.
(6) Pneumonia is observed in 70% of cervical and high thoracic spinal cord injuries. Pneumonia can develop from aspiration of gastric contents at the time of the initial injury or can occur later from nosocomial bacterial infection.
(7) Chest trauma resulting in hemothorax, pulmonary contusions, pneumothorax, and rib fractures could be present in patients who have sustained SCI. These injuries often necessitate prolonged mechanical ventilation with difficulty in weaning and delayed operative intervention to stabilize the spine.
Cardiovascular support. For the first few minutes after SCI, a brief and substantial autonomic discharge from direct compression of sympathetic nerves occurs. This results in severe hypertension and arrhythmias and can cause left ventricular failure, myocardial infarction, and pulmonary capillary leak. This transient phase is usually no longer evident by the time the patient reaches the hospital when hypotension from neurogenic shock and traumatic hypovolemia is commonly seen.
Gastrointestinal (GI) tract. During the acute stages of SCI, the GI tract loses autonomic neural input and becomes atonic. Intestinal ileus (especially after thoracic and lumbar SCI) and gastric atony can cause gastric distention and place the patient at risk for aspiration. Moreover, the dilatation can also cause upward pressure on the diaphragm, adversely affecting ventilation. Insertion of a nasogastric tube limits distention and reduces the risk of regurgitation.
(1) Because hypochloremic metabolic alkalosis can occur with excessive gastric suctioning, careful monitoring of fluid and electrolyte balance must be provided.
(2) Gastritis and gastric ulceration and hemorrhage can occur after SCI, especially in patients requiring mechanical ventilation or as a result of administration of corticosteroids. Preventive techniques include monitoring gastric pH and the use of antacids or H2 blocking drugs.
(3) Other diseases occurring in critically ill patients after SCI include pancreatitis, acalculous cholecystitis, and gastric perforation (especially in those receiving high-dose steroids).
(4) Patients who have acute SCI are characteristically catabolic. Therefore, the initiation of nutritional supplementation within the first few days after injury is advised.
Genitourinary. During the acute stages of SCI, the bladder is flaccid. Insertion of a latex-free (to prevent the development of latex allergy) indwelling urinary catheter is often necessary. Adequate hydration is likely if urinary volume is >0.5 mL/kg/hour in the absence of renal dysfunction.
(1) Bladder flaccidity is followed by bladder spasticity. The abnormalities of bladder emptying predispose the patient to recurrent urinary tract infections, bladder stones, nephrocalcinosis, and recurrent urosepsis.
(2) Although an indwelling drainage catheter is required during the initial 2 to 3 weeks after injury to prevent urinary retention and reflex vagal responses, intermittent straight catheterization of the bladder with latex-free catheters should be instituted as soon as feasible.
(3) Acute renal failure is uncommon but can occur as a result of hypotension, dehydration, sepsis, or associated trauma.
Temperature control. The body temperature of patients who have injuries above C7 tends to approach that of the environment (poikilothermia) owing to the inability to conserve heat in cold environments through vasoconstriction and the inability to sweat in hot ambient conditions. Consequently, these patients are prone to hypothermia if the ambient temperature is lower than normal body temperature. While hypothermia can provide some degree of spinal cord protection, it can also increase the incidence of arrhythmias and prolong the effects of anesthesia. Delayed awakening is problematic because it interferes with prompt neurologic examination.
Deep venous thrombosis (DVT). Without prophylaxis against DVT after acute SCI, patients have an incidence of asymptomatic DVT of 60% to 100%. Venograms become positive within 6 to 8 days after injury. Despite an increased awareness of DVT as a complication of SCI, pulmonary embolism (PE) occurs in 10% to 13% of SCI patients and ranks as the third leading cause of death. Given the high risk of DVT and PE after SCI, a multimodal prophylactic medical management plan is recommended. With effective treatment, the occurrence of DVT can be decreased to 5%. A recent consensus statement on the prevention of DVT in the SCI patient has been published to guide therapy. It includes the following:
(1) Thromboprophylaxis should be provided for all patients after acute SCI.
(2) Single prophylactic modalities such as low-dose unfractionated heparin (LDUH), graduated compression stockings (GCS), and intermittent pneumatic compression (IPC)) should be avoided.
(3) Prophylaxis should be instituted as soon as feasible after primary hemostasis has been ensured. The combination of IPC and either LDUH or low-molecular-weight heparin (LMWH) should be used.
(4) In patients who have an incomplete SCI and evidence of a perispinal hematoma on computed tomographic (CT) scan or magnetic resonance imaging (MRI), the administration of LMWH should be delayed for 1 to 3 days.
(5) IPC and/or GCS should be used when prophylaxis with an anticoagulant is contraindicated.
(6) An inferior vena caval filter should not be used as primary thromboprophylaxis against PE, but should be used when anticoagulation is contraindicated or after a documented PE in a patient already receiving anticoagulant therapy.
(7) During the rehabilitation phase after acute SCI, either LMWH prophylaxis should be continued or the patient should be converted to an oral vitamin K antagonist to achieve an international normalized ratio (INR) of 2 to 3.
(8) DVT prophylaxis should be continued for 3 months.
Neurologic examination. The neurologic examination determines areas that need radiologic evaluation and establishes a baseline for subsequent assessment. The following neurologic examination can be performed quickly and efficiently. A more thorough examination can be performed if indicated.
a. Consciousness. Is the patient alert, oriented, and responsive?
b. Motor system. Function and strength of the major muscle groups are graded with reference to the normal segmental innervation. If possible, cerebellar function can be assessed by having the patient touch finger to nose.
c. Sensory system. This examination includes an assessment of proprioception and the patient's response to light touch and pinprick. Perirectal sensation and the presence of either the bulbocavernosus reflex or the anal-cutaneous reflex are important indicators of the preservation of distal function (sacral sparing), which can mean a more favorable prognosis. A rectal examination is performed to assess voluntary contraction of the anal sphincter. The most caudad level with normal motor and sensory function is designated as the level of injury (Table-5).
d. Cranial nerves. The specific nerves evaluated depend on the patient's level of injury, associated injury, and level of consciousness. The responses most often evaluated include the pupillary reflex, ocular movement, tongue movement, and function of the trigeminal and facial nerves.
e. Reflexes. Commonly tested reflexes include the biceps, triceps, patellar, Achilles, abdominal, cremasteric, and Babinski.
Radiologic evaluation
a. The incidence of cervical spinal injury in comatose trauma patients is 7%. Therefore, radiologic assessment of the spine is essential after traumatic injuries, particularly in those individuals who are either comatose or have signs and symptoms referable to a SCI.
b. Assessment begins with plain X-ray films. The three-view cervical spine series, composed of lateral, anteroposterior, and open-mouth odontoid views, detect most cervical spinal injuries. For C-spine injuries, a useful method of analysis of the plain films addresses the following:
(1) Adequacy and quality of the occipital-cervical junction (C1-2), C3-7, and the C7-T1 junction.
(2) Alignment of the anterior edge of the vertebral body, the posterior edge of the vertebral body, the spinolaminar junction, and the tips of the spinous process (Figure-4).
(3) Bones should be assessed for fractures of the vertebral body, pedicle, lamina, and spinous process.
(4) Cartilage assessment includes analysis of the disk space and the facet joints.
(5) Soft tissue space should be observed for edema and other abnormalities.
As many as 15% to 20% of patients with a C-spine injury do not have an abnormality on the plain film. A more comprehensive radiologic evaluation can be indicated.

 

Table-5. Muscle group with corresponding level of innervation

Injury Level Sensory Deficit Affected Muscle Group
C4 Acromioclavicular joint Diaphragm
C5 Antecubital fossa (lateral) Shoulder rotators and abductors, elbow flexors
C6 Thumb Supinators, pronators, wrist extensors
C7 Middle finger Elbow extensors, wrist flexors
C8 Little finger Finger flexors, distal phalanx
T1 Antecubital fossa (medial) Intrinsic hand muscles
L2 Upper anterior thigh Hip flexors
L3 Medial femoral condyle Knee extensors
L4 Medial malleolus Ankle dorsiflexors
L5 Dorsum of foot Toe extensors
S1 Lateral heel Plantar flexors
S2-5 Popliteal fossa, ischial tuberosity, perianal area Sphincter ani, bulbocavernosus reflex


 

Figure-4. The lateral cervical spine. Spinal column stability after traumatic injury is often based on a system that divides the spine into four longitudinal lines from anterior to posterior, starting with the anterior edge of the vertebral body (AV), the posterior edge of the vertebral body (PV), the spinolaminar junction (SL), and the tips of the spinous process (SP). Each line provides the border for three columns (I, II, and III). Disruption of two or more of these columns indicates spinal instability.


(1) CT scan is helpful to do the following:
(a) Define bony and soft tissue abnormalities
(b) Evaluate the lower C-spine
(c) Measure spinal canal and neuroforaminal diameter
(d) Provide detailed anatomy of the facet joints
(e) Detect hematoma formation
(f) Determine compression of the spinal canal and spinal stability
(g) Detect a unilateral jumped facet or bone fragments in the canal or root foramen
(h) Confirm complete reduction of a dislocation
(i) Demonstrate hyperdense acute blood or retropulsed vertebral body fragments
(2) Axial CT scan through C1 and C2 and through the lower C-spine is indicated in situations in which poorly visualized or suspicious areas are noted on plain films. The negative predictive value of the combination of a normal three-view cervical spine series supplemented with CT scan through areas that are poorly visualized and "suspicious" is 98% to 100%.
(3) MRI is indicated within 48 hours of injury for symptomatic SCI and in comatose trauma patients who can have a cervical spinal injury. MRI is helpful for the following:
(a) Determining the degree of injury to the soft tissue contents of the spinal canal
(b) Identifying ligamentous injury, nerve root compression, and pathologic signals from the spinal cord itself
(c) Predicting functional neurologic outcome in the subacute stage of SCI
(d) Visualizing the epidural and subarachnoid spaces
(e) Detecting elevation of the anterior or posterior longitudinal ligaments
(4) Flexion-extension films performed under fluoroscopic guidance are recommended as an alternative to MRI to evaluate the degree of ligamentous stability in awake patients who have symptoms of cervical spinal injury and in comatose trauma patients.
Neuroprotective strategies
a. Spinal alignment
(1) Studies have shown that movement of the injured segment results in exacerbation of the initial injury. Therefore, an important neuroprotective strategy is to relieve cord compression and ischemia and prevent further neurologic compromise by immediate and effective immobilization of the spine with either tongs or halo traction devices. Failure to accomplish this can lead to either loss of residual neurologic function or even ascension of the patient's level of neurologic injury.
(2) Patients who have unstable injuries are placed in traction to align and immobilize the spine, decompress neural structures, and prevent further injury. Diminished pressure on the cord improves microvascular circulation, which could reduce spinal cord edema. If there is no bony instability, traction is not usually needed for patients who have sustained penetrating injuries.
(3) Thoracic and lumbar fractures and dislocations can initially be stabilized by restricting the patient to bed rest and turning him or her in a log-roll fashion to preserve spinal alignment. Surgical intervention usually stabilizes subluxations in these regions.
b. Surgical reduction and stabilization could be necessary for dislocations that cannot be reduced by traction and/or manipulation because of the nature of the injury. Surgical decompression within the first 2 hours of injury can increase the chances of recovery. The decision as to the timing of surgery after spinal injury depends on these factors:
(1) Assessment of the underlying injury
(2) Failure of medical, manipulative, and bracing procedures to achieve adequate alignment
(3) The documented benefit of early decompression or stabilization of the spine
(4) The presence of progressive neurologic deficits and/or refractory pain
(5) The severity of any coexisting illnesses, infections, or trauma
(6) The documented benefit of earlier patient mobilization and rehabilitation from early surgical intervention (within 8 to 72 hours after injury)
c. Physiologic therapy
(1) Cooling has been shown to be effective in the treatment of SCI. The limitations of the clinical studies are small cohorts and lack of controls. The high mortality is also of concern. The effect of modest hypothermia on spinal recovery after trauma continues to be evaluated, but clinical efficacy in human SCI has demonstrated little benefit thus far. Conversely, hyperthermia is deleterious. Aggressive measures to prevent hyperthermia should be taken to minimize the propagation of secondary neuronal damage after traumatic SCI.
(2) Some advocate hypertension to improve perfusion in the posttraumatic patient who has evidence of impaired autoregulation and hypoperfusion of the spinal cord. Definitive human data are not available. The MAP is maintained in the normal to high-normal range (85 mm Hg) by either volume replacement (nondextrose-containing crystalloid, colloid, or blood products) if hemorrhagic shock predominates or inotropes and vasopressors if neurologic shock is the cause of hypotension. More aggressive achievement of hypertension carries the risk of intramedullary hemorrhage and edema.
(3) Glucose-containing solutions are avoided. Studies in experimental models have shown that even minimally increased blood glucose levels worsen neurologic outcome.
d. Pharmacologic therapy
(1) Corticosteroids administered after acute SCI are currently considered the standard of care. Previous studies have shown that steroids have the potential to stabilize membrane structures, maintain the blood-spinal cord barrier, enhance SCBF, alter electrolyte concentrations at the site of injury, inhibit endorphin release, scavenge damaging free radicals, and limit the inflammatory response after injury.
The current use and dosage of corticosteroids are based on the National Acute Spinal Cord Injury II Study (NASCIS) reported in 1990. This prospective, randomized, placebo-controlled study compared high-dose methylprednisolone (MP) with naloxone and placebo in patients who had complete and incomplete acute SCI. MP, administered within 8 hours of injury as a 30 mg/kg bolus over the first hour and then infused at 5.4 mg/kg/hour for 23 hours, was associated with improvement in motor function and in sensation at 6 months of follow-up as compared to both naloxone and placebo.
The National Acute Spinal Cord Injury III Study, published in 1997, showed that if MP is given within 3 hours of SCI, the steroid infusion need be continued for only 24 hours. If therapy is initiated within 3 and 8 hours of injury, however, the steroid infusion should be administered for 48 hours. Both studies demonstrated an increase in medical complications in steroid-treated patients: longer hospitalizations, increased wound infections, and an increased incidence of pneumonia, GI bleeding, and severe sepsis.
(2) Mannitol, 0.25 to 1 g/kg, can be used to treat cord edema. The ensuing osmotic diuresis necessitates close attention to the patient's intravascular volume.
(3) Hypertonic saline (HS) use in experimental models of acute SCI has suggested that it can enhance the delivery of MP and prevent immunosuppression, leading to improvements in overall neurologic function and survival rates after SCI. No conclusive evidence has yet been published demonstrating similar benefits in human SCI. The use of HS in the setting of acute SCI, therefore, remains largely experimental.
(4) Other pharmacologic agents have been studied in acute SCI as treatment modalities either to limit secondary injury or enhance neurologic recovery. Such agents have included GM1 ganglioside, tirilazad, naloxone, thyrotropin-releasing hormone, and nimodipine. None of these agents has clearly demonstrated an improvement in outcome after acute SCI, and their use is therefore not currently recommended.
Anesthetic management of acute SCI
Preoperative evaluation. The SCI patient frequently has multiple medical complications that can impact the anesthetic plan.
a. Indicated studies include complete blood count, serum electrolytes, blood urea nitrogen, creatinine, glucose, liver function tests, and a urinalysis. A preoperative electrocardiogram (ECG), arterial blood gas, chest x-ray, and pulmonary function tests can also be indicated.
b. Airway evaluation is necessary. Examination of the airway must include the oropharynx with a Mallampati classification and range of motion of the neck with particular attention to any limitation from either pain or neurologic symptoms. If movement elicits any abnormality, the offending position is avoided. Airway problems are most frequently encountered in patients who have atlantoaxial subluxations, traumatic C-spine injuries in combination with facial trauma, severe kyphoscoliosis or spinal deformities, and spinal stabilization devices. When the patient is in a halo brace or other cervical fixation device, plans for either an awake tracheal intubation or other technique to secure the airway should be made.
c. Neurologic evaluation is performed preoperatively to document any preexisting neurologic deficits. Regional anesthesia is chosen only after careful evaluation and review of all preexisting deficits.
d. Pulmonary evaluation must consider the level of SCI. For instance, patients who have a C-spine injury have restrictive pulmonary defects and marked reductions in lung volumes that predispose them to hypoxemia. Injuries of the cervical and high thoracic spine engender difficulties with clearance of secretions, which could also predispose patients to hypoxemia and hypercarbia.
e. Cardiac evaluation is essential to elicit evidence of cardiovascular dysfunction from either the acute SCI or preexisting abnormalities. In addition, an assessment of the degree of orthostatic hypotension and the risk of autonomic hyperreflexia should be made.
Monitoring. Decisions regarding the utilization of advanced monitoring are based on the level of injury and neurologic deficit, the complexity and length of the surgical procedure, and any preexisting underlying medical diseases.
a. Neurophysiologic monitoring is often indicated for patients who have no neurologic injuries but are at high risk owing to the instability of their spinal abnormalities and for patients who have incomplete neurologic injuries and are undergoing operations for spinal stabilization. Neurophysiologic monitoring could consist of an intraoperative wake-up test, somatosensory evoked potential (SSEP) monitoring, or motor evoked potential monitoring. SSEPs monitor the posterior columns of the spinal cord, whereas motor evoked potentials monitor the anterior portion of the spinal cord. For a more comprehensive description of spinal cord monitoring.
b. Intracranial pressure monitoring can be necessary for patients who also have head injuries.
c. Routine monitors (ECG, pulse oximetry, capnography, noninvasive BP, temperature) are employed for every procedure. A latex-free urinary catheter is used to monitor the patient's volume status.
d. In patients who have spinal shock, the institution of direct BP monitoring is indicated, ideally before induction of anesthesia. The arterial catheter is also useful for blood gas measurements and other laboratory determinations that can be necessary intraoperatively.
e. Early use of pulmonary artery catheters during spinal shock is appropriate. Measurement of intracardiac pressures (central venous pressure [CVP], pulmonary capillary wedge pressure [PCWP], left ventricular end diastolic pressure [LVEDP]) in conjunction with cardiac output and BP is necessary to differentiate hypovolemia from low systemic vascular resistance (SVR). The information obtained is helpful in determining the appropriate form of management (fluid versus vasopressors) and in monitoring the response to therapy.
(1) Patients who have low SVR can be treated with titrated infusions of a direct-acting alpha-agonist, as above.
(2) Patients who are hypovolemic can receive fluid boluses of 250 to 500 mL. A Starling curve, identifying the optimal fluid filling pressure, can be derived from the changes in intracardiac pressures (CVP, PCWP, LVEDP), cardiac output, and BP in response to the fluids.
Anesthetic technique
Securing the airway without causing or exacerbating SCI is the principal concern.
(1) An awake intubation has the advantage that the patient acts as a monitor to avoid worsening the SCI. In addition, a neurologic evaluation can document the absence of any new changes. An awake intubation also avoids the use of succinylcholine and the attendant risk of hyperkalemia.
(2) A blind nasal endotracheal intubation is often recommended as one of the best means to avoid spinal manipulation during intubation. This approach is contraindicated with facial trauma or a basilar skull fracture. Topical application of 0.2% phenylephrine hydrochloride in 4% lidocaine is essential to shrink nasal tissues and limit bleeding. Anesthesia of the tongue can be achieved using 2% lidocaine ointment or local anesthetic sprays. Anesthesia of the vocal cords and larynx is achieved by using the combination of a transtracheal injection of 4% lidocaine via a percutaneous puncture of the cricothyroid membrane and superior laryngeal nerve blocks with the bilateral injection of lidocaine 1%, 2 mL, into the thyrohyoid membrane just above the lateral wings of the thyroid cartilage. An alternative technique uses nebulized lidocaine 4% to a maximum dose of no >4 to 5 mg/kg. Calculations of toxicity must include all topical and injected local anesthetics.
(3) Fiberoptic endotracheal intubation can be used in a nonemergent situation after anesthetizing the airway as detailed in the preceding text. With the oral route, the use of either a bite block or large oral airway containing a central passageway for the fiberoptic scope is essential. In addition, oral intubation often mandates the use of mild sedation to facilitate patient acceptance. Blood, debris, and vomitus in the airway mitigate against fiberoptic intubation.
(4) Direct laryngoscopy can be appropriate if the previous methods do not seem feasible. Neutrality of the neck must be maintained to prevent further SCI. Extension or flexion during intubation can cause displacement and worsening of the original SCI. In-line manual cervical immobilization appears to be the safest method to minimize spinal column motion.
(5) When either severe facial trauma or neck instability exists or the airway is lost, a surgical airway via cricothyrotomy or tracheotomy can be necessary. The method selected for intubation depends on perceived airway difficulties, coexisting disease and trauma, and other factors including facial trauma and soft tissue swelling.
Induction
(1) The sympathetic function of SCI patients is unpredictable. Because they are also frequently hypovolemic, the induction should proceed slowly in an elective situation. When the patient has a full stomach, a rapid-sequence induction is indicated after adequate volume replacement has been accomplished.
(a) Ketamine, 1 to 2 mg/kg i.v., provides a more stable hemodynamic profile during induction. It has the added advantage of amplifying the electrophysiologic monitor's signal amplitude, but its use is not generally recommended in the presence of intracranial hypertension.
(b) Etomidate provides cardiovascular stability during induction.
(2) During the induction of general anesthesia, the maintenance of a spinal cord perfusion pressure of at least 60 mm Hg (ideally 80 to 90 mm Hg) is essential. The patient in the early phase of spinal shock after a high cord injury is at risk of developing bradycardia or asystole. Accordingly, some have advocated the use of a prophylactic anticholinergic to avoid this complication.
(3) Excessive fluctuations of cardiovascular parameters should be treated with direct-acting agonists and antagonists. These drugs should preferably be short acting and delivered via intravenous infusion. Sympathetic agonists and antagonists that release catecholamines indirectly are avoided.
Muscle relaxants. The SCI patient whose injury involves skeletal muscles develops a supersensitivity to depolarizing muscle relaxants. With muscle denervation, the number of postsynaptic acetylcholine receptors increases greatly and amplifies any small neuromuscular signal that can be present. When depolarized by succinylcholine, pores on the neuromuscular junction open maximally, allowing massive egress of stored intracellular potassium. The occurrence of succinylcholine-induced ventricular fibrillation secondary to this acute hyperkalemic response has been reported.
Because the time course for the development of the extrajunctional receptors is not known precisely (but can be as short as 24 hours), succinylcholine is best avoided even in recently injured patients. It is also important to realize that the magnitude of the potassium release is more a function of the amount of muscle mass affected than of the dose of depolarizing drug given. Even small doses of succinylcholine have triggered significant hyperkalemia. The administration of succinylcholine should be avoided in patients who have SCI.
Positioning. Spinal operations are most often performed in the prone position. Patients can be anesthetized on the bed or stretcher and then log rolled onto the operating table. Important goals include maintaining the head and neck in a neutral position; providing adequate padding to the chest, abdomen, head, and extremities; and avoiding excessive neck flexion or extension. Special attention should be given to the endotracheal tube because significant movement or obstruction can occur with changes of position. Sudden changes of position should also be avoided because they can have significant hemodynamic consequences owing to the lack of adequate compensatory vasoconstrictor and cardiac reflexes to maintain venous return and cardiac output.
The head is positioned so that the bony prominences support its weight without pressure on the eyes, ears, or nose. The position of the head can be adjusted slightly every 15 minutes or so throughout the procedure to ensure adequate perfusion under the weight-bearing area.
When an awake intubation is employed, the use of nerve blocks instead of sedatives enables the patients to position themselves. This allows a neurologic examination to be performed after positioning and helps ensure that the operative position does not aggravate the injury. Information gleaned from the preoperative neurologic examination (range of motion, motions that worsen symptoms) also helps to prevent the positioning from exacerbating the neurologic injury.
Maintenance. The choice of anesthetic drugs is guided by the patient's underlying condition. The anesthetic drugs selected should maintain optimal SCBF. The use of neurologic monitors necessitates the avoidance of drugs (e.g., volatile anesthetics) that either suppress the monitored responses or cause fluctuations in the anesthetic depth, which can confuse the interpretation of the evoked responses.
In general, drug regimens that utilize opiate infusions serve this purpose. Regional techniques can be considered, but the high incidence of coexisting injury and the frequency of hemodynamic and respiratory compromise virtually guarantee that general anesthesia is preferable.
Some evidence indicates that hypocapnia decreases SCI from ischemia. However, because hypocapnia could also compromise perfusion, normocapnia is recommended.
Fluid management. Fluid administration is based on the estimated preoperative fluid deficits, intraoperative blood and fluid losses, and a knowledge of the effect of the level of SCI on cardiac and pulmonary function. Meticulous fluid management is essential because patients who have high thoracic and cervical spine injuries have an increased propensity for developing pulmonary edema. In addition, cervical spine injury can cause cardiac dysfunction with decreased inotropy and chronotropy (from reduced sympathetic neural input to the heart). Whether to use either crystalloid or colloid for volume resuscitation is of less importance than the need to avoid glucose-containing solutions, which are known to exacerbate SCI.
Temperature regulation. SCI patients have impaired thermoregulation below the level of the injury. Prophylactic measures to prevent intraoperative hypothermia should be aggressively instituted. These include a warm ambient environment, warming of intravenous fluids, standard warming mattresses, humidification of the respiratory circuit, and forced hot-air blankets. Keep in mind, however, that hyperthermia exacerbates neurologic injury.
Postoperative care. Even patients who had adequate respiratory function before surgery could require a weaning period postoperatively before extubation owing to the residual effects of the anesthetics. Because of the potential difficulty in reintubating the trachea of the SCI patient, determination of the appropriate time for extubation should be extremely conservative. Critical care weaning parameters are used in place of routine extubation criteria after most operative procedures. Once the trachea has been extubated, the patient is monitored for several hours to ensure that the respiratory status does not deteriorate.
Extubation criteria include the following:
a. Blood gases
(1) pH >7.3
(2) Pao2 >60 mm Hg
(3) Paco2 <50 mm Hg
(4) Ratio of partial pressure of arterial oxygen to inspired fraction of oxygen (Pao2/fraction of inspired oxygen [Fio2]) >200
b. Pulmonary functions
(1) Maximal negative inspiratory forces <-25 cm H2O
(2) VC >15 mL/kg
(3) Respiratory rate <25/minute
(4) Dead space-to-tidal volume ratio <0.6
c. Other
(1) Patient conscious and oriented
(2) Unlabored, or minimally labored, breathing
(3) Ability to generate a cough
(4) Minimal volume of tracheal secretions
(5) Stable cardiac function
(6) Optimal intravascular fluid volume and electrolyte status
(7) Absence of infection
Chronic SCI. As improved emergency medical care increases the survival of patients who have high-level spinal cord injuries, one is more likely to encounter patients who now have chronic SCIs scheduled for surgical procedures for spinal and other indications. Many issues raised regarding acute SCIs apply equally to patients who have chronic injury. There are, however, a number of additional medical problems (Table-6).

 

Table-6. Medical problems of the patient who has chronic spinal cord injury
 

System Abnormality Relevant Comment
Cardiovascular Autonomic hyperreflexia  Blood volume Orthostatic hypotension Susceptible to hypertensive crisis if SCI level is above T6. Positional changes and intrathoracic pressure can cause hypotension.
Respiratory Muscle weakness Respiratory drive  ↓Cough SCI patient is susceptible to postoperative pneumonia and can be difficult to wean from mechanical ventilation.
Muscular Proliferation of acetylcholine receptors
Spasticity
Hyperkalemia from succinylcholine.
Genitourinary Recurrent urinary tract infections
Altered bladder emptying
Can lead to renal insufficiency, pyelonephritis, sepsis, or amyloidosis. Frequent catheterization can cause latex allergy.
Gastrointestinal Gastroparesis
Ileus
Susceptible to aspiration.
Immunologic Urinary tract infection
Pneumonia
Decubitus ulcers
Watch for subtle signs of infection and sepsis. Questionable risk of seeding an infection from invasive monitoring.
Skin Decubitus ulcers Prevention.
Hematologic Anemia
Risk of DVT
DVT prophylaxis.
Bone Bone density Osteoporosis, hypercalcemia, heterotopic ossification, muscle calcification, pathologic fractures.
Nervous system Chronic pain Perioperative pain can be difficult to control.
SCI, spinal cord injury, DVT, deep vein thrombosis.

Preoperative. Respiratory complications are the most common cause of morbidity in SCI patients. Pneumonia is second only to anoxia at the time of injury as the cause of death. Any fever with a leukocytosis or physical or radiographic evidence of pneumonitis should be treated aggressively.
Patients who have chronic injury are more prone to episodes of hypertension secondary to autonomic hyperreflexia, especially with lesions above T6. Muscle spasms also occur because of hyperactive spinal reflexes without the modulating effect of cortical, brain stem, and cerebellar centers. This "mass reflex" could require the therapeutic use of skeletal muscle relaxants in the awake patient.
Intraoperative
Regional anesthesia can offer some advantage for patients who still have instability of the cervical spine or whose initial repair limits their cervical range of motion. Should general anesthesia prove necessary for this subset of patients, all precautions for airway manipulation should be employed.
General anesthesia and regional anesthesia are equally effective in preventing autonomic hyperreflexia. Techniques based on the use of oxygen/nitrous oxide/narcotics seem to be less efficacious in this regard. When deciding on the appropriateness of a regional technique, one should consider the site of injury as well as the site of surgery. The patient's underlying hemodynamic status should also be considered. Regardless of the technique, direct-acting vasodilators (e.g., nitroprusside), alpha-adrenergic blocking drugs (e.g., phentolamine), antiarrhythmics (e.g., lidocaine, esmolol), atropine, and other antihypertensives (e.g., labetalol) should be readily available.
Chronic SCI puts all patients at risk for a hyperkalemic response to depolarizing muscle relaxants. Decreasing the dose does not reliably prevent the response. Therefore, succinylcholine is to be avoided.
As the receptors at the neuromuscular junction of denervated muscle are upregulated, basing the dose of nondepolarizing muscle relaxants on twitch response from a denervated limb leads to a relative overdose of muscle relaxant. This should be considered when giving the initial dose, when reversing the relaxation at the end of the procedure, and when judging readiness for extubation.
Urinary retention and urinary tract infections are persistent problems. A distended bladder can trigger the hypertensive response of autonomic hyperreflexia. Therefore, in addition to routine monitors, these patients should have a latex-free urinary catheter inserted for most procedures.
Postoperative. Postoperative management, including when to extubate the trachea, should be guided primarily by the requirements of the surgical procedure and the patient's underlying medical condition.

III. Spinal cord tumors

Spinal tumors can be primary or metastatic in origin. The medical problems associated with the patient are determined by the location of the spinal lesion and by the location of the primary tumor in metastatic lesions. Depending on the length of time since the presentation of the spinal lesion and its associated signs and symptoms, these patients could have many of the same complications seen in patients after traumatic injury to the spinal cord.
Preoperative management
Lesions of the upper spinal cord are the most damaging physiologically. Respiratory impairment secondary to loss of activity of the intercostal muscles and/or diaphragmatic is common. A blood gas measurement is indicated to determine the patient's baseline respiratory status. In addition, the decreased ability to clear secretions can frequently result in pneumonitis, which can require further intervention. Such infections are not always associated with elevated temperature, nor does elevated temperature always point to an infection because temperature regulation is frequently impaired as well.
Cardiovascular tone could be diminished with resulting hypotension. This also occurs in patients with acute SCI. One must differentiate neurogenic hypotension from the hypotension resulting from dehydration and malnutrition, commonly associated with patients who have cancer. Such dehydration could be exacerbated in patients who have recently undergone diagnostic radiographic tests that involved the use of contrast dyes because these usually act as diuretics.
In addition to the basic chemistries, preoperative blood determinations should include liver function tests to identify the presence, if any, of metastasis to the liver. The possibility of pituitary and adrenal insufficiency should also be considered because these are frequent sites of metastatic lesions.
Premedication should be kept to a minimum because it is useful to be able to reassess neurologic function immediately before operation. In particular, sedatives are avoided in situations in which the respiratory status is already impaired.
Intraoperative management
The planned procedure and the location of the lesion dictate the choice of monitors beyond the routine. Patients who exhibit signs of spinal shock are managed more effectively with the cardiovascular information provided by a pulmonary artery catheter and an arterial line. Those patients at risk for autonomic hyperreflexia can also require the "beat-to-beat" BP monitoring provided by an arterial line.
The positioning of these patients for the procedures frequently places the surgical site above the level of the heart. This increases the risk for pulmonary air embolism. The anesthetic plan should incorporate a monitor for the detection of air embolism (e.g., precordial Doppler, transesophageal echocardiography, pulmonary artery pressure) as well as an appropriately positioned CVP line to aspirate air.
The risk of hyperkalemia with the use of succinylcholine is increased as it was for the patient who has SCI. The use of nondepolarizing relaxants is recommended to ensure a quiet surgical field. However, because of upregulation of receptors in the neuromuscular junction secondary to denervation, care should be taken to select an appropriate site for monitoring twitch suppression via the nerve stimulator.
Maintenance of anesthesia can be accomplished with any general anesthetic technique. However, in procedures in which the use of SSEPs is anticipated, drugs that suppress the monitored potentials are avoided. In such circumstances, a nitrous oxide/oxygen/narcotic technique is more appropriate. Frequent changes of anesthetic depth are avoided because they interfere with the interpretation of the SSEPs.
Postoperative management. The decision regarding early extubation of these patients is made on a case-by-case basis. Early extubation in a fully awake patient facilitates postoperative neurologic examination. The appropriateness of early extubation depends on the patient's baseline respiratory function, location and size of the tumor, and duration and degree of difficulty of surgical dissection. Patients who were operated for high-level lesions require close monitoring for as long as 48 to 72 hours postoperatively. During this time, edema at the surgical site can cause renewed compression of the spinal cord and lead to progressive respiratory compromise and loss of protective gag reflexes. Reintubation, when necessary, should be done early in the course of respiratory deterioration. This allows accomplishing control of the airway in a patient who has a potentially unstable neck in as nonemergent an environment as possible.

IV. Scoliosis

General
Scoliosis is a structural disease of the vertebral column causing lateral curvature of the spine with rotation of the vertebra.
Scoliosis most frequently involves the thoracic and lumbar regions.
The severity of the disease is expressed in "degrees of lateral angulation." A larger degree of angulation represents more severe disease. The side of the convexity of the curve designates it as a right or left curvature.
Idiopathic scoliosis, accounting for almost 75% of cases, occurs most frequently in adolescent girls. Other types are classified as nonstructural (caused by gait/posture), congenital, neuromuscular, and traumatic.
The degree of severity of scoliosis correlates directly with the degree of respiratory dysfunction. Curvatures of <60° are not usually associated with significant pulmonary involvement, whereas patients who have curvatures of >100° are typically severely impaired.
Pulmonary function testing typically reveals a restrictive pattern owing to the reduction in chest wall compliance with reductions in all measures of lung capacity and volume. The greatest decrease is noted in the VC. Blood gas analysis reveals a lower Pao2, which is primarily because of the ventilation-perfusion mismatch that occurs. Paco2 is not usually altered unless an obstructive pulmonary component has also developed, a condition more common in the elderly.
In patients who have more severe thoracic disease, rib cage deformities lead to the underdevelopment of the pulmonary vasculature. This is exacerbated by hypoxic pulmonary vasoconstriction and can result in potentially significant elevations in pulmonary vascular resistance. Right ventricular hypertrophy and right atrial enlargement can occur as a result of these changes in pulmonary vascular resistance. Eventually patients develop irreversible pulmonary hypertension and cor pulmonale.
Preoperative management
The preoperative assessment should include information about the location and degree of scoliosis as well as its etiology. Both location and degree of disease play a role in determining the amount of pulmonary/cardiac involvement one can expect to find. Scoliosis owing to concurrent neurologic motor deficits can alter the choice of muscle relaxants.
Physical examination indicates necessary testing. Patients who have limited exercise tolerance require further pulmonary function testing to ascertain the extent of their pulmonary insufficiency. Patients who have vital capacities below 25 mL/kg are high operative risks.
Preoperative sedation is avoided in patients who have significant pulmonary compromise.
Intraoperative management
Decisions regarding monitoring are guided by the extent of pulmonary and cardiac involvement. One should consider an arterial line for blood gas measurement in any patient who has even moderately reduced pulmonary reserve. An arterial line is also necessary for closer monitoring of BP when "deliberate hypotension" is employed to reduce intraoperative blood loss.
Pulmonary artery catheter monitoring should be reserved for those patients who have either pulmonary hypertension or significantly diminished right ventricular output.
No advantage can be demonstrated for any particular anesthetic induction or maintenance regimen. The underlying hemodynamic condition of the patient should be used to guide the choice and dose of drugs.
Placement of spinal instrumentation involves traction to correct the curvature. SSEPs are frequently utilized to monitor the sensory component of the spinal cord. However, SSEPs monitor only the posterior cord. Anterior cord elements could be damaged despite normal SSEPs. When SSEP monitoring is utilized, one should limit either the use or the concentration of inhalation anesthetics, which interferes with signal interpretation (see preceding text).
A wake-up test definitively confirms adequate blood flow to, and therefore the function of, the anterior motor portion of the spinal cord. This is accomplished by having the patient awaken and move the lower extremities in response to verbal command. With a multitude of short-acting muscle relaxants and maintenance anesthetics, it has become relatively simple to maintain a deep level of anesthesia until the time of the wake-up test yet to allow for a quick awakening at the appropriate time during the procedure.
Postoperative management. The spinal fusion and rodding procedure prevents further deterioration of pulmonary and cardiac parameters. These abnormalities are not typically corrected by the procedure. Careful consideration of the patient's baseline status helps to determine which patients are suitable candidates for early extubation.

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