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Neurogenic shock is the interruption of autonomic pathways leading to hypotension and bradycardia and hypothermia. Spinal shock is the loss of reflexes below the level of SCI resulting in the clinical signs of flaccid areflexia and is usually combined with hypotension of neurogenic shock.

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There is a gradual return of reflex activity when the reflex arcs below redevelop, often resulting in spasticity, and autonomic hyperreflexia. This is a complex process and a recent four-phase classification to spinal shock has been postulated: A SCI affects the functioning of the spinal cord at the level of injury. It is important to discriminate between complete and incomplete injury. Spinal immobilization is indicated if a patient has sustained an injury with a mechanism compatible with spinal damage. Any patient with spinal pain or tenderness, neurologic deficit, depressed level of consciousness, drug or alcohol intoxication, or a painful distracting injury should be immobilized at the scene with a hard collar.

They should be transferred to hospital with surrounding head blocks on a spinal board. The spinal board is a transport device only and its prolonged use is associated with pressure sores. Patients should be well oxygenated at all times to prevent secondary cord damage and a low threshold for intubation is required.

Patients with SCI are also at increased risk of regurgitation and pulmonary aspiration of gastric contents because of paralytic ileus and loss of gastroesophageal sphincter tone. In the acute setting, a rapid sequence induction RSI should be used. Before induction the patient's hard collar and head blocks should be removed and manual in line cervical spine stabilization MILS should be initiated by a second operator.

Cervical spine movement should be minimized during laryngoscopy, especially flexion, which is thought to be more dangerous to the cord than extension. Associated maxillofacial trauma, blood or vomit in the upper airway, airway oedema secondary to direct trauma, or access problems such as cervical immobilization devices including halo traction can all make intubation difficult. Difficult airway equipment including a fibre-optic bronchoscope should be immediately available and awake fibre-optic intubation AFI may also be considered.

The spine must be immobilized if AFI is undertaken. No individual airway technique is superior, it is more important to avoid hypoxia and use familiar methods. Despite direct and indirect intubation techniques and cricoid pressure all being associated with spinal movement, this movement is unlikely to result in neurological injury providing reasonable care is taken. It must be remembered that after 72 h post-injury succinylcholine should be avoided as it may precipitate life threatening hyperkalaemia.

Gastric emptying remains reduced so a modified RSI or AFI if airway or access limited may be considered in the weeks after initial injury. Cord injury above T1 removes intercostal function and respiration will be entirely diaphragmatic. Lesions involving the phrenic nerves C3—5 will impair diaphragmatic function and if the damage is above C3 the patient will be permanently ventilator dependant unless there is partial recovery of the cord.

Any patient with cervical cord injury or those demonstrating signs of high cord injury with inability to cough or diaphragmatic breathing should be monitored acutely in a critical care setting as they may deteriorate neurologically especially in the first 72 h post-injury and again early intubation should be considered. It is important to remember that in the acute phase high cord-injured patients will have better respiratory function lying flat as the diaphragm has a greater excursion in inspiration as it is pushed into the chest by abdominal contents, whereas if sitting up the diaphragm is pulled down by abdominal contents impeding further excursion in inspiration.

Patients should, therefore, not sit up for the first few days after injury and thereafter only gradually as intercostal paralysis develops and the chest no longer collapses in during inspiration preserving the smaller tidal volumes produced by diaphragmatic descent. It is important that early assessment of respiratory function, vital capacity, pulmonary recruitment, and passive limb movements by an experienced spinal injury physiotherapist is carried out. In the minutes after cord injury a massive release in catecholamines occurs, particularly after high cervical injury producing dramatic hypertension and tachycardia.

Following this phase, paralysis of sympathetic tone leads to hypotension. This is attributable to a combination of vasodilatation, decreased inotropism, and bradycardia if above T5 and cardiac sympathetics are involved. Classically, the patient presents with hypotension and bradycardia, but they may be warm and vasodilated. Systolic arterial pressure will often settle at 80—90 mm Hg but this is unpredictable. Hypotension may be fluid resistant and most patients with high cord injury require vasopressor support.

Overtransfusion of fluid may lead to pulmonary oedema as capillary integrity of the pulmonary circulation may be impaired as a result of the catecholamine surge. Invasive pressure monitoring should be used for cord injuries associated with neurogenic shock, i. The neurogenic shock phase lasts from 24 h to several weeks.

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Early catheterization is essential not only to act as a marker of renal perfusion but also to avoid bladder overdistension that may precipitate bradycardia. Consider supra pubic catheterization if priapism is present. Signs that may indicate spinal injury especially in the patient with the depressed level of consciousness include: A thorough evaluation should be undertaken as soon as possible and should include assessment of motor function, sensation, respiratory function, reflexes, and anal tone on log rolling sacral sparing.

It should also document whether the injury is complete or incomplete and whether a clinical syndrome is suspected. Early total body CT is crucial in excluding other life threatening injuries in trauma patients with a cord injury to exclude occult haemorrhage as usual physiological response to shock is impaired. Spinal reformatting of CT images will aid immediate assessment of vertebral column, assist in spinal clearance, and give some information on cord integrity Fig. Anterior displacement of C5 vertebrae on C6 vertebrae is demonstrated.

This CT is consistent with an unstable hyperflexion injury. Early MRI has a role in investigating cord integrity and guiding early surgery e. It is a balance of risk vs benefit in this unstable group, ventilated patients, and those on vasopressors or inotropes should be carefully monitored by experienced personnel if MRI is undertaken. There are no magic bullets in protecting the cord, but avoidance of hypoxia, hypotension, and hypercarbia are crucial in the days after injury.

Some specific areas of investigation include:. Early vasopressor support has been advocated to ensure adequate spinal cord perfusion pressure and reduce secondary cord injury. There is little evidence for choice of inotrope, although vasoconstriction appears logical as first line. A number of animal studies showing a potential benefit in functional recovery have been reviewed; however, human studies are limited and at present cooling is not recommended.

The high-profile NASCIS II study recommended use of steroids demonstrating a small reduction in the level of injury in those treated early with high dose methylpredisolone, and this has recently been ratified in a review. Stabilization, open or closed reduction, and surgical decompression must be considered to relieve direct pressure on the cord and prevent secondary injury.

Urgent stabilization should be considered in patients with any deterioration in neurology. These patients are at high risk both because of immobility and increased thrombogenicity secondary to trauma. The use of anticoagulants should be restricted in the first 48—72 h because of risk of bleeding around the cord and intermittent calf compression devices or graduated compression stockings should be used instead. Standard prophylactic low molecular weight heparin should be started after 72 h. If anticoagulant use is contraindicated early insertion of an IVC filter may be considered.

Unopposed vagal activity increases gastric acid and therefore rates of peptic ulceration. Despite normal bowel sounds and increased gastric acid secretion, unopposed vagal activity may also lead to a gastroparesis. Feeding patients with high cord lesions may lead to nausea, vomiting, risk of aspiration, and abdominal distension, further impairing respiration.

However, early enteral feeding decreases mortality in polytrauma patients and it is usual practice to feed all intubated patients within 24 h. Glycaemic control is essential to avoid both hypo- and hyperglycaemia. Pressure sores are devastating for cord-injured patients leading to prolonged immobilization or severe sepsis.

These usually develop in the first few days after admission to hospital and are a result of immobility, poor perfusion of the skin, hypoxia, and leaving patients on spinal boards. Appropriate mattresses and good nursing care are essential to reduce pressure sores and early spinal fixation will allow earlier mobilization.

Neurogenic Bladder

Current research is not only focusing on secondary injury prevention, but also investigating more novel ways into the repair, remodelling and remyelination of damaged neurones, the regeneration of lost connections within the spinal cord, and replacement of lost nerve cells. The creation of a spinal neurone from stem cells heralds potential advances for the future. Given the nature of physiological derangement exhibited by SCI patients, the role of the anaesthetist is crucial in optimizing outcome for this high-risk group of patients.

Good quality early treatment and prevention of associated complications can make a dramatic difference to mortality and in particular the patient's functional outcome.

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Management of Intercurrent Disease All Journals search input. Close mobile search navigation Article navigation. This article was originally published in.

Initial management of the SCI. Neuroprotection strategies in SCI. View large Download slide. There is incomplete or complete loss of motor sensory function of the torso, pelvic organs, and the legs. The level of injury will affect which of these are affected. It may occur because of osteophyte impaction on half of the cord producing sensorimotor damage at the level of the injury.

This is most common in the cervical region where it presents as upper motor neurone signs in the legs and mixed upper and lower motor signs in the arms with loss of pain and temperature sensation in the arms. Sacral nerve fibres are positioned laterally in the cord and the patient may demonstrate sacral sparing of sensation. This is associated with damage to the posterior spinal artery and is very rare.

Older patients may need long-term ventilation. In addition, peripheral lesions can affect the parasympathetic supply to the detrusor muscle or the sympathetic supply to the bladder neck as well as somatic innervation to the external urethral sphincter. In order to explain the different types of voiding dysfunction, several different classification systems have been described, which are based on site and extent of the neurologic lesion, urodynamic findings, and classification of bladder function.

These 2 categories are further subdivided based on whether the failure is due to a problem with the detrusor or due to the bladder outlet. Examples of failure to store would be detrusor hyperreflexia or uninhibited bladder contractions or an areflexic bladder outlet.

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Any of these problems may occur at different stages of the acute and chronic period of SCI. Therefore, during the course of a patient's life, bladder management may have to change depending on the bladder dysfunction. The goals of bladder management are to prevent upper and lower urinary tract complications, including hydronephrosis, renal calculi, bladder calculi, and vesicoureteral reflux.

Urodynamic evaluation is helpful in defining urologic problems associated with SCI. This test studies the filling and voiding phases of bladder function. In addition, the detrusor pressure, duration of detrusor contraction, and compliance of the detrusor can be measured. As spinal shock resolves by approximately 3 months after injury, detrusor activity is noted.

Therefore, performing the urodynamic study after that time will provide the most useful information regarding the bladder dysfunction. Bladder drainage is achieved through indwelling catheters, intermittent catheterizations, suprapubic catheters, condom sheath catheters, or a combination of these methods. For example, in a person with a high cervical-level SCI, an indwelling catheter, in our opinion, is probably the most useful at least during the acute phase , because this will allow the patient more independence than the use of other techniques.

In a person with paraplegia who can be taught to self-catheterize, we believe that intermittent catheterization may be the first choice. Pharmacologic management of specific bladder dysfunctions may also be required, and many medications are currently available. For instance, when there is a failure to store due to bladder dysfunction, anticholinergics such as oxybutynin and propantheline have an antispasmodic effect on the smooth muscle. These medications suppress uninhibited bladder contractions, increase bladder capacity, and increase urethral resistance.

Patients with failure to empty due to bladder dysfunction may be treated with cholinergics such as bethanechol. These medications, however, have side effects. This is especially true of the anticholinergic drugs, which can cause dry mouth and constipation. In our opinion, patients who perform intermittent catheterization may require fluid restriction of approximately 2 L per day, and this may be difficult because of the side effects of the drugs. Once catheters and medical management have been tried, surgical options also exist.

Incidence and mortality

In patients with incontinence caused by the detrusor hyperreflexia, the following methods have been suggested. An augmentation cystoplasty may increase bladder capacity and lower intravesical pressure. Intermittent catheterization is then performed on a regular basis. There is often mucus in the urine from the bowel segment that was used to create the new bladder. Neurostimulation for control of bladder function has also been used. The most widely used technique is to apply electrodes to the sacral anterior roots within the cauda equina.

In those patients with incontinence due to incompetence of the sphincter, artificial sphincters may be implanted. Other methods to aid in the treatment of incontinence are timed voiding, pelvic-floor exercises, and biofeedback. Urethral stent placement has also been performed in patients with retention due to problems with failure to empty.

Bowel dysfunction is one of the most devastating sequelae of SCI, because it not only affects morbidity but it also can severely disrupt a person's quality of life. There are numerous gastrointestinal complications of bowel dysfunction, including ileus, gastric ulcers, gastroesophageal reflux, autonomic dysreflexia, pain, distention, diverticulosis, hemorrhoids, nausea, loss of appetite, impaction, constipation, diarrhea, and delayed or unplanned evacuation.

In order to better understand the neurogenic bowel, a brief review of normal anatomy and physiology is needed. The colon is bounded proximally by the ileocecal valve and distally by the anal sphincter. The internal anal sphincter IAS is a continuous smooth muscle layer of the rectum at the end of the colon. The external anal sphincter EAS is a circumferential band of striated muscle that is continuous with the pelvic floor and located proximal to the anus.

The puborectalis muscle loops around the rectum and maintains the anorectal angle by tethering the rectum toward the pubic bone. When the puborectalis muscle contracts, it lifts the rectum upward and forms an angle between the rectum and anus. In the resting state, continence is maintained by the tonic activity of the IAS. The intrinsic nervous system of the gastrointestinal tract, which includes Auerbach's plexus, is situated in the colonic wall between the longitudinal and circular muscle layers. This nerve supply helps coordinate colonic wall movement and the advancement of stool through the colon.

The extrinsic nervous system also innervates the colon and includes the parasympathetic, sympathetic, and somatic nerves. The pelvic nerve carries parasympathetic fibers from S2-S4 to the descending colon and rectum. Some pelvic nerve branches travel proximally and innervate the transverse and ascending colon. Sympathetic innervation is supplied by the superior and inferior mesenteric T9-T12 and hypogastric TL2 nerves. The colon absorbs fluids, electrolytes, and short-chain fatty acids; provides for growth of symbiotic bacteria; secretes mucus for lubrication of feces; and slowly propels stool toward the anus.

Transport of contents may take 12 to 30 hours from the ileocecal valve to the rectum. Small and large intestinal movements are mainly autonomous, with some spinal cord and minimal brain influence. Peristaltic waves travel both toward and away from the ileocecal valve in the ascending colon, but in the descending colon the waves travel mainly to push the contents to the anus. The motility of the colon is performed by 3 primary mechanisms: Most intestinal muscle displays autorhythmicity that causes colonic wall contractions. Chemical control is through the activity of neurotransmitters and hormones.

The chemicals influence the promotion or inhibition of contractions through the action of the central nervous system, autonomic nervous system, or direct action on muscle cells. The local neurogenic mechanism of colonic control is the enteric nervous system, which coordinates all segmental motility and some propagated movement. The nerves in the myenteric plexus cause the muscles above the dilation to constrict and those below the dilation to relax, and this helps propel the contents caudally. The extrinsic nervous system including the vagus nerve, sacral parasympathetics, and pelvic nerve—all help increase colonic motility.

The mechanism of this action is not fully understood. In the resting state, both anal sphincters are active and the anal-rectal canal is maintained in an acute angle by the puborectalis muscle. Voluntary contraction of the EAS also helps to maintain continence. Increased intra-abdominal pressure also causes the EAS to reflexively contract.

A neurogenic bowel occurs when there is a dysfunction of the colon due to lack of nervous control. The enteric nervous system remains intact after SCI; however, depending on the level of the injury, different bowel problems and complications may arise. Stiens et al 38 described 2 main types of neurogenic bowel. The lower motor neuron LMN bowel syndrome or areflexic bowel results from a lesion affecting the parasympathetic cell bodies in the conus medullaris, the cauda equina, or the pelvic nerve. No spinal cord—mediated peristalsis occurs, and there is slow stool propulsion.

Only the myenteric plexus coordinates segmental colonic peristalsis, and a dryer, rounder stool shape occurs. Due to the denervated EAS, there is increased risk for incontinence. The levator ani muscles lack tone, and this reduces the rectal angle and causes the lumen of the rectum to open.

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A lesion above the conus medullaris causes an upper motor neuron UMN bowel syndrome or hyperreflexic bowel. There is increased colonic wall and anal tone. The voluntary control of the EAS is discontinued, and the sphincter remains tight thereby retaining stool. The nerve connections between the spinal cord and the colon, however, remain intact; therefore, there is reflex coordination and stool propulsion.

In designing a bowel program for a patient with SCI, a variety of factors must be considered. A history is used to determine whether any gastrointestinal problems or any other medical conditions—such as diabetes, irritable bowel syndrome, lactose intolerance, inflammatory bowel disease, or rectal bleeding—existed before the SCI. These disorders may affect the choice of medications used in the bowel regimen.

Medications frequently used by patients with SCI for other problems—such as anticholinergics for treatment of neurogenic bladder, antidepressants, narcotics, and antispasticity medications—may also affect the bowel. In addition, we believe the person's dietary habits and preferences as well as the amount of fluid intake allowed should be addressed as part of the bowel management. The diet should be nutritional and provide high-residue foods such as fruits, vegetables, grains, and cereals. Drinking fluids should be encouraged. A full physical examination including rectal examination should be performed to help devise a bowel regimen.

A neurologic examination can reveal the extent of the nerve damage and the completeness of the SCI. The abdomen should be inspected for distention, increased abdominal muscle tone indicative of spasticity and bowel sounds. The rectal examination can provide information regarding external sphincter tone, stool in the rectal vault, and the presence of hemorrhoids or masses, and it assesses the tone and ability to produce voluntary contraction of the puborectalis muscles. We contend that it is also important to take into account the patient's strength in the upper and lower extremities; his or her sitting balance and ability to transfer; the length of the patient's arms, legs, and trunk; and the patient's weight.

These factors will help determine whether the patient can perform his or her own bowel program or whether he or she will need assistance. Prolonged bed rest interferes with bowel motility. The seated position reduces the anorectal angle and facilitates defecation. If it is possible to perform the bowel program in the seated position, after taking into account all the previously mentioned factors, the seated position is preferred.

The time when the person conducts his or her bowel regimen will be determined by his or her lifestyle, and it is arranged around work, school, or other activities. Many people prefer to perform the bowel regimen in the morning and have the rest of the day free. Some people can be assisted only at certain times of the day, and that will determine when the bowel regimen is performed.

There are numerous medications used to aid in the management of the neurogenic bowel. The 4 main categories of medications are stool softeners, colonic stimulants, contact irritants, and bulk formers. An example of a stool softener is docusate sodium, which emulsifies fat in the gastrointestinal tract and, therefore, softens the stool. Senna tablets are colonic stimulants that stimulate Auerbach's plexus to induce peristalsis. Bisacodyl tablets and suppositories act as contact irritants in the mucosa of the colon and produce peristalsis. Psyllium is a type of bulk former. A usual bowel program will consist of a stool softener administered 3 times per day—2 senna tablets and a bisacodyl enema daily.

The times that these medications will be given depends on the time of day the bowel program begins. Many people have had good results with this method; however, most times the medications will require adjustments in order to achieve proper and regular evacuation. In adjusting the medical regimen, the effects of other medications the patient is taking are considered as are the person's diet and the position in which the person performs the bowel program. For a reflexic bowel, the chemical stimulant is placed into the rectum with the patient in the upright or left lateral decubitus position, and digital stimulation is performed until evacuation.

Digital stimulation increases peristalsis and relaxes the EAS. It is performed by inserting a gloved, lubricated finger into the rectum and slowly rotating the finger in a circular movement. Other assistive techniques such as the Valsalva maneuver, push-ups, abdominal massage, or leaning forward may also be used. A bowel care regimen for an areflexic bowel consists of performing gentle Valsalva maneuvers or manual evacuation in the upright or side-lying position.

Medication management also depends, in part, on the type of bowel dysfunction. In a reflexic bowel, the medical regimen should work to produce a soft, formed stool that can be evacuated with rectal stimulation. In an areflexic bowel, firm, formed stool is required to allow the stool to be retained between bowel regimens and to be manually evacuated easily. A surgical approach to bowel management is the placement of a colostomy or ileostomy.

The time spent in bowel care has been reported to decrease from 11 hours to 4 hours per week with ostomies, and fecal incontinence is prevented. Most patients with SCI do not meet these criteria, and, therefore, biofeedback does not appear to be beneficial. Bowel accidents were noted to be the most socially distressing situation in people with SCIs, and bowel and bladder accidents were of primary concern when related to sexual activity. The impact of SCI on sexual response depends on the degree of injury and its location in the spinal cord.

Most of the information available about male sexual response is based on questionnaire studies, 52 — 54 whereas most of the data available about women comes from laboratory-based research. Masters and Johnson 60 provided a framework for studying human sexual response and divided its components into arousal, plateau, orgasm, and resolution. Each of the phases has particular genital and peripheral physiologic characteristics. When we discuss the topic of male sexual response, the components that most frequently come to mind include the occurrence of erections during the arousal phase and ejaculation during the orgasm phase.

As may be expected, most of the literature pertaining to the impact of SCI on male sexual response relates to these 2 phenomena. Nevertheless, in both sexes, heart rate, blood pressure, and respiratory rate also progressively increase during the arousal, plateau, and orgasm phases of sexual response and then return to baseline levels during the resolution phase.

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In order to predict the impact of SCI on male erection, knowing the level and degree of a person's injury and whether the injury is in the UMN or LMN and is affecting the sacral reflex arc is critical. Erectile function can occur 2 ways: Men with a complete LMN injury should not experience reflex erections but may experience psychogenic erection, depending on the degree of preserved neurologic function affecting the TL2 region of the spinal cord.

Ejaculation is a more complicated neurologic process and is more profoundly affected by SCI. Coordinated efforts of the sympathetic, parasympathetic, and somatic nervous systems result in the production of a man's ejaculate. In men with SCI, any of these neurologic pathways can be interrupted, depending on where the injury is located, and the result will often be a retrograde ejaculation in which semen is forced into the bladder instead of out the urethra. Seventy percent of men with incomplete LMN injuries reportedly can ejaculate. Orgasm in men with SCI has only been studied by questionnaire.

In women, the arousal phase of sexual response is characterized by lubrication of the vagina; clitoral swelling; increases in heart rate, respiratory rate, and blood pressure; and other changes. Most of these effects have been confirmed in the laboratory. For women with complete UMN injuries affecting the sacral segments, the ability for reflex but not psychogenic lubrication should be maintained. For women with incomplete UMN injuries affecting the sacral segments, it is thought that they may retain the capacity for reflex lubrication and may maintain the capacity for psychogenic lubrication.

Orgasm in women with SCIs has also been studied in laboratory settings. Furthermore, at no time were unsafe blood pressure responses noted in women with SCI. Descriptions of orgasm were indistinguishable between women with and without SCI. Based on the above research, 30 it is hypothesized that an intact sacral reflex arc is needed to achieve orgasm and that orgasm may be a reflex response of the autonomic nervous system.

Currently, a comprehensive assessment of the orgasms of men with SCIs is under way to determine whether the impact of neurologic injuries on sexual response will be similar to those of women. Although men remain interested in sexual activity after SCI, 53 , 54 , 70 their level of desire has been shown to decrease. Other researchers 71 noted a decrease in the frequency of intercourse in men from 3 to 4 times per week to 1 to 2 times per week. Reasons for the decrease in the frequency of sexual activity have included fewer opportunities for sex, 54 but the level and degree of injury have not been found to affect frequency of sexual activity.