Injury severity
Glasgow coma scale
Post-traumatic amnesia
Structural imaging
Loss of consciousness (LOC)
Alteration of consciousness/mental state
Mild
13–15
<24 h
Normal
0–30 min
A moment up to 24 h
Moderate
9–12
1–7 days
Normal or abnormal
>30 min and <24 h
>24 h
Severe
3–8
>7 days
Normal or abnormal
>24 h
>24 h
Table 26.2
Ranchos los amigos scale
Cognitive level | Outcome | Patient response |
|---|---|---|
I | No response | No response to sounds, sights, touch, or movement |
II | Generalized response | Limited response, which is inconsistent and nonpurposeful; responses to sounds, sights, touch, or movement |
III | Localized response | Inconsistent but purposeful response in a more specific manner to stimuli; may follow simple commands |
IV | Confused and agitated | Confused and often frightened; overreactions to stimuli by hitting or screaming; highly focused on basic needs (e.g., eating, toileting); difficulty following directions |
V | Confused and inappropriate | Appears alert and responds to commands; easily distracted by the environment; frustrated and verbally inappropriate; focused on basic needs |
VI | Confused and appropriate | Follows simple directions consistently; may have some memory but lacks details, attention span of about 30 min |
VII | Automatic and appropriate | Follows a set schedule; does routine self-care without help; attention difficulty in distracting or stressful situations; problems in planning and following through |
VIII | Purposeful and appropriate | Realizes difficulties with thinking and memory; less rigid and more flexible thinking; able to learn new things; demonstrates poor judgment; may need guidance for decisions |
Common Sequelae and Treatment
Traumatic brain injury is associated with a variety of physiologic, physical, cognitive, behavioral, and emotional manifestations post injury [95]. With the exception of amantadine hydrochloride, which has been shown to accelerate recovery for patients with severe TBI [96], all other pharmacological clinical trials have not demonstrated a beneficial effect in the recovery course of TBI, therefore rehabilitative interventions remain the most appropriate management once the patient is medically and surgically stable. Rehabilitative strategies attempt to target symptomatology associated with TBI, particularly those symptoms which most impair function. A discussion of some of the more common symptoms expressed after TBI is presented in the following section:
Headache: Post-traumatic headaches are the most common physical complaint following mild TBI (mTBI). While most patients report symptom resolution within the first month of injury, some patients develop post-traumatic headaches as late as 3–6 months following injury and their symptoms may persist for years [97]. According to the International Headache Society classification system, headaches can be divided into acute post-traumatic and chronic post-traumatic. Pharmacological management may include nonsteroidal anti-inflammatory medications (NSAIDs), beta adrenergic antagonists, calcium channel blockers, and antiepileptics. Botulinum toxin injections and nerve blocks have also shown efficacy.
Agitation/Aggression Behavioral changes after TBI are common and are often both challenging and troubling to families and caregivers. A multifaceted intervention strategy is required, utilizing family counseling, pharmacological interventions, and psychotherapy. Determining the etiology is important, since concurrent neuropsychiatric conditions, depression, or delirium due to medical illness may be present. In addition to correcting any underlying medical conditions, overstimulation of the patient should be avoided, with dim lighting, reduced noise, and establishing a regimented daily schedule. Pharmacological management often includes atypical antipsychotics, tricyclic antidepressants, trazodone, amantadine, and beta blockers [98]. The uses of benzodiazepines are not recommended for acute aggression since these medications may cause confusion, amnesia, poor balance, and even worsening agitation.
Post–traumatic Seizure/Post–traumatic Epilepsy (PTE) Post-traumatic seizures are classified as either: immediate (within the first 24 h); early (from 1 to 7 days); or late (after the first week). The incidence of early seizures after TBI is reported to be between 2.6 and 16.3 %. The majority of post-traumatic seizures (86 %) occur within the first 2 years of trauma [99]. Risk factors for early seizure development include intracerebral hematoma, subdural hematoma in children, younger age, severity of injury, and alcoholism. Risk factors for late seizures include intracranial bleed, severity of injury, and age greater than 65. Mild head injury without skull fracture with either loss of consciousness or post-traumatic amnesia lasting less than 30 minutes has not been found to be associated with PTE [95]. Current guidelines do not recommend seizure prophylaxis beyond 7 days. Frequently used antiepileptic medications include phenytoin (Dilantin) and levetiracetam (Keppra).
Conditions such as contractures, pressure ulcers, spasticity, deconditioning, sleep disturbances, heterotopic ossification, and pain syndromes are also commonly associated with TBI and are discussed in other sections of this chapter.
Spinal Cord Injury (SCI)
Epidemiology
According to the National Spinal Cord Injury Statistical Center (NSCISC), the annual incidence of SCI in the United States is approximately 12,500 new cases each year. The prevalence is estimated to be in the range from 240,000 to 337,000 persons, with the average age at time of injury has increased from 29 years in the 1970s to 42 years currently. Approximately 79 % of all SCI occur among males. The leading causes of traumatic SCI are from motor vehicle accidents, followed by falls, acts of violence, and sports/recreational activities. The estimated lifetime costs associated with SCI vary depending on age, neurological impairment, and preinjury employment, but have been reported to range between $1.1 and 4.7 million [100].
Classification
The American Spinal Injury Association (ASIA) has set forth standards of evaluation for the classification of SCI. According to the NSCISC the most frequent neurologic category is incomplete paraplegia, followed by incomplete tetraplegia, complete paraplegia, and complete tetraplegia. Classification of acute spinal cord injury is standardized by use of the International Standards for Neurologic Classification of Spinal Cord Injury (ISNCSCI) guidelines. A worksheet may be obtained from the ASIA web site [101]. The worksheet details the exam which incorporates the evaluation of key sensory and motor levels on both sides. With this information, a neurologic level of injury may be obtained and determined to be complete or incomplete. AIS classification can be used to communicate with other physicians or healthcare professionals in other facilities.
Acute Management of Spinal Cord Injury
Point of injury care should include spinal stabilization. Early surgical intervention in spinal cord injury is defined as intervention occurring from 8 to 72 h [102]. Although the optimal timing remains unknown, there are purported benefits associated with early surgical intervention in the presence of spinal instability. Current research favors weighing the benefits of early intervention against the greater risks of performing excessive spinal surgeries on patients with multiple injuries [103]. The delay is considered beneficial to provide spinal cord recovery time and optimization of general health. Evidence suggests that a 19 % decrease in odds of mortality was shown with each 24 h increase in time until surgery [104]. While still controversial, high-dose steroid use is not currently recommended [105, 106]. Future research strategies aim to more specifically target post-traumatic inflammation as well as identify biomarkers to better monitor prognosis. Implicated possible biomarkers include: TNFα, IL-1β, IL-6, IL-8, and IL-10 [107].
Functional Outcomes after Spinal Cord Injury
Evidence suggests that the level of injury for patients with SCI has the greatest implication for prognosis. Patients with injuries above C4 will most likely require lifetime ventilation, while an injury at the C5 level may allow a patient to drive independently with a specially adapted vehicle. Independence in transfers, feeding, grooming, and bowel/bladder care are frequently achieved by individuals with complete injuries at below the C7 level. The minimal neurologic level for independent, functional ambulation with bracing is L2 (hip flexion) on one side and L3 (knee extension) on the other.
Common Sequelae and Treatment
Autonomic Dysreflexia/Autonomic Hyperreflexia is a unique phenomenon that occurs in approximately 50–70 % of patients with complete spinal cord lesions generally at or above T6 [108]. Symptoms may include facial flushing, diaphoresis, bradycardia, headache, and blurred vision. The most prominent sign is elevated blood pressure 20–40 mmHg over the patient’s baseline, but may lead to seizure or even death. Because baseline blood pressures may be decreased following SCI, regular monitoring is recommended. Autonomic dysreflexia occurs as the result of a sympathetic nervous system discharge below the level of injury that persists unopposed by central inhibition from above the level of injury. Immediate recognition and treatment is necessary and typically involves identifying noxious stimuli below the level of injury that initiates the sympathetic reflex. Common noxious stimuli include bladder distension, infection, constipation, pressure ulcers, VTE, ingrown toenails, or renal calculi [102, 109]. Treatment guidelines have been published by the Paralyzed Veterans of America and are publicly accessible [110]. The blood pressure should be monitored and treated with a rapid-acting short-duration antihypertensive, if the systolic pressure is at or above 150 mmHg [111]. Pharmacologic interventions include the calcium channel blocker nifedipine or topical nitrates [102, 104]. Other preventative measures include frequent turning to prevent pressure ulcers and regularly checking for possible sources of noxious stimuli, such as ingrown toenails. In the subacute phase, the use of specific α-adrenergic antagonists such as terazosin may prevent serious consequences [112]. For unresponsive patients or those nonresponsive to therapy, anesthesia (regional or general) may be used to successfully ameliorate the sympathetic response driving the phenomenon [113].
Bladder Dysfunction: Urinary retention and/or incontinence are frequently encountered after SCI. Detrusor sphincter dysynergy (DSD) remains a frequent problem, leading to elevated bladder pressures and possible hydronephrosis. Further imaging, cystoscopy, and urodynamics may help guide appropriate treatment. (Please refer to above section “Urinary System Treatment”)
Bowel Dysfunction: Spinal shock, which is characterized by muscular flaccidity and loss of motor reflexes in all parts of the body below the level of injury, can induce an acute decrease in gastric motility, increasing transit times, prolonging gastric emptying and increasing water absorption resulting in constipation and/or fecal incontinence. If not addressed, this can lead to medical complications and poor functional outcomes. Bowel movements should be closely monitored and pharmacological management may help to prevent constipation. A bowel program can be initiated with a goal for a bowel movement daily to every other day. Digital stimulation or digital disimpaction may be sufficient to produce a bowel movement; pharmacologic treatments used may include bulk-forming agents, stool softeners, oral stimulants, and suppositories. Surgical options may include colostomy.
Pain Syndromes: Multiple sources of nocioception are common for patients with SCI, whether centrally or peripherally mediated. Direct injury to the cord or nerve roots may lead to significant neuropathic pain syndromes in a dermatomal or nonspecific distribution. In addition, pain may generate from concomitant fractures, soft tissue, or other organ damage. Two important variants to consider are syringomyelia and cauda equina syndrome. Syringomyelia should be considered whenever there is a delayed onset of segmental pain accompanied by a rising level of sensory loss [74]. Cauda Equina syndrome is associated with lower extremity dermatome pain, bowel and bladder incontinence, and classically saddle anesthesia. Central dysesthesia syndrome may also occur, which typically manifests as diffuse, nondermatomal pain accompanied by hyperalgesia or allodynia.
Other complications of SCI include spasticity, orthostatic hypotension, skin breakdown, heterotopic ossification, and pain which have been addressed previously in this chapter.
Peripheral Nerve Injuries
Etiology
Peripheral nerve injuries may result from direct trauma or as a complication of medical care (e.g., poor fitting orthosis/casts or poor bed positioning) or a complication of surgery (e.g., compression by hardware placement or excessive tourniquet pressure during surgery). Common locations of peripheral nerve injury include: the brachial plexus, ulnar nerve at the elbow (cubital tunnel), and peroneal nerve at the fibular head. In the acute trauma setting, the diagnosis of a peripheral nerve injury may be confounded because of the presence of other more life-threatening injuries. Trauma patients, particularly those with prolonged ICU stays, systemic inflammatory response syndrome (SIRS), and shock [114], may develop a critical illness polyneuropathy (CIP) or critical illness myopathy (CIM), manifesting as generalized weakness, muscle atrophy, and/or impaired sensation. These conditions have been attributed to alterations that occur in the nervous system and/or muscular architecture with loss of protein channels and neural degeneration. There is an apparent increased risk of developing CIM associated with intravenous glucocorticoids used to treat patients with acute respiratory distress syndrome or chronic obstructive pulmonary disease [115]. Other risk factors for the development of long-term critical illness neuropathy include duration of ICU treatment, duration of ventilator support, and a high APACHE score [116]. Recovery from CIM/CIP is generally good although the rehabilitation course typically protracted. Electrodiagnostic testing is often very helpful in the evaluation of peripheral nerve and muscle function. Ultrasound may also be a useful diagnostic tool for the evaluation of peripheral nerves and is also beneficial when used to guide interventional procedures to avoid potential nerve injury.
Treatment
Prevention of peripheral nerve injuries includes proper bed positioning to avoid common compression neuropathies located at the elbow and fibular head. The use of padding at compression points, splints, and/or activity modification may help to prevent further nerve damage to injured peripheral nerves. Nursing staff and therapists can provide assistance and patient/family education for proper bed mobility techniques and/or use of assistive devices for activities of daily living. Regular exercise and rehabilitation therapy sessions are also beneficial in treating critical illness myopathy (CIM). Just as the causes of CIM are varied, the treatment is also multidisciplinary; nutritional intake, stricter glycemic control and removal or minimizing steroid and muscle relaxant medications all may be helpful [117]. For severe neurologic injury, surgical treatment using grafts may be necessary; a more detailed discussion is beyond the scope of this chapter. Rehabilitation after such surgery is prolonged. Neuro-recovery is dependent on the location of injury and distance to the most distal muscle. In general, reinnervation occurs at the rate of one millimeter per day/one inch per month.
Conclusion
Rehabilitation of the neurotrauma patient is complex, requiring the coordinated care of a specialized interdisciplinary team. Interventions are focused on recognizing the negative effects of immobility, mitigating the risk of secondary complications, identifying functional impairments, and implementing education and treatment strategies to promote recovery , independence, and eventual community reintegration. Frequent barriers to successful rehabilitation include impaired cognition, complex pain syndromes, poor home accessibility (particularly for those with mobility challenges), as well as psychological problems. Therefore, treatment strategies should employ patients, families as well as a multitude of specialists, including assistive technology to overcome barriers and foster appropriate goal-directed care to ultimately restore quality of life and dignity after trauma .
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