Chief complaint: “Don't touch me, it hurts.”
History of Present Illness
A 55-year-old unrestrained male driver involved in a minor single vehicle car crash. The emergency medical technician reported the patient's vehicle struck a cement parking post at less than 10 mph, minor damage to the front fender, no air-bag deployment, and no intrusion or damage to the windshield. The patient suffered no loss of consciousness. The patient was actively moving all four extremities. The only visible injury reported was a minor abrasion to the forehead. The patient's only complaint was severe “burning” pain to his upper body and arms, 10 on a scale of 1–10.
Past Medical History
Hypertension and hyperlipidemia.
Past Surgical History
Appendectomy as a child.
- Hydrochlorothiazide/olmesartan (Benicar HCT) 25/40 mg daily, and
- Atorvastatin (Lipitor) 40 mg daily.
No known drug allergy.
Occupation. Accountant; married, with two children; lives in a 2-story house. Drinks 3–4 oz of whiskey a week; and denies smoking or illicit drug use.
Review of Systems
Constitutional. Denies fever or chills; no recent significant weight gain or loss.
HEENT. Denies head pain or visual disturbances, no ear pain or difficulty hearing, no nose pain or epistaxis, no dental pain or malocclusion, and no sore throat or difficulty swallowing.
Neck. Generalized neck pain.
Chest/Heart. Complain of “deep burning” pain to chest, 10 on a scale of 1–10, radiating to bilateral arms/hands. Denies chest pain, pressure or heaviness, denies pleuritic chest pain or shortness of breath, and no cough or hemoptysis.
Abdomen. Denies abdominal pain. No nausea, vomiting, or diarrhea.
Back. Denies back or flank pain.
Genitourinary. Denies dysuria, frequency, or urgency. Denies urinary hesitancy or bowel/bladder incontinence.
Extremities. Complain of severe “deep burning” pain to bilateral arm/hands. Arms feel “heavy” and “can't use” hands/fingers.
Skin. Denies rashes or pruritus.
Neurological. Complain of “burning” sensation and arm/hand weakness. Denies headache, dizziness, or vertigo. Denies recent falls or history of near syncope or syncope.
Psychiatric. Denies history of depression, anxiety, panic attacks, visual or auditory hallucinations, and suicidal or homicidal ideation or prior attempts.
Blood pressure: 167/96 (per thigh cuff); heart rate: 102 beat per minute; respiratory rate: 20; temperature: 99.2 °F oral; and pulse oximetry 98% on room air. Unable to obtain blood pressure per arms or place on a cardiac monitor due to severe pain.
Age, 55 years; white male, well developed and well nourished in extreme distress; unable to lie still in bed, uncontrollable crying and moaning in pain. Any attempts to touch chest or upper extremities caused severe pain.
Head. Minor superficial abrasion to center of forehead. No active bleeding or swelling. No bony crepitus. No other signs of facial injury.
Eyes. Pupils equal, round, and react to light. Extraocular movements intact.
Ears. External auditory canal intact, tympanic membrane intact, no hemotympanum, and positive light reflex.
Nose. Septum midline, no septal hematoma, and no epistaxis.
Throat. No oral or dental trauma, no malocclusion, and uvula midline.
In a rigid cervical collar, trachea midline, no jugular venous distention, diffuse neck tenderness, no crepitus or deformity.
Normal chest contour and lung expansion, no use of accessory muscles, and no retractions. No signs of trauma. Breath sounds clear to auscultation. Unable to palpate the chest wall; patient screams with any palpation.
Tachycardia; regular rhythm; normal S1, S2, no S3 or S4, 2+/4 palpable radial, femoral, and dorsalis pedis. No edema.
Obese but soft, positive bowel sounds, no visible trauma, nondistended, nontender, and no rebound or guarding.
No visible trauma, diffuse tenderness to upper back, and no lumbar vertebral tenderness, crepitus, or deformities.
No signs of trauma, no bony tenderness, and normal range of motion without pain.
No signs of trauma or blood at the meatus; no priapism; no testicular ecchymosis, tenderness or mass; and positive cremasteric reflex.
Normal anal tone with intact sphincter reflex.
No obvious bony deformity.
Minor superficial abrasion to forehead, no other signs of trauma. Normal skin color, warm and dry. No visible bleeding.
Alert; oriented to person, place, and time. Glasgow Coma Scale score 15. Cranial nerves II through XII intact. Bilateral gross upper motor strength diminished deltoids/biceps/triceps 3/5, wrists/fingers 2/5, weak 2/5, but equal hand grasps. Bilateral gross lower motor strength: hip flexors; quadriceps; hamstrings 5/5; dorsiflexion; plantar flexion; inversion; eversion of feet 5/5; and dorsiflexion of toes 5/5. Hypersensation to bilateral upper extremities and upper torso. Bilateral lower extremity gross sensation to light touch and sharp/dull differentiation intact. Unable to assess upper extremity reflexes due to pain. Bilateral patellar and achilles hyperreflexic 4+/4. Negative Babinski.
Differential diagnosis of any trauma patient with a head or neck injury with neurological deficits should include evaluation of a cervical spinal cord injury (SCI). Central cord syndrome (CCS) is an acute form of an incomplete SCI characterized by greater neurological impairment in the arms and hands compared to the lower extremities. Diagnoses to consider in the differential diagnosis of CCS include cervical disk herniation, cervical spondylosis, cervical spine injury, anterior cord syndrome, and brachial plexus injury (Cervical Hyperextension Injuries, n.d.; Bellotte & Wilberger, 2006). Another consideration for this case study was a psychosomatic disorder, in which the pain was out of proportion to the injuries. However, this is a diagnosis of exclusion, and one must rule out all other causes first.
CCS is an incomplete cervical SCI, usually related to trauma involving a hyperextension injury. Common mechanisms of injury (MOI) include sports activities, a forward fall, or a motor vehicle crash. In the case study, when the car struck the cement post, it caused the unrestrained driver to move forward and upward, striking his forehead on the windshield, causing hyperextension of his cervical spine and subsequent CCS.
CCS is the most common type of incomplete SCI, which results in partial motor and sensory deficits (Alpert, 2010; Xin-Feng & Li-Yang, 2010). CCS is differentiated from other incomplete SCI by physical findings, which indicate greater impairment of upper extremity motor function compared with the lower extremities, sensory disturbances below the involved level, and varying degrees of bladder dysfunction. Loss of motor function is especially prevalent in the fine motor movements of the hands (Alpert, 2010).
As with other SCIs, most CCS patients are male patients. The prevalence rate of CCS in patients with a SCI is 15.7%–25% (Lenehan et al., 2010). CCS has a bimodal distribution, affecting those between the ages of 15 and 24 years and individuals older than 50 years. Trauma is the most common cause for both groups, but the specific MOI and underlying causes differ. In the younger population, the MOI is frequently related to sports activities (e.g., wrestling and diving) or motor vehicle crash. In the older population, forward falls from standing height are the most common MOI. Older adults also have preexisting medical conditions, such as arthritis or spondylosis, which increase the risk of CCS (Alpert, 2010; Bellotte & Wilberger, 2006).
Upper extremity motor weakness and hyperpathia, or exaggerated pain response, to the chest and upper extremities are common findings for CCS (Xin-Feng & Li-Yang, 2010). CCS was originally described as a hyperextension injury causing stretching of the cervical cord with subsequent hemorrhage and swelling to the central portion of the spinal cord. It was thought that injury to the central cord caused impaired motor and sensory function of the upper extremities (Alpert, 2010; Xin-Feng & Li-Yang, 2010). Hyperpathia was attributed to injury to the spinothalamic tracts responsible for pain and temperature sensation. However, subsequent studies indicate that the specific pathogenesis of CCS is not clearly defined, and the exact anatomic location of injury is not known (Tator, 2000; Xin-Feng & Li-Yang, 2010).
Initial radiographic studies to evaluate the cervical spine (C-spine) in a trauma patient include plain radiographs or computer tomographic (CT) scans. Plain C-spine radiographs include three views: anterior-posterior; lateral; and odontoid. If the C-spine radiographs do not adequately visualize all seven cervical vertebrae and the top of the first thoracic vertebrae, or if an abnormality is noted, then a cervical CT scan is indicated. A CT scan is superior to plain films and magnetic resonance imaging (MRI) in the evaluation of fractures because of the enhanced image of bony details.
Patients with abnormal neurological findings but negative C-spine radiographs or CT scans require an MRI to assess for SCI. An MRI is the study of choice for evaluating the spinal cord and surrounding tissue and ligaments. Indication of CCS on MRI reveals evidence of narrowing of the spinal canal with spinal cord compression (Albert, 2010; Zwienenberg-Lee, Kim, & Muizelaar, 2005).
No specific laboratory tests are used to diagnosis CCS. The presenting trauma history and physical examination determine whether laboratory tests are necessary. In the case study, basic screening laboratory tests, for example, basic metabolic panel and complete blood count, were drawn. In addition, both serum and urine toxicology screens were obtained to rule out drug- and alcohol-related causes for his abnormal presentation. The laboratory results indicated no abnormal findings.
Initial management of any trauma patient should begin with the assessment of the airway, with simultaneous cervical spine stabilization, followed by the assessment of breathing and circulation (Emergency Nurses Association, 2007). A rigid cervical collar or an Aspen collar should be placed to immobilize the cervical spine. Special care should be taken when moving patients to prevent further damage to the spinal cord. An SCI at or above the fifth cervical vertebrae increases the risk of respiratory insufficiency and may require advanced airway management (Bellotte & Wilberger, 2006). After initial assessment and stabilization have been achieved, the secondary survey or head-to-toe assessment is performed to identify additional injuries (Emergency Nurses Association, 2007).
The goal of management for an SCI is to prevent secondary injury. Attention should focus on avoiding hypoxia and hypotension, both of which can cause further damage to the injured cord (Bellotte & Wilberger, 2006). There are no standard treatment plans for the management of CCS (Fehlings, Wilson, Dvorak, Vaccaro, & Fisher, 2010).
Rehabilitation services are the main therapeutic modality for the treatment of CCS. The focus of physical therapy is to preserve motor function and enhance current functional ability. Strength training of the lower extremities with trunk balance is important in gait training. The goal of occupational therapy is to maximize the use of the patients' upper extremities and their ability to perform basic activities of daily living. Speech therapy's function is to evaluate the patient for dysphagia or aspiration risks. A vocational specialist would evaluate the need for assistive devices and workplace modifications (Alpert, 2010; Bellotte & Wilberger, 2006). Additional services to consult would include social service, clergy, and psychiatry to provide additional resources, counseling, and emotional support.
Use of steroids in the treatment of closed SCI is controversial. The purpose of steroids is to reduce swelling and prevent further damage to the spinal cord. Steroids are thought to block the release of harmful biochemical agents that cause tissue damage at the cellular level (Alpert, 2010; Bellotte & Wilberger, 2006). However, the evidence to support the clinical benefit of steroid use in improving SCI outcomes is inconclusive. The controversy is whether the potential benefits of high-dose steroids outweigh the risks, for example, hyperglycemia, increased infection, and gastrointestinal complications (Zwienenberg-Lee et al., 2005).
Despite weak evidence to support the use of high-dose steroids, their use is an option, and administration is based on the clinician's practice. The literature recommends steroid use only in the cases of nonpenetrating SCI patients with neurological deficits. In addition, the administration of steroids should be started only if the injury is less than 8 hrs old (Alpert, 2010; Bellotte & Wilberger, 2006; Zwienenberg-Lee et al., 2005).
High-dose steroids are initiated within 8 hrs of the injury to provide optimal effect. A methylprednisolone bolus of 30 mg/kg is administered over 15 min. Forty-five minutes after the bolus, a methylprednisolone infusion is started at 5.4 mg/kg/hr. The duration of the steroid infusion is based on the time period between the onset of injury and the time the bolus was initiated. If the bolus is given within 3 hrs of injury, the infusion continues for 23 hrs. If the bolus is given between 3 and 8 hrs of injury, the infusion continues for 48 hrs (Alpert, 2010; Zwienenberg-Lee et al., 2005).
Surgical management of CCS is another controversial topic. There is no consensus on whether CCS should be managed medically or whether surgical stabilization is warranted. If surgery is deemed necessary, it is unclear as to whether the stabilization should take place in the acute phase of injury or be delayed (Fehlings et al., 2010; Lenehan, et al.,2010).
Implication for Practice/Relevance to Advanced Practice Nurses
This case highlights the significance of obtaining a thorough history and physical examination. It is important to obtain information on the MOI to determine the risk of a cervical hyperextension injury and to identify the differences in motor function between the upper and the lower extremities. Early recognition of the signs and symptoms of CCS is a critical factor in providing optimal care and the best long-term prognosis.
SUMMARY AND CONCLUSION
The morbidity and mortality for most patients with CCS is positive, with some degree of neurological and functional improvement (Alpert, 2010; Dvorak et al., 2005). The CCS is an incomplete SCI; therefore, neurological improvement can occur after decompression of the nerves. Factors that affect potential outcomes include initial motor function, underlying comorbidities, age of the patient, and development of complications (Alpert, 2010; Dvorak et al., 2005; Xin-Feng & Li-Yang, 2010). Early return of motor function or sensation indicates a positive recovery. Conversely, neurological deficits for greater than 6 months signify permanent loss of sensation or motor function (Bellotte & Wilberger, 2006).
In conclusion, the patient in the case study did not have a positive outcome. The C-spine x-ray showed straightening of cervical lordosis but no bony fracture or malalignment. The CT scan was negative for spinal fracture or subluxation. An MRI of the cervical spine showed cervical spine compression with edema. Shortly after admission, the patient developed respiratory compromise, requiring intubation and ventilation. He eventually required a tracheotomy. He received high-dose steroids within 3 hrs of his injury without significant improvement in his neurologic recovery. His SCI was managed conservatively with the placement of an aspen collar for 6 months. Despite extensive rehabilitation, the patient had no significant functional recovery. The patient was unable to function independently and was admitted to a nursing home, where he was wheelchair bound, with the loss of both bowel and bladder functions.
Injuries to the spinal cord are not always obvious. The CCS can occur without a fracture; therefore, recognition of signs and symptoms is important. As this case study delineates, even a patient with a minor MOI can have a significant SCI. A high degree of suspicion for cervical SCI should be present for any trauma patient with a head or neck injury who exhibits neurological deficits.