SPINE SGDSAN GABRIEL, SANIANO, SANTOS JJ, SANTOS MS, SISON, SORREDA, SOTALBO

General Data

AA is a 15 year old female from Bacoor, Cavite who came in for consult due to bilateral lower extremity weakness and sensory deficits

DOI: June 21, 2009TOI: 1:30 PMPOI: road in Bacoor, CaviteMOI: vehicular crash

History of Present Illness

June 21, 2009 (1:30 PM)While walking towards the other side of the road, the patient was hit by a jeepney at speed on the back lumbar area. She was flung over the hood and again fell in front of the still moving vehicle and was run over. The vehicle stopped with her pinned under the rear wheel. Bystanders lifted the jeepney and she was pulled out.

She was unconscious at this time and sustained abrasions over her face, arms, legs and back. No gross deformities were seen.

History of Present Illness

She was then brought to Crisostomo Medical Center, 30 minutes away from the site of the accident.

At the CMC, she regained consciousness. Her wounds were cleaned and x-rays of her neck, chest, arms and kegs were done. This allegedly revealed a compression fracture of one of her lumbar vertebrae. Difficulty breathing prompted her to be given O2 support

She was confined at CMC untill...

History of Present Illness

June 28, 2009 She was brought to the PGH ER with an admitting impression of SCI secondary to VC. Repeat labs and x-rays were done.

July 2, 2009She was transferred to the Spine Ward and is awaiting definitive management.

Past Medical History

Left Knee Lacerations secondary to trauma from broken glass (2001) –required stitches, healed with no complications

(-) Asthma(-) TB(-) Hypertension(-) Diabetes

No other past surgeries or hospitalizations

Family Medical History

(+) Asthma(-) HPN(-) DM(-) TB(-) CA(-) Stroke(-) CVD

Personal and Social History

No vices, currently studying in Grade 5 but had to stop schooling since the injury.

She is the 2nd of 3 children and has good relationships with her siblings. She has good social support from both family and friends .

Review of Systems

(+) Pain over lumbar area, VAS 5/10(-) Headache(-) Blurring of Vision(-) Neck Pain/Stiffness(-) Nausea(-) Vomiting(-) Chest Pain(-) Urinary/Bowel Changes(-) Dysuria(-) Abdominal Pain

Physical Examination

General Survey:Found in bed, alert, conscious, coherent and not in cardiorespiratory distress. She speaks in sentences, can follow commands and can converse clearly.

Physical Examination

Vital Signs:HR 84RR 24BP 100/70

HEENT:Anicteric sclerae, pink palpelbral conjunctivae, full EOMs, pupils EBRTL, subconjunctival hemorrhages on both eyes, (-) blurring of vision, (-) CLAD, (-) ANM, (-) masses/tenderness, (-) facial asymmetry

Physical Examination

Chest/Lungs:Clear breath sounds, equal chest expansion, (-) crackles/ rales/wheezes

Heart:Adynamic precordium, regular rate and rhythm, no murmurs

Abdomen:Soft, flabby abdomen with normoactive bowel sounds, (-) bowel changes

Genitourinary:(-) urinary changes, CVA not assessed

Physical Examination

Extremities:Multiple abrasions over facial area, arms, legs and back. No gross deformities on inspections. CRTs <2 secs, good pulses for all extremities. Both legs extended, R foot in extended plantar flexion. Manual muscle testing for UE all 5/5. Lower extremities; left 3/5, right 0/5.

Assessment

Compression Fracture L1 VertebraIncomplete Spinal Cord Injury, ASIA class B, intact sensory perception, Neurologic Level L1

DISCUSSION

Goals

Short TermPrevent SCI complicationsWheelchair mobilityMaintain range of motion of all jointsPrevent bed sore formation

Long TermGo back to schoolingIndependent ADLs

Compression FracturesForce ruptures plates of vertebra & shatters the bodyWedge shaped appearing vertebra on X-rayMay involve injury to nerve root &/or cordFragments may project into spinal canalShearing / Spinal Cord Compression traumatic necrosis of the spinal cord destruction of gray and white matter variable amount of hemorrhage, chiefly on vascular

central parts maximal at the level of injury and 1 or 2 segments

above and below it

Clinical Effects of SCI

1) voluntary movement in parts of the body below the lesion immediately and permanently lost

2) all sensation from the lower (aboral) parts is abolished

3) reflex functions in all segments of the isolated spinal cord are suspended

Clinical Effects of SCI

2 Stages1. Spinal Shock / Areflexia2. Stage of Hypereflexia

Spinal Shock•Reflex arc is not functioning•motor function lost with atonic paralysis of bladder,

bowel, gastric atony•muscles below level of lesion become flaccid and

hyporeflexic• Loss of sensation below the level of the lesion•Duration: Lasts from 24 hours to 3 months after injury.

Average is 3 weeks.

Stage of Hypereflexia• As spine recovers from shock, reflex arc functions

w/out inhibitory or regulatory impulses from the brain, creating local spasticity & clonus

• Reflexes become stronger• Pattern of higher flexion is noted• Dorsiflexion of the big toe (Babinski sign)• Bladder starts to contract irregularly

Complete Lesion

Complete Injury (Waters 1991)Absence of sensory and motor function in the lowest sacral segmentZone of Partial Preservation (only used with complete lesions): dermatomes & myotomes caudal to neurological level of injury that remain partially innervated

Incomplete LesionPartial preservation of sensory and/or motor functions

below the neurological level, whichWith Sacral Sparing —voluntary anal sphincter

contraction or sensory function Due to preservation of the periphery of the SC Sacral sparing indicates possibility of SC recovery

PROBLEMS IN SPINAL CORD INJURY

Orthostatic HypotensionSudden drop in systolic blood pressure (BP) of at least 20 mm Hg or diastolic BP by at least 10 mm Hg within 3 minutes of standing upright or 60 degrees on a tilt table lightheadedness, dizziness, ringing of the ears, fatigue, tachycardia, and sometimes syncopeOccurs more frequently in persons with cervical level or neurologically complete injuriesWhen bedrest is prolonged, the degree of orthostasis tends to be more severeIntensifies after eating, exposure to hot environments, defecation, and rapid bladder emptying

Orthostatic Hypotensionexact mechanism is unknown, but theories include increased sensitivity of baroreceptors and catecholamine receptors in the vessel walls, development of spasticity, improved autoregulation of cerebral vascular perfusion, and adaptations of the renin-angiotensin system

Autonomic DysreflexiaA composite of symptoms, most notably a sudden rise in BP, seen in those with SCI due to autonomic dysfunctionUsually restricted to those with injuries at or above T6Most common source of noxious stimulus is from the bladder, either from overdistension or infection, followed by fecal impaction

HypercalcemiaOccurs when bone resorption is increased in association with an impaired fractional excretion of calcium by the kidney

Risk factors: multiple fractures, age under 18 because of high rate of bone turnover, male gender, high level lesion, complete neurological injury, prolonged immobilization, and dehydration

HypercalcemiaSymptoms: acute onset of nausea, vomiting, anorexia, lethargy, polydipsia, polyuria, or dehydration

Tx: intravenous fluid (normal saline at 100 to 150 cc/hour), as tolerated to increase calcium excretion

Other meds:calcitonin, etidronate, glucocorticoids , pamidronate

Heterotrophic OssificationFormation of lamellar bone within the soft tissue surrounding a joint

Clinical limitation of the range of motion (ROM), joint may also appear warm and swollen

In severe cases, adjacent neurovascular structures may be compromised leading to distal extremity swelling and nerve entrapment

Heterotrophic Ossification

Treatments: passive- and active-assisted ROM with gentle stretching after the acute inflammatory period is over (1 to 2 weeks), nonsteroidal antiinflammatory drugs (NSAIDs) (e.g., indomethacin), bisphosphonates, radiation therapy, and surgical excision

Thromboembolic DisordersDevelopment of DVT is low in the first 72 hours, and occurs most frequently during the first 2 weeks (approximately 80% of cases) following injury

PE is the 3rd leading cause of death in all SCI px in the first-year post injury

Clinical signs: unilateral edema, low-grade fever, and pain in a patient with an incomplete injury

Pressure Ulcers Risk factors: level and severity of the injury, gender,

ethnicity, marital status, employment status, educational achievement, tobacco and alcohol use, nutritional status, and possibly depression Having a previous ulcer is a risk factor as well.

The longer the time a person has been injured the greater the risk of developing an ulcer.

Pressure UlcersThe most common location in persons with SCI within the first 2 years is the sacrum, followed by the ischium, heel, and trochanter.

After 2 years, the ischial tuberosities are the most common site of development

Musculoskeletal PainIn persons with SCI upper extremities are used for weight-bearing activities

Shoulder pain is the most commonly reported painful joint after SCI chronic impingement syndrome rotator cuff pathology

Musculoskeletal PainIf pain develops acutely, then referred pain should be excluded

Pain associated with neurological changes (i.e., weakness, sensory loss or reflex changes) may be due to peripheral nerve entrapment, radiculopathy, or a posttraumatic syrinx.

Neuropathic PainMay be treated with Gabapentin

Opioids are also gaining acceptance as a therapeutic option in nonmalignant pain syndromes and are rated by SCI patients as one of the more effective treatments

Posttraumatic Syringomyelia most common cause of progressive myelopathy after

an SCI may develop at any time, from 2 months to decades

postinjury Presents as neulogical decline or as elongated cavity

in MRI The most common presenting symptom is pain,

usually located at the site of the original injury or may radiate to the neck or upper limbs

Posttraumatic SyringomyeliaPain is described as aching or burning, often worse with coughing, sneezing, straining, and in the sitting rather than in the supine positionEarliest sign is an ascending loss of deep tendon reflexesMRI with gadolinium is the gold standard in dx

MANAGEMENT

Workup

Arterial blood gas measurements• to evaluate adequacy of oxygenation and ventilation Lactate levels •to monitor perfusion status Hemoglobin and/or hematocrit levels •to detect or monitor sources of blood loss Urinalysis •to detect associated genitourinary injury

Imaging

Standard Radiographs•Not as effective as a CT scan but can be obtained faster. It is sometimes sufficient to assess spinal injury particularly in emergent cases•3 standard views

a) Anteroposteriorb) Lateralc) Odontoid (cervical spine)

Imaging

CT Scan•More sensitive, better visualization•For delineating bony abnormalities or fractures•Radiography with CT scanning has a negative predictive value between 99-100%

MRI•best for suspected spinal cord lesions, ligamentous injuries, or other soft tissue injuries or pathology•for evaluation of nonosseous lesions•can visualize soft tissue changes secondary to injury

Treatment

Prehospital Care of Suspected Spinal Injuries

1. assure patient safety and prevent further injury2. stabilize and immobilize the spine on the basis of

mechanism of injury, pain in the vertebral column or neurologic symptoms

3. use a cervical collar or backboard for transport

Treatment

Emergency Department Care

1. assessment and treatment of airway, respiration and circulation

2. assessment of associated injuries or covert/overt bleeding

3. some patients may require intubation

Treatment

4. treatment of neurogenic shocka) fluid replacement with isotonic solutionb) systolic BP of no less than 90-100 mmHg to maintain spinal

cord perfusionc) heart rate of 60-100 bpm with normal sinus rhythmd) atropine treatment of hemodynamically significant

bradycardiae) urine output of 30mL/h; inotropic support with dopamine

for patients with decreased urinary output despite adequate fluid resuscitation

f) prevent hypothermia

Treatment

5. Neurologic assessment with imaging6. Nasogastric tube placement since ileus is common in

SCI patients7. Prevention of pressure sores

Steroid therapy is no longer advocated in the management of SCI

Surgical Management

May require a team approach from different surgical fields depending on mechanism of injury, location, severity and other associated conditions1. Trauma Surgeon•Since the majority of spinal cord injuries are traumatic in nature2. General Surgeon•Patients can present with more than one injury requiring surgical intervention

Surgical Management

Rigid External Orthotic Devices•Stabilize the spine and decrease range of motion•Include cervical collars and halo vests

Goals of Surgical Intervention1. Decompression of spinal cord or nerve roots2. Stabilization of injuries judged too unstable to heal

with external orthotics only (surgical stabilization)

Surgical Management

3. Orthopedic SurgeonFor repair of affected skeletal structures and removal of bone fragments in the case of fracture trauma to the spine4. NeurosurgeonAssessment of affected neurologic structures and appropriate repositioning, repair, anastomosis or other procedures involving the CNS or spinal cordEach surgical team is composed of specific members based on the patient’s condition and type of injury.

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