SPINE SGD

1. SPINE SGD SAN GABRIEL, SANIANO, SANTOS JJ, SANTOS MS, SISON, SORREDA, SOTALBO

2. 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, 2009 TOI: 1:30 PM POI: road in Bacoor, Cavite MOI: vehicular crash

3. 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.

4. 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...

5. 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, 2009 She was transferred to the Spine Ward and is awaiting definitive management.

6. 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

7. Family Medical History (+) Asthma (-) HPN (-) DM (-) TB (-) CA (-) Stroke (-) CVD

8. 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 .

9. 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

10. 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.

11. Physical Examination Vital Signs: HR 84 RR 24 BP 100/70 HEENT: Anictericsclerae, pink palpelbral conjunctivae, full EOMs, pupils EBRTL, subconjunctivalhemorrhages on both eyes, (-) blurring of vision, (-) CLAD, (-) ANM, (-) masses/tenderness, (-) facial asymmetry

12. Physical Examination • Chest/Lungs: • Clear breath sounds, equal chest expansion, (-) crackles/ rales/wheezes • Heart: • Adynamicprecordium, regular rate and rhythm, no murmurs • Abdomen: • Soft, flabby abdomen with normoactive bowel sounds, (-) bowel changes • Genitourinary: • (-) urinary changes, CVA not assessed

13. 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.

14. Assessment Compression Fracture L1 Vertebra Incomplete Spinal Cord Injury, ASIA class B, intact sensory perception, Neurologic Level L1

15. DISCUSSION

16. Goals • Short Term • Prevent SCI complications • Wheelchair mobility • Maintain range of motion of all joints • Prevent bed sore formation • Long Term • Go back to schooling • Independent ADLs

17. Compression Fractures • Force ruptures plates of vertebra & shatters the body • Wedge shaped appearing vertebra on X-ray • May involve injury to nerve root &/or cord • Fragments may project into spinal canal • Shearing / 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

18. 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

19. Clinical Effects of SCI 2 Stages Spinal Shock / Areflexia Stage of Hypereflexia

20. 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.

21. 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

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

23. Incomplete Lesion • Partial preservation of sensory and/or motor functions below the neurological level, which • With 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

24. PROBLEMS IN SPINAL CORD INJURY

25. Orthostatic Hypotension • Sudden 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 syncope • Occurs more frequently in persons with cervical level or neurologically complete injuries • When bedrest is prolonged, the degree of orthostasis tends to be more severe • Intensifies after eating, exposure to hot environments, defecation, and rapid bladder emptying

26. Orthostatic Hypotension • exact 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

27. Autonomic Dysreflexia • A composite of symptoms, most notably a sudden rise in BP, seen in those with SCI due to autonomic dysfunction • Usually restricted to those with injuries at or above T6 • Most common source of noxious stimulus is from the bladder, either from overdistension or infection, followed by fecal impaction

28. Hypercalcemia • Occurs 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

29. Hypercalcemia • Symptoms: 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

30. Heterotrophic Ossification • Formation 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

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

32. Thromboembolic Disorders • Development 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

33. 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.

34. Pressure Ulcers • The 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 ischialtuberosities are the most common site of development

35. Musculoskeletal Pain • In 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

36. Musculoskeletal Pain • If 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.

37. Neuropathic Pain • May 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

38. 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

39. Posttraumatic Syringomyelia • Pain is described as aching or burning, often worse with coughing, sneezing, straining, and in the sitting rather than in the supine position • Earliest sign is an ascending loss of deep tendon reflexes • MRI with gadolinium is the gold standard in dx

40. MANAGEMENT

41. 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

42. 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 • Anteroposterior • Lateral • Odontoid (cervical spine)

43. 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

44. Treatment Prehospital Care of Suspected Spinal Injuries assure patient safety and prevent further injury stabilize and immobilize the spine on the basis of mechanism of injury, pain in the vertebral column or neurologic symptoms use a cervical collar or backboard for transport

45. Treatment Emergency Department Care assessment and treatment of airway, respiration and circulation assessment of associated injuries or covert/overt bleeding some patients may require intubation

46. Treatment • treatment of neurogenic shock • fluid replacement with isotonic solution • systolic BP of no less than 90-100 mmHg to maintain spinal cord perfusion • heart rate of 60-100 bpm with normal sinus rhythm • atropine treatment of hemodynamically significant bradycardia • urine output of 30mL/h; inotropic support with dopamine for patients with decreased urinary output despite adequate fluid resuscitation • prevent hypothermia

47. Treatment Neurologic assessment with imaging Nasogastric tube placement since ileus is common in SCI patients Prevention of pressure sores Steroid therapy is no longer advocated in the management of SCI

48. Surgical Management • May require a team approach from different surgical fields depending on mechanism of injury, location, severity and other associated conditions • 1. Trauma Surgeon • Since the majority of spinal cord injuries are traumatic in nature • 2. General Surgeon • Patients can present with more than one injury requiring surgical intervention

49. Surgical Management • Rigid External Orthotic Devices • Stabilize the spine and decrease range of motion • Include cervical collars and halo vests • Goals of Surgical Intervention • Decompression of spinal cord or nerve roots • Stabilization of injuries judged too unstable to heal with external orthotics only (surgical stabilization)

50. Surgical Management 3. Orthopedic Surgeon For repair of affected skeletal structures and removal of bone fragments in the case of fracture trauma to the spine 4. Neurosurgeon Assessment of affected neurologic structures and appropriate repositioning, repair, anastomosis or other procedures involving the CNS or spinal cord Each surgical team is composed of specific members based on the patient’s condition and type of injury.