Complications - spinal cord injury .pptx

Spinal cord injury complications

1. COMPLICATIONS of SPINAL CORD INJURY Dr. Anit Catherine Charls PG - PMR

2. ACUTE COMPLICATIONS Pulmonary Cardiovascular Bowel and bladder dysfunction Deep vein thrombosis Pulmonary embolism Pressure ulcer Pain Sexual dysfunction

3. CHRONIC COMPLICATIONS Heterotopic ossification Thermal regulation dysfunction Gastrointestinal complications Spasticity Contratures Metabolic dysturbances Pathologic fractures

4. NEUROGENIC SHOCK Neurogenic shock is due to severe hypotension and bradycardia in cervical injuries due to drop in blood pressure in relation to an acute SCI. Because of an intact parasympathetic influence  via  the vagal nerve and a loss of sympathetic tone due to disruption in supraspinal control, neurogenic shock develops as a result of imbalance of the autonomic control. Depending on the severity of the SCI, prolonged and severe hypotension, requiring vasopressive therapy may last up to 5 weeks after injury. In the Trauma Audit and Research Network database , the percentages of neurogenic shock was 19.3% in cervical injuries. In thoracic and lumbar injuries the reported incidence was 7.0% and 3.0%, respectively.

5. Cardiovascular Complications Injuries to the autonomic nervous system are the cause of many of the cardiovascular complications following a SCI. In the acute phase many irregularities of the cardiac rhythm may occur; - sinus bradycardia and bradyarrhythmias (14%-77%) - supraventricular ectopic beats (19%), - ventricular ectopic beats (18%-27%), - orthostatic hypotension (33%-74%), - increased vasovagal reflex. Common autonomic disturbances after 4 to 5 weeks of post-injury are autonomic dysreflexia, orthostatic hypotension.

6. ORTHOSTATIC HYPOTENSION • State of transient reflex depression caused by a lack of sympathetic outflow and triggered by tilting the patient upright > 60 degrees. – Lesion at T6 or above – T1–L2 responsible for tachycardia, vasoconstriction, and increased arterial pressure. – Heart and blood vessels supplied by T1–T7.

7. Mechanism Upright position causes decrease in blood pressure (BP). Aortic and carotid baroreceptors sense decrease in BP (would usually increase sympathetic outflow in neurologically intact individual); however, efferent pathway interrupted following SCI. Brainstem unable to send message through SC to cause sympathetic outflow and vasoconstriction of splanchnic bed to increase BP. Orthostasis lessens with time due to development of spinal postural reflexes whichallow for vasoconstriction due to improved autoregulation of cerebrovascular circulation in the presence of perfusion pressure

8. • Symptoms – Lightheaded – Dizziness – Presyncope – Nausea – Pallor • Signs – Hypotension: loss of sympathetic tone – Tachycardia: aortic and carotid baroreceptors respond to hypotension. – Syncope

9. Treatment Reposition —Trendelenburg/– recliner wheelchair – Elastic stocking/abdominal binder/ace wrap LE – Accommodation–use of tilt table – Fluid resuscitation: increase fluid intake Pharmacological Salt tablets 1 gram QID Midodrine (alpha 1 adrenergic agonist): 2.5–10 mg TID (mineralocorticoid): 0.05–0.1 mg QID

10. AUTONOMIC DYSREFLEXIA (AD) Mechanism: Syndrome of massive imbalanced reflex sympathetic discharge in patients with SCI above the splanchnic outflow (T5–L2). • Occurs in patients with lesions at T6 and above and affects 48–90% of susceptible patients. AD is secondary to the loss of descending central sympathetic control and hypersensitivity of receptors below the level of the lesion. Pathophysiology: – Noxious stimulus—increases sympathetic reflex spinal release – Regional vasoconstriction—causes a marked rise in arterial BP – Increases peripheral vascular resistance—increases cardiac output, increases BP

11. Onset: - After spinal shock. May appear within 2–4 weeks post injury. - If occurs in a patient, will present within the first year in > 90% of cases. - Classically occurs in patients with neurological complete SCI. Cause: - Noxious stimulus below the level of the lesion – Most commonly from bladder (over-distention or infection), followed by bowel (fecal impaction). – Abdominal emergency (appendicitis, cholecystis, pancreatitis) – Pressure ulcers – Fractures – Urinary tract infections

12. Signs and Symptoms: – Headache – Sweating above level of SCI – Flushing above level of SCI – Elevated blood pressure – Piloerection – Pupillary constriction – Sinus congestion Management: Sit patient upright and loosen all tight fitting clothing and devices (ie, elastic band from urine leg bag, TEDS, abdominal binder) 2. Identify and remove noxious stimulus—early bladder evaluation. 3. Monitor BP every 2–5 minutes during episode and monitor for recurrent symptoms for at least 2 hours after resolution to ensure that it does not recur.

13. 4. Pharmacotherapy: – Acute: transdermal nitroglycerin patch: can be removed once noxious stimulus corrected Clonidine: 0.3–0.4 mg Nifedipine:10 mg chew and swallow – ICU Management: Diazoxide Sodium Nitroprusside Labetalol Potential Complications of Autonomic Dysreflexia If hypertensive episodes are not treated, complications can lead to: Retinal hemorrhage,CVA /SAH, Seizure, MI,Death AD predisposes patient to atrial fibrillation by altering normal pattern of repolarization of the atria, making the heart susceptible to reentrant-type arrhythmias

14. PULMONARY CARE AND COMPLICATIONS IN SCI • Respiratory complications occur in up to 67% of acutely injured patients in the first month post injury. • Pulmonary complications are more common in high cervical injuries (C1–C4). The most frequent complications are pneumonia, atelectasis, and ventilatory failure. Respiratory ability based on SCI level: – C3: respiratory failure secondary to disruption of diaphragmatic innervation, usually requiring mechanical ventilation early after injury. May be able to wean off ventilator. – C4: generally able to maintain spontaneous ventilation. – In low cervical (C5–C8) and thoracic (T11–T12) complications are frequently acute. – Injuries above C8: loss of all abdominal and intercostal muscles, impairment of inspiration and expiration

15. – T1 through T5: intercostal volitional function is lost. – T5 through T12: progressive loss of abdominal motor function, impairing forceful expiration or cough • Pulmonary dysfunction occurs for several reasons following SCI: 1. Paralysis of some or all respiratory muscles to varying degrees 2. Loss of ability to cough secondary to varying levels of abdominal muscle paralysis 3. Injury to chest— eg , rib fracture 4. Pulmonary injury— eg , lung contusion

16. Predisposing Factors for Pulmonary Complications • Older age • Obesity—restrictive respiratory deficits • History of COPD, asthma, and smoking • Pneumonia is the leading cause of death among chronic SCI patients. • Left-sided respiratory complications are more common among hospitalized SCI patients. This is due to the left mainstem bronchus branching off at a 40–50° angle from vertical, making it more difficult to clear secretions, especially with suctioning. Pulmonary Compromise Related to Level of Injury • Head trauma may disrupt respiratory drive. • Lesions above C3 (and incomplete lesions initially): – Initially they require ventilatory support – Later they will fall into two groups: 1. No damage to phrenic nerve nucleus 2. Damage to phrenic nucleus

17. No Damage to Phrenic Nerve Nucleus Lesion above Phrenic Nerve (C2 and Above) • Diaphragm is innervated by the phrenic nerve (nerve roots C3, 4, 5 “keeps you alive”). • Lesion affecting the phrenic nerve can be determined by electro diagnostic studies including nerve conduction of the phrenic nerve or EMG of the diaphragm. • If phrenic nerve nuclei are intact and an UMN injury occurs, the patient may be a candidate for phrenic nerve or diaphragmatic pacing.

18. 2. Damage to the Phrenic Nerve Lesions affecting C3– 5 nerve roots or phrenic nerve • Determined by electro diagnostic studies. EMG of diaphram is necessary to rule out damage to phrenic nerve nucleus • C3: Respiratory failure secondary to disruption of diaphragmatic innervation, requiring mechanical ventilation • C4: Generally the highest level of injury at which spontaneous ventilation can be sustained. • T1 through T5: intercostal volitional function is lost • T5 through T12: progressive loss of abdominal motor function, impairing forceful expiration or cough. • Injuries below T12: few complications if there is lung injury ( eg , trauma) otherwise, no respiratory dysfunction

19. Prevention of Respiratory Complications • Use of incentive spirometer. • Monitor CO2 levels with ABGs. • Monitor vital capacity. • Cough assist—placing the hands on each side of the pts. upper abdomen and applying intermittent pressure, coordinated with the initiation of cough by the patient—helps produce forceful cough. • Mechanical cough assist—via use of an insuflattion-exsufflation machine – Advantages include the ability to better clear secretions, since it can clear both lung fields as well as clear out larger mucous plugs than the suction catheter, is easy to use, and patients prefer it.

20. Prevention of Respiratory Complications… • Use of incentive spirometer. – Contraindicated in patients with a history of bullous emphysema, known susceptibility to pneumothorax or pneumo-mediastinum. • Suctioning—tracheal suctioning may cause increased vagal tone leading to cardiac arrest (only suction as you withdraw catheter). • Chest physical therapy— • Strengthening of pectoralis major muscle, clavicular portion, in tetraplegic patients. • Pneumobelt—helps with exhalation. Inflatable, compresses the abdominal wall, diaphragm rises, and active respiration is produced .

21. Sleep Apnea in SCI • 15–60% of patients with SCI. • Common features loud snoring disrupted sleep witnessed apnea nocturnal gasping and choking daytime sleepiness fatigue • In SCI patients, the sleep apnea is primarily obstructive, with a small percentage of patients demonstrating central sleep apnea.

22. Complications daytime sleepiness cognitive changes including poor attention, concentration, complex problem solving, short-term recall, and judgment. • increased risk for the development of hypertension, pulmonary hypertension, congestive heart failure, depression, and mortality. •. Optimal work-up would include an overnight oximetry recording, followed by a formal sleep study, if the oximetry recording is abnormal. • Treatment includes assisted ventilation at night as well as possible use of medications directed towards relief of upper airway symptoms

23. Thermal Regulation Body temperature is controlled physiologically primarily by the hypothalamus and secondarily by personal behavior, to increase or decrease heat loss. Heat and cold signals  afferent nerves  hypothalamus integrated and thermal regulation  mediated by inhibition or activation of the sympathetic nervous system. Increase in core temperature  sympathetic inhibition  vasodilatation and sweating. Decrease in core temperature  sympathetic stimulus  vasoconstriction, and shivering.

24. With high-level and neurologically complete SCI, the afferent and efferent pathways are interrupted  vasomotor control and the ability to shiver and sweat are lost. Commonly seen in complete lesions above T6 , because of loss of supraspinal control. People with SCI therefore tend to have a higher body temperature in warm environments and a lower temperature in cold environments. This is termed poikilothermia. Mx proper heating and cooling of the environment is needed to ensure continuous thermal stability, especially for those with high-level SCI. Appropriate clothing should be worn, strenuous exercise in a hot environment avoided, and cool moist compresses applied when body temperature rises.

25. SWEAT SECRETION The sweat glands are largely sympathetically innervated in the upper part of the body from T1-T5, and in the lower part of the body from T6-L2. Changes in sweat secretion often occur after SCI, and excessive sweating ( hyperhidrosis ), absence of sweating ( anhidrosis ) and diminished sweating ( hypohidrosis ) may all occur. Most common symptoms are minimal/abolished sweating under the level of injury and profuse sweating over the level of injury. This is due to compensatory increase in sweat secretion above the level of injury due to the loss of sympathetic stimulation below the level of injury, which results in reduced sweat production. Sweating may also occur exclusively below the level of injury. This type of sweat is reflex sweating, and is usually a symptom of a massive autonomic response that occurs particularly with cervical and high thoracic injuries (above T8-T10).

26. BLADDER DYSFUNCTION LMN Bladder -Failure to Empty Causes: • Commonly results from flaccid bladder and/or spastic sphincter • Spinal shock: reflex arc not functioning due to initial trauma • Conus medullaris syndrome • Cauda equina syndrome • Syringomyelia • Acute CVA (detrusor areflexia )

27. Lesion: • Lesion involving sacral micturition center (S2–S4) • Lesion exclusively involving the peripheral innervation of the bladder Can Result in: • Large, areflexic, flaccid bladder • Tight, spastic sphincter • Failure to Empty

28. Treatment: • Intermittent catheterization (IC) • Crede maneuver ( suprapubic pressure) • Valsalva maneuver • Drugs to induce urination: – Bethanacol : stimulate cholinergic receptors – Alpha blockers: block alpha adrenergic receptors

29. UMN Bladder-Failure to Store Causes: • Commonly results from spastic bladder and/or incompetent sphincter • SCI: return of reflex arc after initial trauma • Subacute CVA (detrusor hyperreflexia ) • Multiple Sclerosis Lesion: • Lesion above sacral micturition center (above S2)

30. Can Result in: • Small, overactive, spastic bladder • Failure to store Treatment: • Drugs to store urine – Detrol , Pro- Banthine : anticholinergic medications are most commonly used – Ditropan ®: Direct smooth muscle relaxor – Tofranil ®, ephedrine: Stimulates alpha, beta receptors to allow storage

31. Urinary Tract Infections (UTIs) Pathophysiology UTIs are generally caused by the endogenous flora of the host overcoming the competing normal flora and the host defense mechanism. • The presence of the UTI is affected by: – Virulence of the invading microorganism – Condition of the urine as the culture medium – Host defense mechanisms

32. Management of UTIs Asymptomatic UTIs and Prophylaxis of UTIs • Asymptomatic bacteriuria in SCI patients being managed with an indwelling catheter or IC is generally not treated. • In addition, the use of prophylactic antibiotics to prevent UTIs after SCI is not supported. Vitamin C supplementation, cranberry juice, and methenamine salts can be used as acidifying agents.

33. Symptomatic UTIs A UTI is generally treated when there is: 1. Significant bactiuria - Clean catch midstream urine specimen: the presence of > 100,000 organisms per mL Bladder catheterization: the presence of > 100 organisms per mL 2. Pyuria 3. Clinical signs and symptoms (fever, malaise, increased spasticity or neurogenic pain)

34. Most Common Urinary Tract Complications in the Neurogenic Bladder • Irregular, thickened bladder wall and small diverticuli—earliest changes • Vesicoureteral reflux: 10–30% of poorly managed bladders, leads to pyelonephritis, renal stones. • Hydronephrosis and hydroureters caused by outlet obstruction • Overdistended, areflexic bladder • Reduced bladder compliance • Kidney and bladder stones

35. Management of Bowel Dysfunction in SCI Acute Phase complications Adynamic ileus and gastric atony • Occur in 63% of SCI patients, resulting from spinal shock and reflex depression. • Adynamic ileus usually presents immediately following SCI (can be delayed 24–48 hrs ) and typically resolves within 1 week. • Gastric atony may result in vomiting and aspiration. Management – Nasogastric tube (NGT) suction to prevent GI dilation and respiratory compromise for persistent abdominal distention. – Intravenous (IV) fluids – Use of electrical stimulation has been shown to be effective (TENS to stimulate peristalsis of gut). – If longer, Metoclopramide and/or Erythromycin (if other interventions are unsuccessful) can be used to stimulate peristalsis .

36. chronic Phase Complications • Colonic distension: problems with small bowel motility • Pseudo obstruction: no evidence of obstruction on radiographic studies • Abdominal distention, nausea, vomiting, constipation • Secondary causes: electrolyte imbalance and medications (narcotics, anticholinergics). Management: – NG suction if gastric atony – Remove constipating medications. – Oral medications to promote stool propulsion . – Rectal medications (ie, suppositories, enemas) – If cecum is dilated > 12 cm, surgical decompression or colonoscopy may be considered.

37. Long-Term Management • Padded upright commode preferred to side-lying position. • Maintain adequate fluid intake (2–3 L/day). • Minimize medications that decrease bowel motility (opioids, tricyclic agents, anticholinergics). • Diet: moderately high fiber (approximately 30 grams/day) • Medications: – Bulk forming agents – Bowel irritants – Stool softeners

38. Bowel Program Goals • Initially aims for daily bowel movement. As time progresses can be performed daily to every third day . • Ultimate goal is consistent and complete evacuation of the bowel at a specified time, in a relatively short time period, without incontinence between programs. • To assist with defecation, intact reflexes can be utilized: The Gastrocolic Reflex - Contraction of the colon occurring with gastric distention - When feasible, SCI patients should be instructed to perform their bowel programs 20–30 minutes after a meal. - Increased colonic activity occurs in the first 30 to 60 minutes after a meal (usually within 15 minutes). - Therefore, place the SCI patient on the commode within 1 hour subsequent to a meal.

39. T he Anorectal Reflex (Rectocolic Reflex) Occurs when rectal contents stretch the bowel wall reflexively, relaxing the internal anal sphincter. Suppositories and digital stimulation cause the bowel wall to stretch and take advantage of this reflex. Note this reflex can be manipulated by digital stimulation of the rectum. • Key components of a bowel program: – Digital stimulation – Dietary fiber intake – Oral medications – Rectal evacuants • For pharmacological intervention, start with the “3-2-1” program: 1. Docusate sodium: 100 mg 3\ daily 2. senna glycoside: 2 tablets daily (timed approximately 8 hours before suppository) 3. Dulcolax : 1 suppository daily after meal (usually dinner or breakfast)

40. Complications of Neurogenic Bowel Fecal incontinence: Skin breakdown, ulcerations, UTI Fecal impaction: nausea, abdominal discomfort, autonomic dysreflexia. • Anticholinergic meds that are prescribed for failure-to-store bladder, as well as opioid medications, can cause severe constipation. • Bowel dysfunction affects the patient’s community integration—socially, vocationally, and psychologically. • Surgical intervention (e.g., colostomy)—should be considered if diet changes, medications, and physical techniques fail to produce consistent bowel movements .

41. Other Gastrointestinal Complications Gastroesophageal Reflux • Avoid prolonged recumbency; elevate the head of the bed. • Avoid smoking. • Avoid certain medications, such as Ca+ channel blockers, benzodiazepines, nitrates, anticholinergics. Treatment : – Antacids for mild to moderate symptoms – H2 antagonists, Metoclopramide 10 mg qid (short term use only)

42. Gastrointestinal Bleeding • Most frequently secondary to perforating and bleeding ulcers • Most common early after injury • Use of steroids may increase risk. • Diagnosis : endoscopy is the diagnostic method of choice. • Provide prophylaxis with: – Antacids – H2 blockers – Sucralfate—stimulates local prostaglandin synthesis • Treatment : – With active GI bleeding: maintain BP, correct coagulation deficits, monitor CBC, consult GI/surgical service.

43. Cholecystis • Most common cause of emergency abdominal surgery in SCI patients • Increased risk: 3x > in SCI • Possible causes: abnormal gallbladder motility in lesions above T10, abnormal biliary secretion, abnormal enterohepatic circulation • Should be considered if adynamic ileus doesn’t resolve or it recurs. • Treatment: – Medical observation/antibiotics – May opt for surgical removal.

44. Pancreatitis • Most common in the first month post injury • May be related to steroid use—increased viscosity of pancreatic secretions. • May suspect when adynamic ileus doesn’t improve. Clinical symptoms: – Abdominal pain – Nausea – Emesis – Poor appetite Evaluation: – Labs: elevated amylase, lipase – Radiographs – CT of abdomen – Ultrasonogram

45. Superior Mesenteric Artery (SMA) Syndrome • Condition in which the third portion of the duodenum is intermittently compressed by overlying SMA resulting in GI obstruction. • Predisposing factors include: – Rapid weight loss (decrease in protective fatty layer) – Prolonged supine position – Spinal orthosis – Flaccid abdominal wall causes hyperextension of the back • Symptoms: – Postprandial nausea and vomiting – Bloating – Abdominal pain

46. • Diagnosis: UGI Series demonstrates abrupt duodenal obstruction to barium flow. • Treatment: typically conservative – Eat small, frequent meals in an upright position. – Lie in the left lateral decubitus position after eating. – Metoclopramide ( Reglan ®): stimulates motility of UGI tract. – Rarely requires surgery. If conservative treatment fails, surgical duodenojejunostomy should be performed.

47. METABOLIC COMPLICATIONS Hypercalciuria Immobilization, decreased weight bearing promotes bone resorption • Patients become Hypercalciuria—this may continue for 18 months. • Vitamin D and parathyroid hormone are not involved in the process. Hypercalcemia • In rare cases, patients with Hypercalciuria can develop hypercalcemia when the efflux of calcium is massive or the glomerular filtration rate of the kidneys is reduced. Incidence: 10–23% of persons with SCI • Affects adolescent and young adult males. • More common in patients with tetraplegia than with paraplegia • Usually appears 4–8 weeks after SCI, (range 2 weeks to 6 months postinjury ). Clinical presentation : often insidious, and presenting symptoms can be vague, so should maintain a high index of suspicion.

48. • Signs and symptoms: “Bones, stones, and psychic overtones” – Fatigue– Lethargy – Dehydration – Constipation – Anorexia - nausea – Vomiting – Polydipsia – Polyuria – Psychosis Labs : serum calcium level is usually < 10.5. Treatment : – Treat both symptomatic and asymptomatic patients because prolonged hypercalcemia can cause nephrocalcinosis. – Hydration with IV normal saline. Increases urinary excretion of calcium. – Early mobilization. Standing and ambulation as tolerated – Diet Restrictions - Restriction of dietary calcium intake is unnecessary; 1,25-dihydroxyvitamin D levels already are low, suppressing intestinal absorption of calcium.

49. – Medications Pamidronate: inhibits osteoclast-mediated resorption and reduces osteoclast viability. The drug is administered as a single IV infusion 60mg \ 4 hours to 90 mg \ 24 hours) depending on severity of hypercalcemia) and rapidly lowers serum calcium within 3 days. Furosemide increases urinary excretion of calcium (although not routinely used). Avoid thiazide diuretics - cause hypercalcemic effects.

50. Osteoporosis Secondary to disuse–occurs in extremities below the level of the lesion • Approx. 22% bone loss 3 months post injury • Most bone loss occurs over the first year postinjury • Increases risk of fracture throughout the patient’s life Treatment: – Weight bearing early post injury may be of benefit. – Pharmacologic agents may be helpful in reducing rate of bone loss in acute SCI. – Long-term treatment should include calcium and Vitamin D supplementation.

51. Fractures • The cumulative incidence of chronic long-bone fractures is approximately 2.5% over 20 years after SCI. • Fractures are more common in persons with neurological complete injuries, and in paraplegia relative to tetraplegia. • Most fractures are due to falls during transfers, but fractures can result from minor stresses ( eg , long-sitting or ROM) or without any known etiology. • Supracondylar femur fractures are the most common fractures , followed by the distal tibia, proximal tibia, femoral shaft, femoral neck, and humerus, respectively.

52. • Treatment: – Most fractures are treated nonoperatively with soft padded splints. – The patient should be allowed to sit within a few days. Callus formation is usually evident in 3–4 weeks. – Surgery, circumferential casting, and external fixation are usually not indicated unless there is significant deformity or vascular supply is in danger in the SCI population (because of potential complications due to low bone mass, risk of osteomyelitis, recurrent bacteremia, and skin breakdown.) – Femoral neck and subtrochanteric fractures are the most difficult to manage and internal fixation may be considered if a minimal device, such as an intramedullary rod, can be used.

53. Hyperglycemia • Up to 70% of the patients show insulin resistance, with abnormal response to glucose load. • Important to monitor in chronic patient and initiate treatment when appropriate

54. DEEP VENOUS THROMBOEMBOLISM / PULMONARY EMBOLISM IN SCI Deep Venous Thrombosis (DVT) • Predisposing Factors – Virchow’s triad: venous stasis/intimal injury/hypercoagulability – LE fractures – Obesity – History of previous DVT – DM – Arterial vascular disease – Older age – Immobility – Malignancy

55. • Incidence – Ranges 47–100%; varies widely depending on the method of detection and number of cases evaluated in the study. – More common in neurologically complete patients – More common in tetraplegic patients – 10 times more frequent in plegic leg • Onset – Most common during first 2 weeks after SCI. – Incidence decreases after 8–12 weeks post SCI.

56. . Diagnosis – Venogram is the gold standard. – Venous Doppler is used as a screening test for lower extremity DVTs Impedance plethysmography—accurate in assessment of DVTs above the calf – Sensitivity—95%; specificity—98% • Complications – Pulmonary embolism is the leading cause of death in acute SCI. – Postphlebitic syndrome (late complication of DVT): Distal venous hypertension - Spasticity - Chronic pain ( postthrombotic syndrome) - Ulceration - Autonomic dysreflexia

57. Thromboembolism Individuals with SCI have a higher risk of coagulation disorders and venous stasis due to physical inactivity, altered haemostasis with reduced fibrinolytic activity and increased factor VIII activity. They are therefore predisposed to thromboembolism. During the first year post-injury, the incidences of deep vein thrombosis and pulmonary embolism are estimated to be 15% and 5%, respectively. The incidence is highest 2-3 week after the injury, followed by a small peak three months after the injury. During the chronic phase, the incidence of clinically significant thromboembolism is less than 2%.

58. Pulmonary Embolism • Symptoms – Pleuritic chest pain – Dyspnea – Tachycardia – Fever – Hemoptysis – Hypoxemia • Physical Examination 1. Increased S2 sound: severe pulmonary HTN cor pulmonale right heart failure 2. Dullness at bases of lungs • Incidence – Up to 7% of acute/subacute SCI patients – Most cases develop from deep veins of the lower extremities. – PE is not influenced by degree or level of injury.

59. • Diagnosis (PE) – EKG: right axis deviation – Right bundle branch block (RBBB): if massive PE – ABG: O PO2 (PO2 drops severely) – Chest x-ray: wedge shaped opacity fluid vascularity – Perfusion lung scan: V/Q mismatched – Gold standard : pulmonary arteriogram • Treatment (PE) – O2 – Heparin – Vasopressor to treat shock • Surgical Treatment – Embolectomy

60. Prophylaxis for Thromboembolic Disorders • Mechanical Prophylaxis – External pneumatic compression devices (effective) Improves LE venous return, reduces stasis and stimulates fibrinolysis. If placement is delayed > 72 hours, rule out DVT before putting on compression devices. Contraindicated in patients with arterial insufficiency – Electrical stimulation: effective but hardly used • Chemoprophylaxis – Anticoagulants generally withheld for first 72 hours. Incidence then is small and perhaps increases complications. Can still use mechanical devices. – Hold dose morning of surgery and resume the next day. – Options: Enoxaparin ( Lovenox ®) low molecular weight heparin (LMWH)—most highly recommended, Dose: 30 mg SQ BID Low dose unfractionated heparin (UH) Dose: 5000 IU SQ every 8–12 hours or 7500 IU SQ every 12 hours Adjusted dose unfractionated heparin Dose: maintain aPTT at 1.5\ control Better prophylaxis than low dose UH but increases risk of bleeding.

61. • Inferior Vena Cava (IVC) Filter Indications – Failed anticoagulant prophylaxis – Contraindication to anticoagulation – High level complete tetraplegia with poor cardiopulmonary reserve – An IVC is not a substitute for prophylaxis • Duration of DVT Prophylaxis: Current Consortium Recommendations – Incomplete SCI Continued until discharge in persons with an incomplete SCI. – Complete SCI Continue 8 weeks postinjury in uncomplicated complete motor injury. Continue 12 weeks postinjury or discharge from rehab in persons with complete motor injury and other risk factors. (ie, lower limb fracture, history of thrombosis, cancer, heart failure, obesity, or age > 70)

62. • DVT Management – Many centers using LMWH for initiation of treatment. – Therapeutic anticoagulation initially with IV heparin with subsequent transition to warfarin . Heparin—if not contraindicated standard: 5,000 units IV bolus; followed by a constant infusion of 1,000 units/ (25,000 units in 250 mL D5W at 10 cc/hr) maintain PTT 1.5–2 times normal at least 5–10 days of anticoagulation prior to mobilization – If documented proximal DVT, Coumadin continued for 6 months. – If there is a contraindication to anticoagulant therapy or significant risk of hemorrhage, IVC filter is used to prevent pulmonary embolism

63. A Clinical Practice Guideline for the Management of Patients With Acute Spinal Cord Injury: Recommendations on the Type and Timing of Anticoagulant Thromboprophylaxis (1) anticoagulant thromboprophylaxis be offered routinely to reduce the risk of thromboembolic events in the acute period after SCI (2) anticoagulant thromboprophylaxis , consisting of either subcutaneous low-molecular-weight heparin or fixed, low-dose unfractionated heparin (UFH) be offered to reduce the risk of thromboembolic events in the acute period after SCI. Given the potential for increased bleeding events with the use of adjusted-dose UFH, this option is not recommended;”  (3) Commence anticoagulant thromboprophylaxis within the first 72 hours after injury, if possible, in order to minimize the risk of venous thromboembolic complications during the period of acute hospitalization.”

64. HETEROTOPIC OSSIFICATION (HO) Formation of mature lamellar bone indistinguishable from normal bone in soft tissues, most frequently deposited around a joint • As bone matures it becomes encapsulated, not connected to periosteum. • Causes – No definitive explanation established. – Possibly due to alteration in neuronal control over the differentiation of mesenchymal cells into osteoblasts, which form new bone. Incidence – HO has been reported to occur in 16–53% of patients following SCI. – Clinically significant HO that results in significant limitation of joint ROM affects 10–20% of SCI patients – Occurs below the level of neurological injury. – Most common joints involved in SCI (in order of occurrence): hip/knee/shoulder/elbow

65. Onset 1–4 months post injury most common, but can present after first 6 months. Symptoms Heat/warmth Localized soft tissue swelling—may present similar to an acute DVT Decreased ROM of a joint Joint erythema/joint effusion Low-grade fever • Risk Factors Spasticity Completeness of injuries Trauma or prior surgery to joint Age (younger) Presence of DVT

66. • Diagnosis – Can be seen early after onset on bone scan. – Bone scan precedes findings on x-ray. – Plain film detects HO in at least 7–10 days after clinical signs are observed. – Serum alkaline phosphatase increases at 2 weeks, exceeds normal levels at 3 weeks, peaks at 10 weeks, and returns to normal before HO matures. – CPK and ESR: can be elevated but not specific for HO. • Complications – Peripheral nerve entrapment – Decreased ROM/loss of function – progressing to ankylosis – HO overlying a bony prominence will directly predispose to pressure ulcer/skin breakdown secondary to poor positioning • Prophylaxis – Didronel® ( etidronate disodium) 20 mg/kg/day for 2 weeks and then 10 mg/kg/day for 10 weeks, but not frequently prescribed.

67. Treatment Options ROM—the goal is to maintain functional range. Once the acute – inflammatory period is over the affected joint should be gently ranged through functional range. Didronel \ 6 months. Dose may be based upon the initial CPK blood test results. Normal CPK: use Didronel 20 mg/kg/day \ 3 months, and then 10 mg/kg/day for another 3 months. Elevated CPK: use high dose (20 mg/kg/day) \ 6 months. - Surgery is considered when HO severely limits ROM impairing function. - Should only be undertaken after bone is mature (12–18 months post injury with normal bone scan).

68. SPASTICITY Spasticity is a common secondary impairment after SCI characterized by hypertonus, increased intermittent or sustained involuntary somatic reflexes (hyperreflexia), clonus and painful muscle spasms. Spasticity affects 70% of patients with SCI and causes considerable disability for many. The pathogenesis of spasticity in patients with SCI remains uncertain. An alteration in the excitability of various supraspinal inhibitory nerve paths used to be the main explanation. Severe spasticity may contribute to increased functional impairment, contractures, ulcers, posture disorders and pain.

69. Management options of spasticity involve: elimination of exacerbating factors (such as urinary tract infection, constipation, ingrown nails, pulmonary infection, pressure ulcers,  etc .) use of physical agents (heat, cold) physical techniques, systemic medications, chemical neurolysis, intrathecal agents, electrical stimulations surgical interventions. Commonly used antispastic medications are Baclofen, Tizanidine, botulinum toxin, benzodiazepine, dantrolene sodium, gabapentin and Pregabalin.

70. Chemical neurolysis is usually used for localized spasticity. In this intervention, phenol or ethanol solution is used to constitute a nonselective destruction of the nerve axon or motor point that can decrease spasticity. Surgical approaches include many orthopedic procedures ( e.g ., tendon extension, tendon plasty or osteotomy) and the ablation of motor nerves and/or rhizotomy of sensory spinal roots. Surgical treatment of spasticity leads to irreversible changes and can often be avoided if other methods are used at an early stage.

71. PAIN SYNDROMES Chronic pain is one of the frequent secondary complications for individuals with SCI, with up to 80% of patients with SCI reported to suffer from it. Chronic pain may lead to functional disability and emotional discomfort and may impact negatively on community participation and quality of life. The International Association for the Study of Pain has proposed a taxonomy of pain with a tiered classification of pain related to SCI in which pain types are divided into two main groups: nociceptive (from bone, ligaments, muscle, skin, other organs) neuropathic (from peripheral or central neural tissue damage)

72. NOCICEPTIVE PAIN (MECHANICAL/MUSCULOSKELETAL/ORGANS) • More common than neuropathic pain • Damage to non-neural tissue including bone, ligaments, muscle, skin, other organs Musculoskeletal Nociceptive Pain • 70% of individuals with chronic SCI report pain in their UEs. • The shoulder is the most commonly affected joint usually due to use as a weight bearing joint and overuse syndromes: – Tendonitis/bursitis – Rotator cuff impingement/tear– Impingement syndrome – Subacromial bursitis – Capsulitis – Myofascial pain – Cervical radiculopathy

73. • Risk Factors – Tetraplegia > paraplegia – increases with time from injury, older age – Associated with manual WC use and transfers; overuse; overhead activities; inflexibility; muscle imbalances – Shoulder pain is a symptom, NOT a diagnosis! • Etiology – Intrinsic vs. extrinsic sources – Cervical spine changes – Heterotopic ossification Abdominal – pathology (with lesions above T7) – Cervical root compression – Syringomyelia

74. • Diagnosis – Complete history and physical exam, including functional assessment, ROM, flexibility, and sensation testing – Radiological and electrodiagnostic testing as needed • Treatment – Rest to decrease acute pain – Medications (NSAIDs, etc.) – Physical therapy – Modalities – Injections as needed – Address secondary disabilities

75. Visceral Nociceptive Pain • Pain generated from visceral structures located in the thorax or abdomen. • Dull, aching or cramping secondary to visceral pathology or dysfunction ( eg , infection or obstruction). • Should always consider the differential diagnosis. – Examples: UTI, ureteral calculi, impaction, appendicitis

76. PAIN SYNDROMES….. Neuropathic pain Neuropathic pain can occur above the level, at the level or below the level of injury. Above the level neuropathic pain may arise from complex regional pain syndromes and compressive mononeuropathies. At the level neuropathic pain may be due to damage to either nerve roots or the spinal cord itself. Below the level neuropathic pain is also referred to as central dysesthesia syndrome and often presents diffusely caudal to the level of SCI. It is generally characterized as a burning, aching, tingling or stabbing sensation.

77. Characteristics of NEUROPATHIC PAIN • Develops in 60–70% of patients. • Usually more severe • Damage to peripheral or central neural tissue • Characterized as “burning,” “tingling,” “shock-like,” “cold,” etc. • ~ 1/3 have severe disabling pain. • Correlates with increasing age at injury. – Peaks in 30–39 age group and then again > age 50. • Treatment – Identify if underlying cause of pain. – Evaluate psychosocial factors. – Evaluate functional status (activity levels). – Multi/interdisciplinary treatment recommended. – Medications: Tricyclic antidepressants, Anticonvulsants, Anti- arrhythmics , Topical formulation

78. PRESSURE ULCERS • Approximately 25% of SCI patients develop a pressure ulcer. • Pressure ulcers are classified (according to the extent of tissue damage) utilizing the National Pressure Ulcer Advisory Panel (NPUAP) staging system. NPUAP Staging of Pressure Ulcers Stage Description I - Nonblanchable erythema of a localized area usually over a bony prominence. II - Partial-thickness loss of dermis or dry shallow ulcer. III - Full-thickness destruction through dermis into subcutaneous tissue. Subcutaneous fat may be visible but bone, tendon, or muscle is not exposed. IV - Full thickness tissue loss with exposed bone, tendon, or muscle.

79. The most common location in persons with SCI within the first 2 years is the sacrum , followed by the ischium, heels, and trochanters. After 2 years, the ischial tuberosities are the most common site of development. – In children up to age 13 years, the occiput is the site of most frequent development. Risk Factors : – The most important risk factors for the development of PUs are pressure and shear forces. – Others include higher level and greater severity of the injury, immobility, nonemployment status, tobacco and alcohol use, poor nutritional status, smoking, and possibly psychosocial issues (ie, depression).

80. PREVENTION OF PRESSURE ULCERS • Minimize extrinsic factors: pressure, maceration, and friction. • Decrease duration of pressure forces A the patient should initially be turned and positioned every 2 hours. • Pressure relief and repositioning should be done every 20–30 minutes when sitting. • Proper mattress/bed overlay • Proper cushioning and wheelchair seating. • Weight shifts when seated.

81. In general, healing will be promoted if the wound remains clean and moist, with debridement of necrotic and infected tissue as needed. • Medications can be used for supplementation, particularly in severe cases: – Vitamin C 1 g/day – Zinc sulfate 220 mg/day – Copper 2 mg/day (zinc depletes copper) – Arginine (7–15mg/day) and glutamine (10–20 mg/day) – Increase protein intake – Appetite stimulants: Megestrol Acetate 800 mg \ 30 days and then 40 mg/day Dronabinol 2.5 mg 30 min before lunch and dinner – Anabolic steroids: Oxandrolone 2.5 mg BID-QID (not to exceed 20 mg/day)

82. Surgery Intervention Musculocutaneous flap: - most common and most often recommended in severe pressure ulcers in SCI. – Skin transferred with underlying muscle/blood vessels • Rotation flap: – Semicircular flap rotating about a pivot point to close a triangular defect • Transposition flap: – Rectangular flap rotates about its base to fill an adjacent defect • Advancement flap: – Moved into a defect without lateral or rotational movement

83. SEXUAL DYSFUNCTION AFTER SCI • Male erectile and ejaculatory functions are complex physiologic activities that require interaction between vascular, nervous, and endocrine systems, parasympathetic nervous system. Erectile Dysfunction • Men with SCI may obtain reflexogenic (> 90% of men with complete and incomplete UMN lesions; up to 12% with complete LMN lesions) or psychogenic erections. – Approximately 50% of men with incomplete UMN lesions only. – Not achieved with complete UMN lesions. – Approximately 25% with complete LMN lesions.

84. Ejaculatory Dysfunction • In men with SCI, the ability to ejaculate is less than the ability to obtain an erection. • The rate of ejaculation varies depending on the location and nature of the neurological injury. – Approximately 5% of men with complete UMN lesions and 18% with complete LMN lesions have ejaculations. – The percentages are higher with incomplete injuries. • Achieving ejaculation does not ensure successful reproduction, and less than 10% of couples will have successful reproduction. • Semen analysis in men with SCI reveals decreased sperm count and decreased sperm motility.

85. Female Infertility After SCI • Immediately following SCI, amenorrhea occurs in 85% of women with cervical and high thoracic injuries and 50–60% of women overall. •However, 50 and 90% (respectively) have return of menstruation within 6–12 months after injury. • SCI does not affect female fertility once menses return.

86. ANXIETY & DEPRESSION Many patients with SCI experience psychological stress. Patients response is affected by the cause and extent of injury, and the patients current life situation. To prevent or minimize the problems physical, pharmacological or psychological interventions should be available. Interventions will be pain relief, avoidance of sensory and/or sleep deprivation, providing a familiar atmosphere, as well as giving the patient careful explanations and reassurance. If possible the patient should have access to psychotherapy and pharmacological treatment during their rehabilitation.

87. Thank you