Core Strengthening
Disease/ Disorder Definition Once termed “ spinal stabilization”, core strengthening applies to the trunk, transversus abdominis, quadratus lumborum, and paraspinals including the multifidi; secondary muscles include internal and external oblique and pelvic rotator muscles. Strengthening increases intra-abdominal pressure acting as […]
Pain and Placebo Physiology
[…] the establishment and maintenance of neuropathic pain7. Includes but is not limited to diabetic or other peripheral neuropathy, postherpetic neuralgia, spinal cord injury pain, phantom limb (post-amputation) pain, and post-stroke central pain6. Inflammatory pain Pain caused by the activation of the immune […]
Traumatic Lumbosacral Plexopathy
[…] Trauma can result in compression, stretching, or laceration of plexus components, perineural fibrosis, or avulsion of nerve roots from the spinal cord.4 The type and degree of nerve injury within the lumbosacral plexus depends on the mechanism and severity of […]
Spine Infections
[…] to improved imaging technologies, to the growing number of older patients with chronic illnesses, and to the increasing cases of spinal surgery or procedures.1 There are multiple confusing terms that refer to spinal infections, such as discitis, vertebral osteomyelitis, pyogenic spondylitis, septic facet joint, and Pott’s disease. Spondylodiscitis is the correct terminology to describe primary spinal infections, the most common type of spinal infection.2 Etiology Primary spine infections are hematogenous. The infective organism seeds the vertebral bodies during times of bacteremia. Secondary infections are introduced into the spine via non-hematogenous routes, including trauma, surgery, and injections. Primary discitis in adults is not commonly seen because the disc is avascular. It is seen secondary to vertebral osteomyelitis or is iatrogenic following a discogram, surgery, or inadvertent disc injection during a spinal procedure. In a study of 159 patients treated for spondylodiscitis 35% were secondary infections due to previous open spine surgery, and 65% were primary infections. Primary infections progress more severely and result in significantly higher mortality rate than secondary or postoperative infections (12.5% vs. 1.8%).3 Epidemiology including risk factors and primary prevention The incidence of spondylodiscitis varies between 1 to 5 cases per 100,000 and increases with age.1 The mean age of diagnosis is 58.3 years old with 60% of patients being men.4 In this meta-analysis of 4173 patients across 50 studies, the most common comorbidities and risk associated with spondylodiscitis are Concurrent infection (35%, 207/834, 14 studies) Cardiovascular diseases (24%, 260/1083, 13 studies) Diabetes (20%, 651/3272, 33 studies) Intravenous drug abuse (15%, 226/1379, 14 studies) Immunosuppression (11%, 274/2429, 20 studies).4 Pyogenic spondylodiscitis is most commonly caused by Staphylococcus aureus, and secondly by Enterobacteriaceae spp. Escherichia coli is the most common of the gram-negative family.2 Mycobacterium tuberculosis is the most common pathogen to cause spondylodiscitis worldwide.5 The most common infection risk factors in order of most common to least common are 6 Age >65 years – 15/40 (37.5) Prior non-spine infection (in past 1 month) – 12/40 (30.0) Spine surgery (>1 years ago) – 9/40 (22.5) Nonspine malignancy – 9/40 (22.5) Diabetes mellitus – 8/40 (20.0) Current nicotine use 8/40 (20.0) Spine surgery (⩽1 year ago) – 6/40 (15.0) Prior spine infection – 5/40 (12.5) Non-spine surgery (⩽1 year ago) – 5/40 (12.5) Immune suppression or corticosteroid use 5/40 (12.5) Decubitus or other skin ulcer – 5/40 (12.5) Intravenous or other illicit drug use – 3/40 (7.5) Spine fracture / trauma – 1/40 (2.5) Indwelling catheters, intravenous cannulas 1/40 (2.5) Malnutrition Patho-anatomy/physiology The vertebral arteries form end arteries on either side of the disc. This grants the infective organism access adjacent to the endplates. The primary site of infection usually involves the two adjacent vertebra and intervening disc .7 In adults, the intervertebral disc is a relatively avascular structure and provides some protection against hematogenous spread of infection to the disc. In patients under age 20, there is residual blood supply to the disc; if infection does spread to the disc, primary discitis occurs. Infection can spread locally into the disc from the adjacent vertebral osteomyelitis. The anatomy reveals that the outer two thirds of the disc is firmly adherent to the vertebral endplate, however, the central portion of the disc may be more loosely adherent and have endplate openings to allow venous drainage which can be a site of pathogen entry. In the lumbar spine, the Batson Venous Plexus, because of its rich anastomosis with pelvic organs and its network adjacent to the intervertebral disc, is considered the most likely infectious pathway from pelvic and abdominal sources. Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) An infective organism causes localized suppuration also known as pus. This cuts off the nutrient supply to the disc, causing rapid deterioration. The intervertebral disc, which is acellular, offers no resistance, and local tissue necrosis ensues. Collapse of the intervertebral disc space is often early. Infection then spreads anteriorly into the prevertebral space and into the psoas muscle, posteriorly into the epidural space causing an epidural abscess and/or meningitis; it can also spread longitudinally into the adjacent disc and vertebra. Specific secondary or associated conditions and complications In rare cases, the infection is walled off and becomes chronic because of formation of dead bone or involucrum. This can lead to recurrence of infection. Worsened osseous and discoligamentous destruction and deformity causes spinal deformity and results in increased disability score and reduced quality of life.4 In about 12% of cases, especially with Staphylococcus aureus or Mycobacterial infection, systemic dissemination results in paralysis and death. The poor vascularization of the disc makes it a nidus for infection, resulting in prolonged antibiotic treatment. This spread of infection can also be exacerbated by a history of osteomyelitis in which bacteremia and suppuration results in increased intraosseous pressure and decreased blood flow.4 Spread of infection into the epidural space, most commonly in the lumbar spine (48%), can cause cord compression and may lead to permanent cord damage if not decompressed within 72 hours. In extremely rare cases, infection can spread in the subdural space, causing rapid compression of the spinal cord. Once direct involvement of the central nervous system is observed, outcome is poor.1 Essentials of Assessment History The onset of spondylodiscitis can be acute, subacute, and insidious, in the order of decreasing severity of presentation. The progressive nature of the insidious type often delays diagnosis due to unclear time of onset, milder symptoms, and fewer symptoms.7 In adults, spondylodiscitis commonly presents as dull back pain. In children, it can present as inability to walk or move and may be mistaken for muscle strain. Cervical spine infections commonly present with a stiff neck. There may be history of minor trauma. About 50% of patients give a history of fever. Patients with infection often complain of nocturnal pain possibly due to a relative decrease in oxygen saturation while asleep. Radicular symptoms suggest epidural involvement. In subacute and chronic cases there may be weight loss, loss of appetite, and malaise. Physical examination There are no classical clinical signs for spine infections, but a very detailed spine and neurologic evaluation is essential. Tenderness and deformity of the spinous process along with muscle spasm and reduced range of motion is noted. Pseudoparalysis may be noted in children secondary to pain. Pain may be reproduced with vertical pressure on the vertebra and disc (Anvil test). If vertebral collapse occurs, there may be palpable deformity. Positive straight leg raise tests may suggest epidural involvement. Associated abdominal examination might be needed to assess for the presence of psoas abscess. Cardiac examination may be indicated to rule out infective endocarditis. In a meta-analysis of spondylodiscitis in adult patients, the most common findings at presentation were 4 Back pain – 2101/2299 (91%) Fever – 748/2125 (35%) Neurologic deficits – 1009/3422 (29%) Functional assessment One needs to assess if the patient can safely ambulate, whether because of pain or weakness. If there is any question of central nervous system involvement, a formal cognitive assessment would be needed. Laboratory studies Complete blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures x 3 from different sites, including aerobic and anaerobic, especially when febrile. The most common organism responsible for pyogenic infections is Staphylococcus aureus, followed by Escherichia coli.2 Fungal infections are more likely to be seen in immunocompromised individuals and intravenous drug use. Testing for human immunodeficiency virus, syphilis, and tuberculosis are recommended. Imaging Magnetic resonance imaging (MRI) is the test of choice with a 92% sensitivity and 96% specificity.8 MRI sensitivity can increase to 95.4% when performed using galodinium contrast.9 Computed tomography (CT) scan can help look for osteomyelitis, sequestrum, disc space collapse, and prevertebral and psoas abscess. Plain radiographs are a good initial test to evaluate disease progression, but a negative X-ray does not rule out spondylodiscitis.5 Technetium Tc 99m scan is typically positive in a few days following onset of symptoms. Indium-111 labeled white blood cell is a good tool for diagnosis of peridural abscess. Gallium citrate Ga 67 scans have been found to have a sensitivity close to 100%, with increased uptake 1 day earlier than for the Technetium Tc 99m scan. Also, gallium is helpful for chronic osteomyelitis. Gallium-citrate positron-emission tomography (PET)/CT can be useful to differentiate between spinal infections and tumors. PET with fluorodeoxyglucose is not affected by implants and is recommended by the Infectious Diseases Society of America (IDSA) only when MRI is contraindicated.10 Ultrasound has been used to diagnose discitis in infants.11 Its role is primarily to diagnose and follow-up on psoas and other prevertebral abscesses. Supplemental assessment tools CRP has a sensitivity as high as >90%, ESR is positive in 75% of cases, whereas blood cultures are positive only in 50-60% of cases.1,2 Because isolation of the organism will impact treatment, vertebral biopsy is required if the blood cultures are negative. CT or ultrasound-guided biopsy of the lesion is currently the most common and accurate method of securing a histopathologic diagnosis. A combined superimposed MR and CT imaging is recently being reported to help achieve higher detection rate during CT-guided biopsies.2 Open biopsy may also be performed if the patient is being treated surgically.12 Though this is crucial in subacute and chronic cases to rule out a neoplasm, the sensitivity and specificity of CT-guided biopsy or open biopsy is lower than expected, with surgical biopsy and percutaneous biopsy being positive only 58% and 57% of the time, respectively.4 Early predictions of outcomes Generally, the indicators of poor long-term outcome include the following: Presence of neurologic signs Longer time to diagnosis Hospital-acquired infection Level of spine involvement (cervical > thoracic > thoracolumbar > lumbosacral) Social role and social support system Social and home care agencies need to be involved early to prepare for […]
Adult Degenerative Scoliosis
[…] Elastic Tissue Dysfunction Soft tissue contractures (e.g., due to empyema, surgical treatment, burns, radiation, resultant scarring, radiation fibrosis) Neuromuscular Dysfunction Spinal cord injury, syringomyelia Table derived with permission from DeLisa’s Physical Medicine and Rehabilitation: Principles and Practice, p 892-899.8 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Asymmetric degeneration leads to progressively increasing asymmetric load, thereby giving rise to progression of curvature. Curve magnitude in ADS progresses on average 3° per year.10 A patient’s age, sex, and bone mineral density does not affect the rate of curve progression.11 However, patients having a Cobb angle >30 °, lateral listhesis >6mm, apical rotation more than Grade II, or intercrest line through L5 are correlated with higher rate of curve progression.10 […]
Anticoagulant Pharmacology
[…] 30% may have a recurrence in 10 years.1 0.71% develop VTE in the 180 days following orthopedic surgeries.4 In acute spinal cord injury the 91-day cumulative incidence of VTE was 5.4% with appropriate prophylaxis. In SCI the incidence of asymptomatic VTE, can reach 48% to 100% among patients not given any medical thromboprophylaxis.5 In COVID-19 infection the incidence of VTE is thought to be 27-47% in hospitalized patients.6 In cancer among average-risk patients, the overall incidence of VTE has been estimated to be 13 per 1,000 person-years, with the highest risk among patients with cancers of the pancreas, brain, and lung.7 In the US, atrial fibrillation may be responsible for >70,000 strokes each year representing 10%–12% of all ischemic strokes.8 Patho-anatomy/physiology Coagulation Cascade The coagulation cascade can be broken into the extrinsic, intrinsic and common pathways.9 Warfarin is the most commonly prescribed anticoagulant worldwide and is a vitamin K antagonist (VKA) that works by inhibiting γ-carboxylation of factors II, VII, IX, and X in the liver and can take up to 5 days for full effect.10 Heparin and Low molecular weight heparin (LMWH) work by the potentiation of antithrombin leading to the inactivation of thrombin and factors II, VII, IX, and Xa.2,10 Direct Oral Anticoagulants (DOACs) such as Rivaroxaban and Apixaban work by directly inhibiting Factor Xa while Dabigatran is a direct thrombin inhibitor.2,10 Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2. Clopidogrel is an inhibitor of ADP-induced platelet aggregation acting by direct inhibition of ADP binding to its receptor. Aggrenox is a combination of Aspirin and an extended-release Dipyridamole, which inhibits adenosine uptake into cells, increases platelet cAMP, thereby decreasing platelet aggregation. See tables 1 and 2 for additional information regarding DOACs and antiplatelet agents respectively Anticoagulant-Pharmacology-Table-1-Direct-Oral-AnticoagulantsDownload Anticoagulant-Pharmacology-Table-2-Antiplatelet-AgentsDownload Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Venous stasis, vascular injury or a hypercoagulable state can lead to clot formation. Venous stasis is the most important and often related to valvular insufficiency in the deep veins of the legs that results in blood pooling, local hypoxia and expression of certain procoagulants. It manifests as swelling, redness and tenderness. Thrombi can rupture and migrate into the pulmonary vasculature leading to PE and shortness of breath (SOB). Arterial thrombosis is thought to be caused by erosion of an arteriosclerotic plaque, which can rupture and further lead to clotting and embolization. Atrial fibrillation and valvular or septal defects can cause blood turbulence or stasis which can further embolize and lead to strokes. Specific secondary or associated conditions and complications Complications related to anticoagulants include thrombosis (insufficient anticoagulation) and hemorrhage (too much anticoagulation). Both can lead to serious complications including DVT, PE, stroke or death. All anticoagulant medications have an increased risk of bleeding. Warfarin has the highest number of major bleeding events, likely due to the effect of various drugs and foods on CYP 450 enzyme, which breaks down warfarin and/or alters the intestinal absorption of vitamin K.10 Apixaban has demonstrated a statistically significant decreased risk of major bleeds including GI when compared to warfarin and other DOACS.11 Importantly, DOACs are similarly affected by drugs that alter the CYP3A4 enzyme, namely, phenytoin, carbamazepine, phenobarbital and St. John’s wort.10 Essentials of Assessment History Patients may present with affected limb pain, swelling, redness, decreased pulses, arrhythmias, SOB, dizziness, new neurological deficits, ecchymoses or active bleeding.12 Additional history may reveal recent travel, surgeries or other conditions leading to prolonged immobility, infections such as COVID-19, cardiac arrhythmias, valvular or septal defects, history of hypercoagulable state, smoking, morbid obesity, administration of oral contraceptive, and history of VTE (history of DVT was an independent predictor of DVT recurrence) should also be obtained. Physical examination Typical findings of VTE are tenderness, warmth, erythema, cyanosis, edema, palpable cord (a palpable thrombotic vein), and superficial venous dilation of the lower extremity. These can occur in various combinations and evolve over hours to weeks.13 Though with a low specificity and sensitivity in diagnosing DVT, a positive Homan’s sign, described as presence of deep calf pain or tenderness upon palpation of calf during forced dorsiflexion of the foot with the knee flexed 10 degrees, may indicate the presence of a DVT.14 PE can manifest as tachypnea, tachycardia without significant findings on lung auscultation. Tachy or brady-arrhythmias can be detected with precordial auscultation or by irregular pulses. Murmurs can indicate valvular or septal defects. CVA signs include sudden neurological deficits affecting strength, sensation, speech, coordination, cognition. Over-medication with anticoagulants can cause internal or external bleeding. Clinical functional assessment: mobility, self-care cognition/behavior/affective state Patients affected by VTE, PE, CVA and other hypo/hypercoagulable states can present with impaired mobility and ADL’s. Furthermore, when a new DVT/ PE is diagnosed, the patient should be first anti-coagulated prior to restarting mobilization. Early mobilization after therapeutic anticoagulation is indicated over bed rest.15 Currently there is no specific guideline as to when to start mobilization/therapy when a new VTE is diagnosed. However, patients who were encouraged to ambulate within 3 days of diagnosis of VTE were not more likely to develop a progression of DVT, DVT related death or PE than those treated with bed rest after a new DVT/PE diagnosis.16 Laboratory studies D-dimers (>500ng/ml) – low specificity; can be elevated in cancer, after recent surgery, trauma and other conditions.17 Prothrombin time (PT) and activated partial thromboplastin time (aPTT) should be requested in all patients on warfarin, prior to a procedure, or with clinically relevant bleeding. Quantitation tests of specific medications such as the dilute thrombin time, ecarin clotting time, and ecarin chromogenic assay for dabigatran and Anti-FXa assay for apixaban are not widely available.18 Imaging Choosing the correct imaging study depends largely on the differential diagnosis. Imaging studies for VTE, cardiac valvular/septal defects include: Ultrasound Duplex compression vascular ultrasound (non-invasive, can visualize arterial or venous clots) Cardiac ultrasound Radiologic Angiography (invasive, involves injection of radiopaque contrast dye into a blood vessel) X-ray arteriography or venography Computed tomography angiography (CTA) Magnetic resonance angiography (MRA) Nuclear Studies Ventilation/ Perfusion (V/Q) scan: high radiation exposure risk Imaging to detect strokes: Non-contrast Head CT: performed first, to exclude intracranial hemorrhage (ICH), detects ischemic changes in 6-24 hours Head MRI: can detect ischemic changes within 3-30 minutes Contrast Studies: most accurate, but expensive, invasive, difficult to perform contrast materials can be nephrotoxic, irritating to vessel walls and can cause allergic reactions EKG changes can uncover arrhythmias. Supplemental assessment tools Many factors should be taken into account when making a comprehensive treatment decision to anticoagulate, including patient’s age, medical history, comorbidities, interactions with other medications, fall risk, life expectancy, among others. Pretest probability tools such as the Wells Score19 for PE in conjunction with D-dimer can help stratify patient categories based on risk/probability. The Wells score is calculated based on the presence of: clinical signs and symptoms of DVT tachycardia immobilization for >3 consecutive days or surgery in the previous 4 weeks previous PE or DVT hemoptysis malignancy Assessment tools considered in the three-tier Wells score risk-model:19 low risk (0-1): consider PE rule-out criteria (PERC) and D-dimer moderate risk (2-6): consider D-dimer or pulmonary CTA high risk (>6): consider CTA or V/Q scan, D-dimer not recommended In the two-tier model: PE unlikely (4.5): consider pulmonary CTA CHA2DS2-VASc score (0-9) is a tool that estimates stroke risk for atrial fibrillation, based on patient’s age, sex, history of HTN, CHF, stroke/TIA/VTE, vascular disease and diabetes. Oral anticoagulation therapy (OAC) is recommended for a score of 2 and above.20 HAS-BLED score (0-9) is a tool that estimates the risk for bleeding based on patient’s age, bleeding predisposition, abnormal renal/liver function and a history of HTN, stroke, labile INRs and drugs or alcohol use. A HAS-BLED score of ≥3 indicates that caution is warranted when prescribing oral anticoagulation and regular review is recommended.20 Early prediction of outcomes Rehabilitation and medical outcomes may vary based on the patient’s comorbidities. Older age, tobacco use, CHF, chronic lung or kidney disease, cancer or atrial fibrillation can predict worse outcomes.21 Central venous catheters, higher illness intensity scores, history of VTE, higher BMI, and vasopressor therapy are all poor prognostic factors.22 Cancer at baseline, older age, leukocytosis, diabetes mellitus, liver disease, female sex, and initial presentation with massive PE were all independent predictors of all-cause mortality.23 Of the DVT prophylaxis methods, data has shown that sequential compression devices were superior to antiembolic stockings, and that chemoprophylaxis was efficacious in preventing VTE.24 Environmental N/A Social role and social support system Multidisciplinary teams and allied health professionals are essential in supporting patients on anticoagulation during the transition of care between healthcare settings and home. Point of care INR monitoring by general practitioners, pharmacists, combined with patient and family education was found to be beneficial in vulnerable patient groups taking anticoagulants such as warfarin or DOACs.25 Professional issues Warfarin treatment, though inexpensive, requires frequent INR testing. Adherence to INR testing strategies into clinical practice supports the patient-clinician relationship and ensures patient compliance.26 DOACs are more expensive but do not require frequent lab monitoring. Financial assistance programs are however available for those who qualify. Rehabilitation Management and Treatments Available or current treatment guidelines Currently, there is no “standard of care” specific to anticoagulation within the rehabilitation setting. Depending on medical history, admitting diagnosis, weight and lab values, patients are usually started on Heparin or LMWH (i.e., Enoxaparin).27 Below are some anticoagulation recommendations by diagnosis: Neurologic Ischemic strokes Dual-antiplatelet therapy with Aspirin 81 mg and Clopidogrel 75 mg daily for 21 days followed by mono-therapy with Aspirin is recommended.28 Aggrenox can be used as an alternative. DOACs are the preferred anticoagulation strategy for secondary prevention in patients with atrial fibrillation.29 Traumatic Brain Injury (TBI) LMWH or low-dose unfractionated heparin (UH) may be used in combination with mechanical prophylaxis for VTE.30 VTE prophylaxis should be started within 24–72 hours following TBI if no contraindication.31 Weak evidence suggests that anticoagulation after intracranial hemorrhage (ICH) may be initiated between 14 days up to 30 weeks, and not earlier than 7 days post ICH, on a ‘case-by-case basis’.32 Spinal Cord Injury (SCI) LMWH for 3 months post SCI to prevent DVT/PE, after which the risk is similar to that of the general population;33 based on the severity of neurological dysfunction LMWH may be continued for up to 6 months.34 Poly-trauma/Burns Severely ill patients may require increased doses of anticoagulation to prevent VTE. In severe burns with >20% total surface area, LMWH is recommended instead of DOACs.35 Hip/Knee/Spine Surgery Commonly used pharmacologic agents for VTE prophylaxis: LMWH, UFH, fondaparinux, rivaroxaban, apixaban, dabigatran, warfarin, or aspirin.36 LMWH and DOACs are preferred in orthopedic patients after total knee arthroplasty (TKA) or total hip arthroplasty (THA).37 For low post-procedural bleeding risk, anticoagulation can be restarted 24 hours post-procedure. If the risk is higher, it should be delayed for 48 to 72 hours.38 Start DVT prophylaxis within 12hrs or more post-operatively for a minimum of 10 to 14 days and extending for up to 35 days.36,39 For patients after TKA or THA there was no significant difference on DVT or PE prophylaxis between aspirin and rivaroxaban.39 No specific thromboprophylaxis is suggested for isolated lower-extremity injuries requiring immobilization and for patients undergoing knee arthroscopy without a history of VTE. Amputees Currently there have only been two larger studies comparing heparin to LMWH which demonstrated no difference in efficacy or increased side effects.40 Cancer LMWH has been the primary treatment choice for patients with VTE.41 More recently, Apixaban & Rivaroxaban have been recommended in addition to LMWH.42 DOACs are associated with lower intracranial hemorrhage risk than warfarin.41 DVT/PE DVT/PE usually occurs within the first week after stroke and the first 2 weeks after SCI.12 Treatment duration: First unprovoked isolated distal (calf) VTE/ VTE provoked by a reversible risk factor: 3 months Second unprovoked VTE/ VTE associated with active cancer: indefinitely.43 Atrial fibrillation (Afib)/ valvular disease DOACs generally recommended over VKA for Afib.44 Warfarin (target INR 2.5-3.5) is preferred for mechanical heart valve assuming patient’s target therapeutic range (TTR) is > 65%, otherwise DOAC is preferred. Warfarin is preferred in renal impairment if TTR is 65%-70%, otherwise apixaban is preferred.45 COVID-19 The data on VTE prophylaxis in COVID-19 is still evolving. A few studies were completed in 2021 that looked at the use of VTE prophylaxis in patients with COVID-19: In a meta-analysis of 66 observational studies through August 2020, the overall prevalence of VTE in hospitalized patients with COVID-19 was 9.5% without screening, and 40% with ultrasound-screening.46 In the ACTION trial, Lopes et al. did an efficacy and safety analysis by looking at therapeutic versus prophylactic anticoagulation in COVID-19 population with elevated D-dimer levels. They found that compared to prophylactic anticoagulation, in-hospital therapeutic dose anticoagulation with rivaroxaban or enoxaparin followed by 30 days of rivaroxaban did not improve clinical outcomes and was associated with increased bleeding.47 In the RAPID trial, Sholzberg et al. did not find a significant reduction in the primary composite outcome of death, mechanical ventilation, or ICU admission with therapeutic heparin. However, therapeutic heparin decreased the odds of all cause death at 28 days with a low risk of major bleeding, suggesting that it is beneficial in moderately ill patients admitted with COVID-19 and increased D-dimer levels.48 In the HEP-COVID trial, Spyropoulos et al. looked at VTE, arterial thromboembolism (ATE) and death from any cause within 30 ± 2 days after randomization to various heparin formulations. Therapeutic-dose LMWH was found to reduce the composite of thromboembolism and death compared to institutional standard heparin prophylaxis without an increased major bleeding among the patients hospitalized (not in the ICU) with elevated D-dimer levels.49 Renal Impairment There is limited data to support DOAC use. Patients with renal impairment are at higher risk of developing stroke and major bleeds therefore appropriate anticoagulation is essential in this patient population. Studies looking at the safety and effectiveness of apixaban versus warfarin in severe renal impairment found no significant difference in the occurrence of major bleeding as well as of stroke and VTE. Another study found that patients who were prescribed the standard dose (5 mg twice a day) versus the reduced dose (2.5 mg twice a day) demonstrated that unlike the other DOACs, apixaban use in end stage renal disease (ESRD) was associated with a lower risk of major bleeding, thromboembolism and death compared with warfarin.50- 52 Common interventional pain procedures:53 Prior to low-risk procedures (e.g., minor peripheral procedures, trigger point injections, etc.) No need to hold anticoagulation Consider holding Aspirin/ Aggrenox for 4 days, Heparin for 4-8hrs, LMWH for 24hrs prior to procedure Prior to moderate/severe-risk procedures (e.g., spinal facet joint injections, epidurals, spinal cord stimulators, pumps, catheters, etc.) Medial Branch Blocks/ RFAs: No need to hold anticoagulation Epidural injections/ Spinal cord stimulator or pump trials/implants: Aspirin – hold for 4-6 days NSAID’s (COX1, COX2) – may continue or stop 1-10 days Platelet Aggregation Inhibitors – hold for 5-7 days DOACs – hold for 3-5 days Warfarin – hold for 2-5 days LMWH bridge therapy during cessation of the anticoagulant – up to 24 hours before the procedure – can be used if VTE risk is high Anticoagulant may generally be resumed 12 hours after the interventional procedure At different disease stages Below we will focus on the management of common “diseases” that require anticoagulation: Ischemic events New onset/acute ischemic events potential curative interventions clot extraction/ thrombectomies/ tPA anticoagulant pharmacotherapy IV UFH infusion – short half-life, available reversal agent (protamine sulfate) oral/ SQ anticoagulation therapy DOACS preferred for DVT/ PE (LMWH & warfarin as alternatives) non-pharmacological therapy (for high bleeding risk patients)54 left atrial appendage occlusion device inferior vena cava filter (IVCF) avoid sequential compression devices (SCDs) symptom relief pain: analgesics/ anti neuropathics shortness of breath: oxygen supplementation rehabilitation strategies start early mobilization once therapeutic anticoagulation is achieved avoid massage over the limb with DVT Subacute/chronic/stable secondary VTE prevention with pharmacotherapy symptom relief with analgesics rehabilitation strategies – continue therapy while on anticoagulants to optimize function Bleeding events Injectable anticoagulants27 A meta-analysis showed that adjusted-dose LMWH decreased the risk of both DVT and PE but increased risk of ICH. High-dose UFH (>15,000 units/dose) was associated with a reduction in PE but showed an increased risk of ICH/ extracranial hemorrhage (ECH). Low-dose UFH (40 kg/m2 and weight >120 kg from the previous 2016 guidance from the International Society of Thrombosis and Hemostasis (ISTH): The 2021 ISTH guidance […]
Wheelchair and Power Mobility for Adults
[…] EA, Dyson-Hudson TA, Cowan RE, Pedersen JP, Shea M, Boninger ML. Effectiveness of Group Wheelchair Skills Training for People With Spinal Cord Injury: A Randomized Controlled Trial. Arch Phys Med Rehabil. 2016 Oct;97(10):1777-1784.e3. Worobey L, Oyster M, Nemunaitis G, Cooper R, Boninger […]
Spasticity
[…] specific to the type and severity of CNS injury. For example, it is estimated that spasticity affects 65-78% of chronic spinal cord injury (SCI) patients3, 25% of stroke patients,4 80% of patients with MS at some point during their clinical course,5,6 and […]
Neurological Examination and Classification of SCI
Overview and Description The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), or the International Standards, is the standardized examination which clinicians used to classify neurological impairments.1 An international standard was first established in 1982 by the American Spinal Injury […]
Discogenic Lumbar Pain
[…] late degenerative disk disease (DDD) and internal disc disruption.1 DLP symptoms are distinct from those occurring as a result of spinal deformity or radiculopathies. Etiology Strong familial predisposition to DLP2 DDD is associated with advanced age, male sex, and smoking3 […]