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Regional Blocks in Non-

Cancer Patients

Regional Blocks in Non-

Cancer Patients

Richard W. Rosenquist, M.D.

Chairman, Pain Management Department

Cleveland Clinic

Cleveland, OH

USA

W.O. Walker Center

11.09.2015

2

DisclosureDisclosure

• EMMI – Consultant

• UpToDate – Educational Material

Development

• KURE – Board of Directors

ObjectivesObjectives

• Discuss the role of regional blocks

• Describe common regional blocks used

in non-cancer pain

• Analyze the limitations of regional

blocks

• Illustrate the role of regional blocks in

actual patients

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What is the role of regional

blocks in non-cancer pain?

What is the role of regional

blocks in non-cancer pain?

• Diagnostic

- Determine if there is a unique, identifiable pathway

- Determine which portion of the nervous system is carrying or perpetuating the pain signal

• Predictive

- Predict outcome for various ablative techniques e.g. radiofrequency, cryoablation, surgical resection

• Therapeutic

- Local anesthetic and steroid injections

- Signal interruption e.g. sympathetic nerve blocks

- Analgesic blocks to facilitate physical therapy

When are

Diagnostic/Therapeutic Blocks

Indicated for Non-Cancer Pain?

When are

Diagnostic/Therapeutic Blocks

Indicated for Non-Cancer Pain?• Answer specific questions

- Localizing source

- Mechanism of pain

- Range of motion

- Spasticity

- Malingering

• Done with rigorous criteria

- Technically successful

- Objective evidence of successful block

- Reproducible results

- Uncoached responses from the patients

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ThoracotomyThoracotomy

Chronic Pain After

Thoracic Surgery: A

Follow-Up Study

Chronic Pain After

Thoracic Surgery: A

Follow-Up Study

Perttunen K, Tasmuth T, Kalso E.

Acta Anaesthesiologica

Scandinavica 1999;43:563-7

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Perttunen K, et al.Perttunen K, et al.

• 110 pts interviewed before and 1 week

after surgery to find out about

preoperative pain and amount of

postoperative pain

• The amount of postoperative analgesic

used during the 1st 5 postoperative days

• Interviewed by letter 3, 6 and 12 months

after surgery to determine extent of pain

and effect on daily activities

Perttunen K, et al.Perttunen K, et al.

• Incidence of chronic post-thoracotomy pain- 80% at 3 months

- 75% at 6 months

- 61% at 12 months

- 3-5% had severe pain

• Chronic pain interfered with daily life in more than 50%

• High analgesic consumption during the 1st

week was associated with a higher risk of chronic pain

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Chronic Post-Thoracotomy

Pain: A Retrospective

Study

Chronic Post-Thoracotomy

Pain: A Retrospective

Study

Pluijms WA, Steegers MAH, Verhagen AFTM, Scheffer GJ,

Wilder-Smith OHG.

Acta AnaesthesiologicaScandinavica 2006;50:804-8.

Pluijms WA, et al.Pluijms WA, et al.

• 255 patients that had postero-lateral thoracotomy

• Overall incidence of chronic pain was 52% (32% mild,

16% moderate and 3% severe chronic postoperative

pain)

• Patients with chronic post-operative pain reported

acute post-operative pain more frequently than those

without 85% vs. 62%, had more severe acute post-

operative pain, underwent more extensive surgical

procedures, had more constant acute pain and

reported less absence of pain during the first post-

operative week.

• There was no significant decrease in chronic pain

with time after the thoracotomy

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Only Half of the Chronic

Pain After Thoracic Surgery

Shows a Neuropathic

Component

Only Half of the Chronic

Pain After Thoracic Surgery

Shows a Neuropathic

Component

Steegers MAH, Snik DM, Verhagen

AF, van der Drift MA, Wilder-Smith

OHG.

The Journal of Pain 2008;9:955-61

Steegers MAH, et al.Steegers MAH, et al.

• 243 patients that had VAT or thoracotomy

• Chronic pain- 40% after thoracotomy

- 47% after VATS

• Chronic neuropathic pain present in 23% with chronic pain, with an additional 30% having probably neuropathic pain

• Greater probability of neuropathic pain with more intense chronic pain

• Predictive factors for chronic pain were younger age, radiotherapy, pleurectomy and more extensive surgery

• There may be a visceral component apart from nerve injury

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Common Regional Blocks used

in Non-Cancer Pain

Common Regional Blocks used

in Non-Cancer Pain

• Head and neck blocks

• Peripheral nerve blocks

• Truncal nerve blocks

• Spine related blocks

• Sympathetic nerve blocks

Head and Neck BlocksHead and Neck Blocks

• Trigeminal nerve blocks

• Superficial cervical plexus block

• Occipital nerve block

• Glossopharyngeal nerve block

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Peripheral Nerve BlocksPeripheral Nerve Blocks

• Brachial plexus block

- Suprascapular

- Radial

- Median

- Ulnar

• Lumbar plexus block

- Femoral

- Saphenous

• Lumbosacral plexus block

- Sciatic

- Tibial

- Peroneal

- Distal branches

Truncal Nerve BlocksTruncal Nerve Blocks

• Intercostal nerve blocks

• Ilioinguinal nerve block

• Iliohypogastric nerve block

• Genitofemoral nerve block

• Lateral femoral cutaneous nerve block

• TAP blocks

• Pudendal nerve blocks

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Spine Related BlocksSpine Related Blocks

• Medial branch blocks

• Selective nerve root blocks

• Neuraxial blocks

- Spinal

- Epidural

Selective Nerve Root BlockSelective Nerve Root Block

• Diagnostic aid to determine nerve root

involvement

• Volume of injectate can influence

results greatly

• Direct delivery of local anesthetic,

steroid or both to inflamed nerve root

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Selective Nerve Root

Injection

Selective Nerve Root

Injection

Sympathetic Nerve BlocksSympathetic Nerve Blocks

• Stellate ganglion block

• Lumbar sympathetic block

• Splanchnic nerve blocks

• Celiac plexus block

• Superior hypogastric plexus block

• Ganglion impar block

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Limitations of Regional

Blocks

Limitations of Regional

Blocks

Goals and Challenges of

Diagnostic Blocks

Goals and Challenges of

Diagnostic Blocks

• Gain diagnostic information

• Guide therapeutic interventions

• Improve therapeutic outcome

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Diagnostic Neural Blockade

Assumptions I

Diagnostic Neural Blockade

Assumptions I

• Pathology causing pain is located in an

exact peripheral location and impulses

travel via a unique and consistent

neural route

• Injected local anesthetic totally

abolishes function of intended nerves

and does not affect other nerves

Diagnostic Neural Blockade

Assumptions II

Diagnostic Neural Blockade

Assumptions II

• Relief of pain after local anesthetic

block is attributable solely to block of

the target afferent neural pathway

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Local Anesthetic IssuesLocal Anesthetic Issues

• Intensity of blockade

- Variable and partial nature of local anesthetic effects

• Differential blockade

- Selective block has proved elusive

• Systematic effects

- Pain relief can occur from absorption

Psychosocial IssuesPsychosocial Issues

• Diagnostic blocks involve a complex social interaction

• Different goals- Physician - pathophysiologic

information- Patient - reassurance, confirmation,

proof or certification of their disability

• Placebo response is a significant impediment to relying on neural blockade for diagnosis

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Evaluation of BlockEvaluation of Block

• Duration

• Activity

• Undesired spread

• False positive and negatives

• Placebo response

Case ExamplesCase Examples

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Saphenous Nerve Block for

Persistent Pain After Knee

Surgery

Saphenous Nerve Block for

Persistent Pain After Knee

Surgery• 64 year old male with traumatic right femur fracture requiring extensive surgical repair and right total knee replacement. He had persistent medial distal thigh and knee pain and hypersensitivity that limited his ability to bear weight and ambulate. Medical management including high dose opioids, anticonvulsants, antidepressants, topical lidocaine and TENS provided inadequate pain relief.

• Diagnostic right sub-sartorial saphenous nerve block provided complete relief of pain allowing him to stand without pain. Repeat block with local anesthetic and Depo-Medrol provided 3 weeks relief with subsequent recurrence of his symptoms. A right saphenous cryoablation has provided 18 months of pain relief and improved function.

Geniculate Nerve Block for Knee

Pain

Geniculate Nerve Block for Knee

Pain

• 93 year old male with severe right knee osteoarthritis and deformity with associated pain. He did not want to undergo surgical repair, but wanted reduced knee pain.

• Diagnostic geniculate nerve blocks provided more than 50% pain relief on 2 occasions

• Radiofrequency geniculate nerve block performed with 50% reduction in pain and improved tolerance for ambulation.

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Superficial Cervical Plexus

Block

Superficial Cervical Plexus

Block

• 57 year old female with persistent left sided facial pain and headache following a motor vehicle collision resulting in blunt facial trauma and dislocation of left temporomandibular joint. Subsequently, she had difficulty moving the left side of her face and/or eating due to pain. Medical management with opioids, antidepressants and anticonvulsants provided no relief. A diagnostic trigeminal nerve block at an outside clinic produced numbness in the expected distribution, but no pain relief and no improvement in facial function.

• Physical examination demonstrated dysesthesia and pain with palpation in the distribution of the superficial cervical plexus, especially along the posterior border of the sternocleidomastoid muscle.

• Local anesthetic block with 0.5% bupivacaine provided complete relief of her headache and facial pain. She was able to move her face symmetrically and open her mouth far more than normal with almost no pain.

Interscalene BlockInterscalene Block

• 37 year old female with persistent left arm pain following high voltage electrical injury. She had a frozen shoulder and markedly reduced active and passive hand and wrist range of motion and could not tolerate PT due to pain.

• Interscalene block was performed, which provided complete relief of pain and facilitated aggressive physical therapy.

• She had both reduced pain and improved range of motion in all joints of the left arm and hand.

• Repeat blocks have allowed her to maintain improvements and continue to reduce pain and improve function

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Intercostal Nerve BlockIntercostal Nerve Block

• 64 year old male with prior esophagogastrectomywith subsequent development of a diaphragmatic and chest wall hernia at the site of prior thoracotomy requiring surgical repair and partial rib resection.

• No response to medical management with opioids, tricyclic antidepressants, anticonvulsants, topical lidocaine and TENS.

• More than 75% relief of pain with diagnostic T8, T9 and T10 blocks with bupivacaine X2

• Excellent relief of pain with cryoablation of T8, T9 and T10

Lateral Femoral Cutaneous

Nerve Block

Lateral Femoral Cutaneous

Nerve Block

• 44 year old obese nurse with bilateral lateral thigh pain and hypersensitivity. The pain is worse when standing and walking and improving with sitting or lying down. Physical examination demonstrates marked tenderness to palpation over the course of the lateral femoral cutaneous nerve just medial to the anterior superior iliac spine. She continues to work full time, but is having a hard time completing her shift.

• Diagnostic, ultrasound guided, bilateral lateral femoral cutaneous nerve blocks with local anesthetic and steroid provided complete relief of he symptoms and have allowed her to engage in a physical therapy program in addition to diet modification to begin to lose weight to reduce the likelihood of recurrence.

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U/S LFC BlockU/S LFC Block

Tibial Nerve BlockTibial Nerve Block

• 56 year old male with persistent left stump pain following a BKA after traumatic injury in a motorcycle accident. He has a well-healed stump, but has difficulty wearing his prosthetic due to persistent stump pain. Medical management and modification of his prosthetic has not provided adequate relief. Physical examination is remarkable for reproduction of pain with palpation of the distal tibial nerve stump. Ultrasound examination demonstrates a distal neuroma.

• Ultrasound guided local anesthetic neuroma block provided good relief of pain and allowed him to wear his prosthetic without discomfort.

• Subsequent cryoablation of the stump provided him with 6 months of reduced pain and improved function. The cryoablation was repeated with restoration of the previous level of pain control and improved function.

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ConclusionsConclusions

• Regional blocks have a valuable place in the management on chronic non-cancer pain

• They provide unique diagnostic and predictive capabilities

• They must be interpreted carefully

• They can be therapeutic in their own right

• They can utilized to facilitate other forms of pain therapy

• They are frequently underappreciated and underutilized in chronic, non-cancer pain therapy

• The evidence basis is limited as many cases are not reproducible.

MaturityMaturity

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Complications of

Interventional Pain Medicine

Complications of

Interventional Pain Medicine

Richard W. Rosenquist, M.D.

Chairman

Department of Pain Management

Cleveland Clinic

Cleveland, OH

USA

Cleveland ClinicCleveland Clinic

11.09.2015

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DisclosureDisclosure

• EMMI – Consultant

• UpToDate – Educational Material

Development

• KURE – Board of Directors

Learning ObjectivesLearning Objectives

• List factors associated with infectious, vascular, needle-stick and other types of injuries

• Identify approaches to reduce patient risk

• Assess potential treatments for potential complications in order to reduce morbidity and mortality

At the conclusion of this activity, participants

should be able to:

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• The practice of Pain Medicine is associated with increased patient risk

• Issues and trends are identified through numerous venues- Case reports- Peer reviewed publications - ASA closed claims analysis- Malpractice cases under review- Outcomes data- Internal billing data from insurance organizations

- Government agencies – FDA, CDC, CMS- News media

Scope of the ProblemScope of the Problem

• Fitzgibbon et al 1970 – 1999

- 284 chronic pain claims

• Rathmell et al 2005 – 2008

- 294 chronic pain claims

Are we seeing more

complications?

Are we seeing more

complications?

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• Improved training

• Treatment algorithms

• Interventional treatment checklists

• Modified imaging and drug choices

• Advanced assessment

• Modified incentives related to

performance of procedures leading to

reduced numbers of procedures

performed for better indications

Can We Avoid

Complications???

Can We Avoid

Complications???

• Personal hygiene

• Contamination

• Inadequate preparation

• Poor aseptic technique

• Contaminated medications

• Inadequate/inappropriate antibiotics

Infectious ComplicationsInfectious Complications

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Paraspinal Abscess

Complicated by Endocarditis

Following a Facet Joint

Injection

Paraspinal Abscess

Complicated by Endocarditis

Following a Facet Joint

Injection

Hoelzer BC, Weingarten TN, Hooten WM,

Wright RS, Wilson WR, Wilson PR

European Journal of Pain 2008;12:261-5

• 65-yr-old male with low back pain for repeat L5-S1 facet injection and infiltration of L5-S1 intraspinal ligament

• 2 weeks later he had increased pain after lifting heavy objects and a repeat L5-S1 facet injection and L5-S1 interlaminar ESI was performed

• 6-8 hrs after the procedure the patient developed fever and chills

• 1 day later he had malaise, myalgias, lower extremity edema, blisters on his forehead and worsening pain

Hoelzer BC et alHoelzer BC et al

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• 2 days after the procedure he presented to the ED and was admitted. Vital signs stable, temp 37.8 Exam demonstrated Janeway lesions and Osler’s nodes

• Blood cultures positive for methicillin sensitive staphylococcus aureus and diagnosed with L5-S1 paraspinal abscess and infective endocarditis

• Treated with IV Vancomycin 1 day, Cefazolin 9 daywith Gentamicin 4 days and then Nafcillin for 6 weeks

• 2 years after infection he still has renal insufficiency but has no back pain and no neurologic sequela

Hoelzer BC et alHoelzer BC et al

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• Embolic

• Chemical

• Mechanical disruption

Vascular InjuriesVascular Injuries

Posterior Circulation Stroke after

C1-C2 Intraarticular Facet Steroid

Injection: Evidence for Diffuse

Microvascular Injury

Posterior Circulation Stroke after

C1-C2 Intraarticular Facet Steroid

Injection: Evidence for Diffuse

Microvascular InjuryEdlow BL, Wainger BJ, Frosch MP,

Copen WA, Rathmell JP, Rost NS.

Anesthesiology 2010;112:1532-5

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• 64-yr-old man with chronic cervical pain consented to a C1-C2 intraarticular facet steroid injection

• 25-gauge needle advanced with fluoroscopic guidance, iohexol contrast was injected followed by AP and lateral radiographs

• Neither live fluoroscopy or digital subtraction was used

• 2 mls of 40-mg/ml triamcinolone acetonide suspension was then injected

Edlow BL et alEdlow BL et al

• Immediate loss of consciousness with extensor

posturing of the limbs, brief period of apnea and

BP ↑ from 144/85 to 219/110 with a HR of 46.

• Initial CT angiography was normal

• MRI demonstrated multiple hyperintensities

reflecting infarction of the thalami, pons, occipital

lobes, hippocampi, splenium of the corpus

callosum and cerebellum

• On day 4 the patient remained comatose. Given

the poor prognosis, the family withdrew support

and he died shortly thereafter

Edlow BL et alEdlow BL et al

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Anesthesiology, V 112 • No 6 • June 2010

Anatomic ConsiderationsAnatomic Considerations

Anesthesiology, V 112 • No 6 • June 2010

Brain MRI Acutely and on Day

3

Brain MRI Acutely and on Day

3

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Edlow BL et al - ConclusionsEdlow BL et al - Conclusions

• It is clear that devastating neurologic injury can occur during cervical transforaminal or facet injection because of particulate steroid entering the posterior cerebral circulation.

• We call on all practitioners to perform cervical procedures only when the benefits clearly outweigh the risks, to provide adequate explanation of these risks during the informed consent process, and to adopt safety measures to minimize risk.

• In the specific case of cervical intraarticular facet injections, the benefit of this treatment is unclear; thus, practitioners should stop performing these injections altogether until further scientific evidence is available.

Cerebellar Herniation After

Cervical Transforaminal Epidural

Injection

Cerebellar Herniation After

Cervical Transforaminal Epidural

Injection

Beckman WA, Mendez RJ, Paine GF,

Mazzilli MA. Reg Anes Pain Med

2006;31:282-5

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• 31-year-old with cervical radicular pain and right upper extremity radicular symptoms

• Transforaminal epidural steroid injection at the right C8 nerve root

• Following the TFESI he developed a cerebellar infarct and brainstem herniation

• He survived but had residual deficits:

- Persistent diplopia on right lateral gaze

- Difficulties with short-term memory loss and concentration

Beckman WA, et al.Beckman WA, et al.

• Nerve injury

• Spinal cord infarction

Lumbar Transforaminal Epidural

Steroid Injection

Lumbar Transforaminal Epidural

Steroid Injection

Reg Anes Pain Med 2006;31:282-5

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Paraplegia Following Image-

Guided Transforaminal Lumbar

Spine Epidural Steroid Injection:

Two Case Reports

Paraplegia Following Image-

Guided Transforaminal Lumbar

Spine Epidural Steroid Injection:

Two Case Reports

Kennedy DJ, Dreyfuss P, Aprill

CN, Bogduk N

Pain Medicine 2009;10:1389-94

Preventing Vascular

Complications

Preventing Vascular

Complications• Checklist

- Image guidance

- Accurate anatomic placement

- Appropriate needle selection?

• Sharp, round tip, Whitacre or Sprotte configuration

- Aspiration test

- Contrast administration

• Live +/- digital subtraction angiography

- Local anesthetic test dose followed by clinical

examination

- Appropriate drug selection?

• Particulate, small particulate or non-particulate

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InjectionsInjections

• Most common class of procedure

• Associated with the greatest number of complications

• Procedures

- Trigger point injections

- Facet injections

- Epidural steroid injections

• Interlaminar

• Transforaminal

• Seemingly innocuous

• Bleeding

• Pneumothorax 51% of

all claims

Trigger Point InjectionsTrigger Point Injections

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• Accidental dural puncture

• Epidural hematoma

• Nerve injury

• Spinal cord injury

Epidural Steroid InjectionsEpidural Steroid Injections

Desai MJ, Dua S.

Pain Practice 2013;Mar 6. doi:10.1111/papr.12047

Perineural Hematoma Following Lumbar

Transforaminal Steroid Injection Causing

Acute-on-Chronic Lumbar

Radiculopathy:

A Case Report

Perineural Hematoma Following Lumbar

Transforaminal Steroid Injection Causing

Acute-on-Chronic Lumbar

Radiculopathy:

A Case Report

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Injury and Liability Associated

with Cervical Procedures for

Chronic Pain

Injury and Liability Associated

with Cervical Procedures for

Chronic Pain

Rathmell JP, Michna E, Fitzgibbon DR, Stephens LS, Posner KL,

Domino KB.

Anesthesiology 2011;114:918-26

• Compared claims for cervical pain

treatments to all other chronic pain

complaints from 2005 – 2008

• Claims for spinal cord injury underwent

in-depth analysis for mechanisms of

injury and use of sedation during the

procedure.

Rathmell JP, et alRathmell JP, et al

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• Claims related to cervical procedures 22% (64/294)

• Cervical procedure characteristics

- Healthier ASA 1-2

- More frequently women

• Cervical procedure 59% experienced spinal cord injury compared with 11% of those with other chronic pain

• Direct needle trauma was the predominant cause (31%)

Rathmell JP, et alRathmell JP, et al

• General anesthesia or sedation was used in

67% of cervical procedure claims associated

with spinal cord injuries but only 19% of

cervical procedure claims not associated with

spinal cord injuries

• Of the patients who underwent cervical

procedures and had spinal cord injuries, 25%

were nonresponsive during the procedure

compared with 5% of the patients who

underwent cervical procedures and did not

have spinal cord injuries

Rathmell JP, et alRathmell JP, et al

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Injury and Liability Associated with

Cervical Procedures for Chronic Pain

Injury and Liability Associated with

Cervical Procedures for Chronic Pain

Copyright © 2011 Anesthesiology. Published by

Lippincott Williams & Wilkins.

• Injuries related to cervical interventional pain treatment were often severe and related to direct needle trauma to the spinal cord.

• Traumatic spinal cord injury was more common in patients who received sedation or general anesthesia and in those who were unresponsive during the procedure.

• Further studies are crucial to define the usefulness of cervical interventions and to improve their safety.

Rathmell JP, et alRathmell JP, et al

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Intradiscal ProceduresIntradiscal Procedures

Phillips H, Glazebrook JJ,

Timothy J.

Acta Neurochir 2012;154:1033-36

Cauda Equina Compression

Post Lumbar Discography

Cauda Equina Compression

Post Lumbar Discography

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• 29-year-old female dancer with LBP

• MRI and CT myelography demonstrated DDD at L4-5 and L5-S1

• 3-level discogram with fentanyl/midazolam sedation

• L4-5 severe concordant pain L5-S1 milder concordant pain

• 3 weeks after the procedure, admitted with urinary incontinence for 3 weeks, fecal incontinence for 48 hours, lower extremity weakness 3-4/5 and decreased sensation globally on the right and L4-S2 on the left.

Phillips GH, et al.Phillips GH, et al.

Pre-Procedural Imaging and

Discogram

Pre-Procedural Imaging and

Discogram

Acta Neurochir (2012) 154:1033–1036

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MRI Imaging 3-weeks Post-

Discography

MRI Imaging 3-weeks Post-

Discography

• Lumbar laminectomy and L4-5, L5-S1

microdiscectomy

• She subsequently underwent elective

L4-5, L5-S1 ALIF with removal of the

discs followed by bilateral L4-5, L5-S1

facet joint screw fixation

• Discharged from clinic 4 years and 1

month after initial presentation with no

pain and no residual neurologic deficits

Phillips GH, et al.Phillips GH, et al.

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Subach BR, Copay AG, Martin

MM, Schuler TC, DeWolfe DS

The Spine Journal 2012;12:e1-4

Epidural Abscess and Cauda

Equina Syndrome after

Percutaneous

Intradiscal Therapy in

Degenerative Lumbar Disc

Disease

Epidural Abscess and Cauda

Equina Syndrome after

Percutaneous

Intradiscal Therapy in

Degenerative Lumbar Disc

Disease

• 61-year-old male with LBP due to DDD involving the lumbar spine (annular tears L3-4, L4-5 and L5-S1)

• No response to conservative treatment or strong analgesics

• Underwent bone marrow aspiration from the left iliac crest and aspiration of autologous fat

• The bone marrow aspirate, unseparated adipose tissue and plasma from a peripheral blood draw were combined and injected into the L3-4 and L5-S1 disc spaces.

• 2 weeks later he developed fever, increasing low back pain and new onset left lower extremity radicular pain associated with weakness and urinary retention – cauda equinasyndrome

• MRI – discitis, myelitis, epidural abscess and paraspinal abscess

• Surgical treatment X 2 with evidence of herniated disc material found at the L3 pedicle

• One year later – normal strength, hypoactive reflexes, patchy sensory loss and normal bladder function

Subach BR, et al.Subach BR, et al.

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Vertebroplasty and KyphoplastyVertebroplasty and Kyphoplasty

Tran I, Gerckens U, Remig J, Zintl G, Textor J.

Spine 2013;38:E316-8

Pericardial Tamponade and

Right Ventricular Cement

Embolus due to Right Ventricle

Perforation During Kyphoplasty

Pericardial Tamponade and

Right Ventricular Cement

Embolus due to Right Ventricle

Perforation During Kyphoplasty

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• Procedural complications

• Infection

• Direct neural trauma

• Pump errors

- Programming error

- Drug overdose

- Drug error or contamination

• Granuloma formation

• Catheter breakage or disconnect

Intrathecal or EpiduralIntrathecal or Epidural

Spinal Cord Stimulation

Devices

Spinal Cord Stimulation

Devices

• Infection

• Epidural hematoma

• Nerve injury

• Spinal cord injury

• Equipment failure

- Lead breakage

- Disconnect

• Battery failure

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A Report of Paraparesis Following

Spinal Cord

Stimulator Trial, Implantation and

Revision

A Report of Paraparesis Following

Spinal Cord

Stimulator Trial, Implantation and

Revision

Smith CC, Lin JL, Shokat M,

Dosanjh SS, Casthely D

Pain Physician 2010;13:357-63

• 4 cases

- 1 – cord contusion

- 3 – cord compression

• 2 – epidural hematoma

• 1 – implantation in the setting of broad based thoracic disc herniations

- All electrodes and neurostimulators successfully removed

• 1 – complete paraplegia

• 2 – incomplete paraparesis

• 1 – complete recovery of neurologic function

Smith CC, et alSmith CC, et al

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Wloch A, Capelle HH, Saryyeva A, Krauss JK.

Stereotact Funct Neurosurg 2013;91:265-9

Cervical Myelopathy due to an Epidural

Cervical Mass after Chronic Cervical

Spinal Cord Stimulation

Cervical Myelopathy due to an Epidural

Cervical Mass after Chronic Cervical

Spinal Cord Stimulation

Retrospective Review of 707

Cases of Spinal Cord

Stimulation:

Indications and Complications

Retrospective Review of 707

Cases of Spinal Cord

Stimulation:

Indications and Complications

Mekhail NA, Mathews M, Nageeb F,

Guirguis M, Mekhail MN, Cheng J

Pain Practice 2011;11:148-53

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• Trials

- Lead migration 0.7%

• Permanent Implants

- Hardware related complications

• Lead migration 22.6%

• Lead connection failure 9.5%

• Lead breakage 6%

- Biological complications

• Pain at the generator site 12%

• Clinical infection 4.5%

• Failed back surgery and diabetics were at highest risk

Mekhail NA, et alMekhail NA, et al

Reducing Neuromodulation

Complications

Reducing Neuromodulation

Complications

• Appropriate training, credentialing and

privileging

• Algorithmic approach to patient

selection

• Checklist procedural approach

• Algorithmic trial and postoperative

management

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• Complications of Pain Medicine practice

are common

• Interventional techniques carry significant

complications and risk

• Careful patient selection, excellent

anatomic knowledge and meticulous

technique may reduce risk and maximize

benefit

Conclusions IConclusions I

• We must codify and enforce the basics

• We must develop and use a uniform set of

outcome measures that allows broad

comparisons

• We must develop and implement a

method of tracking outcomes and

complications to improve patient safety

• We must innovate to survive healthcare

reform without sacrificing patient safety

Conclusions IIConclusions II

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50

Treatment of 1

Michael Stanton-HicksMB;BS Dr. med, FRCA, FCAI (hon), ABPM, FIPP

Department of Pain Management

Shaker Pediatric Rehabilitation

Cleveland Clinic

European Pain Federation Klagenfurt Pain School

6th – 11th September 2015; Parkvilla Wörth, Pörtschach

Ambroise Paré

as surgeon to Charles IX,

during multiple bloodletting

for smallpox, caused nerve

injury that led to causalgic Sx

1557

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51

Weir Mitchell

“symptom amplification” causalgia

“Gunshot Wounds and other Injuries”

with Moorhouse and Keen 1864

Paul Sudeck

“..über die akute

Knockenatrophie..”

1900

René Leriche

Related pain to

SNS dysfunction

1879-1955

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52

participants

� Wilfrid Jänig

� Martin Zimmermann

� Terrence Murphy

� Edmond Charlton

� William Roberts

� Martin Kolzenberg

� Hans Nolte

� Ilmar Jurna

� Jennifer Kelly

� Hermann Kreuscher

� Peter Wilson

� Karen McCann

� Gabor Racz

� Ronald Tasker

� Stephen Butler

� Erik Torbjörk

� Prithvi Raj

� Ulf Egle

� Robert Boas

� Helmut Blumberg

� Stephen Abram

� David Haddox

� Hannington-Kiff

� Christopher Glynn

� Albert van Steenberge

� Hans Gebershagen

� Michael Stanton-Hicks

Orlando concensus conference1993

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53

Pain. 1995 Oct;63(1):127-33.

Reflex sympathetic dystrophy: changing concepts and taxonomy.Stanton-Hicks M1, Jänig W, Hassenbusch S, Haddox JD, Boas R, Wilson P

� CRPS: 3 stages originally proposed

� Inflammatory: early

� Dystrophic: 3-6 months

� Atrophic: Late

� INACCURATE! (Level 4)

Bruehl S. et al., Pain. 2002 Jan;95(1-2):119-24

Maleki J. et al., Pain. 2000 Dec 1;88(3):259-66

� Most cases � Sxs actually remain stable or improve with time (“spread” in 10%)

CRPSmild severe

no progression of Sx

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• Terms Reflex Sympathetic Dystrophy and Causalgia lost clinical utility

• Taxonomy emphasizes clinical characteristics– Complex: varied clinical features

– Regional: majority of cases involve a region of the body, usually an extremity

– Pain: essential to the diagnosis

– Syndrome: repetitive nature of clinical features

Taxonomy CRPS - 1994 IASP

Merskey H, Bogduk N eds. IASP Press, 1994, Stanton-Hicks et al. Pain, 1995

Sympathetic Contribution

� A favorable response to a sympatholysis is NOT required for

the diagnosis of CRPS

Merskey H and Bogduk N eds. IASP Press 1994

Stanton-Hicks et al., Pain. 1995 Oct;63(1):127-33

SMP

SIP

Magnitude of Pain

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“Budapest” Criteriaat least I SYMPTOM in 3 of 4 categories and 1 SIGN in 2

or more categories. (SENS. 0.99: SPEC. 0.68)

Harden et al. Pain (2010);150: 268-

274

CATEGORY SYMPTOM SIGN

SENSORY Hyperesthesia,

allodynia

hyperalgesia (PP)

allodynia – mech. /

thermal / deep

VASOMOTOR ∆ skin / color

∆ temperature

> 1˚ C / ∆ skin color

SUDOMOTOR

EDEMA

∆ sweating / edema ∆ sweating / edema

MOTOR

TROPHIC

motor dysfunction

ROM

∆ trophic

motor function

ROM (weak,

dystonia, tremor) /

trophic

Lancet. 1993 Oct 23;342(8878):1012-6.

Signs and symptoms of reflex sympathetic dystrophy:

prospective study of 829 patients.Veldman PH1, Reynen HM, Arntz IE,

Goris RJ.

« 7In its early phase, reflex sympathetic dystrophy is

characterised by regional inflammation, which increases after

muscular exercise. Pain was present in 93% of patients, and

hypoaesthesia and hyperpathy were present in 69% and 75%

respectively7 »

«7Tremor was found in 49% and muscular incoordination in

54% of patients. Sympathetic signs such as hyperhidrosis are

infrequent and therefore have no diagnostic value3»

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MVF, GMI

Reactivation

Contrast Baths

Desensitization

Exposure therapy

Edema control

Flexibility (active)

Isometric strengthening

Correction of postural abnormalities

Dx & Rx of secondary MFPS

Stress loading

Isotonic strengthening

ROM – gentle – resistant

General aerobic conditioning

Postural normalization & balanced use

Ergonomics

Movement therapies

Normalization of use

Vocational / Functional Rehabilitation

Core

Treatment

Algorithm

LLLL

EEEE

VVVV

EEEE

LLLL

1111

Flor H et al., Pain 1992; 49: 221–30

Guzman J et al., BMJ 2001; 322: 1511–6

Interdisciplinary

Management

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The algorithms were discussed in Milan

SIG, Pain & SNS : “A comprehensive analysis of CRPS treatment : the new, the old. what works and what doesn’t”

World Congress, IASP, Milan, August 25 –31, 2012

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problems of management

� Non-uniform Rx strategies

� wide range of practice habits

� patient heterogeniety

� Scale of treatment options

� limited evidence

� always something new

� Non responders

� mismatch of treatment with patient

ddddifferent CRPS symptoms have different ifferent CRPS symptoms have different ifferent CRPS symptoms have different ifferent CRPS symptoms have different

mechanisms mechanisms mechanisms mechanisms

•Changes in color, temperature, edema due to

malfunction/pathology of microcirculation

•Changes in bones due to osteoclast/blast

dysregulation

•Pain can be nociceptive and/or neuropathic

•Regional changes in muscle, skin, hair, nails

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vasomotor inflammation

dystonia

Neuropathi

c

sudomotor

treat

clinical

features

pathology

florid

Pathophysiology CRPS

Brain

Spinal

cord

Inflammation

Nerve

damage Tissue damage

Genetic

Immune acquired

cGRP

Blood vessel

Central Sensitisation

allodynia. Dystonia

autonomic dysfunction

Mast cells

CNS

NO/endothelial

dysfunction

IL6

TNFα

neuropeptides

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Levels of Evidence

� Level 1: Meta-analysis or systematic reviews.

� Level 2: One or more well-powered randomized, controlled

trials.

� Level 3: Retrospective studies, open-label trials, pilot studies.

� Level 4: Anecdotes, case reports, clinical experience, etc.

Harden RN et al., Complex regional pain syndrome: practical diagnostic

and treatment guidelines, 4th edition. Pain Med. 2013 Feb;14(2):180-229.

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Before Algorithms

� Treatment reflected the specialty of the clinician

� Carlson (1987) emphasized physical modalities� “stress-loading, isometrics”

� Interdisciplinary management

� 3 consensus meetings� Malibu (1997), Minneapolis (2001), Budapest (2005).

CRPS - treatment

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Psychological interventions

� Psychological/social issues: Important

� Rationale

� Utility in non-CRPS

� ? direct interaction with pathophysiological mechanisms

� Sympathetic/catecholamines

� Both anxiety and anger expressiveness have been

found to be significantly stronger in CRPS patients

than in non-CRPS

� Inflammatory mediators

Harden RN et al., Complex regional pain syndrome: practical

diagnostic and treatment guidelines, 4th edition. Pain Med. 2013

Feb;14(2):180-229.

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McCabe CS et al., Rheumatology (Oxford). 2003 Jan;42(1):97-101

Daly AE, Bialocerkowski AE. Does evidence support physiotherapy

management of adult complex regional pain syndrome type one? A

systematic review. Eur J Pain 2009;13:339–53.

Subject viewing non-reflective surface

with painful limb hidden

Subject viewing non-painful limb in

mirror with painful limb hidden

• Daly and Bialocerkowski: meta-analysis

�good quality level 2 evidence

E

A

R

L

Y

Mirror Box Therapy

Anti-inflammatories

� NSAIDs: level 4

� Anecdotal +

� Small CRPS trial � naproxen not effective

� Oral Corticosteroids: level 2

� High dose: ~30 mg/day

� Long duration: ~12 weeks

� Use when inflammation present

� Beware of contraindications

Rico H et al., Clin. Rheumatol 1987 Jun;6(2):233-7

Christensen K et al., Acta Chir Scand 1982;148:653–5

Braus DF et al., Ann Neurol 1994;36:728–33

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Antidepressants

� NNT = 3 for TCA in neuropathic pain

� There is no evidence that antidepressants are

effective in reducing pain in patients with CRPS-I

(level 4)

Perez RS et al., Evidence based guidelines for complex regional pain

syndrome type 1. BMC Neurol. 2010 Mar 31;10:20

Anticonvulsants

� Gabapentin: mild effect (level 2)

� Adult case series and pediatric case report

� 1 DBRCT: mild effect with improvement in sensory

deficits

� pregabalin, topirimate, zonisamide, levetiracetam,

carbamazepine, oxcarbazepine etc.

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Sympathetic Blocks

� First line treatment but poor quality studies

� DB cross-over study, 7 CRPS pts, SGB

� Onset of analgesia: <30 min, both LA & saline

� duration of pain relief: LA > saline

� Testing for sympatholysis: CRUCIAL

� Temperature >34 0C

� Within 3 0C of core temperature

Cepeda MS et al., Clin J Pain. 2002 Jul-Aug;18(4):216-33

Price DD et al., Clin J Pain. 1998 Sep;14(3):216-26

Malmqvist EL et al., Reg Anesth 1992;17:340–7

Tran KM et al., Anesth Analg 2000 Jun;90(6):1396-401

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Antihypertensives and α-Adrenergic

Antagonists

� Clonidine:� Systematic review: no evidence (level 1)

� Nifedipine:� 2 uncontrolled case series found doses of up to 60 mg/day

useful for CRPS (level 4)

� Phenoxybenzamine:� Treatment of complex regional pain syndrome type 1

with oral phenoxybenzamine: rational and case reports

α1 & α2 non-competitive block

Kingery WS et al., Pain 1997;73:123–39

Muizelaar JP et al., Clin Neurol Neurosurg 1997;99:26

Prough DS et al., Anesthesiology 1985;62:796–9

Inchiosa M, Kizelshteyn G Pain Pract 2008; 8 : 125

Successful treatment of CRPS 1 with anti-TNF.

Huygen FJ, Niehof S, Zijlstra FJ, van Hagen PM, van Daele PL.

J Pain Symptom Manage. 2004 Feb; 27(2):101-3.

Case Report n = 2

Infliximab 3mg/kg

Both Signs and Sx

6 weeks

A Double Blind, Randomized, Placebo Controlled Trial of

Anti-TNFα Chimeric Monoclonal Antibody in CRPS

At 10 wks sig.

TNFα in blister

fluid

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Tadalafil Placebo P-value P-value

start end start end 10 wks Between groups

Pain intensity VAS (0-100mm)

61.3 ± 14.1 52.3 ± 19.1 57.0 ± 12.1 56.5 ± 10.8 0.03 0.04

Effect of tadalafil on blood flow, pain, and function in chronic

cold complex regional pain syndrome: a randomized

controlled trial. BMC Musculoskelet Dis 2008; 20

Groeneweg G1, Huygen FJ, Niehof SP, Wesseldijk F, Bussmann JB, Schasfoort FC,

Stronks DL, Zijlstra FJ

n=24

Rx, 20 mg po /daily

for10 weeks

Rheumatology (Oxford). 2013 Mar;52(3):534-42. doi:

10.1093/rheumatology/kes312. Epub 2012 Nov 30.

Treatment of complex regional pain syndrome type I with

neridronate: a randomized, double-blind, placebo-

controlled study.

Varenna M1, Adami S, Rossini M, Gatti D, Idolazzi L, Zucchi F, Malavolta

N, Sinigaglia L.

• n=82, neridronate IV 4 X for 10 days

• @ 20 days VAS 4.6 cf. 2.2

• @ 1 year – no CRPS pts. had CRPS Sx

Biphosphonates

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Free Radical Scavengers

� Vitamin C prevents CRPS (level 1)

� 4 RCTs, 3 UE (wrist) and 1 LE (ankle)� A minimum dose of 500 mg/day is recommended

� Limited to prophylaxis immediately after fx

Zollinger PE et al., J Bone Joint Surg Am. 2007 Jul;89(7):1424

Besse JL et al., Foot Ankle Surg. 2009;15(4):179-82

Shibuya N et al., J Foot Ankle Surg. 2013 Jan-Feb;52(1):62-6

DMSO (50% cream 5 x/day for 2 months) significant

pain vs. placebo (level 2)

It is likely that 600 mg tab of N-acetylcysteine TID

will CRPS Sx (level 3)

Perez RS et al., Pain 2003, 102:297-307

Zuurmond WW et al., Acta Anaesthesiol

Scand 1996, 40:364-367

Fourouzanfar T et al., Eur J Pain

2002;6:105–22

Hyperbaric Oxygen (level 2)

� DBRCT, 15 x 90-minute sessions, 5 d/wk

� 37 patients HBO vs. normal air

� 34 patients room air (2.4 Atm. P)

Kiralp MZ et al., Effectiveness of hyperbaric oxygen therapy in the

treatment of complex regional pain syndrome.J Int Med Res. 2004 May

Jun;32(3):258-62

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neuromodulation

� SCS - (as an extended trial)

� When CMM has either failed or when

confronted with florid CRPS

� Intrathecal ziconotide for complex regional pain

syndrome: seven case reports.

Kapural L, Lokey K, Fiekowsky S, Stanton-Hicks M, Sapienza-

Crawford A, Webster L Pain Pract 2009; 9: 296

Why SCS?

� CRPS

� Peripheral adrenergic-nociceptor coupling

� DRG Aβ-adrenergic coupling in CRPS II

� peripheral ischemic pathology

� α1- adrenoceptor population on keratinocytes, mast cells

and immune cells

� Neuropeptide release in DH & periphery (SP, CGRP, VIP)

� Inhibition of inflammatory response

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Neuromodulation of α1- adrenoceptor

sites

NE

1

2

3

4

Sympatheticefferent

Sensory afferent

Macrophage

Jänig and Baron Lancet Neurology 2003

Stimulation of the dorsal route ganglion for

the management of complex regional pain

syndrome: a prospective case series.

Van Buyten JP, Smet L, Liem, L, Russo M, Huygen F. Pain Pract

2014 Jan 23 (Epub ahead of print)

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71

� 8 patients – prospective, randomized controlled trial

� Average Pain Reduction (VAS):

75.0% Foot

65.0% Overall

Clinical Mentor Course 2013

© 2013 Spinal Modulation, Inc.* Data courtesy of JP Van Buyten, I Smet, L Liem, M Russo, F Huygen 2014

CRPS of the Foot

CRPS of the Foot

� 60 year-old male

� CRPS type-1 after minor fracture

� Pain in left leg and foot showing

signs of severe erysipelas.

* Data courtesy of JP Van Buyten & I Smet.

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72

� Baseline VAS

� Overall: 67 mm

� Leg: 69 mm

� Foot: 91 mm

� Single lead at L5

DRG

Clinical Mentor Course 2013

© 2013 Spinal Modulation, Inc.

* Data courtesy of JP Van Buyten & I Smet.

Data from van Buyten et al*

6 months

Baseline

1 month

* Data courtesy of JP Van Buyten & I Smet.

data from Van Buyten et alal

CRPS of the Foot

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Autoimmun Rev. 2013 Apr;12(6):682-6.

Complex regional pain syndrome, prototype of a novel

kind of autoimmune disease

Goebel and Blaes 2013; 12: 682

Emerging Rx: IVIG

• IgG serum autoantibodies against autonomic receptors

• CRPS includes an autoantibody-mediated autoimmune process

• Suggests novel Rx modalities in future

Pharmacotherapy for CRPS

� Inference from neuropathic pain trials

� Complex pathophysiology � unlikely one medication will control all pain

� Rational polypharmacy: often necessary

� Specifically trialed in CRPS:

� Calcitonin and bisphosphonates

� Corticosteroids

� intravenous immunoglobulin (IVIG)

Harden RN et al., Complex regional pain syndrome: practical diagnostic and

treatment guidelines, 4th edition. Pain Med. 2013 Feb;14(2):180-229.

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Scrambler therapy

Predictive Factors Associated with Success and Failure for Calmare (Scrambler) Therapy: A Multi-Center Analysis.

Moon JY, Kurihara C, Beckles JP, Williams KE, Jamison DE,

Cohen SP.

Clin J Pain. 2014 Sep 17. [Epub ahead of print]

Suggests relief in neuropathic and mixed

neuropathic/nociceptive pain

Traumatic/surgical etiologies and anti depressant use

correlated with failure

38.1 % success

Emerging: Botulinum Toxin

� DBPRCT, 25 pts

� 0.2ml or 5 units per site

� Limit: 40 sites or 200 U

� spontaneous pain, brush allodynia, and cold pain thresholds

� LSB with BTx-A in 9 CRPS patients with SMP

� pain relief 71 days vs. < 10 days for bupivacaine

Ranoux D et al., Botulinum toxin type A induces direct analgesic effects in

chronic neuropathic pain. Ann Neurol. 2008 Sep;64(3):274-83

Carroll I et al., Sympathetic block with botulinum toxin to treat complex

regional pain syndrome. Ann Neurol 2009 Mar;65(3):348-51

11.09.2015

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Pathophysiology

InflammationTNFα

IL-6

(Immune

modulator)

Infliximab

thalidomide

IVIG

Hypoxia

NO/ endothelin

dysfunction

O2 radicals

vasoconstriction

NO donation

eNO synthase

Isosorbidedinitrate

PDE-5 inhibition

Tadalafil

Neuromodulation

O2 radical scavengers

Movement

Disorder

tremor

dystonia

IT Baclofen UE’s

SCS

Central sensitization

DH

microglia

astrocytes

locus coeruleus

anticonvulsants

antidepressants

minocycline

WP9QY

naltrexone (TLR4)

Phenoxybenxamine (α1α2)

neuromodulation

Autonomicblood vessels

sweat glands

keratinocytes

mast cells

NE’s

α1anatagonist

Ca+ blockers

phenoxybenzamine

neuromodulation

Psychologicno pre-morbid Hx

cause

consequence

Beerthuizen et al

2011

Psychologic interventions

MVF

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Functional restoration

algorithm

REACTIVATION

CONTRAST BATHS

DESENSITIZATION

EXPOSURE THERAPY

FLEXIBILITY

EDEMA CONTROL

ISOMETRICS

ROM

STRESS LOADING

POSTURAL CORRECTION

AEROBIC XC’s

GAMES

WATER THERAPY

FUNCTIONAL REHAB

MUSIC THERAPY

COGNITIVE BEHAVIORAL

GROUP THERAPY

PSYCHOLOGICAL COUNSELING

OF PATIENT / PARENTS

SCHOOLING

SYMP. BLOCK

CON’T. RA

SCS

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PAIN

Joint, Muscle, Bone

Rheumatoid Arthritis ?

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Cheiropathia Diabetica

Osteoarthritis

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Yes Inflammation No

• Rhematoid Arthritis

• Psoriasis

• Lupus erthematodes

• PSS

• Haemosiderosis

• Lyme

• Septic

• Osteoarthritis

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11.09.2015

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Figure 1 A schematic showing the simplified pathophysiologic pathways in

rheumatoid arthritis and their main clinical consequences

van Vollenhoven, R. F. (2009) Treatment of rheumatoid arthritis: state of the art 2009

Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2009.182

Proinflammatorische Cytokine:

Il- 1, Il-6, TNF

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Serology

•ESR

•CrP

•Elpho

•Fe/Ferritin

•etc

•RF

•a-ccP

•HLA B27

•Borrelien

•ANA, dsDNS

•ANCA

•(Parvo B29)

Ultrasond, MRI, etc.

ENA

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11.09.2015

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Destruktion

11.09.2015

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Synovitis

11.09.2015

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Psoriasis-Arthritis

11.09.2015

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Psoriasis

11.09.2015

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11.09.2015

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Assessment of risk of psoriatic arthritis in patients

with plaque psoriasis

Prey S, et al. J Eur Acad Dermatol Venerol

2010 Apr

• 7% - 26%

2171 Papers

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91

Lupus erythematodes

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Tendinitis

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Wladimir Michailowitsch Bechterew

1857-1927

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Spondylarthropathy

• 75 % get

Low back pain

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Gonarthritis

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Uveitis anterior

25-40% of the SpA patients

50% of those having a

uveitis anterior

will once get a SpA

X-ray

• 10a after onset 40%

are positive

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MRI

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Therapy

• PsA

• RA

1999 DMARDs

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2000 TNF blocking

TNF-Blocking

• Golimumab SIMPONI 1x monatlich sc, iv

• Certolizumab CIMZIA 1-2x monatlich sc

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TCR=T-cell receptor; IL=interleukin; IgM=immunoglobulin M; RF=rheumatoid factor; TNF=tumour

necrosis factor; PMN=polymorphonuclear leucocyte; LT=leukotrienes; MMP=matrix metalloproteinases

Adapted from Voulgari PV. Expert Opin Emerging Drugs 2008;13:175–96.

TNF inhibitor

XAnakinra X

Rituximab

X

Abatacept

X Tocilizumab

Rheumatoid Arthritis

Rituximab

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Orencia

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Autoimmune Diseases

11.09.2015

105

Systemic lupus

Pleuritis

11.09.2015

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Pericarditis

Lupus erythematodes

11.09.2015

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Alopecia areata

Lupus erythematodes

11.09.2015

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11.09.2015

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SLE: Therapy 1, Standard

NSaid Arthralgia

Steroide topic skin

systemic

1mg/d bis 1000mg/d

„the lower – the better“?!?

Antimalaria´s OH-Chloroquin flarereduction

better survival

skin

arthralgia/arthritis

Immunmodulation/ Methotrexat arthralgia/arthritis

Immunsuppression

Azathioprin haematology

Cyclosporin

Cyclophosphamid nephritis, cerebritis, etc.

MMF nephritis

SLE: Therapie 2

Immunmodulation/ Methotrexat arthralgia/arthritis

Immunsuppression

Azathioprin haematology

Cyclosporin

MMF nephritis

Cyclophosphamid nephritis, cerebritis, etc.

Immunablation stemcell tx

Anti-B-Zell-Therapy Rituximab

Belimumab

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Anti-B-Cell-Therapy

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Thank you