06 Rheumatology

SECTION 6

Rheumatology 32.

Approach to the Patient with Polyathritis Ved Chaturvedi, Molly M Thabah

169

33.

Practical Approach to a Person with Low Backache Pradeep Kumar Maheshwari, Anjana Pandey, Rosmy Jose

174

C H A P T E R

32

INTRODUCTION

Polyarthritis is a cardinal manifestation in rheumatology. It is essential to recognize and find the most correct cause for polyarthritis in an individual patient. The diagnosis of the cause of inflammatory polyarthritis relies heavily on good history taking and physical examination. Rheumatology as a speciality is unique in that inflammatory rheumatic diseases evolve over time. Hence one rheumatologist may label a patient of polyarthritis as undifferentiated arthritis which over a few months or years may manifest signs of rheumatoid arthritis (RA) or psoriatic arthritis (PsA).

This is also true for connective tissue diseases such as undifferentiated connective tissue disease (UCTD) which may evolve in to systemic lupus erythematosus (SLE).

GENERAL APPROACH TO A PATIENT WITH MUSCULOSKELETAL (JOINT) PAIN

Does the patient have arthritis?- A patient is said to have arthritis if one has joint pain and swelling, and the origin of “joint pain” (true arthritis) is from the joint (articular) structures, in contrast to pain arising from peri-articular synovium, structures.1 Articular structures include synovial fluid, cartilage, intra-articular ligaments, the joint capsule, and adjacent bone.2 RA a disease of synovium, is a classic example of polyarthritis. Osteoarthritis (OA) of hands a disease of articular cartilage, presents with joint pain is also polyarthritis.

Joint pain also arises from involvement of peri-articular structures: ligaments, tendons, bursae, muscle, fascia, bone and nerve.2 Examples of peri-articular (nonarticular) origin of joint pain include Baker’s cyst (bursitis) producing knee pain, Achilles tendinitis can produce ankle pain, carpal tunnel syndrome can produce wrist pain. In arthritis the pain is deep or diffuse, with limited and painful range of motion on both passive and active movement of the involved joint, there is palpable swelling due to synovial proliferation (synovitis), joint space effusion, crepitation, and deformity. By contrast non-articular disorders tend to be painful on active (but not passive assisted) range of motion, example is periarthritis of shoulder (frozen shoulder). Also there is no swelling, deformity, crepitus or instability.2 Local tenderness is present in regions away from the joint line.

Patients with arthritis tend to hold the joint in partial flexion, hence contractures may develop. Therefore the finding of contracture is a sign of inflamed joint.3 How many joints are involved? - Single joint arthritis is monoarthritis. A person with 2-3 joint involvement is

Approach to the Patient with Polyathritis Ved Chaturvedi, Molly M Thabah

oligoarthritis, while poyarthritis is defined as pain (and swelling) involving 4 or more joints.

What is the duration of arthritis? Conventionally if the duration of arthritis is less than 6 weeks it is acute arthritis, and more than 6 weeks it is chronic arthritis.1 Inflammatory versus non-inflammatory arthritisProbably most important is to decide whether it is inflammatory or non-inflammatory.1,3 This is so because inflammatory arthritis especially RA if not diagnosed and treated early will cause bony erosion, deformity to the joints and impair the patient’s quality of life. SLE can have life threatening major organ involvement.

The classical signs of inflammation are pain, warmth, swelling, and erythema.2,3 All patients may not have all these signs. Inflammatory arthritis is characterized by presence of prolonged morning stiffness. Morning stiffness is defined as the time to maximal improvement after an extended period of inactivity, and typically improves with movement. In inflammatory arthritis early morning stiffness (after waking up in the morning) is prolonged and is present at least for 30 min, some patients may have morning stiffness lasting for hours. The pain and stiffness of inflammatory arthritis often improve on gentle use of joints and activity. An example is the low back pain, or buttock pain of ankylosing spondylosis which worsens with rest and improves with activity. By contrast noninflammatory conditions such as OA is characterized by pain which is precipitated by brief periods of rest (gel phenomenon), exacerbated by use of the joint (activity) and stiffness is brief. Inflammatory arthritis is characterised by spontaneous “flares”.1 In clinical practice we often see inflammatory arthritis patients (prototype RA) whose disease appears well controlled but then they present with arthritis flare. So a spontaneous up and down course is indicative of inflammatory disease. Most inflammatory arthritis is accompanied by constitutional symptoms especially fatigue, low-grade fever, weight loss. Fatigue is an important symptom of RA, SLE, polymyalgia rheumatica.

On investigations a patient with inflammatory arthritis may have one or more of the following;1 High erythrocyte sedimentation rate (ESR), high C-reactive protein (CRP) levels. There may be normocytic normochromic anaemia.

Thrombocytosis i.e. platelet count of more than 400,000/ cumm is also a sign of inflammation. The total leukocyte count (TLC) may be high. A reversal of albumin /

170

Musculoskeletal complaint- Joint pain

Non-articular pain/ Periarticular pain

RHEUMATOLOGY

Trauma, fracture Bursitis Tendinitis Nerve entrapment

Arthritis/Arthralgia†

Monoarthritis (1joint)

Polyarthritis

Oligoarthritis (2-3 joints)

Non-inflammatory

Inflammatory

Acute Viral arthritis Palindromic rheumatism Onset of CTD Acute Rheumatic fever Polyarticular gout RS3PE Drug induced Serum sickness Paraneoplastic

Chronic RA Undifferentiated arthritis SLE SSc Poly JIA AOSD Inflammatory OA Polyarticular gout Sarcoidosis Brucella

Acute

Chronic

Amyloid arthropathy Hemoglobino pathies

OA

†See text on how to differentiate arthritis from peri-articular/non-articular pain Abbreviations- CTD, connective tissue disease; RS3PE, remitting seronegative symmetrical synovitis with pedal edema; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; SSc, systemic sclerosis; Poly JIA, Polyarticular juvenile idiopathic arthritis; AOSD, adult onset still’s disease; OA,osteoarthritis;

Fig. 1: Approach to the patient with joint pain and differential diagnosis of polyarthritis globulin ratio and moderate elevations of serum alkaline phosphatase are all seen in inflammatory arthritis.

APPROACH TO POLYARTHRITIS

Polyarthritis is arthritis of 4 joint or more. Using the broad principles outlined above we have the following 4 diagnostic categories in polyarthritis (Figure 1).1,4 a.

Acute inflammatory polyarthritis b) Chronic inflammatory polyarthritis c) Acute non-

inflammatory polyarthritis and c) Chronic noninflammatory polyarthritis.

Point to consider while taking the history of a patient presenting with polyarthritis

Investigations cannot replace the diagnostic clue one can get from detail history and physical examination.3 Demographic parameters are important. Some types of arthritis are seen more commonly in young people while some are more common in older people. A young woman

Box 1: Conditions that mimic polyarthritis Acute polyarthritis mimics Fibromyalgia Neuropathies Carpal tunnel syndrome Tarsal tunnel syndrome Bone secondaries Myeloma Leprosy Parkinson’s disease Tendonitis Polymyalgia rheumatic Chronic recurrent multifocal osteomyelitis Multifocal osteonecrosis with painful swelling of the joints of her hands and history of Raynaud’s phenomenon suggest a connective tissue disease. Whereas an older man who has diabetes and hypertension with history of polyarthritis of large suggest crystal induced arthritis.

Apart from musculoskeletal history the respiratory, cardiovascular, gastrointestinal, central nervous system, has to be reviewed.4 In addition involvement of the airways, lungs, eye, skin, mucous membranes, and renal system involvement is closely linked to rheumatology.

A past or present history of psoriasis suggests psoriatic arthritis. Eye involvement (uveitis, scleritis, conjunctivitis) is very common in the SpA family of diseases. History of nasal or ear discharge or hemoptysis helps to point toward a systemic necrotizing vasculitis. History of oral ulcers especially on the hard palate suggests SLE, while recurrent oral aphtous ulcers and scrotal ulcer suggest Behcets syndrome. Presence of diarrhoea, abdominal pain may indicate mesenteric ischemia. History of urethritis or diarrhoea preceding the arthritis helps to diagnose reactive arthritis (ReA). History of edema feet and other features of renal disease like cola coloured urine, frothy urine can suggest glomerulonephritis of SLE. The CTDs and systemic vasculitis can present with fever of unknown origin (FUO). History of dry cough and presence of bibasal rales on lung auscultation is diagnostic of interstitial lung disease (ILD). ILD is particularly common in systemic sclerosis (SSc). A patient may present only with polyarthralgias, raynaud’s phenomenon and evidence of synovitis on physical examination. If lung auscultation on such a patient reveals bibasal rales we are almost sure of dealing with SSc or a mixed connective tissue disease (MCTD) as the cause of polyarthritis.

Pattern of joint involvement3

During physical examination one can know the extent and pattern of joint involvement.3 A pattern of inflammatory polyarthritis involving large and small joints including

171

A pattern of asymmetrical polyarthritis predominantly lower limb oligoarthritis (2-3 joint involvement), with or without root joint involvement (either hip or shoulder), presence of inflammatory back pain, alternating buttock pain in a young male strongly suggest SpA. Peripheral arthritis can be the first manifestation of ankylosing spondylitis in India.

A gout patient will give history of attacks of great toe arthritis (podagra). Subsequent attacks can be polyarticular and involve the hands also. Therefore when a middle aged, maybe obese man with hypertension and/ or diabetes presents with polyarthritis one should not forget to enquire for past history of podagra.

DIP joint involvement without inflammation is characteristic of primary nodal OA. Involvement of the first carpometacarpal joint is also very common in OA. The pattern of DIP joint involvement with nail findings is typical of PsA. The pattern of bilateral ankle arthritis, and ankle edema, with erythema nodosum is almost diagnostic of sarcoidosis or tuberculosis. Further distinctions between these two conditions depend on tuberculin test, findings of chest radiographs, and computed tomography (CT) of chest.

Cause of Acute Inflammatory Polyarthritis- In acute inflammatory polyarthritis there is involvement of 4 or more joints, and the duration is less than 6 weeks. This category often poses a diagnostic challenge because the causes for acute inflammatory polyarthritis could either be a self-limiting viral arthritis or it could be the onset of a chronic illness such as RA.3,4 There are several conditions which can mimic acute polyarthritis.4 In the authors experience the conditions listed in box 1 can mimic acute polyarthritis. The causes for acute inflammatory polyathritis are viral arthritis, acute rheumatic fever, infective endocarditis, onset of RA, onset of CTDs (SLE, SSc, MCTD), ReA. It could also be due to palindromic rheumatism, which is characterized by attacks of arthritis of short duration. Some patients with palindromic rheumatism can develop RA. Another possibility is a syndrome called RS3PE the acronym for remitting seronegative symmetrical synovitis with pedal edema.5 This condition which is seen maily in older individuals is characterised by a remitting symmetrical synovitis of the upper limbs with pitting edema of dorsum of hands. Patients respond very well to steroids and can be associated with polymyalgia rheumatica, other CTDs, and neoplasia.

Presence of high grade fever at onset could be a pointer to a viral illness such as Chikungunya arthritis.6 Viral arthritis could be related to HBV or HCV infection. Presence of features of heart failure and heart murmurs in a young individual with arthritis suggest acute rheumatic fever or infective endocarditis, where an echocardiogram may reveal valvular regurgitation and vegetations. Reactive

CHAPTER 32

Multiple sclerosis

hands and feet, (with sparing of the DIP joints) in a bilateral symmetrical fashion is almost diagnostic of RA.

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arthritis (ReA) although classically is oligoarticular often have explosive acute onset, predominant lower limb involvement and there is preceding history of urethritis or diarrhoeal illness.

RHEUMATOLOGY

Drugs like hydralazine, isoniazid, pyrazinamide can produce a lupus like syndrome with the clinical presentation of mayalgia, arthralgia, arthritis, and ANA positivity.7 Therefore drug history is important.

But many times such clues are not forthcoming and we may have to wait and watch while the disease evolves. For many such patients we may initially give an open label of “undifferentiated arthritis” or “early inflammatory arthritis”, the diagnosis of which may evolve in to RA or it may go in to spontaneous remission.8 However these labels can be applied after ruling out conditions like septic polyarthritis or infective endocarditis.

Acute non-inflammatory polyarthritisAcute polyarthritis (less than 6 weeks duration), without any signs or symptoms of inflammation (i.e. no palpable synovitis, no prolonged morning stiffness, normal ESR, CRP, and platelet counts etc.) is probably due to fibromyalgia, pain amplification syndromes, or rarely psychogenic/malingering. Fibromyalgia is an important clinical condition which accounts for many rheumatology consultations.9 Although it is not life threatening the condition can impair the patients’ quality of life. It can occur on its own or it secondary to RA or SLE. Patients with fibromyalgia present with widespread pain including both joint and muscle, accompanied by fatigue, headaches and un-refreshed sleep. It is often accompanied by irritable bowel syndrome, headache, and migraine.

Clinical examination reveals widespread tender points, but there will be no synovitis.

Chronic inflammatory polyarthritis which is arthritis of more than 4 joints and present for more than 6 weeks is probably the most important among these 4 categories because of the implications of long term treatment. The patient with chronic inflammatory polyarthritis can have predominant articular involvement the most common cause of which is RA.4 Chronic inflammatory polyarthritis with prominent extra-articular manifestations are discussed.4 In SLE polyarthritis is an important manifestation but more prominent are mucosal, dermatological, haematological, renal, and CNS manifestation.

Patients with early Sjögren’s syndrome may not only have arthralgia/arthritis without sicca symptoms. They often times are mistaken for RA. However with progression of disease there are prominent symptoms of dryness (sicca) due to lacrimal, salivary and parotid gland involvement.

Another clue for diagnosis is presence of purpura.

In SSc the first manifestation is Raynauds’s phenomenon.

At the same time many patients will have history of swelling of the joints, examination of which confirms presence of inflammatory polyarthritis. Detail examination will show

sclerodactyly, ulcerations of finger tips, digital pits, and ILD. Psoriatic arthritis (PsA) can have a polyarthritis pattern very similar to RA. The clue for diagnosis is skin psoriasis, pitting of the nails, other nail changes with distal phalangeal (DIP) joint involvement. Skin involvement may not be obvious. One should examine the scalp, behind the ears, the natal cleft, and the navel for any evidence of psoriasis.

Behcets syndrome is a disease characterised by recurrent genital and recurrent aphtous oral ulcers. ReA arthritis can have an explosive onset of inflammatory polyarthritis predominantly in lower limbs, with preceding diarrhoea or urethritis and conjunctivitis. Dermatomysositis is an inflammatory condition where apart from arthralgias/ arthritis the patient has prominent proximal muscle weakness and characteristic skin changes specific to dermatomyositis (Gottron’s sign, Gottron’s papules, shawl sign, V sign, heliotrope rash etc).

Sarcoidosis where the patient has tender nodules on the lower limbs (erythema nodosum), chest radiograph will show bilateral hilar lymphadenopathy. Multicentric reticulohistiocytosis is a rare condition characterized by destructive arthritis involving hands including DIP joints.

The clue for diagnosis is presence of nodules on the skin, the arthritis involves the DIP joint, and patient can have underlying malignancy.

Systemic necrotizing vasculitides are a group of multisystem disease where renal failure manifested by hypertension and presence of active sediments on urine examination is prominent. Other manifestations of vasculitis are involvement of upper and lower airway, parenchymal lung involvement, mononeuropathy multiplex, and mesenteric ischemia. Adult-onset Still’s disease is a differential when there polyarthritis and PUO along with skin rash, serositis, hepato-splenomegaly and lymphadenopathy.

Chronic tophaceous gout often presents with polyarthritis.

The clue to diagnosis is history of involvement of the great toe (podagra) in the past, presence of tophaceous deposits, and demonstration of monosodium urate crystal in synovial fluid analysis.

Carninomatous polyarthritis is another unique situation where a patient presents with polyarthritis which is actually the expression of a malignancy.10 Carcinomatous polyarthritis is suspected when the arthritis has is of short duration, rapidly progressing, disproportionate weight loss, hepatosplenomegaly, or poor response to steroids and disease modifying agents. Polyarthritis similar to RA has been reported to occur in association with cancer of lung, stomach,colon,ovary and leukemia. The arthritis generally predates the cancer by few months.

CHRONIC NON-INFLAMMATORY POLYARTHRITIS

The classic example of a chronic non-inflammatory polyarthritis is primary OA of the hands.2,3,4 The patient is typically an elderly person, with predominant

involvement of the DIP and PIP joints of the hands in a symmetrical fashion.3 On examination bony enlargement (nodules) are present over the DIP (Heberden’s nodules) and over the PIP joints (Bouchard’s nodules) with sparing of the MCP joints. Primary OA of the hands is often mistaken for seronegative RA. The differentiating point is patient have no systemic symptoms and all inflammatory markers are negative. Other causes of chronic noninflammatory polyarthritis are rare conditions such as hemochromatosis, where there is characteristic involvement of both hand MCPs. The other causes are oochronosis, hypothyroidism, and amyloidosis.

In suspected connective tissue disease such as SLE one should ask for ANA by indirect immunofluorescence technique. ANA is a very good screening test for SLE and but is also present in SSc, dermatomyositis, ILD etc.

ANA may also be present in low titre in up to 15% normal individuals or elderly population.2,3 It can also be present in chronic liver disease and chronic infections. Hence the practice of asking for ANA routinely for all arthritis should be avoided.

When the clinical suspicion for vasculitis is high, i.e. patient has arthritis, proteinuria, and active sediments in urine, suspicious nodules on the chest radiopraph, antineutrophil cytoplasmic antibody (ANCA) test can be ordered. Over 90% of patients with active granulomatosis with polyangiitis (Wegener’s granulomatosis) have a positive c-ANCA.12 However the presence of ANCA should be to support the diagnosis, and should not replace tissue diagnosis. Other routine (but relevant) investigations should also include complete hemogram to look for cytopenias which can be a sign of active SLE. Blood counts are also useful to monitor for drug toxicities. All patients with chronic inflammatory polyarthritis should also have baseline liver function tests, renal function tests, examination of urine for proteinuria and active sediments, plain chest radiograph, ECG and echocardiogram.

Imaging by plain radiographs during acute inflammatory polyarthritis is often normal. Plain radiographs are useful if there is history of trauma and one suspects fracture.3 However in a situation of chronic inflammatory polyarthritis plain radiographs of hands and feet are indicated to look for soft tissue swelling, juxta articular osteopenia, and bone erosions. In gout bony erosions are typically present on the first metarsophalangeal joint with

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CONCLUSION

Evaluation of inflammatory polyarthritis is a challenge because of the wide differential diagnosis. The cornerstone in achieving a diagnosis is good history, review of all systems, recognizing the pattern of arthritis, and followed by relevant investigations. This approach of trying to achieve a clinical diagnosis first will reduce the number of investigations ordered and benefit most to both patient and treating physician.

REFERENCES

1.

Malaviya AN. Clinical approach to patients with joint disease: importance of distinguishing inflammatory from non-inflammatory conditions. APLAR Journal of Rheumatology 2006; 9:11-7.

2.

Cush JJ. Approach to Articular and musculoskeletal disorders. In: Kasper DL, Fauci AS, Longo DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine, 19th edition. New York: McGraw-Hill; 2015. pp 2216-25.

3.

Cush JJ, Dao KH. Polyarticular arthritis. In: Firestein GS, Budd RC, Gabriel SE, McInnes IB, O’Dell JR editors. Kelly’s Textbook of Rheumatology, 9th edition. Philadelphia: Elsevier Saunders; 2013. pp 587-98.

4.

Malaviya AN. Approach to the Patient with Polyarthritis.

In Medicine Update Volume 18, 2008. Published by Association Physicians of India.

5.

Cantini F, Salvarani C, Olivieri I, Barozzi L, Macchioni L, Niccoli L, Padula A, Pavlica P, Boiardi L. Remitting seronegative symmetrical synovitis with pitting oedema (RS3PE) syndrome: a prospective follow up and magnetic resonance imaging study. Ann Rheum Dis 1999; 58:230-6.

6.

Devaux CA. Emerging and re-emerging viruses: A global challenge illustrated by Chikungunya virus outbreaks.

World J Virol 2012; 1:11-22.

7.

Adwan MH. An update on drug-induced arthritis.

Rheumatol Int 2016; 36:1089-97.

8.

Verpoort KN, van Dongen H, Allaart CF, Toes RE, Breedveld FC, Huizinga TW. Undifferentiated arthritis-disease course assessed in several inception cohorts. Clin Exp Rheumatol 2004; 22(5 Suppl 35): S12-7.

9.

Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. J Rheumatol Suppl 2005; 75:6-21

10. Racanelli V, Prete M, Minoia C, Favoino E, Perosa F. Rheumatic disorders as paraneoplastic syndromes.

Autoimmun Rev 2008; 7:352-8.

11. Ravindran V, Rachapalli S. An overview of commonly used radiographic scoring methods in rheumatoid arthritis clinical trials. Clin Rheumatol 2011; 30:1-6.

12. McKinney EF, Willcocks LC, Broecker V, Smith KG. The immunopathology of ANCA-associated vasculitis. Semin Immunopathol 2014; 36:461-78.

CHAPTER 32

INVESTIGATIONS

Once a clinical diagnosis is achieved based on history and examination one can go for relevant investigations. If the clinical suspicion is RA we can ask for rheumatoid factor (RF), and anti-citrullinated peptide antibodies (ACPA), plus plain radiographs of the both hands and feet to look for bony erosions. The presence of ACPA in high titres is predicts erosive disease. Presence of RF, ACPA are considered poor prognostic markers in RA.

overhanging margins. Plain radiographs of hands and feet are particularly useful in follow up of RA to assess joint damage in the longterm.11

Practical Approach to a Person with Low Backache

C H A P T E R

33

Pradeep Kumar Maheshwari, Anjana Pandey, Rosmy Jose

Backache is a price we pay for our upright posture. It affects about 60-80% of world population1. Most patients with acute low back pain, with or without radicular symptoms, have musculoskeletal or degenerative disorders that do not require specific treatment and are often self-limited. Approximately 85% of patients with low back pain cannot be given a definitive diagnosis.

However, the possibility of more serious abnormalities that require specific treatment should always be excluded.

Although there is no evidence that back pain prevalence has increased, reported disability and absence from work due to back pain have increased g. significantly in the last 30 years2.

b.

g.

Psychosocial risk factors like job dissatisfaction, unhealthy relations result into fear/avoidance behaviour and reduced activity levels, excessive reliance on aids and appliances, depressed mood, withdrawal from social interaction and various somatisation disorders particularly low back pain.3

NON MECHANICAL CAUSES4,6,7

Infection (#)

1. Osteomyelitis 2.

Septic discitis

Paraspinous abscess unhealthy h. Psychosocial risk factors 3. like job dissatisfaction,

RISK FACTORS

a.

f. Obesity

Older age

4.

Epidural abscess

relations result lifting into in fear/avoidance behaviour and reduced Heavy labour (in particular jobs requiring 5. Shingles an awkward position).

activity levels, excessive Inflammatory(*) reliance on aids and appliances,

c.

Long-distance driving and whole-body vibration such as experienced by a lorry driver

d.

Lower education and income

e.

Smoking

1.

Ankylosing spondylitis

2.

Rheumatoid depressed mood, withdrawal from socialarthritis interaction and 3.

Psoriatic arthritis

various somatisation disorders particularly low back pain.3 4. Reiters CLASSIFICATION4

MECHANICAL (97%)

NON MECHANICAL (1) %

1) Lumbosacral strain / sprain 2) Lumbar canal stenosis 3) Traumatic 4) Diskogenic pain 5) Bony deformity (kyphosis/scoliosis)

1)infection (#) 2)inflammatory(* ) 3)neoplastic(Ă—) 4)metabolic(â‚“)

PELVIC

RENAL

a) prostatitis

a) pyelonephritis

b) endometriosis c) chronic pelvic inflammatory disease(40%) 55 9dddisease40(40%disease(40%)

VISCERAL (2%)

5

GIT a) penetrating ulcer

b) perinephric abscess

b) cholecystitis

c) nephrolithiasis

c) pancreatitis

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Table 1: Mechanical causes

Symptoms and Signs

Lumbosacral sprain/strain Post traumatic pain confined to lower back with paraspinal muscle spasm.

History of trauma, point tenderness and paraspinal muscle spasm present. Features of radiculopathy present.

Lumbar canal stenosis

History of buttock and low back pain (Pseudoclaudication). Pain relieved with rest.

Lumbosacral disc disease

History of limitation of spinal flexion. The pain is located in the low back only or referred to the back of leg,back of thigh and buttock. Features of radiculopathy are present. All symptoms exaggerated by maneuvers. Cauda equina syndrome signifies an injury of multiple lumbosacral nerve roots within the spinal canal distal to the termination of the spinal cord at L1-2. Low back pain, weakness and areflexia in the ankle, saddle anesthesia, or loss of bladder function may occur.

Non mechanical causes Infection

Fever with other constitutional symptoms, pain worsens on movement; primary source of infection can be often associated.

Inflammatory

This spinal disease has young onset,patients are often males below age 45 years.

Insidious onset of low back and buttock pain accompanied with morning back stiffness, nocturnal pain, pain unrelieved by rest but improving with exercise. Loss of the normal lumbar lordosis and exaggeration of thoracic kyphosis develop as the disease progresses. Similar to ankylosing spondylitis, restricted movements may accompany reactive arthritis (formerly known as Reiter’s syndrome), Psoriatic arthritis, and chronic inflammatory bowel disease.

Neoplastic

Pain constant dull in character worsened at night with no improvement on rest.

Neurologic deficits may be seen.

Metabolic

Pain (localized or radicular) and compression fractures which are seen on radiological imaging and are often asymptomatic. Precipitating factors like steroid abuse, immobilization, thyroid disorders etc. may be present.

Visceral causes GIT, Renal, Pelvic organs

Referred pain particularly to the posterior spinal segments that innervates the organ.

Local signs are absent with little pain on movements.

Postural back pain

Nonspecific chronic vague pain with no anatomical lesions on exhaustive investigations. Most common cause is poor posture or malingering.

5.

Inflammatory bowel disease

Waddell Test

Neoplastic(×) 1.

Metastatic malignancy

Tenderness

2.

Lymphoma/ leukemia

Simulation

3.

Multiple myeloma

4.

Spinal cord and retroperitoneal tumours.

Axial loading

Vertical loading on a standing patient’s skull produces low back pain

Rotation

Passive rotation of shoulders and pelvis in same plane causes low back pain

Distraction

Discrepancy between findings on sitting and supine straight leg raising tests

Metabolic (x)

1. Osteoporosis 2. Osteomalacia 3.

Paget’s disease of bone

CLASSIFICATION (BASIS OF DURATION )4

A.

Acute (1 day - <6 weeks)

B.

Subacute (6 weeks - ≤12 weeks)

C.

Chronic (> 12 weeks)

CLINICAL FEATURES6,7

Low backache is defined as pain related to the area between lower ribs and gluteal folds with or without non neuropathic leg pain. It can be a symptom in any age

Superficial, non anatomic tenderness to light touch

Regional disturbances Weakness

“Cogwheel” (give-way) weakness

Sensory

Non dermatomal sensory loss

Overreaction Disproportionate facial expression, verbalization or tremor during examination Three or more inappropriate responses suggest complicating psychosocial issues in patients with low back pain.

group from 20-55 years. According to etiology the pain may vary or improve on attaining various postures.

CHAPTER 33

Vertebral fracture

176

Nerve Root

Pain

Sensory

Motor

Reflex

L4

Antero lateral thigh and medial calf

Medial part leg

Knee extensors,hip adductors

Knee

L5

Lateral calf, dorsal foot, buttocks

Dorsum of foot

Foot evertors, foot dorsiflexors and hip abductors

S1

Buttocks, posterior thigh, calf Sole and lateral border foot

RHEUMATOLOGY

RED FLAG SIGNS ASSOCIATED WITH LOW BACKACHE7

1.

Progressive motor weakness

2.

Gait disturbances

3.

Faecal incontinence

4.

Saddle anaesthesia

5.

Signs of radiculopathy

6.

Motor, sensory or reflex signs.

DIAGNOSIS 3,6,7,9

A good examination of the lumbar spine and relevant nerves can be accomplished in less than 5 min if it is done systematically.

A complete and thorough history(with emphasis on mood and sleep cycle of the patient) and clinical examination is must and investigations are necessary to pinpoint the etiology of the disease.

Examination of the spine begins with inspection of the entire spinal curvature, lower limbs and the gait of the patient. Apart from musculoskeletal system examination, neurological (especially tone and deep tendon reflexes) and vascular system examination should also be done thoroughly. Complete examination includes thorough examination of abdomen and rectum to rule out any visceral cause if present.

INSPECTION

A.

Standing posture

i.

Any exaggerated or flattened spinal curvatures,

ii.

Asymmetry of skin folds,

iii.

Spinal deformities,

iv.

Muscle atrophy

v.

Abnormal hair growth in the area.

B.

Sitting posture: look for asymmetry of pelvis

C.

Recumbent posture

Look for limb length discrepancy (apparent or true). True length discrepancy (lengthening and shortening) is measured from ASIS (anterior

Ankle

superior iliac spine) to a distal fixed landmark like tibial tuberosity or medial malleolus.

PSYCHOGENIC LOW BACK PAIN8

If the distribution of pain is nonanatomic, a psychogenic cause is highly likely. The Waddell tests is a set of five maneuvers performed during a routine physical examination to identify patients in whom non organic issues play an important role in the persistence of low backache.

Hip extensors, toeflexors, foot plantar flexion

Gait

Should be evaluated while standing in front, to the side and behind the patient.

Range of motion

At lumbar spine this is evaluated with the patient standing upright. If full range of active motion is achieved by the patient, gentle pressure to be applied to check for a further passive range of motion. Care to be taken when applying pressure, as it could exacerbate the patient’s symptoms.

Range of motion at the hip joint also to be examined. Hip pain and symmetry in motion should be noted.

PALPATION

Purpose of palpation of the lumbar spine— i.

To locate tender areas

ii.

To confirm findings previously demonstrated in the inspection.

Palpation along the midline is used to check for bony tenderness and for deformity. Muscles just lateral to the spinous processes should also be palpated for tender points or spasms. In this position, the transverse processes, which are positioned deep to paraspinal muscles, can also be appreciated.

The patient is instructed to lie supine, and the anterior superior iliac spine, anterior inferior iliac spine, and pubic bones should be palpated.

STRAIGHT LEG RAISING TEST

It is used to evaluate for lumbar nerve root irritation. In this test lower limb is passively flexed at hip with knee held in extended position. It is said to be positive if patient’s symptoms can be reproduced. While performing the straight leg raise test, sometimes symptoms may be produced in the contralateral leg. This is termed ascrossed straight leg raise test and indicates central lumbar disc herniation.

LASEGUE TEST

It is also used to evaluate lumbar nerve irritation. It is performed in the same fashion as the straight leg raise test. Once a complaint of pain or tightness is achieved, the leg is slowly lowered 5˚-10˚ or until radicular symptoms disappear. While holding the leg in this lowered position, passively dorsiflex the foot. The test is positive if there’s reproduction of symptoms in this position.

PATRICK TEST

The test is used to evaluate for pathology of the sacroiliac joint and hip joint. The patient lies supine on the examination table and is asked to place one foot on the opposite knee by placing the hip in flexion abduction external rotation. While supporting the pelvis with one hand, the physician presses firmly down on the flexed knee while supporting the pelvis at the opposite anterior superior iliac spine. A positive test is when pain in the sacroiliac joint of the leg can be demonstrated. It is a common finding in inflammatory arthritis.

Is associated with neurological symptoms or signs.

2.

CT SCAN

It is diagnostic study when the spinal and neurological levels are clear and bony pathology is suspected. CT scan is superior to routine x-rays for the detection of fractures involving posterior spine structures, craniocervical and craniothoracic junctions, C1 and C2 vertebrae, bone fragments within the spinal canal, or misalignment

3.

MRI OR CT Myelography: Spine MRI’s yield exquisite views of intraspinal and adjacent soft tissue anatomy.

NEUROLOGICAL EXAMINATION

The neurological examination is an important part in the lumbar spine evaluation. The spinal cord and the nerve roots can contribute to or cause lumbar pain. The neurological examination consists of 3 elements: motor, sensory, and reflex.

VASCULAR SYSTEM

Check peripheral pulses of dorsalis pedis artery and tibialis posterior artery. The character should be compared bilaterally.

LABORATORY EVALUATION

It is useful in following scenarios i.

when the exact spinal and neurologic levels are unclear,

ii.

when a pathological condition of the spinal cord or soft tissues is suspected,

iii.

when postoperative disc herniation is possible, or

iv.

when an underlying infectious or neoplastic cause is suspected.

Biochemical Investigations I.

CBC with ESR: The sedimentation rate is the most useful blood test in patients suspected of having spinal infection since it is elevated in up to 80 per cent of cases. Neutrophilia and anaemia are also commonly seen in patients with neoplasia and infection.

CT Myelography is useful in identifying nerve root pathology, particularly in patients with previous lumbar spinal surgery or with a metal fixation device in place. It provides elucidation of neural compression or arachnoiditis when several spinal operations have been undertaken and for the treatment of foramina and spinal canal stenosis.

II.

RA factor/ CRP.

III.

HLA B-27.

IV.

Urine routine microscopy.

V.

Markers for malignancy (PSA, CEA, etc.).

VI.

Laboratory evaluation of patients with osteoporosis and/or pathological fractures should include serum calcium, phosphorus, alkaline phosphatase as well as serum and urine.

RADIONUCLIDE BONE SCINTIGRAPHY with technetium-99m is helpful in conditions characterized by increased bone turnover. These include bone metastases, fracture, Paget’s disease, and infections. Gallium-67 binds to polymorphonuclear leucocytes and can be helpful in the evaluation of vertebral osteomyelitis and sacroiliac septic arthritis. Typically, bone scans are negative in patients with multiple myeloma which is characterized by lytic lesions.

RADIOLOGICAL INVESTIGATIONS

In general, imaging procedures are not required for patients with uncomplicated neck or back pain of less than 1 month’s duration 1.

Spinal X-rays are required only if the pain is associated with certain ‘red flag’ symptoms or signs, which indicate a high risk of more serious underlying problems:

a.

Starts before the age of 20 or after 50 years.

b.

Is persistent and a serious cause is suspected.

c.

Is worse at night or in the morning, when an inflammatory arthritis (e.g. ankylosing spondylitis), infection or a spinal tumour may be the cause.

d.

Is associated with a systemic illness, fever or weight loss.

Neurophysiological studies are rarely indicated except in patients in whom it is difficult to distinguish between a neuropathy, radiculopathy, or plexopathy. Fibrillations in the para spinous muscles are the most common and earliest findings seen in radiculopathy. Their presence indicates a lesion proximal to the vertebral foramen and excludes a plexopathy. The H reflex noted on is used to evaluate for an S1 radiculopathy or to distinguish from an L5 radiculopathy.

TREATMENT

A.

Non pharmacological

B. Pharmacological C.

Surgical

NON PHARMACOLOGICAL 10

Bed rest was advised previously, however latest teaching if allowing early mobilization with back strengthening

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e.

178

exercises, aerobics and stretching exercises. Supervised intense physical exercise has been found to be effective in alleviating symptoms.Yoga in its many forms has been found to effective alternative to these exercise regimens.

RHEUMATOLOGY

Cognitive behavioural therapy that includes helping patients to identify and modify his/her thinking regarding pain and disease per say. These interventions often encourage self-management, assist in staying active, and reduce potential concerns about LBP.

volume of drug to be injected into the pathological site.

IV.

Epidural injections have been widely used in direct placement near the involved nerve root.

V.

Vertebroplasty is a percutaneous technique that involves the placement of a needle (or needles) into a fractured vertebral body, and then bone cement is injected to strengthenthe structures, lessens the deformity, and reduces associated pain.

Kyphoplasty is another similar technique for pain alleviation.

Spinal manipulation, massage accupunture and TENS are the other available options.

PHARMACOLOGICAL6

About 90 per cent of patients with a herniated lumbar disc will improve significantly with limited rest, analgesics, and anti-inflammatory drugs. The role of epidural steroids remains unclear. They may afford short-term improvement in leg pain but they do not reduce the need for surgery.

Drugs that are commonly used are NSAID (acetaminophen) are effective. The risk of renal and gastrointestinal toxicity is increased in patients with preexisting comorbidities.

Benzodiazepines like clonazepam operates via GABAmediated mechanisms provide muscle relaxation as well as benefit in anxiety.

Skeletal muscle relaxants like cyclobenzapramine, methocarbamol, carisoprodol, chlorzoxazone, and metaxalone provide symptomatic relief. However sedation is a very common and disturbing side effect.

SURGICAL3,11,12

Indications for surgery include persistent disabling buttock and/or leg pain despite 2 to 3 months of conservative management, and/or severe or progressive worsening neurological deficit whilst on treatment. Surgery may also be indicated in patients with neurological claudication due to spinal stenosis, but only after all attempts with conservative management have failed.

Patients with spinal stenosis who are more incapacitated by back pain than by neurological claudication probably should not be operated on, since surgery is rarely effective and may even worsen back pain.

Surgical procedures can further be classified as minimally invasive and invasive techniques.

MINIMAL INVASIVE TECHNIQUES

I.

II.

III.

Intradiskal electrothermal therapy a minimally invasive technique where the annulus is subjected to thermo modulation. The proposed mechanism is shrinkage of collagen fibers and coagulation neural tissues, thereby improving the pain.

Percutaneous adhesiolysis with or without spinal endoscopy is another interventional technique used to manage chronic low backache.

Transforaminal corticosteroid injectionsis another method for pain alleviation. It requires minimal

Apart from these methods, procedure like spinal fusions are also being performed.The need for such procedure is doubtful because segmental instability cannot be demonstrated in all cases.

CONCLUSION

Backache, though a common complaint should neither be ignored nor over zealously investigated and treated.

The art of diagnosing and treating this condition lies in the physician’s awareness about this symptom, his ability to elicit a detailed history, conducting a meticulous examination and judicious use of available investigatory modalities. Majority of patients can be treated by offering lifestyle modifications like graded back exercises, yoga and cognitive behavioural therapies as definitive diagnosis is not possible in majority of cases.The corner stone of treatment is staying active and early mobilization if no contraindication exists.

REFERENCES

1.

Hoy D, Brooks P, Blyth F, Buchbinder R. The Epidemiology of low back pain. Best Pract Res Clin Rheumatol 2010; 24:76981.

2.

Goldman: Cecil Medicine, 25th edition.

3.

Kumar & Clark: clinical medicine, 8th edition.

4.

EULAR Textbook on rheumatic diseases, 2nd edition.

5.

Sutton MY, Strenberg M, Zaida A, et al. Trendsin pelvic inflammatory disease hospital dischargesand ambulatory visits, United States 1985-2001. Sex Trans Dis 2005; 32:778784.[PubMed].

6.

Harrison’s Principles of Internal Medicine, 19th edition.

7.

Davidson’s Principle & Practice of medicine, 22nd edition.

8.

Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine 1980; 5:117–25.

9.

Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med 2007; 147:478-491.

10. Chou R1, Huffman LH; Nonpharmacological therapies for acute and chronic low back pain. Ann Intern Med 2007; 147:492-504.

11. Lamb SE et al: Group cognitive behavioural treatment for low-back pain in primary care: A randomised controlled trial and cost-effectiveness analysis. Lancet 2010; 375:916.

12. Mummaneni PV et al: Clinical and radiographic analysis of cervical disk arthroplasty compared with allograft fusion: A randomized controlled clinical trial. J Neurosurg Spine 2007; 6:198.