The limping or non-weight bearing child is a common general practice and emergency department presentation, that can cause a lot of stress for parents.

There are also a wide range of differentials, although most of these can easily be narrowed down by age. Thankfully, most of the differentials are not emergencies, but there are some serious things not to be missed.

The majority of cases will likely be transient synovitis (or no cause identified). This is a benign disorder

Differentials

• Non-accidental injury – NAI
• Developmental dysplasia of the hip – DDH
• Transient synovitis
• Perthes disease
• Slipped capital femoral epiphysis (SCFE)
• Septic arthritis
• Viral myositis
• Toddler’s fracture
• Reactive arthritis or other rheumatological disorder

History

• Duration of symptoms
• Speed of onset
• Limp or complete refusal to weight bear?
• History of trauma?
  • There may often be a history of (typically mild) trauma that is incidental
• Preceding illness?
  • Recent viral infection? (Transient synovitis or reactive arthritis)
• Any fever?
• Location of pain
  • Often difficult to localise, especially in children <5 years
• Morning stiffness? (Rheumatological disorder)
• Any previous injuries or other child protection concerns?

Examination

• General appearance
• Temperature
• Gait
• Neurological examination
  • Weakness
• Bruising
  • Excessive or not in keeping with accidental injury
• Abdomen
  • Check for tenderness, including inguinal area (masses)
  • In boys – if any abdominal pr inguinal pain – check the scrotum!
• Lower limb
  • Bony tenderness
  • Assess hip, knee and ankle
    • Hip pathology suggested by restricted internal rotation and abduction
  • Check lumbar spine and sacrum

Investigation

• If limp <3 days duration, no history of trauma and afebrile, investigation is not typically required
• If septic arthritis suspected (fever, often severely restricted movement), then consider:
  • FBC
  • CRP / ESR
  • Blood cultures
  • USS – can show effusion in septic arthritis of hip joint
• If limp >3 days duration, or history of trauma, consider imaging:
  • X-ray, typically of hip and knee, “frog leg lateral view” is good for spotting SCFE
  • Bone scan can spot areas of increased bone turnover, and as such may help to identify:
    • Osteomyelitis
    • Discitis
    • Perthe’s disease
    • Occult fracture

Management

• Depends on the underlying disorder
• See individual topic articles

In the case of transient synovitis, or no cause identified:

In my experience, many non-specific cases in otherwise well toddlers improve dramatically with NSAIDs and a short wait (an hour or so) and can be safely discharged from the Emergency Department or GP surgery. In cases with a fever, give NSAIDs whilst the results of FBC and CRP are awaited, and if normal this is typically enough to exclude septic arthritis if the child’s walking improves, and I would discharge these patients home with NSAIDs and close FU (e.g. advise review with the GP the following day). The cases of septic arthritis I have seen tend to be pretty obvious – with a clearly distressed child refusing to move the limb at all, but be wary that early septic arthritis may not be so severe – Dr Tom Leach

Summary of disorders

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Child with limp – RCH

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Spondylolisthesis refers to an anterior or posterior movement of a vertebrae in relation to its adjacent vertebrae.

Spondylolisthesis affects about between 5-12% of the population but most cases are asymptomatic. It is thought that in the cases where pain results, the pain is due to degeneration of the affected intervertebral disc.

Pain is typically exacerbated by prolonged standing, walking or exercise.

There are several causes, but many cases are thought to be secondary to laxity of the interspinous ligaments.

Generally spondylolisthesis is a relatively benign, although chronic disorder. Chronic pain can result in disability and reduced quality of life. Most cases respond well to conservative management, especially in teenagers. Surgery may be considered in resistant or more severe cases.

Epidemiology

There are several types of spondylolisthesis:

• Isthmic – the most common form. Acquired, usually in teenage years, and secondary to spondylosis (see below)
• Degenerative – due to facet joint degeneration and osteoarthritis which can both cause bone remodelling
• Traumatic
• Pathological – from metastasis
• Dysplastic – congenital and rare

Dysplastic, traumatic and pathological causes are rare.

• Spondylosis(a common precursor to spondylolisthesis – see below) typically occurs between the ages of 6 and 16, and affected about 5% of the population. The incidence is as high as 15% in young athletes an gymnasts, thought to be the result of trauma-induced stress fractures. Particular at risk activities include:
  • Gymnastics
  • Rugby
  • Cricket
  • Footbal
  • Weight lifting
  • Diving
  • Tennis
• F>M
• 60-80% of people with spondylosis also have spondylolisthesis
• 90% of cases affect L5, almost all other cases affect L4
• Degenerative spondylolisthesis affects older patients

Aetiology

Risk factors include:

• Female gender
• Young age of onset
• Wedge shaped vertebra
• Hyperlordosis
• Family history
• High impact sports

 Pathology

• Spondylosis is a separate disorder, but often precedes, and is associated with spondylolisthesis. It describes a Bony defect in the pars interarticularis, which results in the body of the vertebrae becoming partially separated from the vertebral arch and thus the normal support mechanisms in pace to prevent the body of the vertebrae from moving are reduced. It can be congenital, or the result of a stress fracture. It may be unilateral or bilateral.

Grading

Types of spondylolisthese are typically graded by the degree to which the vertebrae have slipped (there are 5 grades, from I-V, with grade V being the worst).

Other grading systems may differentiate types by the cause.

Presentation

• Most cases are asymptomatic and may be discovered incidentally
• Low back pain, particularly with extension of the lumbar spine
• Spondylosis is typically NOT visible on x-ray – as the changes are subtle. Once it progresses to spondyolisthesis, then the degree of vertebral slippage may be visible on x-ray
• Isthimic
  • Exercise related back pain
  • Pain received by rest
  • Tight hamstrings
  • Enhanced lordosis
  • “Waddling gait”
  • Gluteal muscle wastage
  • Typical onset in adolescent years
  • Pain may radiate to buttocks or thighs, or have other features similar to that of vertebral disc prolapse
  • In severe cases, the slippage can cause cauda equina syndrome
• Degenerative
  • Aching lower back pain
  • Insidious onset
  • Neurological claudication
  • Symptoms chronic and progressive
• Trauma. pathological and dysplastic
  • Features typically similar to other causes
  • Traumatic will obviously have a history of trauma, and if significant, , may have signs of cauda equina syndrome

Differential Diagnosis

Differentials are broad and I highly recommend reading the lower back pain article for an overview of assessing lower back pain.

Differentials include:

• Mechanical lower back pain
• Sciatica – caused by disc prolapse
• Inflammatory arthritis – including ankylosing spondylitis and psoriatic arthritis
• Osteoarthritis of the spine
• Myeloma
• Bony metastases
• Osteoporotic crush fractures
• Discitis

Investigations

Most presentations of lower back pain do not warrant investigation. However, be wary of cases presenting in people <20 and >50 years old – relevant to spondylolisthesis because in these patients, isthimic and degenerative spondylolistheses are relatively more common. In such patients, or in those with other back pain red flags or in other patients in whom back pain is not settling after 6-12 weeks, consider the following:

• Bloods
  • CRP and FBC – for signs of infection (discitis)
  • FBC – myeloma
  • Calcium – hypo/herpcalcaemia
• Lateral spine x-rays
  • Will show spondylolisthese and can help to give a grade
  • Perform x-rays at the position of maximum pain
• CT +/- radionuclide scan – can better define the lesion than on x-ray, and is often used to assess if the lesion is stable of progressive
• MRI may be performed pre-operatively

Management

The aims of treatment are to:

• Reduce pain
• Maintain or improve function
• Prevent further slippage / stabilise the spine

>80% of symptomatic children will have complete resolution of symptoms with conservative management

Conservative management

• Suitable or cases with <50% slippage, with no neurological signs
• Sleep
  • Advise sleeping on the side with a pillow between the knees
• Activity modification
  • If >25% slippage, patients should avoid high risk activities (typically weight lifting, contact sports, gymnastics)
• Analgesia
  • Paracetamol 1g QID
  • NSAIDs – e.g. ibuprofen 400mg TDS
• Steroid injection
  • May receive symptoms if there is nerve root compression
• Brace
  • A brace may be advised if there is a part interarticularis fracture which has a good chance of healing
  • Some debate over whether or not this actually improve long-term outcomes
• Physiotherapy
  • Biomechanical correction
  • Flexibility and strengthening exercises
  • Core stability exercises
  • Graduated return to activity levels

Surgical Intervention

Surgical intervention is indicated in:

• Patients who fail to respond to conservative management
• Evidence of progression (typically defined on x-rays several months apart)
• Significant neurological deficit
• Significant pain resulting in disability

Surgical procedures

• There is often a long rehabilitation period following surgery
• Surgery typically involves fusing the affected vertebrae with an adjacent vertebra. The damaged intervertebral disc is usually removed
  • The benefit or realignment surgery is controversial. Especially in slow or prolonged cases. Over time, there are associated changes in the surrounding musculature, and thus surgical realignment of the spine may not necessary provide benefit
  • In younger patients, or more acute episodes of spondylolisthesis, then realignment is likely to be of more benefit
  • Complication rates are high, especially in older patients
• Decompression of nerves that have becomes squashed as a result of spoondylolisthesis is of more proven benefit
• Neurological complications and chronic pain are potential complications

References

• Spondylolisthesis – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Complex regional pain syndrome (previously known as reflex sympathetic dystrophy (RSD) or Sudeck atrophy) is a poorly understood condition which typically affects the extremities (arms and legs), causing severe pain, disability and sometimes swelling. It most commonly occurs after trauma, such as a fracture or sprain, but the trauma can be fairly trivial and in some cases no trauma at all is identified.

It is caused by sustained sympathetic activity, and characterised by symptoms that are out of proportion to any original injury.

It usually affects a single limb, but in 5-10% of cases it may spread to another limb.

Although very poorly understood, it is not a psychological disorder, although sometimes misinterpreted as such – especially as it is often associated with depression.

It can be divided into two types, although the type present does not affect the management:

• CRPS I – without an identified underlying nerve injury
• CPRS II – with an underlying identified nerve injury

It typically settles after time, but it can last for several years. Activity and mobility should be encouraged, and patients often require referral to the pain clinic.

Epidemiology

• Incidence of 25 per 100 000 per year
• Incidence increases with age
• 4x more common in women
• Arm: 60% of cases
• Leg: 40% of cases
• In children
  • Very rare before the age of 6
  • Tends to affect the lower limb
  • Even more common in females than in adults

Aetiology

• Fracture – 45% of cases
• Sprain – 20% of cases
• Elective surgery – 10% of cases
• Spontaneous – 10% of cases
• Other risk factors:
  • ACE-inhibitor use at the time of trauma
  • Limb immobilisation >4 weeks
  • Hx of migraine
  • Hx of asthma
  • Sibling of an affected child (genetic predisposition)
  • Smoking
  • Pre-existing anxiety or depression
  • Fibromyalgia

Pathology

• Not well understood
• An abnormal inflammatory response is thought to result in vasomotor dysfunction and alterations in neuroplasticity in the peripheral nerves
• There is some evidence that prophylactic vitamin C 500mg daily for 50 days reduces the incidence – in distal radius fractures, and foot and ankle surgery

Presentation

Typically presents within one month of traumatic event or immobilisation. In the early stages, there may be very few identifiable physical signs, which can make diagnosis difficult.

• Throbbing, burning pain which is usually worse at night
  • Out of proportion to the original injury
  • Pain often worsened by light touch or other sensations that do not usually cause pain (allodynia)
• Parasthesia (“pins and needles”)
• Spontaneous sweating
• Spontaneous formation of goosebumps
• Change in appearance of hand and skin
  • At first: red, warm, swollen hand or foot with dry skin
  • Later: cold, often cyanosed and mottled, moist skin
  • These changes are often demarcated by an obvious boundary line (very specific for complex regional pain syndrome)
• Muscle wasting
• Reduced strength and ROM of the hand – typically secondary to pain and swelling. Joint are also often described as being painful
• Loss of hair and nails in very advanced cases

Diagnosis

Diagnosis is made using the Budapest Criteria. These require:

• Pain that is out of proportion to any initial causative event PLUS
• At least ONE symptom from each of the THREE following categories AND at least ONE sign from at least TWO of the categories:
  • Sensory – hyperalgesia or allodynia
  • Vasomotor – temperature difference, skin colour changes / asymmetry
  • Oedema / abnormal sweating
  • Motor – reduced ROM, weakness, tremor, dystonia
• PLUS
• No other diagnosis is more suitable

The problem with these diagnostic criteria, is that signs must be present at the time the patient is seen, which often causes a delay in diagnosis.

Imaging studies are often completely normal.

• Occasionally patchy decalcification of bone may be seen on x-ray.
• Bone scan may show increased uptake and can assist diagnosis in some cases
• EMG / nerve conduction studies – may show changes in nerve conduction but are often too painful tome tolerated by the patient and not routinely adivised

Differential Diagnosis

• Improperly placed cast or splint
• Nerve entrapment
• DVT
• Carpal tunnel syndrome
• Psychiatric illness

Management

• Prompt diagnosis is associated with a better prognosis. 
• The most important factor is to keep using the affected limb. Prolonged periods of disuse are associated with a longer duration of illness and worse prognosis.
• Involve a multidisciplinary team – typically the GP, pain specialist and perhaps orthopaedics or rheumatology.
• Aim to improve function, and reduce fear about pain, particularly use-related pain.
• Multiple analgesics are often required. Consider use of the analgesia ladder, for example:
  • Paracetamol, plus
  • NSAID, plus
  • Neuropathic agent – e.g. amitriptyline, gabapentin plus
  • Opiates
• Consider the use of bisphosphonates in those with evidence of bone resorption. Has bene proven to improve pain in these patents.
• Avoid the use of capsaicin – which is often severely painful.
• Considering screening for and treating depression and anxiety which are associated with CRPS.
• Occasionally surgery may be indicated:
  • Surgical decompression – in cases where local nerve compression is implicated (most commonly if there is carpal tunnel involvement)
  • Surgical or surgical sympathectomy – stellate ganglion (upper limb) or lumbar spinal (lower limb)

Prognosis

• Pain will typically flare up and down during the duration of the illness. These are NOT a sign that the condition is progressing
• Rates of resolution vary widely from study to study
  • 75% at one year in one study
  • 35% at 6 years in another
• Good prognostic features
  • Upper limb
  • CRPS after fracture seems to have a better prognosis than other causes
  • Warm type CRPS (usually indicates an early diagnosis)
  • Children
• In severe cases CRPS can spread to all extremities and be completely disabling
• Be wary that many patients may develop opiate dependency after long periods of opiate treatment

Complications

• Mental health complications – such as anxiety and depression
• Immobilisation often makes the condition worse
• Skin infections are common

References

• Complex regional pain syndrome – patient.info
• Complex regional pain syndrome – orthobullets
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Trigger finger (and trigger thumb) is a type of flexor tenosynovitis. It is a relatively common disorder – with a lifetime risk of about 2.5%.

It is most common around the age of 40-60. Predisposing factors include:

• Type I diabetes
• Rheumatoid arthritis
• Gout
• Hypothyroidism
• Amyloidosis

The mechanism is thought to be related to abnormal tendon repair from the normal stresses and strains of use. Normal use causes small tears and minor damage to the tendons. As they repair, fibrosis can occur, along with oedema and swelling, which leads to the formation of hard nodules in the tendons. These hard nodules and then unable to freely slide through the normal fibrosseous tunnels (“pulleys”) that hold tendons down against the bones in the hand. The affected pulley is the A1 pulley. This causes a sensation of “popping” and “clicking” as these nodules squeeze through these tunnels, as indicated in the middle and right images below:

Presentation

• Finger that “locks’ into position when flexed
• Finger may appear to make suffer jerking movements when flexed and extended
• Can’t be extended, but can be manually extended with use of the other hand to pull the finger straight (only when severe).
• Tender firm nodule may be felt in the palm – at the level of the metacarpal head
• Thumb, 3rd and 4th fingers most commonly affected

Differential diagnosis

Dupuytren’s contracture

• May be tricky to differentiate from trigger finger. The following are features NOT typically seen in Dupuytren’sm but commonly seen in trigger finger:
• Tender nodule at the base of the finger
• Usually causing clicking or popping sensations when moving the finger
• Pain when moving the finger
• Symptoms often are worse after periods of inactivity – e.g. when first waking in the morning

Management

Conservative management

Is often first-line treatment for the thumb, and may be used in milder cases in fingers.

• Splinting – especially overnight
• NSAIDs
• Activity modification

The two main interventional options for management os corticosteroid injection and surgery. Surgery is not frequently required.

Corticosteroid injection is often used first-line for fingers

• Corticosteroid injection
  • About 70% effective for complete resolution
  • Injection into the palmar surface, with the finger extended, injection is made just distal to the nodule
  • Palpate the tendon sheath during injection – you can usually feel the fluid entering the tendon sheath
  • Encourage the patient to exercise the fingers for 1-2 minutes to spread the steroid along the tendon sheath
  • Typically begins to work within 48 hours
  • If it is not effective or recurs, a second injection may be attempted after 3 weeks (or more)
  • Repeated failure of the procedure indicates need for surgery
• Surgery
  • Release of the A1 pulley is performed
  • May be first line in paediatric cases (rare)

References

• Trigger finger – orthobullets
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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• The Achilles tendon is the largest tendon in the body. Tendinopathy and rupture can affect both athletes and those with sedentary lifestyles
• Acute injury (i.e. rupture) to the Achilles tendon usually occurs from sudden acceleration or deceleration. This is different to Achilles tendinopathy – which is often a chronic overuse condition
• Achilles tendon rupture occurs in athletes in 80% of cases. It is more common in those who have had previous Achilles tendon problems
• Achilles tendon rupture can be partial or complete
• Complete tears are usually managed surgically, but in older sedentary patients may be managed conservatively. Surgical management reduces the risk of re-rupture, but has a higher acute complication rate

Aetiology

• Usually in athletes
  • Most commonly in sports that involve a quick acceleration – e.g. sprinting, tennis, basketball, football
• Typically aged 30-50
• M > F
• May also occurs as a result of a fall with forces dorsiflexion
• More common in chronic Achilles tendinopathy
• Drugs
  • Corticocosteroids
  • Fluoroquinolones – e.g. ciprofloxacin
  • Avoid use of both of these medications together!
• Pre-existing conditions
  • Rheumatoid arthritis or other inflammatory rheumatological disorders

Pathology

• The Achilles tendon connects the gastrocnemius and soles muscles to the posterior of the calcaneus
• It begins at the mid calf
• It has slightly unusual anatomy – there is not true synovial sheath and instead it is surrounded by a sheath called the paratenon.This is a highly vascular structure and it allows for a sliding action of the tendon inside the paratenon
• The blood supply is least around the mid tendon – defined as the region 2-6cm proximal to the insertion. This is the area most likely to rupture

Presentation

• Sudden onset Achilles tendon pain. Initially sharp pain, often settles within hours to days to more of a dull ache
• A loud “snap” or “bang” is sometimes heard when the tendon ruptures!
• Some patients report feeling as though they were hit on the back of the tendon
• Usually occurs with a pushing-off motion – in contact to ankle sprain, which is often due to impact on landing
• Inability to stand on tip toe on affected side

Examination

• Often localised swelling
• Altered gait
• Inability to stand on tip toes
• Reduced plantar flexion
• Simmond’s Triad. Ask the patient to lay prone on the couch, with their feet dangling off the end of the bed. Compare both sides. Check:
  • Altered “angle of dangle” – in Achilles tendon rupture the affect foot will naturally “dangle” in a more dorsiflexed position than the unaffected side
  • Calf squeeze (aka Thomson’s calf squeeze test) – in a normal, intact Achilles tendon, a calf squeeze should cause plantar flexion of the ankle. In Achilles tendon rupture, there will be minimal or no plantar flexion
  • Palpable notch or gap in the Achilles tendon at this site of the rupture

Investigation

• Often a clinical diagnosis
• USS (usually first line) or MRI can help to differentiate a partial from a complete tear, or to narrow down differentials

Management

• Non-weight bearing – immediately
• Urgent referral to orthopaedics – surgery is usually required
  • Surgical repairs reduces the risk of subsequent recurrent rupture, but also carries risks – such as wound infection
  • Following surgery, rehabilitation plan is often similar to conservative management outlined below
  • 80% of athletes return to sport
  • Athletes may not be able to resume full activity for up to 1 year
  • There is often some loss of function – even small amount of functional loss can have a significant impact for athletes
• Conservative management is an option for older more sedentary patients – but decision should be made by orthopaedic specialist
  • Plaster cast for 2 weeks
  • Can be changed to immobilising boot from 2 weeks
  • Weight bear as pain allows from 4-6 weeks
  • Physiotherapy involvement from the start
• Partial tears are usually managed conservatively, with an immobilisation boot from the start, and earlier weight bearing

Complications

• Achilles tendon scarring and contracture – especially if there is not early mobilising and range of movement exercises – best direct by physiotherapist
• Re-rupture
  • 3-5% after surgical treatment
  • 8-12% with conservative management
• DVT

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• The Achilles tendon is the largest tendon in the body. Tendinopathy and rupture can affect both athletes and those with sedentary lifestyles
• Achilles tendinopathy is usually an overuse condition, causing pain, swelling and stiffness of the Achilles tendon. It is common in runners – in long distance runners the lifetime risk is 50%. In other athletes, the lifetime risk is about 25%
  • Acute injury to the Achilles tendon usually occurs from sudden acceleration or deceleration
• Symptoms vary from mild, to severe disabling pain that can interfere with normal daily activities
• Treatment involves avoidance of aggravating activities, rest, ice, compression, simple analgesia, as well as stretching and strengthening exercises
• It does not typically cause a lot of inflammation and thus anti-inflammatory medication (NSAIDs) and corticosteroid injections are of little value – in fact corticosteroids are associated with an increased risk of rupture
• Most cases resolve in weeks to months
• There is an increased risk of Achilles tendon rupture during a flare of Achilles tendinopathy – although it is rare because the pain of tendinopathy usually prevents activities that can cause rupture

Aetiology

• Overuse – e.g. in runners, dancers, tennis players, or any individual who does a lot of jumping type activity
  • Often associated with an increase in training duration or intensity
  • May be due to poor footwear and / or poor technique
  • Training on steep slopes
  • Cold weather training
• M > F
• More common with increasing age
• Associated with inflammatory arthritis – e.g. ankylosing spondylitis or psoriatic arthritis
• More common in individuals with other chronic conditions
  • Hypertension
  • Hypercholesterolaemia
  • Diabetes Mellitus
• Drugs
  • Fluoroquinolones – e.g. ciprofloxacin – known to predispose to Achilles tendinopathy and rupture
• Family history
  • 5x increased risk

Pathology

• The Achilles tendon connects the gastrocnemius and soles muscles to the posterior of the calcaneus
• It begins at the mid calf
• It has slightly unusual anatomy – there is not true synovial sheath and instead it is surrounded by a sheath called the paratenon. This is a highly vascular structure and it allows for a sliding action of the tendon inside the paratenon
• The blood supply is least around the mid tendon – defined as the region 2-6cm proximal to the insertion. This is where most cases of tendinopathy occur
• In Achilles tendinopathy there is thickening, inelasticity, scarring and stiffness of the tendon, and sometimes adhesions to the paratenon or other surrounding structures
• The exact mechanism of this is not well understood

Tendinitis vs tendinosis

• Tendinopathy is a term that refers to any pathology of the tendon. This encompasses both tendinitis and tendinopathy
• Tendinitis refers to inflammation of the tendon. More specifically it refers to inflammation of the tendon sheath. Tendons with tendinitis are not structurally affected on a microscopic level, and the tendons themselves are not weakened. Tendinitis can be treated with rest and anti-inflammatories, and is an acute process that should resolve with treatment.
• Tendinosis is a long-term degeneration of a tendon, and damage to the tendon fibers themselves. It is not an inflammatory process. It leads to tendons that are both microscopically and macroscopically (to the naked eye) different in appearance to healthy tendon. Tendons suffering from tendinosis are weakened and pre-disposed to rupture. Tendons have very limited blood supply, and thus have little capacity for healing.

It is believed that in cases of Achilles tendinopathy, short-term cases probably involve only tendinitis, but in longer-term cases there may be a combination of both tendinitis and tendinosis, or tendinosis alone. Tendinitis may lead to tendinosis.

Cases consisting primary of tendinitis will resolve within a period typically of days to weeks. about 95% of cases resolve with conservative management.

Cases of tendinosis can last for several months. About 80% of cases will improve with conservative management.

Presentation

• Pain in the area of the Achilles tendon
  • About 60% of cases in the mid-tendon
  • About 20% at the insertion
• Pain usually gradual onset and improves with rest
  • Be cautious of Achilles tendon rupture in sudden onset pain, or sudden worsening of pain
• May improve with gentle exercise – i.e. walking – and worsen with more strenuous activity

Examination

• Tenderness of the Achilles tendon – either at the site of insertion, or up to 3-4cm proximal to the site of insertion
• Calf raise – will elicit pain
  • Ask patient to stand just on the affected leg, and then stand on tip toes on this leg
• ALWAYS check for Achilles tendon rupture – Simmond’s Triad. Ask the patient to lay prone on the couch, with their feet dangling off the end of the bed. Compare both sides. Check:
  • Altered “angle of dangle” – in Achilles tendon rupture the affect foot will naturally “dangle” in a more dorsiflexed position than the unaffected side
  • Calf squeeze (aka Thomson’s calf squeeze test) – in a normal, intact Achilles tendon, a calf squeeze should cause plantar flexion of the ankle. In Achilles tendon rupture, there will be minimal or no plantar flexion
  • Palpable notch or gap in the Achilles tendon at this site of the rupture

Investigations

• Usually a clinical diagnosis
• USS or MRI can be useful to determine rupture or to rule out other differentials if clinical examination is inconclusive
• X-ray may demonstrate calcification of the tendon in up to 60% of cases but is not required for diagnosis

Differential Diagnosis

• Calcaneal Bursitis – most commonly in older patients, usually due to poorly fitting footwear, rubbing around the area of insertion of the Achilles tendon. Tends to resolve more quickly than Achilles tendinopathy with change of footwear, rest and ice.
• Sever’s Disease – aka Calcaneal apophysitis – an overuse injury, usually seen in boys, between ages of 8 and 15. Present with pain in the heel, and can be unilateral or bilateral. Usually pain and tenderness are 1-2cm distal to the insertion of the Achilles tendon. Again, symptoms tend to resolve with cessation of provoking activity and simple conservative measures, within a few weeks.
• Ankle Sprain
• DVT

Management

• Rest – avoid high impact sports (e.g. running and jumping). Encourage patients to stay moderately active (e.g. walking and weight bearing). Complete rest probably prolongs recovery. Increase level of activity in line with pain reduction.
• Analgesia – paracetamol 1g QID recommended. NSAIDs have been shown to reduce the strength of the Achilles tendon after recovery and should be avoided.
• Ice – is useful for analgesia in the early stages. Recommend 10-30 minutes. Less than 10 minutes is not effective and greater than 30 can cause skin damage. Do not put ice directly on skin – bag of peas wrapped in a tea towel works well!
• Exercises – e.g. gentle calf stretches, calf raises. Usually introduced about 1-2 weeks after the onset of pain, after a period of rest. Usually performed daily, and increasing in intensity.
• Physiotherapy to direct exercises and tailor a specific programme to the patient can be useful if not responding to self directed therapy
• Corticosteroid injections – are strongly contraindicated. Although useful in other tendinopathies, in Achilles tendinopathy they increase the risk of rupture
• The earlier treatment is started, the shorter the duration of symptoms
• Some cases become chronic. In these cases, specialist treatments may be attempted:
  • Extracorporeal shock-wave therapy – a type of sound wave therapy. Studies prove benefit in cases that have not responded to other treatments. Small risk of causing rupture. Should only be performed after discussion with specialist.
  • Autologous blood injection – also occasionally used under specialist supervision. Efficacy is unclear. It is thought that growth factors contained in the blood may stimulate healing.
  • Plaster cast – may be useful in difficult to treat cases
  • Surgery – sometimes considered as a last resort. Surgery can remove nodules and scarring, and remove adhesions of the tendon capsule. In certain cases, a longitudinal incision is made in the tendon to encourage healing.

References

• Achilles Tendinopathy – Patient.info
• Achilles Tendinopathy and Rupture – Patient.info
• Achilles tendinopathy and tendon rupture – UpToDate
• Achilles Tendinopathy: Advice and Management – Oxford University Hospital NHS Foundation Trust

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Perthes disease (also Legg-Calvé-Perthes disease) is a childhood hip disorder that results in avascular necrosis of the femoral head.

The cause is unknown.

It can be differentiated from adult onset osteonecrosis because in Perthes there is healing and bone remodelling, whilst in osteonecrosis there is not.

Epidemiology and Aetiology

• Can occur between ages of 2 and 12, but most commonly between 4 and 8
• 10 -20% of cases are bilateral – but often has at different stages of disease
• M:F – 5:1
• 1 in 10,000
• Higher incidence in urban areas
• Higher incidence amongst lower socioeconomic class
• Higher incidence at high latitude (low at equator)
• Associated with thrombophilia – in up to 50% of patients (and 75% of patients have some sort of clotting abnormality) – thought to be related to protein C and S deficiencies (controversial)
• Other risk factors include
  • Low birth weight
  • Second hand smoke
  • Caucasian, Asian, Inuit descent

Pathology

• Disruption of blood supply causing avascular necrosis of the femoral head
• Self-limiting process – an initial ischaemic event with later healing. The whole process can take 2-5 years
• Subsequent revascularization which causes reabsorption of the bone and collapse of the femoral head
• Then, there is remodelling of the femoral head
• Good prognostic factors
  • Younger age at presentation
  • Spherical femoral head (i.e. it has not yet collapsed)
  • Female
• Long term
  • 50% of patient develop OA
  • Most patient maintain good function until 5th or 6th decade of life

Presentation

• Pain and limp – often chronic and insidious course. Early detection can be difficult
• Restricted ROM on hip examination
• Antalgic gait
• Trendelenburg gait
• Limb length discrepancy (late finding)

Differentials

• Slipped Capital Femoral Epiphysis (SCFE)
  • Usually older children (mean age around 12)
  • Can be acute or chronic
  • Associated with obesity
• Septic Arthritis
  • Child often unwell
  • Signs of sepsis
  • Bloods suggestive of infection (raised WCC and CRP)
• Transient Synovitis
  • Usually younger children
  • Always acute
  • Resolves within a few days
  • Investigations normal

Investigations

• X-ray – AP and frog leg lateral
  • Joint space widening
  • Irregularity of femoral head
  • Crescent sign
• Bone scan
  • Can be diagnostic
  • Can show level of femoral head involvement
• MRI
  • Can show early features when other investigations are negative
  • More sensitive than x-ray
• Bloods – wil be normal

Management

• Usually non-operative
  • NSAIDs
  • Traction
  • Crutches
  • Physio
• Aim to restore ROM and limit disability
• Younger patients are least likely to benefit from surgery
• Surgical management
  • Indicated in children over 8 and severe disease

Complications

• Femoral head deformity
• Lateral hip subluxation
• Premature arrest of epiphyseal plate – causing leg length discrepancy
• Labral injury
• Osteochondritis Dessicans
• Degenerative Arthritis

References

Perthes’ Disease Factsheet – SCHN

Legg-Calve-Perthes Disease (Coxa plana) – Orthobullets

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Slipped Capital Femoral Epiphysis (SCFE), also sometimes called Slipped Upper Femoral Epiphysis (SUFE) is a disease of childhood, typically seen in late childhood and early adolescence.

In the condition, the head of the femur ‘slips’ out of alignment due to shearing forces across the physics (growth plate).

SCFE is associated with obesity, and often presents as hip and / or knee pain. It is usually unilateral but can be bilateral. The affected leg may be shortened and external rotated.

It can be diagnosed with a frog leg lateral view x-ray of the hip and always requires surgical intervention. Left untreated, there is often further slippage and permanent disability.

Epidemiology

• Weight often >90th percentile (at least 50% of cases)
  • Obesity more likely to cause earlier age of onset, more severe disease and bilateral disease
• Between 0.2 and 10 per 100,000
• Slightly more common in boys (60% of cases)
  • Boys mean age – 13.5
  • Girls mean age – 12
• Left hip is more commonly affected
• Bilateral in 20-50% of cases
• Sometimes associated with endocrine disorders – check for hypothyroidism

Pathology

• Capital femoral physis is displaced from the metaphysis
• Due to mechanical forces on a susceptical physis
• Exact aetiology is unknown
• Capital femoral physis is displaced from the metaphysis

  

Presentation

• Pain in the groin, thigh or knee. Often vague
  • Knee pain is often the only presenting complaint
• Antalgic gait
• Externally rotated hip / “out toeing”
• Affected leg may be shortened
• Can be acute, chronic, or acute on chronic
• Child may or pay not be able to weight bear
  • 85% of cases are chronic (>3 weeks gradual onset of symptoms)
• Drehmann sign – there is passive flexion of the hip during obligatory external rotation – this is highly suggestive of SCFE
• Thigh atrophy may be present

Differentials

• Transient Synovitis
  • Usually younger children
  • Always acute
  • Resolves within a few days
  • Investigations normal
• Septic Arthritis
  • Child often unwell
  • Signs of sepsis
  • Bloods suggestive of infection (raised WCC and CRP)
• Perthes Disease
  • Usually younger children (age 4-8)

Investigation

• X-ray – AP and frog leg lateral views of the hip
• Always x-ray both sides!
• Usually diagnostic
• MRI performed rarely – where there is high clinical suspicion but negative x-rays it can identify pre-slip pathology such as growth plate widening and oedema of the metaphysis
• Bloods – normal

Management

• Surgical management is always required – refer urgently for orthopaedic assessment
• If SCFE is suspected, then the child should be kept non-weight bearing until the diagnosis is made
• Surgical techniques – usually screws to prevent any further slipping

Complications

• Osteonecrosis – even with surgical treatment – 50% risk without treatment, about 5% risk with treatment
• Chondrolysis
• Osteoarthritis – earlier risk of OA
• Impingement – femoral acetabular impingement due to severe deformity of the femoral neck. Further surgery may be required
• Chronic pain (5-10%)

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Transient synovitis (a.k.a. Irritable Hip) is the most common cause of hip pain in children aged 3-8.  It can be difficult to differentiate from the much more serious septic arthritis, and as such, transient synovitis should be a diagnosis of exclusion.

Other causes of hip pain in children include viral arthritis (common), juvenile arthritis (rare),

It is caused by inflammation of the synovium of the hip.

The condition is self limiting and usually resolves within a few days.

Epidemiology

• Most common cause of hip pain in children aged 3-8
• Can occur between ages of about 1-10
• M:F – 2:1

Pathology

• Non specific inflammation of the synovial lining of the hip – often 1-2 weeks after an upper respiratory tract infection (URTI)

Presentation

• Child reluctant to weight bear, complaining of hip pain
• Often still able to walk with difficulty (unlike septic arthritis where they often cannot walk at all)
• Usually 1-2 weeks after a viral URTI
• Otherwise, afebrile and systemically well
• Pain often worse first thing in the morning – usually improves throughout the day
• Child often sits or lies in position with least pressure on the hip – flexion, abduction and external rotation

Examination

• Reduction in ROM of hip, particularly internal rotation
• Often still able to weight bear with encouragement
• More severe limitation of movement suggest septic arthritis

Investigations

• X-ray – request AP, lateral and frog leg views
  • Usually normal
  • May show some joint space widening
  • Should always be performed
• Bloods – including FBC and CRP – to rule out a septic arthritis
• USS – not routinely performed – can show effusion (more likely septic arthritis) or synovial inflammation (suggest synovitis as most likely diagnosis)
• MRI – not routinely performed – can show osteomyelitis or myositis

Differentials

• Viral Arthritis
  • Most similar to synovitis and also a benign course. Other viral symptoms (e.g. a rash or URTI symptoms) usually still ongoing at time of presentation
• Slipped Capital Femoral Epiphysis (SCFE)
  • Usually older children (mean age around 12)
  • Can be acute or chronic
  • Associated with obesity
• Septic Arthritis
  • Child often unwell
  • Signs of sepsis
  • Bloods suggestive of infection (raised WCC and CRP)
• Perthes Disease
  • Usually younger children (age 4-8)

Management

• Firstly – make sure you are confident it is not septic arthritis!
  • No fevers
  • Weight bearing
  • Systemically well
  • Inflammatory markers (WCC and CRP) are not raised
• NSAIDs – e.g. ibuprofen 10mg/Kg TDS
• Symptoms usually resolve in less than a week

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Epidemiology and Aetiology

• M>F (slightly)
• Increased incidence in Pet Owners
• Genetic susceptibility – increased risk in a family history of the disease
  • Disease also often occurs in local geographical clusters
• Essentially unknown aetiology; environmental factors in a predisposed individual (possibly viral infection is the environmental factor)
• Incidence increases with age
  • Rare under 50

Clinical features

• Chronic progressive disease
• Often asymptomatic, and discovered incidentally with a raised ALP in the blood, or discovered incidentally on x-ray
• Only 15-40% of cases have symptoms
• Bone pain – the most common symptom
  • Occurs in 40% of presentations
    Pain is usually due to impingement on other localised structures
  • Bone pain is a late feature. It is typically a deep constant aching pain, worse with weight bearing, and may persist through the night
  • Consider Paget disease of the bone in elderly patients presenting with persist back pain
  • Bony deformity may cause warm skin overlying the lesion due to increased blood flow
• Deformity – up to 30% of patients
• May affect bones anywhere in the skeleton, but common sites include; pelvis, lumbar spine, femur, thoracic spine, sacrum, skull, tibia, humerus
• Usually only affects one site – it is not ‘systemic’ like osteoporosis, and does not spread to other sites.
• Osteoarthritis
• Fractures – bones are prone to fracture because they become more brittle. Affect 15% of patients
• Deafness / Headaches – occurs in some patients due to compression of the vestibulocochlear nerve, when the skull is affected
  • More rarely there may be other non-specific neurological features – e.g. dizziness, altered gait
• Osteosarcoma – used to be more common, now only affects 1% of patients
• Bowing deformity is seen in Paget disease of the long bones
  • This can cause altered gait, and may result in other joint pains, particularly of the hips and lower back
  • Traumatic fracture are also most likely to occur in Paget disease of the long bones

Pathology

• Increased number of osteoclasts. Osteoclasts also often larger. The osteoblasts are normal, but are often over active, due to increased factors released by osteoclasts.
  • Osteoclasts are also often oversensitive to vitamin D
• Essentially, an accelerated rate of bone turnover – with subsequent rapid new bone formation – and this new bone does not have a normal bone matrix – the matrix is disorganised
• The bones increase in size, but become more brittle, and thus more prone to fracture.
• Unclear why some areas of bone are affected and others are normal

Investigations & Diagnosis

Diagnosis is usually made radiologically. Blood tests and other investigations are suggestive or supportive of the x-ray findings.

Once diagnosis is confirmed, radionuclide bone scan is often performed to check for any other areas of involvement.

Bone biopsy is not usually required.

Blood tests

• Raised alkaline phosphatase – ALP can be an indicator of osteoblastic activity
  • Remember to ask for bone specific ALP – increased ALP can also be of liver origin
  • Consider checking gamma-GT – to rule out a liver cause if bone specific ALP is not available
  • The level of ALP is correlated to the severity of the Paget disease
• Serum calcium and phosphates are usually normal
  • Abnormal levels may be an indicator of unrelated parathyroid disease  (hyperparathyroidism)
• Vitamin D levels are normal tested. This is for two reasons:
  • To help rule out another cause of raised ALP
  • To ensure levels are sufficient to undertake bisphosphonate therapy

X-ray

• Widening of the cortical region – i.e. the hollow cortex at the centre of the bone (where marrow is produced) is wider
• Mixed areas of sclerosis and lysis – on the x-ray will look like lots of opaque dark splodges in the bone
  • Seen in early disease
  • This can make differentiation between Paget Disease and malignancy difficult in the early stages of the disease
• Bone thickening and enlargement
  • Seen in later disease
  • Easier to differentiate
• Bone deformities
  • Bone bends anteriorly in the tibia
  • Bone bends laterally in the femur
• May also show what appears to be localised osteoporosis in areas of very high osteoclast activity – called osteoporosis circumscripta – this is particularly apparent in the skull
• MRI or CT may also be used to better define unusual bone lesions

Bone scan

• Increased isotope uptake in affected bones
• Often performed after the initial lesions has been diagnosed to assess the extend of the disease
• Any areas that appear to show ‘uptake’ on a bone scan should then be further investigated with x-ray to confirm if there is Paget’s disease at these sites

Urine

May contain collagen due to very high bone resorption

Differentials

• Bone malignancy
• Osteoarthritis
• Osteoporosis

Treatment

• Severe pain
• Nerve compression from expanding bone, or other neurological complications
• Fractures
• Asymptomatic disease with significant biochemical abnormalities, e.g.
  • ALP >2x normal
  • Raised ALP and Paget Disease at a site that commonly results in fracture (e.g. long bones, vertebrae or base of skull)
• In some cases it can be difficult to detainee if pain is arising from Paget Disease or osteoarthritis. In these patients, I trial of bisphosphonates may be indicated.

Bisphosphonates are the ‘mainstay’ of treatment. They inhibit osteoclast activity, and cause osteoclast apoptosis. They damage the cytoskeleton of the osteoclast, so the cell is then unable to bind to bone, and to perform its bone resorption duties.

Serum calcium and vitamin D levels should be checked before therapy is initiated and all patient should be started on supplemental vitamin D (1,000 international units daily) and calcium (this often comes combined).

Bisphosphonates are often able to induce disease remission. Typical regimen will last 2 months. The agents described below are sometimes called the “newer” bisphosphonates, or the “nitrogen containing bisphosphontes”. Older agents are less effective and rarely used.  Options include:

• Zolendronic acid
  • Given via IV infusion – e.g. 5mg given on 15 minutes
  • Induces remission for up to 2-3 years after a single dose
  • Usually first line choice – more effective than oral agents
  • Up to 90% remission rate, <1% relapse rate
  • Resistance can develop after multiple doses
  • Can cause flu-like symptoms after first dose
  • Pamidronate is an alternative IV bisphosphonate but is less effective (“older” bisphosphonate). It may be considered if resistance has developed to zolendronate
• Oral therapy – e.g. risedronate, alendronate
  • May be considered in younger patients or those with less severe disease
  • About 60% remission rate, 20% relapse rate
  • Usually oral doses are given daily for a limited period – e.g.:
    • Risedronate 30mg daily for 2 months
    • Allendronate 40mg daily for 3-6 months
  • Much more cumbersome dosing than the IV preparations:
    • Must be taken with water
    • No food should be taken for at least 30 minutes afterwards
    • Patients should not lie down for 2 hours after taking them to avoid oesophageal irritation and gastroesophageal reflux
  • Any required dental work should be performed before initiation of therapy as this reduces the risk of a rare but serious side effect of bisphosphonates – oestonecrosis of the jaw
• Calictonin
  • Can be used in patents who do not tolerate bisphosphonates
  • Does not induce remission but can reduce disease progression
• Adverse effects of bisphosphonates
  • Osteonecrosis of the jaw – extremely rare in the short durations of therapy used in Paget Disease. Approximate risk is 1 in 100 000
  • Bone Pain
  • Flu-like symptoms – transient, occurs in 25% of patients

• Simple analgesia – e.g. paracetamol 1g QID, ibuprofen 400mg TDS PRN
• Orthoses – braces, usually plastic that support and protect a bone
• Orthotics – show inserts that help to correct deformity and altered gait
• Analgesia
• Education
• Treat the complications – e.g. joint replacement, hearing aids, physiotherapy

Ongoing Management

• Consider repeating ALP at 3-6 months to assess the effectiveness of treatment
• Repeat annually
• Initiate treatment again when ALP starts to rise or patient becomes symptomatic again

Complications

• Increased risk of bone tumours – particularly osteosarcoma
  • Incidence of up to 1% of PBD patients
  • Consider this in lesions that do not respond to medical therapy – particularly pain
  • If osteosarcoma develops it is often advanced and fatal
  • More common in long standing disease

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Paget Disease of the Bone – UpToDate
• Paget Disease of bone – AFP

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