Gout

  • Gout is an inflammatory arthritis caused by deposition and accumulation of monosodium urate crystals in tissues, mainly synovium, cartilage and skin with or without symptoms as a result of long standing hyperuricemia.
  • 90% of gout is due to under excretion and 10% is due to increased synthesis.
  • The stages of gout are hyperuricemia, asymptomatic gout, acute gout, inter-critical gout and chronic gout.
  • It is often associated with metabolic syndrome with insulin resistance, hypertension and diabetes mellitus.
  • Gout and asymptomatic hyperuricemia is associated with significantly elevated risk of chronic lifestyle diseases such as obesity, hypertension, ischaemic heart disease, type 2 diabetes, chronic kidney disease etc.
  • Nephropathy and disorders associated with increased cell turnover can be associated.

Metabolism


  • Uric acid is the end metabolite of purine metabolism in humans.
  • In other species, presence of the enzyme called uricase converts uric acid into highly water soluble allantoin.
  • In humans, the uricase gene is inactivated by the presence of 2 mutations.
  • The level of uric acid in humans is 10 times higher than other species due to the absence of uricase.
  • It is a weak acid and at the physiologic pH exists in the ionic form called urate.
  • Uric acid levels depend on the dietary intake, synthesis and excretion.
  • The limit of solubility of urate is 6.8mg/dL.
  • When exceeded, urate crystal deposition occurs in tissues.
  • Solubility of urate is determined by the following factors
    • pH
    • Body temperature
    • Level of hydration
    • Presence of nucleation factors
    • Concentration of cations

Clinical Features


  • Episodic urate crystal induced acute inflammation of joints, tendons and bursa is the classic picture of acute gout.
  • Acute attack which peaks within just 6–12 hours with overlying erythema is highly suggestive of crystal inflammation though not specific for gout.
  • In recurrent podagra with hyperuricemia, a clinical diagnosis is reasonably accurate but not definitive without crystal confirmation.
  • Lower limbs are more commonly affected than upper limbs.
  • Peripheral joints are more commonly affected than central joints.
  • First metatarsophalangeal joint is the site of presentation (Podagra) in more than 50% of cases. Other sites of first attack are the tarsal joints ankle and knee.
  • More than 80% of the site of first episode is in the lower limbs.
  • The first episode is monoarticular in 90%.
  • Polyarticular onset is seen in less than 1%.
  • Olecranon bursa is the commonest site of first attack in the upper limb.
  • First metatarsophalangeal joint is affected in more than 80% of patients with uncontrolled or untreated gout.
  • Acute attacks are preceded by prodromal symptoms such as mild pain, limitation of motion and discomfort.
  • Acute attacks have an abrupt onset with rapid development of acute inflammation with excruciating pain during the first 24-48 hours.
  • Provocative factors for acute attacks include severe dietary restriction, high purine diet, local trauma and initiation of treatment.
  • Sudden drop in uric acid level results in disintegration of solid aggregations leading to local inflammation.
  • Macroscopic collections of urate crystals is called tophi. More commonly seen in areas subjected to pressure or friction.
  • Limitation of joint movement is due to accumulation of tophaceous deposits in the joints and periarticular tissues.
  • Intraarticular tophi may present with mechanical symptoms mimicking meniscus tear or loose body.
  • Rupture of intradermal tophi may mimic pustules.
  • Persistent joint swelling is called chronic gouty arthritis. It is due to chronic granulomatous inflammation induced by urate crystals. X-rays usually show only minimal destruction, but MRI or USG show extensive soft tissue deposits.

Natural history of untreated gout


  • More than 75% develop subsequent acute attacks.
  • Frequency of attacks increase in 50%.
  • Severity of attack increases in 30%.
  • Polyarticular involvement develops in 40%.
  • Tophaceous burden increases.

Investigations


Diagnostic investigations are done for

o          Confirmation of gout.

o          Determination of burden of disease.

o          Identification of complications.

o          Identification of other associated rheumatic conditions.


Confirmation of diagnosis

  • Demonstration of MSU crystals in synovial fluid or tophus aspirates is the gold standard for the diagnosis of gout.
  • Synovial fluid should be send for total count, differential count, analysis, gram stain, bacterial culture and biochemical analysis.
  • MSUC are water soluble and is dissolved if preserved in formalin, hence tissue samples to be examined for urate crystals should be fixed in 100% alcohol.
  • In all synovial fluid samples obtained from inflamed joints for diagnosis, search for MSU crystals.
  • During the intercritical period, definite diagnosis can be made by identification of MSU crystals in the asymptomatic joints.
  • Gout and sepsis may coexist, hence do gram staining and culture
  • Serum uric acid levels alone do not confirm or exclude gout, as many with hyperuricemia do not develop gout, and the serum levels may be normal in many with acute attack.
  • In those with a family history of young onset gout, onset of gout under age 25, or with renal calculi determine the renal uric acid excretion.

Determination of burden of disease

  • Number of acute exacerbations.
  • Number and location of joints ever involved by acute attacks.
  • Presence, size, and location of superficial tophi.
  • Persistence of pain, joint swelling, limitation of motion, and deformities.
  • Short 4-joint USG of both knees and first metatarsophalangeal joints.

Look for comorbidities such as obesity, hyperglycaemia, hyperlipidaemia and hypertension.


Imaging


  • Conventional x-ray
  • Ultrasonography
  • Three-dimensional (3D) multislice imaging via computed tomography (CT),
  • Dual-energy computed tomography (DECT)
  • Magnetic resonance imaging (MRI)

Radiography

  • Radiographs are not useful in confirming the diagnosis of early or acute gout.
  • Play a minor role in diagnosis.
  • Nonspecific initially.
  • Acute gout attack produces soft tissue swelling.
  • Asymmetric erosive arthropathy especially of the first MTPJ is the characteristic appearance of chronic gouty arthritis.
  • Gouty deposits cause well corticated erosions with typical overhanging margins.
  • New bone formation can be seen in the form sclerosis, osteophytes, bony spurs and, rarely, periosteal deposition and ankylosis.

CT Scan

  • Multislice helical CT scanning can show tophaceous deposits with a typical density of 160–170 Hounsfield units. They are found close to the erosions extending into the soft tissues.

Dual Energy CT

  • Uses 2 X-ray tubes arranged perpendicular to each other using different voltages. It has the potential to detect intra-articular and extra-articular urate crystals which would have been otherwise undetectable.

High resolution ultrasound scan.

  • Serial high resolution ultrasound may be used to assess response to treatment.
  • Highly sensitive for detection of erosions.
  • Double contour sign seen

Diagnosis Criteria


Rome criteria – 1963

(2 of 4 required for diagnosis)

  • Serum uric acid > 7mg/dl in males and >6mg/dl in females
  • Tophus
  • Urate crystals demonstrated in the synovial fluid
  • History of recurrent attacks of joint swelling of abrupt onset which resolves within 2 weeks.

New York criteria – 1968

  • Demonstration of urate crystals in the synovial fluid or tissue.

OR

More than 2 of the following criteria.

  • Tophi
  • History or observation of podagra.
  • History or observation of at least 2 attacks of painful limb swelling of abrupt onset which resolves within 1-2 weeks.
  • History or observation of good response to colchicine within 24 hours.

Continue reading “Gout”

Haemophilia for the orthopaedic surgeons

Haemophilia is an X-linked genetic coagulation disorder due to deficiency of either coagulation factor VIII or IX. About 80% is due deficiency of factor VIII (Haemophilia A), 15% is due to deficiency of factor IX (Haemophilia B, Christmas disease) and the rest is due to von Willebrand disease. Haemophilia A & B are inherited as X-linked recessive and von Willebrand disease as autosomal dominant inheritance.

heemophilia types

About 400,000 people are affected across the world. Incidence is 1 per 5000 male live births. Mortality rate in haemophiliacs exceed that of normal population by 2.6 times. 2/3rd have family history but 1/3rd of cases are due to new mutations.

Clotting factor VIII is also known as anti-haemophilic factor or globulin. It is encoded by the f8 gene in the long arm of X chromosome (Xq28). It is synthesized by the sinusoidal cells of liver and by the endothelial cells of the body. In the blood, it circulates in an inactive form bound to von Willebrand factor. When activated it separates from von Willebrand factor and plays a key role in the intrinsic coagulation pathway.


History

  • Hopff in 1828 coined the term haemophilia.
  • Wright first described the prolonged clotting time.
  • Patek and Tailor isolated Factor 8.
  • It is called the royal disease as Queen Victoria (1819-1901) was a carrier who passed on the X-linked gene to 2 out of her 4 daughters as carriers and one of her 5 sons died of haemophilia. One of her grandsons, Alexei born to the Russian tsar Nicholas II also died of the disease.

Milestones in the treatment

1840s – Whole blood transfusion

1923- Plasma transfusion

1950s- Fresh frozen plasma

1960s- Cryoprecipitate

1970- Freeze dried clotting factors

1980s- Transfusion related HIV/AIDS

1990s- Transfusion associated HCV infections

1987- Heat treated factor VIII to reduce HIV

1989- Genetically engineered Factor VIII

2000- Genetically engineered Factor IX

2011- Gene therapy human trials started for Factor IX deficiency using viral vehicle Adeno Associated Virus 8 (AAV8)

2013- First extended half-life clotting factors approved by FDA


Continue reading “Haemophilia for the orthopaedic surgeons”

Ward Rounds- A recently neglected part of inpatient care

 

More than two decades back when I did my house surgeoncy, I had tough time with the length of ward rounds. Ward rounds started at 7:45AM and it would continue beyond 12noon without a coffee break. My feet ached, mind was numb with hypoglycemia. In those moments I used to think why rounds can’t be faster and why it was taking so much of time. But later with a personal experience, that impression changed.

During my early PG days, my grandmother got admitted in the pay ward with a minor surgical problem in the busiest surgical unit. Each day I noticed that she was waiting for the time of rounds. One day, on the operation day of the unit; rounds was not taken till afternoon. My grandmother was unhappy and was wondering why no one has come so far for rounds. I tried to console her by informing her that it was the operation day. Initially she was comforted but soon she started grumbling. Soon it was a full blown tantrum and she refused lunch.

The time flew past the afternoon to evening, I did my best to comfort her without any response. I tried to contact the members of the concerned unit. They were held up in the OT. I gave up the hope of pacifying her and told her that probably there won’t be any rounds as it was already very late. She remained inconsolable. Then there was a knock on the door and the unit chief was standing outside the door. He peeped inside without even stepping in and asked “How are you grandmother? Are you better enough to go home? My grandmother was beaming and became an unrecognisably different person.

From that day I understood the psychological importance of ward rounds to the patient. But it is important for the treating team as well. It helps to establish a rapport with the patient, helps in early detection of complications and often saves one from embarrassment or even legal proceedings.

Over the years I have noticed that doctors as a community have become unaware of the importance of rounds. Rounds is often delegated to junior colleagues and many regard it as a nuisance. The patient is forgotten and more attention is given to the case sheets, investigation reports and the x-ray or MRI images. Some even think it is the best time to catch up with missed calls, emails, Facebook or Whatsapp messages.

To continue…..

https://learningorthopaedics.com/wardrounds/

Meniscus Lesions Tied to Neuropathic Pain in Knee OA

SOMEONE SOMEWHERE

Meniscal extrusion on MRI significantly associated with increasing pain scores in knee osteoarthritis.

Meniscus lesions, specifically extrusions, were a risk factor for neuropathic pain in patients with knee osteoarthritis (OA), results of a pilot study suggested.

The presence of meniscal extrusion on MRI, in both medial (P=0.006) and lateral (P=0.023) compartments, was significantly associated with increasing neuropathic pain (NP) pain scores in knee OA patients, according to Camille Roubille, MD, of the University of Montreal Hospital Research Center in Quebec, and colleagues.

The presence of meniscal tears in the lateral compartment (P=0.011) was also significantly associated with pain scores, they wrote online in Arthritis Research and Therapy.

“Our finding of an association between NP and lateral meniscal tear is somewhat unexpected as literature indicates that meniscal tears are not usually associated with symptoms,” the authors wrote.

The multicenter, cross-sectional, observational study included 50…

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Scapular dyskinesis

Definition

Scapular dyskinesia is defined as observable alterations in the static position of scapula or abnormal patterns of motion of scapula during coupled scapulohumeral movements in relation to the thorax.

Introduction

  • Due to inhibition or disorganization of activation patterns of scapular stabilizing muscles.
  •  Disrupts the normal rhythm of scapulohumeral motion and shoulder kinematics.
  •  Associated with various shoulder pathologies such as impingement, adhesive capsulitis, instability, SLAP lesions, rotator cuff injuries and acromioclavicular disorders.
  • May be the cause, effect or compensation. Exact role in shoulder dysfunction unknown.
  • It may exacerbate symptoms or adversely affect the outcomes of treatment.
  • Other causes are pectoralis minor contracture, Glenohumeral internal rotation deficit (posterior capsule of shoulder contracture), excessive thoracic kyphosis or excessive lumbar lordosis.
  • Frequently seen in athletes with shoulder injuries. It is also in asymptomatic individuals.
  • Treatment directed towards underlying cause and by kinetic chain based rehabilitation protocols to restore normal muscle activation protocols.

Functions of scapula

  • Provision of a stable but mobile foundation for humeral head during glenohumeral motion
  • Scapulothoracic motion
  • Elevation of acromion during abduction to prevent impingement of supraspinatus.
  • As a link in the kinematic chain for proximal-to-distal sequencing of velocity, forces and energy of shoulder function.

Scapular kinematics

  • Scapula, shoulder and humerus are either stabilized or moved during various activities to generate, absorb or transfer forces.
  • To optimize function, the scapula should move in coordination with the movements of humerus to maintain the instant centre of rotation and the alignment of glenohumeral joint. This has been likened to the balancing of a ball on seals nose.

To read more

https://learningorthopaedics.com/scapular-dyskinesis/

Ulnar nerve palsy

Anatomy

  • Ulnar nerve is a branch of medial cord of brachial plexus which arises from C8 and T1 ventral rami.
  • It lies between the axillary artery and vein.
  • It lies posteromedial to the brachial artery.
  • In the arm at the level of coracobrachialis insertion, it pierces the medial intermuscular septum to enter the extensor compartment where it lies anterior to the medial head of triceps.
  • At the elbow it lies in the retrocondylar groove behind the medial epicondyle.
  • It enters the cubital tunnel between the 2 heads of flexor carpi ulnaris to reach the flexor compartment where it lies on the anterior surface of flexor digitorum profundus. It supplies the FCU and the medial half of FDP.
  • 7 cm proximal to the wrist it gives off the dorsal branch which supplies sensation to the ulnar part of dorsum f hand up to the proximal interphalangeal joints.
  • 5 cm above the wrist it gives off the palmar branch which supply the ulnar side of palm.
  • Nerve passes superficial to the flexor retinaculum, medial to the ulnar artery and radial to the FCU through the Guyon’s canal which lies between the pisiform medially and the hook of hamate laterally.
  • In the Guyon’s canal it divides into superficial and deep branches.
  • Superficial branch supplies the palmaris brevis and provides sensation to medial one and a half fingers.
  • Deep branch passes along with the deep branch of ulnar artery between the FDM and ADM. It pierces the ODM to reach the deep surface of flexor tendons.
  • Along with deep palmar arch it passes transversely.
  • Deep branch supplies hypothenar muscles, interossei, medial two lumbricals and ends by supplying adductor pollicis, deep head of flexor pollicis brevis and first dorsal interossei.
  • Ulnar nerves supplies
    • FCU
    • Medial half of FDP
    • Hypothenar muscles
    • Interossei
    • Medial 2 lumbricals
    • Adductor pollicis
    • Deep head of flexor pollicis brevis

Pathoanatomy

  • Martin-Gruber anastomosis
    • Seen in 15%
    • Between ulnar and either median or AIN in the forearm.
    • Carry motor fibres from median to ulnar for intrinsic muscles.
    • May result in intact intrinsic function in proximal ulnar lesions.
    • 4 Patterns
      • Type I 60%- Motor from median to ulnar to supply median innervated muscles
      • Type II 35%- Motor branch from median to supply ulnar
      • Type III 3%- Motor from ulnar to median to supply ulnar innervated muscles
      • Type IV- Motor from ulnar to median to supply median innervated muscles
  • RichieCannieu anastomosis
    • Between deep branch of ulnar and recurrent branch of median nerve.
    • Ulnar to median
    • May result in intact thenar muscle function in presence of median nerve injury.
  • Sites of nerve entrapment
    • At the elbow
      • Arcade of Struthers- Myofascial band extending from medial intermuscular septum to the medial head of triceps, 8 cm above medial epicondyle
      • Medial intermuscular septum where it pierces
      • Medial head of triceps
      • Medial epicondyle
      • Epicondylar groove
      • Cubital tunnel between 2 heads of FCU which are connected by aponeurotic Osborne’s ligament
      • Flexor pronator aponeurosis between FDP and FDS.
    • At the Guyon’s canal
      • Zone I- Proximal to bifurcation
      • Zone II- Distal to bifurcation. Contains deep branch.
      • Zone III- Contains the superficial branch
  • Functional losses in ulnar nerve injury
    • Loss of key pinch due to paralysis of adductor pollicis and first dorsal Interossei.
    • Clawing due to paralysis of Interossei and lumbricals in presence of functioning extrinsic extensors leading to MCPJ hyperextension and functioning long flexors leading to flexion of IPJ.
    • Loss of forward flexion of mobile fourth and fifth carpometacarpal joints lead to loss of transverse palmar arch manifested as inability to cup the hand to hold water.
    • Loss of normal integrated MCPJ and IPJ flexion. Normal finger flexion starts at MCPJ followed by IPJ. In ulnar nerve palsy IPJ flexes first followed by MCPJ. This rolling motion will lead to inability to grasp objects.
    • Loss of FDP function of medial 2 digits in high ulnar nerve palsy leads to diminished grip strength.

Clinical Features

  • Duchenne sign- Clawing
  • Cross finger test- Inability to cross index and middle finger over each other.
  • Pitres Testut sign- Inability to abduct middle finger to either side.
  • Wartenberg sign- Abduction of little finger.
  • Loss of normal sequence of finger flexion- Normally MCPJ flexes then the IPJ flexes. In ulnar nerve palsy MCPJ flexes last.
  • Loss of key pinch
  • Jeannes sign- MCPJ of thumb hyperextended during key pinch.
  • Masse sign- Loss of hypothenar eminence and flattened palmar metacarpal arch.
  • Pollock sign- Inability to flex DIPJ of little and ring fingers.
  • Froments sign- Substitution of adductor pollicis by FPL during key pinch.
  • Bouvier manoeuvre- Correct the hyperextension of MCPJ and ask the patient to extend IPJ. If IPJ extension is improved then Bouvier test is positive and claw and is termed simple claw hand. If IPJ extension doesn’t improve then test is negative and clawing is called complex claw hand.
  • Associated sensory loss over medial aspect of arm and forearm indicate medial cord lesion.
  • Systemic conditions mimicking ulnar palsy
    • Charcot Marie Tooth disease
    • Syringomyelia
    • Leprosy
    • Klumpke’s paralysis
    • Pancoast tumour
    • Cervical IVDP

To continue

https://learningorthopaedics.com/ulnar-nerve-palsy/