Prophylaxis for Venous Thromboembolism in patients undergoing THR and TKR

 THR and TKR

• Indications 

• PAST

• Present

Total hip replacement (THR) surgery,
as we know it, began in 1960.

Total knee replacement (TKR), as currently performed, was first described in 1971.

• While these operations are very successful,deep-vein thrombosis (DVT) and pulmonary embolism (PE) have been significant complications.

The reported prevalence of

• DVT in patients not receiving prophylaxis in clinical trials using mandatory venography has been 45%–57% after THR and 40%–84% after TKR.

• The reported prevalence of PE in other trials has been 0.7%–30% after THR (prevalence of fatal PE, 0.1%– 0.4%), and 1.8%–7% after TKR (prevalence of fatal PE, 0.2%–0.7%).

Patients with thrombophilic syndromes show even higher rate of venous thromboembolism as evident from the table above.

Based on AHA 

• VTE consists of 2 related conditions: deep vein thrombosis (DVT) and pulmonary embolism (PE).

• In 1884, Rudolph Virchow first proposed that thrombosis

        was the result of at least 1 of 3 underlying etiologic factors:

• Vascular endothelial damage, Stasis of blood flow, and Hypercoagulability of blood.

• In assessing whether prophylaxis is indicated, physicians should consider both the strength of individual risk factors and the cumulative weight of all risk factors.

Risk factors to consider for VTE , according to Canadian Orthopaedic association

Guidelines for Starting Pharmacologic Treatment in patients undergoing THR and TKR. 

Preventing Venous Thromboembolic Events in Patients undegoing THR/TKR

 

• A variety of strategies to prevent venous thromboembolism are available: 

• Pharmacological

• Oral antiplatelet agents

• Injectable low-molecular-weight heparins

• Injectable unfractionated heparin

• Injectable or oral factor Xa inhibitors

• Injectable or oral direct thrombin inhibitors

• Oral vitamin K antagonists 

• Mechanical modalities

• Graduated compression

• Intermittent pneumatic compression

• Venous foot pump 

• Combinations of these

Patients with a high risk of bleeding should be started on mechanical methods of prophylaxis (intermittent pneumatic compression and/or elastic stockings) at least until bleeding risk is reduced. In general, patients with one of the weak or moderate risk

• Whereas VTE prophylaxis has generally been recommended for 7 to 10 days, recent studies have found that extending preventive treatment through the 4 weeks after hospital discharge is beneficial in patients undergoing surgery for cancer or total hip replacement. Additional data are needed to define the optimal duration of VTE prophylaxis in other high-risk.

see the timing of anticoagulation required on the first box above , how long does medicine require . 

Thank You.

Viva topics Grilling - Ac. Osteomyelitis,CTEV,CP, Gait Analysis ,ABC,Supracondylar fracture, Perthes Disease , Bone

 Viva 1

A child has hx of fever, malaise & painful walking on his right side. 

How to approach patient ? 

Assess in line of Septic Arthritis and Acute Osteomyelitis 

How do you manage ? 

Detailed Hx. taken including Treatment Hx.,  Past Hx. -allergy to Amy medications if any 

Examination- BP , pulse , Temperature 

Local examination 

Gait 

Inspection 

Resting Posture of Hip (FABER ) 

ROM 

local tenderness 

        Inv. 

AP / Lateral radiographs of hip - to r/o fractures , any structural abnormality

USG - hip effusion 7 mm  

note -  

Predictive markers of hip sepsis 

1. Temperature> 38 .5 deg. Celcius 

2. WBC > 12,000 cells /mm3 

3. ESR > 40 

4. NWB 

Based on above findings , chances of hip sepsis (combination increases accuracy of  diagnosis)

    1 = 3 % , 2= 40 % , 3 = 93 % , 4= 96.6 % 

What's the treatment ? 

Surgery 

Anterolateral Approach to hip 

Remove ellipse of capsule , allow free drainage 

Samples for c/s 

Irrigation 

Hip Spicas - post operative -to prevent subluxation and dysplasia 

Approximate Abx. - Initially broad spectrum abx then adjusting 

Prolonged course 

Guided by Serial infiammation markers

Larger f/u - to assess growth and development of acetabulum 

Viva 2 

Photograph of a normal child with a club foot deformity .Describe it. 

Describe the deformity as Cavus & adductus of mid foot , Varus and Equinus Hindfoot. 

How do you classify  severity of the deformity ?

Pirani Score 

Midfoot - Severity of Medial Crease

- Coverage of talar head

- Curvature of lat border

Hindfoot - Rigidity of Equinus 

     -Severity of posterior crease 

            -Degree of emptyness of heell

    All deformities are given points 0, 0.5 and 1. 

          They are sum up. Maixum is 6 and lowest 0. Higher the score , severe the deformity. 

 

How to manage club foot in babies ? 

History in depth including history of  deformity in Parents

Examination

Classify - syndromic vs Idiopathic 

          Investigations- X-ray of feet  

        Treatment 

Ponseti cast 

 

Pirani casts are above knee casts with foot areas moulded into corrected position . 

        Start with manipulation & serial cating    

     

        Ist cast. 

                                    Dorsiflexion of foot

                                    - 1st ray unlock forefoot and mid foot. 

                                    - Elevation & Ist ray supination

                                   2nd Cast

                          -Abduct at mid foot level, using hand of talus                                         fulcrum

                                     Midfoot corrects after 4 to 5 casts 

Achilies tenotomy for residual Equinus 

Final cast for further 3 weeks .

Denis Browne boots with a bar (23 hours a day for 3 months , then night time until 5 years. It holds foot at 70 degrees ER. 

It also avoids need of surgical release . 

25 % require TA transfer laterally for Inversion in swing after age of about 5 years. 

Be clear that , different treatment is required for grown up child , requires bony procedures. 

Viva 17

What is Cerebral Palsy ? 

Neuromuscular disorder cused by non Progressive leison to immature developing brain before age of 2 yrs ( although neurological injury non Progressive ,MSK features evolve ) 

Types-

Anatomical - Hemiplegia (40 %) , Diplegia (30 % ) , Total Body Involvement (30 % ) 

Physiological 

 Spastic (60 %), Dystonic (20%) , Ataxic (10 %),

Hypotonic (10%) 

GMFCS Classification is also there. 

What is Spasticty?

Velocity dependent increased tone of muscles . Represents as increase response to stretch reflex.

    Management of spasticity 

1.Multidisciplinary approaches- family and patient in goal planning decissions about treatment ,Exploring expectations.

2.Non-operative 

PT -Physiotherapy 

Botulinum toxin -

                                Cl. Botulinum toxin prevents release                                 of Acetylcholine at NMJ .

Effective for 3 to 6 months Combined with plasters & targeted PT/ Orthotics to maintain stretch . 

Baclofen Pump and Injections 

 GABA Agonist / inhibitory neurotransmitter 

It acts  centrally and peripherally to decrease spasticity 

 Intrathecal injections - can increase dose and reduce systemic side effects

        

                                Orthoses 

     3.  Surgery 

SEMLS- Avoid Birthday Operation 

1.Soft tissue lengthening to tight muscles. 

                    2.Muscle transfer

                   3.Osteotomy 

What is Gait Analysis?

Systemic discription , assessment and measurement of quantities that characterizes human locomotion.

Involves Kinematics ( movement of individual parts of body) & kinetics (forces how they interact and & produce the movement ) as well EMG and energy consumption .

Gait analysis- 

2 D Video

3D computer analysis 

 - Breaks movement of individual parts into graphic form .     -Use force plates, measures ground reaction force & EMG records muscle firing patterns

-Gait analysis looked at in conjuction with a Static detailed physical examination. 

Viva- 3

You got an X-ray 

Reads like

AP Radiograph of skeletally immature child showing a multiloculated lytic lesion in proximal metaptysis. The zone of transition in Sharp indicating benign lesion & no associated periosteal reaction . 

           Fallen Fragment inside ?  , see it .  

What is your Diagnosis ? (Prof.)

     X-ray is suggestive of 

Simple Bone Cyst 

ABC 

Infection 

He presensts after few weeks with severe pain . What might have happened?

Pathological fracture 

 

How do you manage ? 

 Detailed histroy 

 Examination 

        Investigations  

  Manage expectantly 

          (# stimulates new bone formation, bear this in this chapter )

Patient treated expectantly but lesion persists . How to manage ? 

        Follow up and see 

        Aspiration of cyst done-If expectant non operative measures            fail

Inject steroid on bone graft, marrow to try and stimulate new bone formation.

        -If it fails , repeated attempt is worthwhile.

Surgery - Curette out lining of cyst through a cortical window and Stabilizing bone to prevent fractures 

        Flexible IM nails across lytic area.

        If cavity adjacent to growth plate , important not to damage                 physis.

Viva 4 

You got an X ray Gartland type IIIA , supracondylar fracture . 

Questions 

How do you manage the case ? 

Hx. - MOI , Other injuries ,drug allergy 

Examn . - assess presence of open injury 

Assess distal NV (Hand colour , capillary refill of finger tips , radial pulse ,sensation in specific dermatomes , motor function in ulnar ,median ,radial and AIN nerves ) 

Treatment 

Analgesia 

Temporary back slab 

Consenting 

OT set up with C-arm back up 

 CR -technique

Continuous traction in 20 degrees flexion , several minutes.

-- correct valgus /varus and rotational deformity 

-flex arm 

-Pronate forearm to lock fragments 

-Insert a lateral wire 1.6 mm k wire first 

Extend arm a bit to plan a mini open approach to medial side .

Bend and cut wires in clinic in 3 to 4 weeks time. 

Splint arm in back slab in near extension 

       Reassess perfusion of hand and watch for compartment                      syndrome 

Not able to feel pulse after pinning. What to do ? 

Assess colour of hand and warmth , capillary refill time

for a pink and warm hand , with adequate Capillary refill of finger tips , I would monitor situation with a regular review. 

Artery in spasm (if) will lead to loss of pulsation.

 If hand white and CR reduced , remove splint, extend elbow and see situation. 

If not contatct vascular /plastic surgery for urgent review as artery has been caught up in fracture and has been occluded by rdeuction.

       If requires exploration anteriorly.

Viva 5 

You are shown an AP Pelvis of skeletally immature child with flattening of femoral head with deformity suggestive of Perthes disease. 

What is underlying disease ? Who gets it ? 

Idiopathic AVN of Proximal femoral epiphysis in childhood . 

Unknown actiology, sequeale of acetabulum procedure

Boys & Girls = 4: 1, Bilateral -20%

Classification

            Based on Staging     

1. Initial  Avascular event (crescent sign presenting subchondral fracture )

2. Fragmentention

3. Resolutions and re-ossification

4. Remodelling

 

Herring’s classification 

Piller height on AP radiograph  during fragmentation .

 >50% maintained 

<50 % maintained 

Caterall’s classification - depending on head involved on lateral Radiograph 

Also Added head at risk sign . 

Clinically

Obese 

Progressive and decrease ROM 

Abduction contracture 

ER with flexion 

Radiographically 

Horizontal Physis 

Lateral Subluxation of epiphysis

Lateral calcification

Diffuse Metaphyseal Sign 

+ Gaze Sign-inverted  V shaped lucency in lateral Metaphysis 

Stullberg's classification based on shape of femoral head 

I- normal 

II - head spherical which is spherical (magna / Bevel ) fits in socket which is congruent 

III - mushroom head congruent 

IV - flat head and flat socket careongruemt mont

V - flat head incongruent .

What is the Principle of management ? 

Goals

Symptomatic Parf

Containment of femoral head 

Restore ROM

Goals achieved by non operative and operative measures.

Management based individual basis taking into accounting their age, clinical  signs & radiological appearances on X-ray .

Viva 5 

What is bone ?

Bone is a dynamic form of specialized connective tissue 

Cells - 10 % 

Osteoblasts 

Osteoclasts 

Osteocytes 

 ECM - 90 % 

Organic 

    Collagen- type I 

Inorganic 

Calcium phosphate 

Osteocalcium phosphate 

Function of Bones

Movement 

support & polkrotect internal organs 

Production - WBC/ RBCs

Storage of Calcium and Phosphate

Osteoblasts short explanation 

Derived from undifferentiated mesenchymal cells

Bone forming ,lay down osteoid ( type I collagen ) 

Contains RANK Receptor activator of nuclear factor kappa - B

Osteocytes osteoblasts that have beame trapped in bone

 

About Osteocytes 

     Osteoblasts that have become trapped in bone matrix ( making         upto 90 % of cells in bone ) , 

     Important role in homeostasis of calcium and phosphate 

Jolius Wolff , German anatomist FIRST  described metabolic change in bone according to demand and hence name as Wolff's law.

Wollf's Law

If loading on bone increases , bone remodels itself over time to become stronger to resist load. 

 

About Osteoclasts 

Monocyte call lineages that multinucleated giant cells that resorb bone

Location - Small pits called Howship Lacunae, bonee surfaces. & lead culting cones.

Ruffled brush border , increase surforce area, create ? low PH to disolve inorganic constituents 

Enzymes Release - tartarate resistant acid phosphatase - break down organic matrix components,

inhibitors to Osteoclast are Osteoproteogerin. 

Bone | Perthes disease |Supracondylar Fracture | ABC | Gait Analysis |Cerebral Palsy (CP )|Congenital Talipes Ewuinovarus (CTEV)|Septic Arthritis |Acute Osteomyelitis|