May 30, 2024

Total hip arthroplasty can be complicated with serious problems which are challenging and should be keenly evaluated

Complications after Total Hip Arthroplasty

Discussed topics are

Mortality

Dreadful complication following THA.

Incidence of 1-3 %

Common cause: cardiovascular complication followed by cerebrovascular complication

Reduced by postoperative thromboprophylaxis  use

Heterotrophic ossification following Total Hip Arthroplasty

Aberrant bone formation in the place where the bone doesn’t exist normally

(Muscle, capsule, and soft tissue)

Causes

  1. Head injury (neurological injury)
  2. Genetic causes ( ossificans progressive/ fibrous dysplasia)
  3. Post-traumatic causes ( surgery/ injury)

Incidence of 1–2 %

90% with risk factors

  1. Male
  2. Traumatic brain injury
  3. Perioperative stroke
  4. Diffuse idiopathic skeletal hyperostosis (DISH)
  5. Ankylosing spondylitis
  6. Past history of Heterotrophic ossification

Surgical trauma to soft tissue will cause stimulus in some way and primitive mesenchymal cells into osteoblastic tissue within 16 hr after the surgery procedure

Maximum stimulus occurs in 32 hr

So, prophylactic measures should be done 24-48 hr post-injury

Brooker classification of Heterotrophic ossification

Class I: Island of bone within the soft tissue of the hip

Class II: Bony spurs at the pelvis of the femur with > 1cm intervening space

Class III: Bony spur at < 1 cm intervening space

Class IV: Bony ankylosis

Class 0: No ossifications ( added later)

Brooker classification of Heterotrophic ossification

Pain is present during rest and interferes with sleep

Pain present initially present in 6 months which resolves spontaneously

Reduction in the arc of motion

Sciatic nerve irritation

Risk patient (Preventive measures should be applied)

  1. Should remain pre-operative prophylaxis
  2. Surgical approach to hip (modified Hardinge has high risk and postero-lateral has low risk)
  3. External beam irradiation (pre-operative)
  4. NSAIDs esp. Indomethacin

Surgical excision of established H.O. is warranted because of pain and limitation of movements

The procedure must be delayed ideally 12-18 months post-index procedure to permit the maturation of H.O.

Nerve Injury in Total Hip Arthroplasty

Incidence of 0.1-1.9 %

Sciatic, Femoral, Obturator, and Superior gluteal nerve are commonly injured

Risk Factors

  • Female genders
  • Dysplastic Hip
  • Revision surgery

Early diagnosis is key to treatment

If intraoperative lengthening is planned, measures should be taken to prevent nerve injuries

Sensory deficit: First sign of compartment syndrome

Should be placed in a position that minimizes tension of the affected nerve

If the sciatic nerve is injured àhip should be extended and the knee should be flexed.

Mechanical causes

  1. Wrongly placed acetabular screw
  2. Lengthening of limb
  3. Developing hematoma

Should be ruled out

Electro-diagnostic studyàlocalizing nerve injury

Paucy evidence of wound exploration unless there is a clear mechanical cause of obstruction.

Dislocation

Disheartening complication

Incidence of dislocation is

0.3-10 %: Primary surgery

14-28 %: Revision surgery

Cause

Multifactorial

Patient Factors

  1. Female gender
  2. Neuromuscular and cognitive disorder
    1. Cerebral palsy
    1. Muscular dystrophy
    1. Psychosis
    1. Dementia
    1. Alcoholism
  3. Pre-operative diagnosis of fracture: Higher incidence of dislocation (Due to loss of thick capsule in Osteoarthritis of the hip)

Surgical Factors

  • Surgical approach: (Posterior: Increase chance)
  • Positioning of acetabular/ femoral components

Excessive anteversion ( ant. d/o)/ retroversion(post. d/o) of acetabulum

Safe zone of cup: 30-50°cup abduction; 15-25° of cup anteversion

  • Larger head size: ↓ chance of dislocation, seated deep within acetabular liner requiring greater translation before dislocation: Jump distance
  • Improved head-to-neck ratio: ↓ dislocation
  • Proper balancing of soft tissue achieved by restoration of offset and leg length
  • Deficiency of the soft tissue/ soft tissue tensionàresult of trochanteric non-union, avulsion of abductors: A risk factor for dislocation
  • Infection
  • Experience of surgeon
  • Timing of dislocation
    • Early: 1st 3 month
    • Late: After that

Management

Early / 1st time dislocation: CR + bracing for 6 weeks

Late dislocation: Assessment of cause

Usually need planned revision surgery + Component change

Recurrent dislocation: Constrained liners

Venous thromboembolism in Total Hip Arthroplasty

Ranges from 42-57%

Blood flow

Patients factors

  • Previous ho VTE
  • Obesity
  • Smoking
  • Carconimas
  • Prolonged inability prior to surgery
  • Inflammatory bowel disease
  • Age > 60 yr
  • Congestive heart failure
  • MI stroke
  • Varicose veins
  • Hormone RT
  • Hypercoagulability stage (antithrombin III deficiency, protein C, S deficiency, dysfibrinogenemia)
  • Lupus
  • Myeloproliferative disorder
  • Plasminogen disorder

So, prophylaxis needed

General Measures

  • Early mobilization
  • Tourniquet
  • Surgical techniques (avoid rough handling)
  • Neuraxial anesthesias

Non –pharmacological

  • Gradual compression stocking
  • Venous foot pump
  • Intermittent pneumatic compression of calf and thigh
  • Inferior venocava filters
  • Electric stimulation

Pharmacological methods

Warfarin

 Inhibits Vit K dependent factors II, VII, IX, and X in liver

Antidote:- Vitamin K

Required regular monitoring of PT/INR

It is dependent on cytochrome P450–>lots of drugs interaction

NSAIDs use, Limited with ↑ gastric bleed

Heparin exerts its anticoagulant activity principally by binding antithrombin III. This causes increased exposure of the antithrombin active site that, in turn, inactivates the coagulation enzymes, Factor IIa, IXa and Ca. Fractioned heparins also bind to antithrombin III but have greater anti-factor Xa activity rather than greater antithrombin activity. The frequency of heparin-induced thrombocytopenia varies greatly on other factors, type of heparin administered, and type of population. Aspirin is contraindicated in the patient under the age of 16 years when used as a antiplatelet agents ( due to risks of Reye's syndrome)

Low molecular weight Heparin (LMWH)

Made by unfractured heparin by chemical/ mechanical depolymerization

Acts on Factor Xa

Once or twice daily dose doesn’t require blood parameter monitoring

Antidote : Protamine sulfate

Metabolite in the kidney, cautiously used with renal dysfunction

Fondaparinux

Antithrombotic action by binding to antithrombin III : factor Xa

No known antidote

Metabolished in the kidney (caution in renal patient)

Side effects: Bleeding / Thrombocytopenia

Acetylsalicylic Acid:

Aspirin

Limits platelets aggregation by inhibiting

↓ thrombus formation

Antiplatelet oral agent required monitoring

Low dose and long-term aspirin use will irreversibly block the formation of thromboxane A2 in platelets, producing inhibitory effects on platelet aggregation. Aspirin inhibits collagen-induced platelet aggregation and ADP-induced platelet aggregation as well as blocking the release of ADP from platelet aggregating substances. Aspirin acts on cyclooxygenase by causing irreversible acetylation of the enzyme so the effect is irreversible for the life of platelets (7-10 days). Other NSAIDs have reversible action.

  • Oral anticoagulants:
  • Oral anti-factor Xa: Eg. Apixaban, rivaroxaban
  • Direct thrombin inhibitor: Eg. Dobigatron

Dextran is a polysaccharide that has antithrombotic effects by binding to the erythrocytes, platelets, and vascular malformation, increasing their electronegativity and thus reducing erythrocyte aggregation and platelets adhesiveness. Dextran also reduces factor VII-Ag von Willebrand Factor, thereby decreasing platelet function.

Infection

2.5% : After introduction of antibiotics

Infection an a complications of THA
Infectious agent

Risk factors

S.aureus + S.epidermidis are common organisms (85% in peri-prosthetic infections)

Other organisms like Streptococcus, Pseudomonas, Klebsiella, and E. coli

Pre-operative dose: 2 hr prior to incision

Peak bone concentration: 35-40 min after IV injection

Intra-operative redosing if surgery > 4 hr

Three Stages

Stage 1: Acute infection probably cause by infection during surgery; seen within 1st three months

Stage 2: Delayed presentation; after several months

Stage 3: Infections from the remote site to hip; urinary, dental, or respiratory–> hematogenous spread

Diagnosis of infection

  • Suggestive history
  • Blood parameters (non-specific parameters)
    • Utility of TLC is less (↑ seen in 15% pts)
    • CRP: a sensitive indicator
      • Max in 48 hr after surgery and returns normally in 2-3 weeks
    • ESR may be elevated for months
  • Normal ESR and CRP exclude infection

In case ↑ ESR and CRP ( but no etiology)àHip joint aspiration advised  (AAOS), send for culture/TC/DC, Put off antibiotics for a minimum of 2 weeks prior to aspiration to maximum culture aid and accuracy

Threshold

Indicators of infections

  1. >4200 cells/ml
  2. >80% PMNs

Nuclear medicine: Isotope scanning: Technetium 99c/ Ga

Aids to diagnosing infections

If still debatable: – Fluid and tissues sample obtained during the time of reoperation is assessed

Purulence in joint: Not absolute indicator:- As seen in metal hypersensitivity

Intra-operative frozen section

Definition of periprosthetic infections according to Musculoskeletal infections Society

  1. Presence of sinus tract communicating with prosthesis
  2. Identification of organisms isolated by culture from 2 or more separate tissue or fluid samples from prosthetic joints
  3. Any 4 of 6
    1. Elevate CRP and ESR levels
    2. Elevated synovial WBC count
    3. Elevated synovial PMN %
    4. Presence of purulence in joints
    5. Isolation of organism in one culture or fluid of joints
    6. > 5 neutrophils/HPF @400 x magnifications form prosthetic tissue

One of the following 3 criteria met

Managements

The goal of treatment is to eradicate the infection + restoration of function

Options

  1. Debridement + retention of components
  2. Single-stage revision
  3. 2 stage revision
  4. Long-term suppressive antibiotics
  5. Salvages procedure
  6. If patients cannot/are unable to tolerate surgery: Antibiotics suppressive is tried
  7. If infections are of short duration: Prosthetics well fit, Overlying skin is normal

And patient immune status is good, careful debridement, copious lavage, change of modular components, Prevent biofilm formation

  • One-stage revision arthroplasty
  • Two stage reimplantation
    • Gold standard

Reimplantation into sterile bed

1st step:

IV antibiotics for 6 weeks

Prosthesis removed with adequate debridement and antibiotics spacer kept

2nd step:

The spacer is removed and definitive implants are kept with the reconstruction of bone ( once ESR and CRP come in normal )

Limitations

  1. Bone pain
  2. Bone stock loss
  3. Prolonged time
  4. Patient ability to tolerate 2 surgeries

Osteolysis and aseptic loosening after THA

Osteolysis and aseptic loosening is another complication following THA

Area of radiolucency in the bone adjacent to implant characterized osteolysis

Wear particlesàinduce biological responseàactivates macrophages, a critical event in the procedure

Cytokines:

  • Prostaglandins E2
  • TNF α
  • IL-1
  • IL-6

RANKL and OPG has a key factors for osteolysis i.e. ↑RANKL and ↓OPG

In THR if the wear rate is >0.3mm/yr all cases of Osteolysis

If < 0.1 mm/yr, no osteolysis

Ceramics-ceramics articulation: The lowest rate of osteolysis

Metal on metal articulation has a lower rate than metal and polyethylene articulation

Initial MOM articulation has ↑ osteolysis in wear particles so-called

[Run in period articulation]

Leading to adverse effects

ALVAL

Managements:

Radiographic evaluations

NSAIDs and COX-2 inhibitors are used in osteolysis

Bisphosphonates tried showed no success

Surgical management

Extends of osteolysis/ stability of implants

Loose/ unstable implants ,revision is done

Femoral osteolysis may lead to periprosthetic fractures

Periprosthetic fractures

Incidence : 0.1-4 %

Classifications

Vancouver classification

Vancouver classification
Vancouver classification

Management Options

Type A

ORIF: Will maintain abductor function + wide displacement

Severe polyethylene tear needs a revision of acetabular components

Type B1

Usually Internal Fixation :

  • Wires/ cables
  • Plates/ screws
  • Cortical Onlay grafts
  • Combinations

Type B2

Revision arthroplasty + ORIF

Uncemented prosthesis: Extensive coated local stem curved prosthesis

Cemented prosthesis

Fluted long-stem prosthesis

Modular implants

Type B3

No sufficient bone stock support the revision prosthesis

Options include:

  • Proximal femoral reconstruction
  • Composite allografts
  • Scaffold techniques

Proximal femoral replacement

Type C

Treat independently of arthroplasty

Bypass stemmed implants

In knee Arthroplasty

Supracondylar fracture in TKA: Classifications

Type 1: Undisplaced fracture, prosthesis stable

(Treatment is nonoperative with immobilization with brace/cast)

Type 2: Displaced fracture, prosthesis stable

Treatment is the fixation of the fracture

Type 3: Unstable prosthesis with/without fracture displacement

Treatment is the revision of femoral components with stemmed prosthesis

Tibial fracture in TKA: Classification

Type 1: Involving Tibial plateau

Type 2: Fractures around the stem of the prosthesis

Type 3: Fractures distal to the stem of the prosthesis

Type 4: Fractures involving the tibial tubercle

Other classification

Type Features
Type AThe prosthesis is well fixed
Type BThe prosthesis is loose
Type CIntra-operative fracture

Treatment Options

In loose prostheses, revision surgery with a stemmed implant should be done

Undisplaced fractures with an intact prosthesis: Conservative treatment

Displaced fractures with an intact prosthesis: Open reduction with internal fixation

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