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➢ Most common joints replaced are the hip, knee and shoulder.
➢ Most patients are elderly, with associated problems such as HTN, IHD, COPD
or renal disease.
➢ There are specific types of pts who are more likely to have orthopedic surgery and
are more likely to have perioperative complications.
➢ geriatric pts
➢ Although all bones are at risk, thoracic and lumbar spine, proximal femur,
proximal humerus, wrist are at highest risk.
Osteoarthritis
➢ Most common type of arthritis loss of articular cartilage, inflammation.
➢ Clinical manifestations pain, crepitance, reduced mobility, and deformity of involved joints.
➢ Hands – spurring, swelling of the distal IP jts (Heberden's nodes) and PIP jts (Bouchard's
nodes).
➢SC rheumatoid nodules may surround joints, extensor surfaces, and bony
prominences.
➢ Restrictive pericarditis (dyspnea, RHF, fever, chest pain, pericardial friction rub,
pulsus paradoxus). ›
➢Pleural disease and intrapulmonary nodules.
➢ diffuse interstitial fibrosis with pneumonitis – PFTs restrictive ventilatory pattern
respiratory insufficiency, pulmonary HTN, RHF.
➢Overlapping CTDs Sjögren's syndrome, Felty's syndrome.
Extraskeletal manifestations
1. aortic insufficiency
2. cardiac conduction abnormalities
3. Iritis
4. upper lobe fibrobullous disease ,pleural effusions.
Musculoskeletal
1. Advanced age
2. Obesity
3. Previous PE and DVT
4. Cancer
5. Prolonged bed rest
➢TECHNIQUE
1. Nerve supply to hip joint includes obturator, inferior gluteal, and superior
gluteal nerves - RA best achieved with SAB/ epidural anesthetic.
• When LMWH has been instituted for the prevention of DVT, patient-
controlled epidural anesthesia cannot be continued postoperatively, and
instead continuous femoral nerve catheters are used
TOURNIQUET APPLICATION
➢ Routinely inflated over thigh during TKA to reduce intraop blood loss,
provide a “bloodless” field for cement fixation of femoral and tibial
components.
➢ When deflated, blood loss usually continues for next 24 hours.
➢ Tourniquets are usually inflated to a pressure 100 mm Hg above pt's SBP
for 1 to 3 hours.
➢ Nerve injury after extended tourniquet inflation (>120 minutes) has been
attributed to combined effects of ischemia and mechanical trauma.
➢ Peroneal nerve palsy, a recognized complication of TKR caused by
combination of tourniquet ischemia and surgical traction.
➢ When prolonged tourniquet inflations are required, deflating the
tourniquet for 30 minutes of reperfusion may reduce neural ischemia.
➢ Cuff should be applied over limited padding.
• Hypothermia:
• orthopaedic theatres colder than other theatres, with a
higher velocity airflow leading to more rapid patient cooling.
• Hypothermia causes poor wound healing, infection,
coagulopathy and CVS dysfunction.
• Fluid warmers, blankets and patient hats should be used
routinely.
Blood loss:
➢ Average blood loss in THR ranges from 300-1500 ml and may double in
the first 24 hours postop.
➢ During TKR with an intraoperative tourniquet, most blood loss occurs in
the recovery area.
➢Careful fluid balance is essential because compensation for hypovolaemia
is poor in the elderly.
Cement reactions:
➢ At the time of cementing, a drop in blood pressure and oxygen saturation
is often seen.
➢ Originally thought to be caused by a directly toxic effect of the methyl
methacrylate monomer component of the cement, but now known to be
caused by a shower of microemboli of blood, fat or platelets forced into
circulation by high intramedullary pressure during cement packing and
prosthesis insertion.
➢Subsequent embolisation to the lungs produces a raised
pulmonary vascular resistance and reduction in left ventricular
return, resulting in hypotension.
➢Microemboli are toxic to the lung parenchyma, causing
haemorrhage, alveolar collapse and hypoxia.
➢May be severe enough to cause cardiovascular collapse,
cardiac arrest and death.
➢Reactions are more common and more severe in bilateral joint
replacements
➢Therefore check vitals to ensure that the patient is not
hypovolaemic before cementing.
Fat Embolism Syndrome
➢ Well-known complication of instrumentation of medullary canal.
➢ Physiologic response to fat within systemic circulation.
➢ Clinical manifestations of FES include respiratory, neurologic, hematologic,
and cutaneous signs and symptoms.
➢ Presentation of FES can be gradual, developing over 12 to 72 hours, or
fulminant leading to ARDS and cardiac arrest.
➢ Gurd and Wilson in 1974 suggested major and minor criteria to be used
for the diagnosis of FES.
➢ Presence of any 1 major + 4 minor criteria and evidence of fat
macroglobulinemia was required for diagnosis of FES.
➢ More recent investigations have indicated that quantity of fat in
circulation does not correlate with the severity of FES or development of
ARDS
Gurd's Diagnosis of Fat Embolism
Syndrome
• Major Features (at least one)
➢ Respiratory insufficiency
➢ Cerebral involvement
➢ Petechial rash
• Minor Features (at least 4)
➢ Pyrexia
➢ Tachycardia
➢ Retinal changes
➢ Jaundice
➢ Renal changes Laboratory Features
➢ Fat microglobulinemia (required)
➢ Anemia
➢ Thrombocytopenia
➢ High erythrocyte sedimentation rate
Schonfeld Fat Embolism Syndrome Index
Sign Score
• Petechial rash 5
•Diffuse alveolar infiltrates 4
Hypoxemia Pao2<70 mm Hg
•Fio2 100%3Confusion 1
• Fever >38°C (>100.4°F) 1
Heart rate >120 beats/min 1
Respiratory rate >30 1
• pts receiving warfarin or LMWH, combined anticoagulant and antiplatelet effects may
increase risk of periop bleeding.