PERIOPERATIVE MANAGEMENT CONSIDERATIONS IN ORTHOPEDIC SURGERY
Bone cement, polymethylmethacrylate,
is fre-quently required for joint arthroplasties. The cement interdigitates
within the interstices of cancellous bone and strongly binds the prosthetic
device to the patient’s bone. Mixing polymerized methylmethac-rylate powder
with liquid methylmethacrylate monomer causes polymerization and cross-linking
of the polymer chains. This exothermic reaction leads to hardening of the
cement and expansion against the prosthetic components. The resultant
intramedullary hypertension (>500 mm Hg) can cause embolization of fat, bone marrow, cement, and air
into venous channels. Systemic absorption of residual methylmethacrylate
monomer can produce vasodilation and a decrease in systemic vascular
resistance. The release of tissue thromboplastin may trigger platelet
aggregation, microthrombus forma-tion in the lungs, and cardiovascular
instability as a result of the circulation of vasoactive substances.The
clinical manifestations of bone cement implantation syndrome include hypoxia
(increased pulmonary shunt), hypotension, arrhyth-mias (including heart block
and sinus arrest), pulmo-nary hypertension (increased pulmonary vascular
resistance), and decreased cardiac output. Emboli most frequently occur during
insertion of a femoral prosthesis for hip arthroplasty. Treatment strategies
for this complication include increasing inspired oxygen concentration prior to
cementing, monitor-ing to maintain euvolemia, creating a vent hole in the
distal femur to relieve intramedullary pressure, performing high-pressure
lavage of the femoral shaft to remove debris (potential microemboli), or using
a femoral component that does not require cement.
Another source of concern related to the use of cement is the potential
for gradual loosening of the prosthesis over time. Newer cementless implants
are made of a porous material that allows natural bone to grow into them.
Cementless prostheses generally last longer and may be advantageous for
younger, active patients; however, healthy active bone formation is required
and recovery may be longer compared to cemented joint replacements. Therefore,
cemented prostheses are preferred for older (>80 years) and less active patients
who often have osteoporosis or thin cortical bone. Practices continue to evolve
regarding selection of cemented versus cementless implants, depending on the
joint affected, patient, and surgical technique.
Use of a pneumatic tourniquet on an extremity
creates a bloodless field that greatly facilitatessurgery. However, tourniquets
can produce poten-tial problems of their own, including hemodynamic changes,
pain, metabolic alterations, arterial throm-boembolism, and pulmonary embolism.
Inflation pressure is usually set approximately 100 mm Hg higher than the
patient’s baseline systolic blood pressure. Prolonged inflation (>2 h) routinely leads to
transient muscle dysfunction from ischemia and may produce rhabdomyolysis or
permanent periph-eral nerve damage. Tourniquet inflation has also been
associated with increases in body temperature in pediatric patients undergoing
lower extremity surgery.
Exsanguination of a lower extremity and tour-niquet inflation cause a
rapid shift of blood volume into the central circulation. Although not usually
clinically important, bilateral lower extremity exsan-guination can cause an
increase in central venous pressure and arterial blood pressure that may not be
well tolerated in patients with noncompliant ven-tricles and diastolic
dysfunction.
Awake patients predictably experience tour-niquet pain with inflation
pressures of 100 mm Hg above systolic blood pressure for more than a few
minutes. The mechanism and neural pathways for this severe aching and burning
sensation defy precise explanation. Tourniquet
pain gradually becomes so severe over time that patients may require
substantial supplemental analgesia, if not general anesthesia, despite a
regional block that is adequate for surgical anesthesia. Even during general
anesthesia, stimulus from tourniquet com-pression often manifests as a
gradually increasing mean arterial blood pressure beginning approxi-mately 1 h
after cuff inflation. Signs of progressive sympathetic activation include
marked hyperten-sion, tachycardia, and diaphoresis. The likelihood of
tourniquet pain and its accompanying hypertension may be influenced by many
factors, including anes-thetic technique (regional anesthesia versus general
anesthesia), extent of dermatomal spread of regional anesthetic block, choice
of local anesthetic and dose (“intensity” of block), and supplementation with
adjuvants either intravenously or in combination with local anesthetic
solutions when applicable.
Cuff deflation invariably and immediately relieves tourniquet pain and
associated hyperten-sion. In fact, cuff deflation may be accompanied by a
precipitous decrease in central venous and arterial blood pressure. Heart rate
usually increases and core temperature decreases. Washout of accumulated
metabolic wastes in the ischemic extremity increases partial pressure of carbon dioxide in arterial blood (Paco2), end-tidal carbon dioxide
(Etco2), and serum lactate and potassium levels. These meta-bolic alterations
can cause an increase in minute ventilation in the spontaneously breathing
patient and, rarely, arrhythmias. Tourniquet-induced isch-emia of a lower
extremity may lead to the develop-ment of deep venous thrombosis.
Transesophageal echocardiography can detect subclinical pulmonary embolism
(miliary emboli in the right atrium and ventricle) following tourniquet
deflation even in minor cases such as diagnostic knee arthroscopy. Rare
episodes of massive pulmonary embolism dur-ing total knee arthroplasty have
been reported dur-ing leg exsanguination, after tourniquet inflation, and
following tourniquet deflation. Tourniquetshave been safely used in patients
with sickle cell dis-ease, although particular attention should be paid to
maintaining oxygenation, normocarbia or hypocar-bia, hydration, and
normothermia.
Some degree of fat embolism probably occurs
with all long-bone fractures. Fat embolism syndrome is less frequent but
potentially fatal (10–20% mortality).It classically presents
within 72 h following long-bone or pelvic fracture, with the triad ofdyspnea, confusion, and petechiae. This syndrome can also be seen
following cardiopulmonary resusci-tation, parental feeding with lipid infusion,
and lipo-suction. The most popular theory for its pathogenesis holds that fat
globules are released by the disruption of fat cells in the fractured bone and
enter the circu-lation through tears in medullary vessels. An alter-native theory
proposes that the fat globules are chylomicrons resulting from the aggregation
of cir-culating free fatty acids caused by changes in fatty acid metabolism.
Regardless of their source, the increased free fatty acid levels can have a
toxic effect on the capillary–alveolar membrane leading to the release of
vasoactive amines and prostaglandins and the development of acute respiratory
distress syn-drome. Neurological mani-festations (eg, agitation, confusion,
stupor, or coma) are the probable result of capillary damage in the cerebral
circulation and cerebral edema. These signs may be exacerbated by hypoxia.
The diagnosis of fat embolism syndrome is
sug-gested by petechiae on the chest, upper extremities, axillae, and
conjunctiva. Fat globules occasionally may be observed in the retina, urine, or
sputum. Coagulation abnormalities such as thrombocyto-penia or prolonged
clotting times are occasion-ally present. Serum lipase activity may be elevated
but does not predict disease severity. Pulmonary involvement typically
progresses from mild hypoxia and a normal chest radiograph to severe hypoxia or
respiratory failure with radiographic findings of dif-fuse pulmonary opacities.
Most of the classic signs and symptoms of fat embolism syndrome occur 1–3 days
after the precipitating event. During general anesthesia, signs may include a
decline in Etco2
and arterial oxygen saturation and a rise in pulmonary artery pressures.
Electrocardiography may show ischemic-appearing ST-segment changes and a
pat-tern of right-sided heart strain.
Management is two-fold: preventative and
sup-portive. Early stabilization of the fracture decreases the incidence of fat embolism syndrome and, in par-ticular,
reduces the risk of pulmonary complications. Supportive treatment consists of
oxygen therapy with continuous positive airway pressure ventila-tion to prevent
hypoxia and with specific ventilator strategies in the event of ARDS. Systemic
hypoten-sion will require appropriate pressor support, and vasodilators may aid
the management of pulmonary hypertension. High-dose corticosteroid therapy is
not supported by randomized clinical trials.
Deep vein thrombosis (DVT) and pulmonary
embolism (PE) can cause morbidity and mortality following orthopedic operations
on the pelvis and lower extremities. Risk factors include obesity, age greater
than 60 years, procedures lasting more than 30 min, use of a tourniquet, lower
extremity fracture, and immobilization for more than 4 days. Patients at
greatest risk include those undergoing hip surgery and knee replacement or
major opera-tions for lower extremity trauma. Such patients will experience DVT
rates of 40–80% without prophy-laxis. The incidence of clinically important PE
fol-lowing hip surgery in some studies is reported to be as high as 20%,
whereas that of fatal PE may be 1–3%. Underlying pathophysiological mechanisms
include venous stasis with hypercoagulable state due to localized and systemic
inflammatory responses to surgery.
Pharmacological prophylaxis and the routine
use of mechanical devices such as intermittent pneu-matic compression (IPC)
have been shown to decrease the incidence of DVT and PE. While mechanical
thromboprophylaxis should be consid-ered for every patient, the use of
pharmacological anticoagulants must be balanced against the risk of major
bleeding. For patients at increased risk for DVT but having “normal” bleeding
risk, low-dose subcutaneous unfractionated heparin (LUFH), war-farin, or
low-molecular-weight heparin (LMWH) may be employed in addition to mechanical
prophy-laxis. Patients at significantly increased risk of bleed-ing may be
managed with mechanical prophylaxis alone until bleeding risk decreases. In
general, anti-coagulants are started the day of surgery in patients without
indwelling epidural catheters. Warfarin may be started the night before surgery
depending on the particular orthopedic surgeon’s routine.Neuraxial
anesthesia alone or combined with general anesthesia may reduce
thromboembolic complications by several mechanisms. These include
sympathectomy-induced increases in lower extremity venous blood flow, systemic
antiinflam-matory effects of local anesthetics, decreased plate-let reactivity,
attenuated postoperative increases in factor VIII and von Willebrand factor,
attenuated postoperative decreases in antithrombin III, and alterations in
stress hormone release.
According to the Third Edition of the
American Society of Regional Anesthesia and Pain Medicine Evidence-Based
Guidelines on regional anesthesia and anticoagulation, patients currently
receiving antiplatelet agents (eg, ticlopidine, clopidogrel, and intravenous
glycoprotein IIb/IIIa inhibitors), throm-bolytics, fondaparinux, direct
thrombin inhibitors, or therapeutic regimens of LMWH present an unac-ceptable
risk for spinal or epidural hematoma fol-lowing neuraxial anesthesia.
Performance of neuraxial block (or removal of a neuraxial catheter) is not
contraindicated withsubcutaneous LUFH when the total daily dose is 10,000 units
or less; there are no data on the safety of neuraxial anesthesia Neuraxial
anesthesia alone or combined with general anesthesia may reduce thromboem-vary
based on regimen. With once-daily dosing, neuraxial techniques may be performed
(or neurax-ial catheters removed) 10–12 h after the previous dose, with a 4-h
delay before administering the next dose. With twice-daily dosing, neuraxial
catheters should not be left in situ and should be removed 2 h before the first
dose of LMWH. Patients on warfarin therapy should not receive a neuraxial block
unless the international normalized ratio (INR) is normal, and catheters should
be removed when the INR is 1.5 or lower. The Third Edition of the guidelines
alsosuggests that these recommendations be applied to deep peripheral nerve
and plexus blocks and cathe-ters (see Suggested Reading). Revisions to these
guidelines occur regularly.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2024 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.