The document discusses anesthesia considerations for orthopedic surgery involving bone cement implantation syndrome (BCIS) and fat embolism syndrome (FES). BCIS is a potentially fatal complication characterized by hypoxia and hypotension occurring during bone cementation. Proper management includes patient risk stratification, intraoperative vigilance, communication and prompt resuscitation. FES presents 12-72 hours after injury with a triad of hypoxemia, neurological abnormalities and petechial rash.
The document discusses anesthesia considerations for orthopedic surgery involving bone cement implantation syndrome (BCIS) and fat embolism syndrome (FES). BCIS is a potentially fatal complication characterized by hypoxia and hypotension occurring during bone cementation. Proper management includes patient risk stratification, intraoperative vigilance, communication and prompt resuscitation. FES presents 12-72 hours after injury with a triad of hypoxemia, neurological abnormalities and petechial rash.
The document discusses anesthesia considerations for orthopedic surgery involving bone cement implantation syndrome (BCIS) and fat embolism syndrome (FES). BCIS is a potentially fatal complication characterized by hypoxia and hypotension occurring during bone cementation. Proper management includes patient risk stratification, intraoperative vigilance, communication and prompt resuscitation. FES presents 12-72 hours after injury with a triad of hypoxemia, neurological abnormalities and petechial rash.
The document discusses anesthesia considerations for orthopedic surgery involving bone cement implantation syndrome (BCIS) and fat embolism syndrome (FES). BCIS is a potentially fatal complication characterized by hypoxia and hypotension occurring during bone cementation. Proper management includes patient risk stratification, intraoperative vigilance, communication and prompt resuscitation. FES presents 12-72 hours after injury with a triad of hypoxemia, neurological abnormalities and petechial rash.
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Anesthesia considerations specific to
orthopedic surgery (BCIS,FES)
Prepared and presented by: Dr Muhammad Adeel Khalid
Bone cement implantation syndrome
INTRODUCTION: BCIS is a potentially fatal complication of orthopedic surgery, involving pressurized bone cement. characterized by hypoxia and hypotension (with potential loss of consciousness), occurring around the time of bone cementation. the incidence of a severe reaction may result in cardiovascular collapse. 20% of cemented hemiarthroplasties have BCIS, with around 1% of these resulting in cardiovascular collapse requiring CPR. What is bone cement
It is a radio-opaque compound composed of polymethyl methacrylate) (90%) and
a small quantity of radio-opaque crystals Polymethylmethacrylate (PMMA) is a sterile acrylic polymer usually supplied as two component systems made up of a fine powder and a liquid. These two components are mixed to start a chemical reaction called polymerization, which forms the polymethylmethacrylate (PMMA) cement. The two components are mixed and the bone cement viscosity changes over time from a runny liquid into a dough like state (2-3 minutes) that can be safely applied (5-8 minutes) and then finally hardens into solid hardened material. Proposed definition of bone cement implantation syndrome: No agreed standard definition. Donaldson and colleagues* have proposed a standard definition of BCIS: “BCIS is characterized by hypoxia, hypotension or both and/or unexpected loss of consciousness occurring around the time of cementation, prosthesis insertion, reduction of the joint or, occasionally, limb tourniquet deflation in a patient undergoing cemented bone surgery.” Clinical features:
It results in reduced arterial oxygenation, characterized by a combination of
clinical features: • Hypoxia • Sudden loss of arterial pressure • Pulmonary hypertension • Arrhythmias • Loss of consciousness • Cardiac arrest Classification and incidence: Classification is based on the degree of hypoxia, hypotension and conscious level, as per Donaldson.
BCIS Grade Hypoxia Hypotension Loss of Incidence
Consciousn ess Grade 1 Moderate: Moderate: Decrease in SBP ≥ None 21% SpO2 20% <94% Grade 2 Severe: Severe: Decrease in SBP ≥ 40% Unexpected 5.1% SpO2 loss of <88% consciousne ss Grade 3 Cardiovascular collapse 1.7% requiring CPR Risk factors for the development of BCIS:
Patient factors: Surgical factors:
ASA III–IV Pathological fracture
Pre-existing pulmonary hypertension Intertrochanteric fracture Significant cardiac disease Long-stem arthroplasty Osteoporosis Male sex Increasing age The causes of BCIS:
There is no proven cause of BCIS but several theories exist. The most commonly accepted cause is the embolic model. Embolic model: During surgical cementation and prosthesis insertion, the cement is intentionally pressurized to force into the small gaps/spaces of the bone, improving bonding between the cement and bone. cement then expands in the space between the bone and the prosthesis, further pressurizing air and the bone contents into the circulation. These debris may reach the lungs, heart or coronary circulation. pulmonary emboli are the cause of the characteristic hypoxia and right ventricular dysfunction leading to hypotension. Other causes:
The direct effect of the exothermic reaction of cement temperature
Air or gas embolism caused by polymerisation of methyl methacrylate monomer. Hypersensitivity/anaphylactic reaction to the monomer. The effect of anesthetic technique on the severity of BCIS: The general principles of management include the maintenance of normovolaemia to avoid the cardiovascular consequences of cementing and the maintenance of high inspired concentrations of oxygen. use of high anesthetic vapor concentrations should be avoided as it is associated with greater hemodynamic compromise. The use of intraop CO monitoring has been recommended in patients with one or more risk factors for BCIS. It can be in the form of semi-invasive transoesophageal Doppler monitor or invasive CO monitor like PA catheter. Role of surgery in prevention of bone cement- associated complications Surgical measures that can reduce the incidence of complications associated with bone cement, especially BCIS, include: • thorough lavage of the femoral canal to remove debris. • Brushing and drying of the intramedullary canal of the femoral shaft before cementation • Use of a suction catheter to depressurize the intramedullary canal • Utilizing a bone-vacuum technique (mixing cement in a vacuum and using a retrograde cement introduction) • the use of non-cemented prostheses in high risk patients. Key intraoperative roles for managing potential BCIS Anesthetic team Surgical team Ensure adequate hemodynamic optimisation pre- and intra- Inform the anaesthetist prior to cement application operatively Aim for a SBP within 20% of pre-induction value Wash and dry the femoral canal Prepare vasopressors in case of cardiovascular collapse Apply cement retrograde, utilising a suction catheter and intramedullary plug in the femoral shaft
Confirm awareness that cement is about to be prepared/applied Avoid excessive pressurisation
Maintain vigilance for cardiorespiratory compromise
Cement Curfew:
A ‘Cement Curfew’ protocol has been adopted at some institutions, which
involves all members of the operating theatre team assuming specific roles and focus around the time of prosthesis insertion. important steps during the process are formally verbalized by the lead surgeon including the start and end of the curfew. The management of BCIS
BCIS is a reversible time-limited phenomenon recovery time ranges from few
seconds to 24 hours. The patient’s chance of survival is increased if immediate recognized and supportive measures are rapidly initiated. aggressive resuscitation and supportive treatment is essential to reduce the morbidity and mortality of this life-threatening situation. A fall in end tidal carbon dioxide concentration may be the first indication of BCIS in the anaesthetized patient and should alert the anesthetist. Early signs of BCIS in an awake patient undergoing regional anesthesia include dyspnea and ALOC The management of BCIS
Grade 1 BCIS can be treated with increased increasing the oxygen to 100%, fluids and vasopressors if needed. In cases of severe BCIS (when the patient has arrested, or in a peri-arrest condition), standard (ACLS) algorithms and procedures should be followed. Fluid resuscitation to maintain right ventricle preload, and inotropes to support ventricular contractility are recommended. Vasopressors (such as phenylephrine and noradrenaline) can be used as they primarily cause peripheral vasoconstriction, increase aortic blood pressure, which in turn supports coronary artery blood flow, and thus improve myocardial perfusion and contractility. Use of vasopressors and inotropes should be continued into the postoperative period as necessary, under the management of the intensive care unit (ICU). The AAGBI guideline recommendations Delivery of 100% oxygen Fluid resuscitation (guided by CVP measurement) Vasoactive ⁄ inotropic support
SUMMARY: • BCIS is a potentially fatal complication of orthopaedic surgery. • Pulmonary embolisation from intramedullary contents is the likely aetiology of BCIS. • Rapid hypoxia, hypotension and loss of consciousness are the key signs. • Good management of BCIS includes: patient risk stratification, intraoperative vigilance, good team communication, and prompt resuscitation. FAT EMBOLISM SYNDROME: Clinical manifestations: FES typically presents 12 to 72 hours after the initial insult. The classic triad of FES includes hypoxemia, neurological abnormalities, and petechial rash. Pulmonary manifestations are the most common initial signs of FES which include dyspnea, tachypnea, hypoxemia, and respiratory failure. Neurological defects typically manifest after the respiratory changes and include focal deficits, confusion, lethargy, restlessness, coma. The petechial rash is classically located in nondependent regions (conjunctivae, head, neck, anterior thorax, or axillae). Other nonspecific findings: Systemic Fever Cardiovascular Tachycardia Hypotension Intraoperative arrhythmias Myocardial ischemia Pulmonary hypertension (PH) Right-sided heart failure Ophthalmic Purtscher’s retinopathy (cotton wool exudates, macular edema and hemorrhage)
Two theories have been proposed regarding the causes of FES 1. Mechanical theory 2. Biochemical theory Mechanical theory:
Obstruction of vessels and capillaries
• Increase in intramedullary pressure forces fat and marrow into bloodstream • Bone marrow contents enter the venous system and lodge in the lungs as emboli • Smaller fat droplets may travel through the pulmonary capillaries into the systemic circulation. • Embolization to cerebral vessels or renal vessels also leads to central nervous system and renal dysfunction Biochemical theory:
Toxicity of free fatty acids
• circulating free fatty acids directly affect the pneumocytes, producing abnormalities in gas exchange • Coexisting shock, hypovolemia and sepsis impair liver function and augment toxic effects of free fatty acids Diagnosis:
Differential diagnosis include pulmonary or cement emboli, vasculitic disorders,
bacterial pneumonia, sepsis, and ARDS. FES is a clinical diagnosis. Two classification schemes may be used for diagnosis. 1. Gurd’s criteria 2. Schonfeld FES Index Gurd’s criteria: Schonfeld FES Index: Laboratory Studies:
Hematological Tests: Anemia, thrombocytopenia, high ESR. Biochemical tests: LFTs, Renal profile, Serum electrolytes Urine and sputum examination: may detect fat globules(non specific) Diagnostic Imaging: Imaging can help to confirm fat embolism or rule out alternative diagnosis. Chest CT is superior for diagnosing pulmonary fat emboli and may show ground-glass appearance. Chest x-ray may show diffuse bilateral pulmonary infiltrates. Brain MRI( preferred imaging modality)should be considered in patients with neurologic symptoms. Diffusion-weighted MRI can reveal a classic “star field” pattern of fat micro embolism within one hour of symptoms onset. Several hours later, foci of vasogenic edema in an embolic distribution can be seen on T2-weighted MRI. CT head is usually normal but could show diffuse white-matter petechial hemorrhages. Trans esophageal or transthoracic echocardiogram may show fat emboli as dense echogenic material. Management:
Respiratory support: intubation/ventilation, indications for respiratory support:
• Sustained SaO2 <90% and PaO2 <8 kPa on oxygen • Respiratory rate of >35 breaths/min Hemodynamic support: • Maintain a systolic blood pressure > 90 mmHg • Avoid hypovolemia with fluid resuscitation and vasopressors • Apply invasive monitoring • TEE Early surgical stabilization of fractures Perform operative correction rather than traction alone Limit the intraosseous pressure during an orthopedic procedure Pharmacological treatment:
Corticosteroids may reduce the risk of a fat embolism in patients with long bone fractures of the lower limbs Heparin clears lipemic serum by stimulating lipase activity, thereby reducing pulmonary complications Albumin use is considered potentially therapeutic in its ability to bind free fatty acids THANK YOU .
