Mod10: Bone Cement - Fat Embolism Syndrome - Venous Air Embolism

Question 1

Orthopedic surgery

Characteristics of Bone Cement:

Answer 1

Frequently used in joint arthroplasties

Used to affix implants and remodel lost bone

Cement interdigitates with the intertices of cancellous bone (spongy inner layer of bone; found at the ends of long bones) and strongly binds prosthetic device with patient’s bone

Mixing polymerized methylmethacrylate powder with liquid methylmethacrylate causes polymerization and cross-linking of the polymer chains

Exothermic reaction occurs and leads to hardening of the cement and expansion against the prosthetic components

Question 2

Orthopedic surgery

Effects of Bone Cement placement:

Answer 2

Exothermic reaction occurs and leads to hardening of the cement and expansion against the prosthetic components

What results is Intramedullary HTN (> 500mmHg)=> this can cause embolization of fat, bone marrow, cement, and air into the venous channels

Question 3

Orthopedic surgery - Bone Cement placement

If residual methylmethacrylate monomer gets absorbed systemically =>

Answer 3

can produce vasodilation and a decrease in SVR

Question 4

_{Orthopedic surgery - Bone Cement placement}

Systemic embolization of bone cement triggers the release of

Answer 4

Tissue thromboplastin

=>

triggers PLT aggregation

microthrombus formation in the lungs, and

CV instability as a result of the circulation of vasoactive substances

Question 5

_{Orthopedic surgery - Bone Cement}

What should you monitor carefully during placment?

Answer 5

Changes in oxygenation, ventilation, and hemodynamics!

Question 6

_{Orthopedic surgery - Bone Cement Syndrome}

Clinical manifestations of bone cement implantation syndrome:

Answer 6

Hypoxia (due to increased pulmonary shunt)

Hypotension (vasodilation)

Arrhythmias (including heart block & sinus arrest)

Pulm HTN (increased PVR)

Decreased CO

Question 7

_{Orthopedic surgery - Bone Cement Syndrome}

Emboli a/w Bone Cement implantation most frequently occur during:

Answer 7

Insertion of a femoral prosthesis for hip arthroplasty

Question 8

_{Orthopedic surgery}

What can the anesthtist do to minimize effects of Bone Cement Syndrome

Answer 8

Being proactive prior to insertion…..

anticipate…you will know by the fumes released with mixing

Increase FiO2 before cement put in joint

Maintain euvolemia

Question 9

Orthopedic surgery

What the Surgeon do to minimize effects of Bone Cement Syndrome

Answer 9

Create a vent hole in distal femur to relieve intramedullary pressure

Perform high-pressure lavage of femoral shaft to remove debris (and potential microemboli)

Use femoral component that doesn’t require cement

Question 10

_{Orthopedic surgery}

Cement vs Cementless protheses; which last longuer?

Answer 10

Cement can loosen over years,

whereas cementless implants are made of porous material, allowing natural bone to grow into them

Cementless protheses generally last longer

Question 11

_{Orthopedic surgery - Cement vs Cementless protheses}

Difference in lenght of recovery

Answer 11

Cementless protheses are better for younger, active pt’s but longer recovery

Cementless implants require healthy active bone formation and recovery may be longer

Cemented prostheses preferred for those patients who are > 80, less active, have osteoporosis

Question 12

_{Orthopedic surgery}

Joint replacement articular surfaces can be:

Answer 12

Metal, plastic, or ceramic

In many cases cemented and cementless components are used in the same patient (eg, total hip arthroplasty).

Articular surfaces on modern prostheses may be metal, plastic, or ceramic.

Question 13

_{Orthopedic surgery - Fat Embolism}

Some degree of fat embolism probably occurs with which types of fractures?

Answer 13

All Long-bone fractures

Question 14

_{Orthopedic surgery - Fat Embolism}

Incidence and mortality of Fat embolism syndrome

Answer 14

Less frequent (about 3-10% of orthopedic trauma patients)

but has a high mortality rate (10-20%)

Question 15

_{Orthopedic surgery - Fat Embolism syndrome}

Presentation of Fat Embolism syndrome

^when?

Answer 15

Usually within 72 hours of fracture of long-bone or pelvis

Can also occur after CPR

After parenteral nutrition with lipid infusion (TPN/PPN)

after liposuction

Question 16

_{Orthopedic surgery - Fat Embolism syndrome}

Triad of symptoms

Answer 16

Dyspnea - Confusion - Petechiae

Question 17

_{Orthopedic surgery - Fat Embolism syndrome}

Triad of symptoms & Other symptoms

Answer 17

Dyspnea - Confusion - Petechiae

Petechiae on chest, upper extremities, axilla, conjunctiva

Sometimes globules of fat can be seen in retina, urine, sputum

Thrombocytopenia, prolonged clotting times

Serum lipase may be high

Pulmonary presentation usually starts as mild hypoxia

^{=> progresses to severe hypoxia and respiratory failure}

CXR normal at first => can progress to the appearance of diffuse pulmonary opacities

Question 18

_{Orthopedic surgery - Fat Embolism syndrome}

Theories of pathogenesis

Answer 18

Exact mechanism still not known

Fat globules or droplets released by disruption of fat cells in the fx’d bone

=> enter bloodstream thru tears in medullary vessels and can be deposited into pulmonary capillary beds and travel to the brain through AV shunts

Droplets can deposited in the microvasculature and this causes

=> local ischemia and inflammation, and at the same time

=> inflammatory mediators and vasoactive amines are released, and PLT aggregation occurs

Metabolic changes cause normal circulating fat to become free fatty acids

=> These FFAs ultimately aggregate to become fat globules or chylomicrons

=> behave in same way as just mentioned (deposited in pulmonary capillaries)

Regardless of source => increased FFA levels can have toxic effect on capillary-alvelolar membrane leading to the release of vasoactive amines and prostaglandins and the development of ARDS

Question 19

_{Orthopedic surgery - <strong>Fat Embolism syndrome</strong>}

Neurological symptoms:

Answer 19

Agitation - Confusion - Stupor - Coma

These symptoms likely due to capillary damage in cerebral circulation and cerebral edema

Hypoxia exacerbates this

_{Review question on fat embolism syndrome: Connelly page 277}

Question 20

_{Orthopedic surgery - Fat Embolism syndrome}

Neuro sx’s d/t:

Answer 20

Capillary damage to cerebral circulation

Cerebral edema may be exacerbated by hypoxemia

Question 21

_{Orthopedic surgery - Fat Embolism syndrome}

Presentation under GA:

Answer 21

Hypoxia with increased A-a gradient

^{(A-a gradient is difference between alveolar concentration of oxygen and arterial concentration of oxygen => increased A-a gradient means Oxygen is not moving from the Alveoli to the blood)}

Tachycardia

Petechial rash on upper body

Decreased pulmonary compliance

Increased PA pressures

Decreased CO

ECG

^{[ST changes (ischemia)]}

Question 22

_{Fat Embolism Syndrome - Triad of presenting symptoms}

Petechiae

Answer 22

Petechiae on chest, upper extremities, axilla, conjunctiva

Question 23

_{Fat Embolism Syndrome - Triad of presenting symptoms}

Sometimes globules of fat can be seen in

Answer 23

Retina - Urine - Sputum

Question 24

_{Orthopedic surgery - Fat Embolism syndrome}

Diagnosis:

Answer 24

Gurd Diagnostic Criteria

Schonfeld Fat Embolism Index

Question 25

_{Orthopedic surgery - Diagnosis of Fat Embolism syndrome} ## Footnote **Gurd Diagnostic Criteria:**

Answer 25

_**1 majo**r_ + **_4 minor_** + **_fat microglobulinemia_** ^{(Petechial rash not seen on all patients with fat embolism)} **_Major_**: respiratory insufficiency, cerebral impairment, petechial rash ***_Minor_:*** Tachycardia - Fever - Jaundice - Retinal changes - Renal alterations **_Labs_:** **Fat microglobulinemia** ^{[required for diagnosis]} **Thrombocytopenia** **Elevated ESR (erythrocyte sedimentation rate)** ^{[The rate at which RBCs sediment in one hour time period => Increases any time there is inflammation]} Anemia

Question 26

_{Orthopedic surgery - Diagnosis of Fat Embolism syndrome} ## Footnote **Schonfeld Fat Embolism Index:**

Answer 26

**5 + points needed** **_Points_:** 5 =\> Petechial rash 4 =\> Diffuse alveolar infiltrates 3 =\> Hypoxemia (PaO2 \< 70 mmHg on 100% O2) 1 =\> confusion, fever, tachycardia, tachypnea

Question 27

_{Orthopedic surgery - Management of Fat Embolism syndrome} How to Decrease incidence of fat embolism syndrome?

Answer 27

**Stabilizing the fracture early** Reduces risk of pulmonary complications

Question 28

_{Orthopedic surgery - Management of Fat Embolism syndrome} ## Footnote **Supportive treatments:**

Answer 28

**Oxygenation** and ventilation ^{Avoid barotrauma - Minimize hypoxia} **Hemodynamic** support for hypotension ^{Pressors - Volume Possible use of vasodilators if pulmonary HTN present} No current evidence to support the use of **steroids**

Question 29

_{Orthopedic surgery} Sub atmospheric pressure within open vein:

Answer 29

**Venous Air Embolism (VAE)**

Question 30

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **VAE can occur when:**

Answer 30

The **pressure** within an open **vein** is **below** atmospheric pressure This can happen in any position and during any procedure in which the **incision or surgical site is above the level of the heart** Particularly at risk during **craniotomies** and other **neurosurgical** procedures

Question 31

_{Orthopedic surgery - Venous Air Embolism (VAE)} Incidence of VAE during neurosurgical procedures:

Answer 31

Sitting (25%) Supine (18%) Prone (10%) Lateral (8%) *_(Barash)*

Question 32

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Presenting signs of VAE:**

Answer 32

Unexplained **hypotension** Increased End tidal nitrogen concentration (but this is rarely available) Very rapid **decrease in EtCO2** So remember =\> hypotension + decreased EtCO2 Decreased EtCO2 is reflection of **dead space** – continued ventilation of alveoli no longer being perfused – vascular supply is obstructed by air bubbles *_(Barash)*

Question 33

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Pathogenesis of VAE:**

Answer 33

Air enters pulmonary circulation =\> gets trapped in small vessels =\> causes acute increase in dead space (ventilated but not perfused) Large VAE =\> can get trapped in RV and cause complete RV failure Microvascular bubbles may cause a reflex bronchoconstriction and activate release of endothelial mediators =\> leads to pulmonary edema Death usually caused by CV collapse and arterial hypoxemia

Question 34

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Paradoxical air embolism:**

Answer 34

Air travels to coronary and cerebral circulations via PFO PFO present in 20-30% of adults Can result in MI or CVA Even in the absence of PFO =\> transpulmonary passage of venous air is possible

Question 35

_{Orthopedic surgery - Venous Air Embolism (VAE)} **Two prerequisites** that initiate VAE Pathogenesis:

Answer 35

**Direct communication** between source of air and vasculature **Pressure gradient** favoring passage of air - pressure within an open vein is below atmospheric pressure

Question 36

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Other conditions a/w VAE:**

Answer 36

CV catheterization Penetrating or blunt chest trauma High-pressure mechanical ventilation Thoracentesis Hemodialysis

Question 37

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Manifestations of VAE:**

Answer 37

Chest pain (awake) Coughing (awake) Sudden attempt to initiate breath (mech. vent.) ^{[If mechanically ventilated => patient may suddenly attempt to initiate breaths/gasp for air – may be first indication]} Hypotension and decreased EtCO2 ↓SpO2 Increased PAP

Question 38

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Late signs of VAE:**

Answer 38

Hypotension Tachycardia Cardiac dysrhythmias Cyanosis “Mill wheel” murmur ^{(with precordial stethoscope)}

Question 39

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Monitors for detection:**

Answer 39

**TEE** ^{Visual representation of air} **Precordial doppler stethoscope** ^{Mill wheel murmur} **Capnography** ^{↓ ETCO2} **Mass spectrometry** ^{Detects ETN2 (↑ in VAE)} **Pulmonary artery catheter** ^{↑ PAP}

Question 40

_{Orthopedic surgery - Venous Air Embolism (VAE)} Which monitor is most sensitive for detecting VAE? A.Capnography B.Mass Spectrometry C.Precordial doppler D.Pulmonary artery catheter E.TEE

Answer 40

A.Capnography (4) B.Mass Spectrometry (5) C.Precordial doppler (2) D.Pulmonary artery catheter (3) **E.TEE (1)** **^{TEE most sensitive (out of these) – can detect 0.25 mL of air}** Many cases are subclinical – actual incidence is unknown Physiological consequences directly related to volume and rate of air entry Based on case studies 200-300 mL (3-5 mL/kg) air needed for lethal dose human (some animal studies on rabbits and dogs) The ***closer the vein of entrainment to the heart***, the **smaller the dose necessary to harm the patient**

Question 41

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote **Management of intra-op VAE:**

Answer 41

**Notify surgeon** ^{Flood/pack surgical field - Wax bone edges Notify surgeon so he/she can irrigate operative site with fluid as well as apply occlusive material to all bone edges so that sites of venous air entry are occluded} **Compress neck veins** ^{Slow further air entrainment Gentle IJ vein compression (increases cranial venous pressure => may slow air entrainment and cause back bleeding, which might help surgeon identify the entry point of the embolus)} **Change position** ^{Place patient in left lateral, head down position Surgical site below level heart - Left lateral decubitus with head down Dislodge air lock/trap air in R atrium} **Fi02 100%** ^{If N2O => D/C => place patient on 100% FiO2 (and remember nitrous can increase size of air bubble)} **Aspirate CV catheter** ^{If CV catheter present => aspirate it – attempt to retrieve entrained air} **Pressors and volume** ^{Give pressors and volume as needed} CPR if needed **PEEP?** ^{Some clinicians advocate for the use of PEEP to decrease entrainment of air (by increase CVP), BUT the efficacy of this has not been confirmed AND reversal of the normal pressure across the atria may lead to a paradoxical air embolus}

Question 42

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote You are providing a general anesthetic. You are using N2O, 50% in O2, and sevoflurane. Suddenly, air is heard on the precordial Doppler ultrasound. Other observations consistent with venous air embolism include: A.Decreased PaO2 B.Increased end-tidal nitrogen C.Decreased arterial BP D.Decreased end-tidal CO2 E.All of the above

Answer 42

A.Decreased PaO2 B.Increased end-tidal nitrogen C.Decreased arterial BP D.Decreased end-tidal CO2 **E.All of the above**

Question 43

_{Orthopedic surgery - Venous Air Embolism (VAE)} ## Footnote Which of the following statements regarding venous air embolism is TRUE? A.The sitting position carries little risk of VAE B.A multi-orifice catheter placed in the SVC is optimal C.The presence of a patent formen ovale (PFO) increases the risk of paradoxical emboli D.Precordial Doppler has not been shown to help detect VAE E.Patient position should not be changed when treating VAE

Answer 43

A.The sitting position carries little risk of VAE ^{Sitting carries the greatest risk for VAE.} B.A multi-orifice catheter placed in the SVC is optimal ^{A mutli-orifice catheter should be placed in the right atrium to evacuate air} **C.The presence of a patent formen ovale (PFO) increases the risk of paradoxical emboli** D.Precordial Doppler has not been shown to help detect VAE ^{A doppler device should be placed on the chest, EtCO2 should monitored, and plans should be made for treating VAE if it occurs} E.Patient position should not be changed when treating VAE ^{Patient should be placed in left lateral decubitus position with head down}