FAT EMBOLI IN LIPOSUCTION

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1 FAT EMBOLI FAT EMBOLI SYNDROME SYNDROME IN LIPOSUCTION IN LIPOSUCTION Magda Hutagalung

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FAT EMBOLI IN LIPOSUCTION

Transcript of FAT EMBOLI IN LIPOSUCTION

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FAT EMBOLI FAT EMBOLI SYNDROMESYNDROME FAT EMBOLI FAT EMBOLI SYNDROMESYNDROME

IN LIPOSUCTIONIN LIPOSUCTION

Magda Hutagalung

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REFERENCES

Grazer FM. Abdominoplasty. In McCarthy JG, editor. McCarthy Plastic Surgery Gordon JB. Liposuction, trunk

Available from: http://www.emedicine.com/; March 2006Kirkland L. Fat Embolism

Available from: http://www.emedicine.com/; August 2005Laub DR. Fat embolism and fat embolism syndrome. In Hetter GP, editor. Lipoplasty 2nd ed. Moser KM. Pulmonary Thromboembolism. In Braunwald E, editor. Harrison’s Principle of Internal Medicine 11th ed. Pitman GH. Liposuction and body contouring. In Aston SJ, editor. Grabb and Smith’s Plastic Surgery 5th ed. Vistnes MD. Liposuction, large volume: safety and indications

Available from: http://www.emedicine.com/; March 2006

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DEFINITION

Clinical entity characterized by sudden cardiopulmonary & neurological deterioration following precipitating event, usually bone fracture/other trauma to marrow (Laub,1990) fat material, through the circulation obstructs blood flow via a smaller calibre vessel (for ex. stroke, pulmonary embolism, central retinal artery occlusion).

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CAUSES

Blunt trauma (90%)

Acute pancreatitis

Diabetes mellitus

Burns

Joint reconstruction

Cardiopulmonary bypass

Parenteral lipid infusion

Sickle cell crisis

Liposuction

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MORBIDITY/MORTALITY IN LIPOSUCTION/ABDOMINOPLASTY

Grazer & Goldwyn (1977):

- 1 in 100 px serious thromboembolic episode

- 1 in 1000 px die

Patients with increased age, multiple underlying medical problems, and/or decreased physiologic reserves have worse outcomes than other patients.

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Grazer (2000): surveyed 1200 actively practicing aesthetic plastic surgeons in USA, 917 reported from 1994-1997, after 496,245 lipoplasties 95 fatalities mortality rate of 1/5224 ~ < 0.5%. (similar to rates quoted elsewhere.)

Pulmonary thromboembolism major cause of death in 23.4±2.6% of these deaths.

Mortality rate of fat emboli generally= 10-20%. (Kirkland 2005)

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PATHOPHYSIOLOGY

Figure 1:

(McCarthy)

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I. Mechanical theory:

Large fat droplets venous system deposited in pulmonary capillary beds arteriovenous shunts brain local ischemia & inflammation + release of inflammatory mediators, platelet aggregation & vasoactive amines (Kirkland, 2005).

II. Biochemical theory:

Trauma &/or sepsis hormonal changes systemic release of FFA as chylomicrons coalesce due to acute-phase reactants, such as CRP reactions above

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DIAGNOSISGurd:

Major Respiratory insufficiency Cerebral involvement Petechial rash Minor Pyrexia Renal changes Tachycardia Jaundice Retinal changes

+ 1 major + 4 minor + fat macroglobulinemia

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Lindeque et al:

Sustained PaO2 < 60 mmHg

Sustained PaCO2 > 55 mmHg or pH < 7.3

Sustained RR > 35 X/mnt, after sedation

Dyspnea, tachycardia & anxiety

+ Clinical history + 1 of above criteria

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Clinical Respiratory consequences: Embolic obstruction

cessation of pulmonary capillary blood flow bronchoalveolar hypocapnia ventilated but not perfused lung zoneintrapulmonary deadspace pneumoconstriction: homeostatic mechanism to

↓ wasted ventilation

Loss of alveolar surfactant within 2 – 3 hrs atelectasis within 24 – 48 hrs

Tachypnea, dyspnea & hypoxia within 12-72 hrs.

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Hemodynamic consequences: Obstruction pulmonary arterial bed area ↓ resistance to pulmonary blood flow ↑ pulmonary hypertension R ventricle failure cardiac output ↑

Early persistent tachycardia at onset.

AbN heart sounds

Fever with high-spiking temperatures.

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Dermatologic– Reddish-brown nonpalpable petechiae:upper body esp. in axillae; within 24-36 hours; in 20-50%; resolve quickly.– Subconjunctival & oral hemorrhages & petechiae

Neurologic:– CNS dysfunction: initially as delirium stupor, seizures, or coma; frequently is unresponsive to correction of hypoxia.– Retinal hemorrhages with intra-arterial fat globules on funduscopic examination

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Lab Studies

BGA: An otherwise unexplained in pulmonary shunt fraction alveolar-to-arterial O2 tension difference, esp within 24-48 hrs.

Thrombocytopenia, anemia & hypofibrinogenemia, yet nonspecific.

Urinary fat stains, not specific enough. Fat globules in urine : common after trauma. Preliminary studies of cytology of pulmonary

capillary blood from wedged pulmonary a. catheter fat globules in px with FES (may be beneficial in early detection)

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Chest X-rays: diffuse bilat interstitial/alveolar infiltrates (Snow storm pattern) within 24-48 hours of onset.

Noncontrast head CT: may be N / reveal diffuse white-matter petechial hemorrhages ~ microvascular injury.

Helical chest CT: may be N / parenchymal changes ~ lung contusion, ALI/ ARDS.

Imaging studies

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Nuclear medicine ventilation/perfusion imaging of the lungs: may be N / show subsegmental perfusion defects.

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MRI: in 1 small study, multiple, nonconfluent, hyperintense lesions.

Transcranial Doppler sonography: In small study, 5 px with trauma monitored with intracranial Doppler sonography, 2 during intraop nailing of long bone fractures Cerebral microembolic signals detected up to 4 days after injury.

Transesophageal echocardiography (TEE): evaluates intraop release of marrow contents into the bloodstream during intramedullary nailing. Density of echogenic material passing via R side of heart ~ degree of ↓ in SaO2.

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DIFFERENTIAL DIAGNOSIS

Hypervolemia

Pulmonary contusion

Cardiogenic pulmonary edema

Aspiration pneumonia

ARDS due to hypovolemic shock

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PREVENTION 5 Pillars of safety in liposuction

1)Surgeon: properly trained & knowledgeable in liposuction technique

2)Anesthesiologist: well trained & have complete understanding of physiology ~ with infusion & removal of large fluids volumes.

3) Facility: completely equipped

4) Support staff: thoroughly trained.

5) Patient: selected appropriately for procedure.

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Patient Selection

In either American Society of Anesthesiologists (ASA) class I (healthy with no medical problems) or ASA class II (medical problems well controlled on medications).

Weight: stable or decreasing with diet & exercise. Px with rapid or persistent weight gain are started on a program of exercise & nutrition.

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Evarts et al (1976), Peltier (1971), Grazer (1990): 5% Dex & 5% alcohol (total 50 gr alcohol), IV, in 30 min – 3 hrs, at start of abdominoplasty 80 mg/100cc blood level

Alcohol: - Prevents breakdown of released fat FFA - Stimulates tissue plasminogen activator & prostacyclin : @ antiplatelet activity, @ antithromboembolic activity, @ vasodilator

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Corticosteroids: – Several studies varying results, usually

with methylprednisolone, in patients identified at high risk

– Optimal timing, duration & dose: undetermined.

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Anesthetic and Fluid ManagementAnesthetic and Fluid Management

General endotracheal anesthesia for large vol liposuction. Intraop monitoring: blood pressure, ECG, pulse oximetry, temperature, end-tidal CO2, urine output, fluid balance. Continuous communication between surgeon & anesthesiologist provided with running balance of wetting solution infused, fat & saline aspirated, blood loss & urine output.

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Fluid balance uses residual vol theory. Residual vol: Total fluids received (IV fluid + crystalloid wetting sol)

– [saline portion of aspirate (without fat) + urine output]. residual crystalloid vol remaining in px as fluid resuscitation source in postop period (Vistnes MD,2006)

Divide this no by preop weight in kg value in cm3/ kg. This no usually is 90-120 mL/kg no signs of intravascular vol depletion or overload.

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IV fluid usually unnecessary because large vol of sc. inj gradually absorbed Subcutaneous crystalloid inj vol = 2 X aspirate vol Total fluid replacement Total/near-total fluid replenishment (Grabb).

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Surgical Technique

4 techniques: Dry

No fluid injected into subcutaneous fat layer. ± 25-45% of aspirated vol is blood. not used commonly except for small vol suctions.

Wet (Illouz, 1980s) Infusion of 100-300 cm3 of saline into each site of fat to be removed . aspirated blood vol ↓ to 20-25% of total aspirate. Addition of 1:200,000 or 1:400,000 epinephrine to fluid (Hettler,1983) < 15% of aspirate was blood.

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Superwet (late 1980s):

infusion of fluid containing epinephrine & low dose

local anesthetic in 1:1 ratio to vol of expected aspirate.

Blood loss was ± 2% of aspirated vol.

Tumescent (Klein, 1990)

Large vol of saline + 1:1,000,000 epinephrine + 0.05%

lidocaine injected sc. to tense tissues.

injected fluid vol > that expected to be suctioned.

Blood loss ± 1% of aspirated volume.

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Post operative care

• Close monitoring: pulse oximetry, hemodynamics, pulmonary function & fluid vol status + control of postop pain & nausea.

Ambulation as soon as possible & lower extremity muscle-contracting exercises while in bed to ↓ risk of deep venous thrombosis & pulmonary embolus.

Compressive postoperative garment ↓ fluid sequestration into tissues, as access incisions are closed to prevent wound drainage.

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THERAPY

Supportive respiratory care

Supportive medical care

Methylprednisolone

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PROGNOSIS

Mild to coma & deathHas improved in 30 yrs, from 15 – 20% mortality rare today due to improved supportive tx

Depends on px’s respiratory function > severe in px with pulmonary disease or shock

As in ARDS, pulmonary sequelae usually resolve almost completely within 1 yr.

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Neurological changes: almost always reversible in days or weeks

Residual neurologic deficits: nonexistent subtle personality changes memory & cognitive dysfunction long-term focal deficits.

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CONCLUSION

Incidence of subclinical fat embolization post liposuction unknown

Common to clinical fat emboli syndrome:

inadequate blood & fluid replacement, pulmonary pathology, obesity, systemic illness

Appropriate px selection, limited resection size, aggressive postop blood, fluid & lung management greatly ↓ incidence

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