Acute Respiratory Distress Following Liposuction

Written By: Sam Savage

Published Date: June 28, 2007 Last Edited: June 28, 2007

By Wessman, Dylan E Kim, Thu-Thuy T; Parrish, John S

An active duty male presented to the emergency room with dyspnea for 2 days after undergoing liposuction surgery. Upon presentation, the patient was afebrile, tachycardie, tachypneic, and hypoxemic. The initial chest radiograph demonstrated bilateral patchy opacities and the PaO^sub 2^/FiO^sub 2^ ratio was

A 31-year-old African-American male with no major medical problems except sickle cell trait presented to the emergency room (ER) with shortness of breath for 2 days’ duration after having undergone liposuction surgery. He also complained of a cough productive of clear sputum, but he denied experiencing fevers, chills, diaphoresis, hemoptysis, rash, confusion, sick contacts, or recent travel. He also denied any anginal or pleuritic chest pain.

The patient underwent liposuction for the removal of “love handles.” The procedure was performed at an outpatient surgical center, lasted several hours, and involved the use of general anesthesia, but the perioperative records were not available. The patient’s dyspnea began immediately after the surgery. He reported wearing compression stockings perioperatively and postoperatively, but denied being treated with any anticoagulants such as heparin or enoxaparin.

The patient was discharged to his home on the day of surgery without any specific treatment for his dyspnea. On postoperative day 1, he returned to the surgical center where he was seen by the plastic surgeon, who prescribed prednisone, reportedly for upper airway edema following the recent intubation. Again, the patient was discharged home, but his dyspnea became progressively worse, such that he sought attention in the ER on postoperative day 2.

The patient’s past medical history was notable for sickle cell trait. His surgical history was notable only for the recent liposuction. He had no known drug allergies. His current medications included cephalexin, acetaminophen/hydrocodone, and prochlorperazine, which were prescribed after the surgery. The patient’s family history was notable for a mother with sickle cell disease. He denied cigarette smoking, alcohol consumption, and illicit drug use. The patient served as an enlisted member in the U.S. military.

Upon presentation to the ER, vital signs included: temperature, 99.3[degrees]F; heart rate, 111 beats per minute; blood pressure, 157/73 mm Hg; respiratory rate, 26 breaths per minute; and pulse oximetry, 53% on room air. The patient was well-developed and well- nourished. He was alert and oriented and he appeared to be in mild respiratory distress. The head was normocephalic and atraumatic. His pupils were equal, round, and reactive to light. The sclerae were anicteric and the conjunctivae were pink. The oropharynx was clear and the mucous membranes were moist. The neck was supple without lymphadenopathy. There was no jugular venous distension or hepatojugular reflux.

The lungs were clear to auscultation without stridor, inspiratory crackles, or expiratory wheezes. The apical impulse was nondisplaced and there was no left ventricular lift or right ventricular heave. Auscultation of the heart revealed a rapid rate with a regular rhythm. There was no murmur, rub, or gallop. The peripheral pulses were 2+ and symmetric.

The abdomen was soft, nondistended, and nontender. Four surgical dressings had been placed over the incision sites in the hypogastrium, suprapubic region, and bilateral flanks; these dressings were clean, dry, and intact. Inspection of the extremities revealed no clubbing, cyanosis, or edema, although the patient was wearing compression stockings over the bilateral lower extremities. The patient had several tattoos on his chest and bilateral upper extremities. There was no appreciable petechial rash. The neurological examination revealed no focal deficits.

Routine laboratory tests were notable for mild leukocytosis with a left shift and microcytic anemia. Cardiac markers and brain natriuretic peptide were not measured. The initial arterial blood gas revealed significant hypoxemia with a widened A-a gradient (Table I). An electrocardiogram demonstrated sinus tachycardia without the signs of right ventricular strain. A chest radiograph demonstrated bilateral, multifocal air space opacities (Fig. 1). The Pa02/Fi02 ratio was 168, consistent with acute respiratory distress syndrome.

The patient was admitted to the medical intensive care unit for supportive care. He was started on intravenous azithromycin and ceftriaxone for possible pneumonia and subcutaneous enoxaparin for possible pulmonary embolism. Blood and sputum cultures were negative. A computed tomography (CIl angiogram of the chest revealed no evidence of pulmonary embolism, but did confirm bilateral, perihilar ground glass opacities (Fig. 2). An echocardiogram was not obtained and bronchoscopy was not performed.

The patient’s oxygen requirement improved and the abnormal chest radiographie findings resolved over the next 48 hours (Fig. 3). Given his acute respiratory distress following liposuction, negative workup for pneumonia and pulmonary embolism, and rapid recovery, a presumptive diagnosis of pulmonary fat embolism was established, although he did not manifest the mental status changes and petechial rash characteristic of the fat embolism syndrome (FES).

Discussion

During the past 20 years, liposuction has become an increasingly popular and widely used cosmetic procedure. Liposuction was developed originally in France and introduced in the United States in the early 1980s. Although the surgical techniques have been refined, liposuction is not a benign procedure. Major complications include bleeding, infection, skin necrosis, vital organ injury, adverse anesthesia reaction, pulmonary embolism, and fat embolism.1 A census survey of North American cosmetic surgeons in the mid- 1990s revealed a perioperative mortality rate of 20 per 100,000 cases; death was attributed to pulmonary embolism in 23% of the fatal cases and fat embolism was identified as the cause of death in 8.5% of cases.2

Fat embolism occurs when adipocytes and small blood vessels are damaged during the procedure, introducing lipid microthrombi into the circulation.3 Patients may present with lowgrade fever, tachycardia, tachypnea, hypoxemia, hypocapnia, and mental status changes. The differential diagnosis includes venous thromboembolism, aspiration pneumonitis, and pneumonia.4

Trauma-related conditions associated with fat embolism include long bone fractures, pelvic fractures, orthopedic procedures, bone marrow harvest, soft tissue injuries, burns, and liposuction. Non- trauma-related conditions include pancreatitis, osteomyelitis, panniculitis, bone tumor lysis, sickle cell disease, fatty liver disease, and lipid infusion.

The FES is characterized by the triad of acute hypoxemic respiratory distress, central nervous system dysfunction, and a petechial rash involving the head, neck, anterior thorax, or axillae. It typically occurs 24 to 72 hours after trauma involving the long bones or pelvis and it is more frequent in closed rather than open fractures. FES is much less likely to occur after damage to adipose tissue.5

Pulmonary fat embolism results from the oxidative effects of large amounts of circulating free fatty acids, which damage endothelial cells and pneumocytes in the lungs. The risk of mortality is significant, ranging from 5 to 15%.4 Approximately 10 to 44% of patients with pulmonary fat embolism develop acute respiratory distress syndrome requiring mechanical ventilation.5

The diagnosis of pulmonary fat embolism is largely clinical, based on a predisposing condition plus typical symptoms and signs. Bronchoalveolar lavage and high-resolution CT have been investigated as diagnostic modalities for FES, but neither is used widely for that purpose.6

The mainstay of treatment for pulmonary fat embolism is supportive care, with close monitoring of respiratory and hemodynamic status. The symptoms and signs of FES typically resolve in 3 to 7 days. The administration of intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin is not recommended and the use of corticosteroids remains controversial.5

Conclusions

Clinicians should maintain a high suspicion for pulmonary fat embolism whenever a patient presents with acute dyspnea following liposuction. The diagnosis is a clinical one and the treatment is supportive. Morbidity due to fat embolism after liposuction can be significant, but mortality is rare. References

1. Iverson RE, Lynch DJ: Practice advisory on liposuction. Plast Resconstr Surg 2004; 113: 1478-90.

2. Grazer FM, De Jong RH: Fatal outcomes from liposuction: census survey of cosmetic surgeons. Plast Reconstr Surg 2000; 105: 436-46.

3. Fourme T, Vieillard-Baron A, Loubieres Y, Julie C, Page B, Jardin F: Early fat embolism after liposuction. Anesthesiology 1998; 89: 782-4.

4. Ross RM, Johnson GW: Fat embolism after liposuction. Chest 1988; 93: 1294-5.

5. Mellor A, Soni N: Fat embolism. Anaesthesia 2001; 56: 145-54.

6. Georgopoulos D, Bouros D: Fat embolism syndrome: clinical examination is still the preferable diagnostic method. Chest 2003; 123: 982-3.

Guarantor: LT Dylan E. Wessman, MC USN

Contributors; LT Dylan E. Wessman, MC USNf; LT Thu-Thuy T. Kirn, MC USN*; CAPT John S. Parrish, MC USN[double dagger]

*Department of Internal Medicine, Naval Medical Center San Diego, San Diego, CA 92134.

[dagger]DMsion of Cardiology, Naval Medical Center San Diego, San Diego, CA 92134.

[double dagger]Division of Pulmonary and Critical Care Medicine, Naval Medical Center San Diego, San Diego, CA 92134.

The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, or the U.S. government.

This manuscript was received for review in July 2006. The revised manuscript was accepted for publication in February 2007.

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