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DE AT HS REL ATED TO LIPOSUC TION

DEATHS RELATED TO LIPOSUCTION
RAMA B. RAO, M.D., SUSAN F. ELY, M.D., M.P.H.T.M.,

ABSTRACT
Background The technique of tumescent liposuction involves the subcutaneous infusion of a solution
containing lidocaine, followed by the aspiration of fat
through microcannulas. Although the recommended
doses of lidocaine are as high as 55 mg per kilogram
of body weight, few safety data are available. Since
reporting of adverse events associated with tumescent liposuction is not mandatory, the incidence of
complications and deaths is unknown.
Methods We identified 5 deaths after tumescent
liposuction among 48,527 deaths referred to the
Office of Chief Medical Examiner of the City of New
York between 1993 and 1998. The patients’ records
and postmortem examination results were reviewed
to identify common contributory factors.
Results The five patients had received lidocaine in
doses ranging from 10 to 40 mg per kilogram. Other
drugs, such as midazolam, were also administered.
Three patients died as a result of precipitous intraoperative hypotension and bradycardia with no definitively identified cause. Postmortem blood lidocaine concentrations in two of the patients were 5.2
and 2 mg per liter. One patient died of fluid overload,
and one died of deep venous thrombosis of calf
veins with pulmonary thromboembolism after tumescent liposuction of the legs.
Conclusions Tumescent liposuction can be fatal,
perhaps in part because of lidocaine toxicity or lidocaine-related drug interactions. (N Engl J Med 1999;
340:1471-5.)
©1999, Massachusetts Medical Society.

L

IPOSUCTION is the most common cosmetic operation in the United States.1 The
technique of tumescent liposuction is a relatively new procedure that has gained popularity in the past decade, in part because of its purported safety.2,3 Tumescent liposuction involves the
subcutaneous infusion of a solution containing a local
anesthetic drug, followed by the aspiration of fat
through microcannulas.4 The infusate typically consists of 1 liter of normal saline containing 500 to
1000 mg of lidocaine, 0.25 to 1.0 mg of epinephrine,
and 12.5 mmol of sodium bicarbonate.4,5 Its components provide prolonged local anesthesia and minimize blood loss. Large-volume liposuction, defined as
the removal of more than 1500 ml of fat, may require
the infusion of several liters of this solution.6 Depending on the extent of liposuction and the patient’s
preference, it can be performed with the patient under
conscious sedation or epidural or general anesthesia.4,5,7 In contrast, older liposuction techniques were

AND

ROBERT S. HOFFMAN, M.D.

performed under general anesthesia, used larger cannulas and no infusate, and often necessitated blood
transfusions.6,8
Despite doses of lidocaine as high as 55 mg per
kilogram of body weight,9 few complications have
been reported.10-14 Fatalities have been alluded to in
medical correspondence but not described.15-18 We report here a series of five deaths related to tumescent
liposuction.
METHODS
We reviewed all autopsy reports from January 1, 1993, through
December 31, 1996, and death-notification records from January
1, 1993, through March 1, 1998, at the Office of Chief Medical
Examiner of the City of New York that had been identified by a
computer search using the key words “liposuction,” “cosmetic,”
“lipoplasty,” “plastic,” “lipectomy,” “abdominoplasty,” and “therapeutic complication.” We also queried city medical examiners
about liposuction-related deaths currently under investigation. Five
cases were identified. We then sought information about concomitant drug therapy, medical conditions other than obesity, and the
details of the liposuction procedures from the patients’ medical and
autopsy records. The amount of lidocaine each patient received
was calculated from the volume and concentration of lidocaine in
the infusate, or the total number of milligrams of lidocaine infused, if available in the medical record. A total dose of lidocaine
per kilogram was then calculated.

RESULTS

During the period investigated, a total of 48,527
deaths were accepted under the jurisdiction of the
Office of Chief Medical Examiner of the City of New
York. Of these, 1001 deaths were certified as due to
therapeutic complications, 5 of them related to liposuction. All five occurred during or after tumescent
liposuction. Four of the procedures were performed
by plastic surgeons and one by a general surgeon, and
anesthesiologists were present during all of them.
Family consent was obtained to describe four of these
cases. The fifth death was caused by complications
of hypotension and bradycardia; specific data regarding this case are omitted, however, owing to our inability to obtain consent. In one of the four cases
described here, both the liposuction and the autopsy
were performed in another jurisdiction and subsequently referred to the medical examiner’s office in
New York for review and consultation.
Each patient underwent a complete autopsy, includ-

From the New York City Poison Control Center, Department of Surgery–
Emergency Medicine, New York University Medical Center and Bellevue
Hospital Center (R.B.R., R.S.H.); and the Office of Chief Medical Examiner of the City of New York and the Department of Forensic Medicine,
New York University Medical Center (S.F.E.) — all in New York. Address
reprint requests to Dr. Rao at the New York City Poison Control Center,
455 First Ave., Rm. 123, New York, NY 10016, or at [email protected].

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The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

ing appropriate microscopical examination and collection of blood from the heart. Pertinent data regarding the four patients are summarized in Table 1.
Resuscitation was attempted in all patients. Only the
postmortem findings thought to be functionally important are described. None of the autopsies identified
laryngeal edema consistent with anaphylaxis. Complete cardiac examination in each patient revealed a
normal heart weight for body mass and no contributory cardiac cause of death. Postmortem toxicologic
testing of blood, urine, and other available fluids and
tissues did not identify illicit substances in any patient.

tabolite of atracurium (0.3 mg per liter); meperidine
(0.7 mg per liter); and lidocaine (5.2 mg per liter)
(Table 1).
Patient 2

Patient 2 was a 40-year-old woman with asthma
and normal liver function who underwent conscious
sedation for tumescent liposuction of the flanks and
back while prone as an outpatient. While speaking at
a time when her arterial oxygen saturation was 96 to
97 percent, 2.3 hours into the procedure, she rotated to a supine position. Within 30 seconds, a widecomplex infranodal bradycardia developed; asystole
ensued. Postmortem examination revealed no gross or
microscopic abnormalities consistent with acute asthmatic bronchitis. Blood samples drawn 22.5 hours
after death revealed midazolam and fentanyl, in concentrations too low to be quantified, and lidocaine
(Table 1).

Patient 1

Patient 1 was a 33-year-old man with a remote
history of appendectomy who underwent tumescent
liposuction of the abdomen and flanks under general
anesthesia with elective intubation as an outpatient.
Preoperative serum potassium, creatinine, and aminotransferase concentrations were normal. Despite an
arterial oxygen saturation of 100 percent, bradycardia
and hypotension developed simultaneously 2.5 hours
into the procedure; asystole ensued. Postmortem examination revealed 250 ml of peritoneal fluid without an identifiable cause, and no fluid overload, as
determined by normal lung weights. Staining for fat
emboli was negative. A blood sample collected 47
hours after death was positive for laudanosine, a me-

TABLE 1. DEATHS RELATED

PATIENT
NO.
HEIGHT WEIGHT

ANESTHETIC ADJUNCT (DOSE)

Patient 3

Patient 3 was a 33-year-old woman with an unspecified psychiatric disorder who was being treated with
lithium, nortriptyline, buspirone, clonazepam, sertraline, trazodone, and carisoprodol. Her hemoglobin
concentration was 12 g per deciliter. As an outpatient she received parenteral analgesia for bilateral augmentation mammoplasty and tumescent liposuction

TO

TUMESCENT LIPOSUCTION.*

DOSE OF
DOSE OF DURATION OF
LIDOCAINE EPINEPHRINE PROCEDURE

FLUID VOLUME

TIME TO
CARDIAC
ARREST†

LIDOCAINE
CONCENTRATION‡

SUBCUTANEOUS

IV
m

kg

1

1.75

100

2

1.57

84

3

1.68

4

1.83

INFUSION

ASPIRATE

liters

Midazolam (5 mg IV),
3
meperidine (100 mg IV),
propofol (20 mg IV),
isoflurane, nitrous oxide

Midazolam (5 mg IV),
1.7
fentanyl (150 µg IV),
methohexital (40 mg IV),
droperidol (125 mg IV)
95.5 Morphine (18 mg IV), di7.3
phenhydramine (25 mg
IV), oxycodone–acetaminophen (2 tablets po)
102.3§ Meperidine, zolpidem,
NA
promethazine

mg/kg

mg

hr

4

4

10

2

2.5

2.5

2.4

2.4

14.3

1.2

2.3

2.3

6

6.7

31.4

3

4.5

6

5.6

40

NA

7

>48

*IV denotes intravenous, po oral, and NA not available.
†Time was measured from the start of the procedure.
‡The concentration was measured by gas chromatography.
§The weight was measured post mortem.

1472 ·

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25

Blood: 5.2 mg/liter;
brain: 4.7 mg/kg;
liver: 5.2 mg/kg;
peritoneal fluid:
17 mg/liter
Blood: 2 mg/liter



Blood: 2.9 mg/liter;
brain: 4.9 mg/kg;
liver: 14.8 mg/kg;
gastric contents:
2.7 mg/kg

DE AT HS REL ATED TO LIPOSUC TION

of the posterolateral thorax, arms, back, abdomen,
thighs, buttocks, and knees, with an estimated blood
loss of 700 ml. Because of postoperative pain she was
hospitalized, at which time her hemoglobin concentration was 5.8 g per deciliter. She received 2 units
of packed red cells, morphine sulfate through a patient-controlled analgesic pump, and 5 percent dextrose in Ringer’s lactate (100 ml per hour, intravenously, throughout a hospitalization of two days).
Furosemide was administered for hypoxia, wheezing,
and peripheral edema.
Two hours after hospital discharge, she reported
worsening dyspnea and had a syncopal event. She
was found in ventricular fibrillation; resuscitation restored her circulation but she remained unresponsive.
Her serum potassium and creatinine concentrations
were normal. A chest radiograph revealed pulmonary edema, an echocardiogram was normal, and serum cardiac-enzyme concentrations were normal. She
remained in an anoxic coma and was pronounced
dead three days later. Postmortem examination revealed severe pulmonary edema with a combined lung
weight of 1560 g. No pulmonary thromboemboli
were identified. Toxicologic testing for lidocaine was
not performed.
Patient 4

Patient 4 was a 54-year-old woman who underwent tumescent liposuction of the back, flanks, abdomen, and thighs under general anesthesia. Eighteen
hours postoperatively, she arose from bed and became “lightheaded” and then unresponsive. Cardiac
electrical activity was identified, but the patient’s pulse
was unobtainable. Postmortem examination revealed
deep venous thrombosis of the left calf with saddle
and distal pulmonary thromboemboli. Blood drawn
22.6 hours post mortem was positive for meperidine
(0.8 mg per liter), normeperidine (0.1 mg per liter),
and promethazine (0.1 mg per liter). The gastric contents (123 g) included the following amounts of drug:
0.3 mg of zolpidem and 0.4 mg of meperidine. Lidocaine values are shown in Table 1.
DISCUSSION

The most striking aspect of this series is the incompletely explained deaths of Patients 1 and 2. Both had
hypotension and bradycardia and then cardiac arrest.
The differential diagnosis of hypotension and concomitant bradycardia includes primary myocardial
dysfunction, disruption of the autonomic nervous system, end-stage systemic disorders (such as sepsis, hypoxia, and anaphylaxis), and toxic–metabolic causes.
In these two cases, the first three categories can be
ruled out by the case histories and pathological findings. Metabolic disturbances such as hypermagnesemia, hyperkalemia, and hypercalcemia are unlikely, because neither patient received any of these substances.
High doses of many drugs can cause hypotension

and bradycardia. These include beta-adrenergic antagonists, the non-dihydropyridine calcium-channel
blockers, cardiac glycosides, and centrally acting alphaadrenergic agonists, to name a few. In rare instances,
propofol causes hypotension and bradycardia during
induction,19 but it is unlikely to account for the
death of Patient 1, who tolerated the induction of
anesthesia without incident.
Lidocaine can cause hypotension and bradycardia.
It suppresses myocardial automaticity and causes some
vasodilatation. When lidocaine is given to treat cardiac dysrhythmias, therapeutic plasma concentrations
range from 2 to 5 mg per liter, and concentrations
above 5 mg per liter are considered toxic.20 Typically,
neurologic signs such as paresthesias, somnolence,
and seizures are correlated with antemortem plasma
concentrations of 5 to 9 mg per liter, and cardiovascular collapse has been described at concentrations
above 10 mg per liter.20
In tumescent liposuction, reported doses of lidocaine range from 10 to 88 mg per kilogram,8 several
times higher than the maximal recommended dose of
4.5 mg per kilogram (or up to 7 mg per kilogram
with epinephrine) typically used for subcutaneous
infiltration.21,22 The 1991 guidelines of the American
Academy of Dermatologists for tumescent liposuction suggested a maximal dose of 35 mg of lidocaine
per kilogram,23 which was increased to “at least 55 mg
per kilogram” in 1997.24 This increase was based on
studies demonstrating that most patients had plasma
concentrations below the toxic range, despite being
given these high doses.5,9,25,26
In tumescent liposuction, plasma lidocaine concentrations have been found to rise for 16 hours,6,9,25-27
or even 23 hours.28 The sampling intervals were often
wide,6,9,27 and regression analyses were used to extrapolate maximal safe doses of 35 mg per kilogram27 and
55 mg per kilogram.9 These analyses failed to consider that hepatic metabolism of lidocaine by means
of CYP3A4 is saturable.29 Once saturation occurs,
absorption exceeds elimination, and plasma lidocaine
concentrations increase precipitously. Administration
of other drugs that are metabolized by or inhibit
CYP3A4 can also alter lidocaine metabolism.29 Midazolam, in particular, may compete with lidocaine
for enzymatic metabolism, protect against lidocaineinduced seizures, and alter mental status,29 delaying
the diagnosis of lidocaine toxicity until the onset of
cardiovascular collapse. General anesthesia or conscious sedation can also mask the early clinical signs
of toxicity, as may have occurred in the cases of Patients 1 and 2. In some reports, “drowsiness” or
“syncope,” which may represent neurotoxicity, was
attributed to other causes.6,30
Interpreting the postmortem blood lidocaine concentrations in Patients 1 and 2 is difficult.31 No data
regarding the stability of lidocaine in postmortem
blood and tissue are available31,32; concentrations as
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low as 4 and 6 mg per liter have been reported in
deaths attributed to the drug.32,33 In our series, the
reported values may not reflect the concentrations in
myocardial tissue at the time of cardiovascular collapse, owing to the redistribution half-life of the drug
(8.5 minutes)20 and the effects of attempted resuscitation. Data on the active metabolite of lidocaine,
monoethylglycinexylidide, are unavailable and may be
relevant. Given the available clinicopathological information, we think lidocaine toxicity or lidocainerelated drug interactions are a possible explanation for
the deaths of Patients 1 and 2.
The American Society of Plastic and Reconstructive Surgeons reports that the number of liposuction
procedures performed by plastic surgeons increased
by 200 percent from 1992 to 1997, with 149,042
procedures performed in 1997.2 The proportion involving the tumescent liposuction technique was not
reported. The most recent survey from the American
Academy of Cosmetic Surgery, representing several
surgical disciplines, reported that 292,942 liposuction procedures were performed in 1996, an increase
of more than 300 percent from 1990. Of these, 92
percent involved tumescent infusions, roughly half
with general anesthesia.3
Deaths associated with earlier liposuction methods
resulted primarily from pulmonary thromboembolism
or fat emboli.34,35 A forerunner of tumescent liposuction, the “wet technique,” involved the subcutaneous
infusion of a dilute solution of epinephrine.28 We
found no reports of concomitant hypotension and
bradycardia during or after liposuction with these
methods.
During earlier liposuction procedures, the amount
of intravenous hydration was based on the volume of
fat aspirated. In tumescent liposuction, however, the
infusate not only serves as a potential source of absorbable fluid, but also provides a tamponading effect,
limiting fluid losses.5,6,30 Overhydration puts patients
at risk for serious or fatal consequences,13 as occurred
in Patient 3, whose severe hemodilution was erroneously attributed to blood loss alone.
Extensive tumescent liposuction of the abdomen
and lower extremities can cause impedance of venous
flow, release of local tissue factors, and postoperative
immobilization. These can contribute to venous stasis and thrombogenesis, as occurred in Patient 4.
Anecdotes in the lay press suggest that these deaths
after tumescent liposuction are not unique. According to press accounts, patients have died from “tumescent anesthesia,” epinephrine or lidocaine toxicity, hypothermia, and fluid overload.36-39 Editorials in the
medical literature have mentioned deaths secondary
to tumescent liposuction that were due to cardiac
“depression,” pulmonary edema, and lidocaine toxicity,15-18 but these cases were not formally reported.
There is no mandatory reporting or review of adverse events associated with this privately performed
1474 ·

procedure, so the true incidence of complications and
death is unknown.
Tumescent liposuction is not a trivial procedure,
because it has the potential to kill otherwise healthy
persons. Drug absorption and drug interactions, fluid
management, prothrombogenic factors, and liposuction volume should be reevaluated for this popular
cosmetic procedure. Deaths due to cosmetic surgery
should be a matter for serious public concern.
Presented as a poster at the North American Congress of Clinical Toxicology, Orlando, Fla., September 14, 1998.

We are indebted to Charles S. Hirsch, M.D., and David R.
Schomburg, R.P.A.-C., Office of Chief Medical Examiner of the
City of New York, Mary Ann Howland, Pharm.D., of St. John’s
University, Jamaica, N.Y., and Lewis S. Nelson, M.D., of the New
York City Poison Control Center, for their support in the preparation
of the manuscript.

REFERENCES
1. Dolsky RL. State of the art in liposuction. Dermatol Surg 1997;23:
1192-3.
2. Number of liposuction procedures increase by 200 percent over fiveyear span. Arlington Heights, Ill.: Plastic Surgery Information Service,
April 1998. (See http://www.plasticsurgery.org/mediactr/lipo-sta.htm.)
(Also available from NAPS [document no. 05513 for three pages], c/o
Microfiche Publications, 248 Hempstead Turnpike, West Hempstead, NY
11552.)
3. 1996 National cosmetic surgery statistics. Chicago: American Academy
of Cosmetic Surgery, 1997:1-8.
4. Klein JA. Tumescent technique chronicles: local anesthesia, liposuction,
and beyond. Dermatol Surg 1995;21:449-57.
5. Pitman GH, Aker JS, Tripp ZD. Tumescent liposuction: a surgeon’s
perspective. Clin Plast Surg 1996;23:633-41.
6. Klein JA. Tumescent technique for local anesthesia improves safety in
large-volume liposuction. Plast Reconstr Surg 1993;92:1085-98.
7. Knize DM, Fishell R. Use of preoperative subcutaneous “wetting solution” and epidural block anesthesia for liposuction in the office-based surgical suite. Plast Reconstr Surg 1997;100:1867-74.
8. Lillis PJ. Liposuction surgery under local anesthesia: limited blood loss
and minimal lidocaine absorption. J Dermatol Surg Oncol 1988;14:1145-8.
9. Ostad A, Kageyama N, Moy RL. Tumescent anesthesia with a lidocaine
dose of 55 mg/kg is safe for liposuction. Dermatol Surg 1996;22:921-7.
10. Bernstein G, Hanke CW. Safety of liposuction: a review of 9478 cases
performed by dermatologists. J Dermatol Surg Oncol 1988;14:1112-4.
11. Hanke CW, Bernstein G, Bullock S. Safety of tumescent liposuction in
15,336 patients: national survey results. Dermatol Surg 1995;21:459-62.
12. Hanke CW, Bullock S, Bernstein G. Current status of tumescent liposuction in the United States: national survey results. Dermatol Surg 1996;
22:595-8.
13. Gilliland MD, Coates N. Tumescent liposuction complicated by pulmonary edema. Plast Reconstr Surg 1997;99:215-9.
14. Klein JA, Kassarjdian N. Lidocaine toxicity with tumescent liposuction: a case report of probable drug interactions. Dermatol Surg 1997;23:
1169-74.
15. McShane RH. Whole blood loss in liposuction: a protocol for handling liposuction specimen. Plast Reconstr Surg 1997;100:281.
16. Stone A. Tumescent technique with local anesthesia for liposuction.
Plast Reconstr Surg 1995;95:603-5.
17. Grazer FM, Meister FL. Complications of the tumescent formula for
liposuction. Plast Reconstr Surg 1997;100:1893-6.
18. Klein JA. Titanic tumescent anesthesia. Dermatol Surg 1998;24:691.
19. Bryson HM, Fulton BR, Faulds D. Propofol: an update of its use in
anaesthesia and conscious sedation. Drugs 1995;50:513-59.
20. Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland
MA, Hoffman RS, eds. Goldfrank’s toxicologic emergencies. 5th ed. Norwalk, Conn.: Appleton & Lange, 1994:717-9.
21. Catterall WA, Mackie K. Local anesthetics. In: Hardman JG, Limbird
LE, eds. Goodman & Gilman’s the pharmacological basis of therapeutics.
9th ed. New York: McGraw-Hill, 1996:331-47.
22. Physicians’ desk reference. 52nd ed. Montvale, N.J.: Medical Economics,
1998:582-5.

May 13 , 19 9 9
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Downloaded from nejm.org by niniadiany ansari on October 29, 2014. For personal use only. No other uses without permission.
Copyright © 1999 Massachusetts Medical Society. All rights reserved.

DE AT HS REL ATED TO LIPOSUC TION

23. Drake LA, Ceilley RI, Cornelison RL, et al. Guidelines of care for
liposuction. J Am Acad Dermatol 1991;24:489-94.
24. Guiding principles for liposuction: the American Society for Dermatologic Surgery, February 1997. Dermatol Surg 1997;23:1127-9.
25. Samdal F, Amland PF, Bugge JF. Plasma lidocaine levels during suctionassisted lipectomy using large doses of dilute lidocaine with epinephrine.
Plast Reconstr Surg 1994;93:1217-23.
26. Klein JA. The tumescent technique: anesthesia and modified liposuction technique. Dermatol Clin 1990;8:425-37.
27. Idem. Tumescent technique for regional anesthesia permits lidocaine
doses of 35 mg/kg for liposuction. J Dermatol Surg Oncol 1990;16:24863.
28. Burk RW III, Guzman-Stein G, Vasconez LO. Lidocaine and epinephrine levels in tumescent technique liposuction. Plast Reconstr Surg 1996;
97:1379-84.
29. Parkinson A. Biotransformation of xenobiotics. In: Klaassen CD, ed.
Casarett and Doull’s toxicology: the basic science of poisons. 5th ed. New
York: McGraw-Hill, 1996:113-86.
30. Pitman GH. Liposuction & anesthetic surgery. St. Louis: Quality
Medical Publishing, 1993:67-9, 249, 335, 375, 389.

31. Prouty RW, Anderson WH. The forensic science implications of site and
temporal influences on postmortem blood-drug concentrations. J Forensic
Sci 1990;35:243-70.
32. Peat MA, Deyman ME, Crouch DJ, Margot P, Finkle BS. Concentrations of lidocaine and monoethylglycylxylidide (MEGX) in lidocaine associated deaths. J Forensic Sci 1985;30:1048-57.
33. Christie JL. Fatal consequences of local anesthesia: report of five cases
and a review of the literature. J Forensic Sci 1976;21:671-9.
34. Teimourian B, Rogers WB. A national survey of complications associated with suction lipectomy: a comparative study. Plast Reconstr Surg
1989;84:628-31.
35. Christman KD. Death following suction lipectomy and abdominoplasty.
Plast Reconstr Surg 1986;78:428.
36. Lasswell M. As she lay dying. Allure. August 1997:128-33, 151.
37. Allen JE. The ugly side of liposuction surfaces: California probes
deaths of 3 from surgery. Star-Ledger. August 26, 1997:20.
38. Doctors’ licenses taken after liposuction death. New York Times.
November 29, 1997:10.
39. Chase M. Extreme liposuction is exposing patients to unnecessary risk.
Wall Street Journal. January 18, 1999:B1.

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