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The Tumescent Technique By Jeffrey A. Klein MD



Chapter 9:
Superwet Liposuction and Pulmonary Edema

The routine use of intravenous (IV) fluids is unnecessary and relatively contraindicated with tumescent liposuction. Liposuction patients have died from unnecessary administration of IV fluids. This chapter examines the kinetics of tumescent fluids and the pathophysiology associated with unnecessary IV fluid infusions.

Substances such as sodium chloride (NaCl) have a crystalline structure and are known as crystalloids. Unlike a colloid substance, a crystalloid substance in solution (e.g., lactated Ringer’s) can easily pass through membranes.

Superwet liposuction uses general anesthesia or IV sedation-analgesia, infusion of significant volumes of IV crystalloids, and infiltration of moderate volumes of subcutaneous crystalloids.1 A syndrome of superwet disseminated intravascular coagulation (superwet DIC) can result from the combination of excessive liposuction trauma, general anesthesia with hypothermia, and hemodilution from excessive IV fluid infusion (see Chapter 14). Each of these factors alone can precipitate a consumption coagulopathy. When they are combined in a single surgical misadventure, the result may be a fatal episode of DIC.

No Third Space

In the true tumescent technique for liposuction, or liposuction totally by local anesthesia, subcutaneous fluids routinely produce hemodilution. If IV fluids are infused as well, a significant risk of systemic fluid overload and pulmonary edema exists.

The traditional theory of liposuction assumes that tissue damage as a result of surgery creates a “third space” phenomenon, in which intravascular fluids are lost into a “black hole” of traumatized tissue. An excessive loss of intravascular fluid precipitates loss of cardiac output, loss of blood pressure, and death. With safe volumes of tumescent liposuction, there is no third space phenomenon. The assumption that tumescent liposuction creates a third space may prompt surgeons to overcompensate and give the patient potentially life-threatening doses of IV fluids.

The tumescent technique prevents the creation of a third space. Tumescent infiltration fills the local interstitial tissue with isotonic fluid and preempts the need for filling the wound with intravascular isotonic fluid. Epinephrine constricts arterioles, decreasing intravascular hydrostatic pressure, which in turn decreases local hemorrhage and distal transcapillary leakage of plasma; the tumescent hydrostatic pressure compresses venules and veins and further decreases hemorrhage.

Intravascular fluid deficits occur with tumescent local anesthesia principally because of excessive amounts of liposuction. These deficits are prevented by avoiding excessive liposuction, not by overcompensating with IV fluids. Administration of IV fluids to prevent intravascular fluid loss is especially dangerous when intravascular fluid volume is already increased as a result of systemic absorption of subcutaneous tumescent fluids.

Fluid Volume and Overload

The sodium-potassium (Na-K) pump maintains a sodium concentration gradient between the intracellular fluid volume and the extracellular fluid volume (ECFV) such that intracellular sodium ion (Na+) concentration is approximately 10% of the Na+ concentration in the ECFV. Because of the osmotic pressure gradient created by the Na-K pump, most of a dose of isotonic crystalloid, such as lactated Ringer’s solution (LR) or 0.9% NaCl (IV infusion or subcutaneous tumescent infiltration), will be distributed throughout the ECFV. The difference is that an IV infusion is rapidly redistributed, whereas a subcutaneous tumescent dose is slowly absorbed and distributed. The duration of the expansion of the ECFV is limited by the rate of renal excretion of sodium and water.

Because plasma is only 20% of the ECFV, any IV or tumescent dose of LR or normal saline (NS) will increase the blood volume by only 20% of the volume given.2 The residual 80% of the given volume enters the interstitial space. For example, a 3-L dose of NS will produce only a 600-ml expansion of the intravascular space, whereas 2400 ml will enter the interstitial space, including the pulmonary interstitium.

Tumescent Fluid and Hemodilution

When delivered into subcutaneous fat by tumescent infiltration, physiologic saline (0.9% NaCl) or LR can be regarded pharmacologically as a drug. This is best represented by a one-compartment pharmacokinetic model, with the pharmacokinetic volume of distribution essentially equal to the ECFV.

Subcutaneous infusion of the tumescent technique, without IV fluid supplementation, results in moderate hemodilution.3 For example, when a 75-kg female was given 35 mg/kg of tumescent lidocaine in 5.25 L of NS (500 mg of lidocaine/L), sequential measurements revealed that the maximum decrease in hematocrit was approximately 10% with or without liposuction. After tumescent liposuction, no clinical evidence indicates an intravascular fluid deficit. The urine specific gravity is not decreased, and hourly urine output is more than 70 ml/hr.

When a reasonable volume of supranatant fat is removed with tumescent liposuction (3% to 4% of total body weight or less than 4 L), no third space is clinically detectable. Any significant IV infusion is unnecessary and can produce intravascular fluid overload and pulmonary edema.

The tumescent technique essentially eliminates problems associated with the shift of IV fluids out of the intravascular space. Thus replacing significant volumes of IV fluids is unnecessary.4 Only minimal amounts of IV fluids are given, although IV access is always established to administer emergency medications. Patients need only an IV access maintained by a heparin lock, flushed with plain physiologic saline containing no heparin.

I recommend no IV fluids during or after tumescent liposuction surgery. If a liposuction patient requires perioperative IV fluids, it is likely that the liposuction removed an excessive volume of aspirate or that tumescent infiltration was insufficient.

Intravenous Crystalloids and the Lungs

A dose of IV crystalloid (e.g., LR, NS) enters the pulmonary interstitial space by a circuitous route. When a large IV dose (2 L/hr) of LR or NS is infused, it flows directly to the right side of the heart, through the lungs, and into the left side of the heart. Standard doses of LR do not cause pulmonary edema in healthy persons, which indicates that most of the dose merely flows through the pulmonary vessels back to the left side of the heart, finally entering the arterial circulation. For humans the maximum pulmonary lymphatic flow rate is only 200 ml/hr. If a significant proportion of the IV dose of LR did enter the pulmonary interstitial space on its first pass through the lungs, the result would be fulminant and fatal pulmonary edema.

A limited amount of IV crystalloid can be safely infused before the risk of pulmonary edema becomes significant. After IV infusion of just 1 L of 0.9% NaCl, sufficient fluid enters the pulmonary interstitium to cause decreased pulmonary compliance.5 The infusion of 3 to 5 L of LR or NS into an adult increases the risk of pulmonary edema.6

Any IV infusion of LR is rapidly redistributed into the interstitial space. In young men, for example, to achieve a steady-state 10% blood volume dilution, the infusion rate must be at least 50 ml/min for at least 40 minutes (2000 ml); in healthy females, IV infusion of LR at 100 ml/min over 15 minutes causes symptoms of fluid overload.7 The risk for iatrogenic pulmonary edema (pulmonary interstitial fluid overloading) is proportional to the degree of excess fluid in the interstitial space. Any IV infusion of crystalloid enters the interstitial space so rapidly that it is generally unnecessary and potentially dangerous with tumescent technique.

If a large volume of IV crystalloid solutions is given to a patient after a significant dose of subcutaneous crystalloid, the postoperative ECFV will be larger than the preoperative ECFV. Healthy patients usually tolerate large volumes of IV crystalloid infusion well. High-compression garments over infiltrated areas increase interstitial fluid pressure and shift ECFV out of the compressed interstitial space and back into the intravascular space, where it is redistributed to other interstitial tissues, including the pulmonary interstitium. This increases the risk of pulmonary edema.

Interstitial Edema

Interstitial edema is the result of excessive water accumulating in the interstitial space. The lymphatic system is the principal means of removing extravasated plasma proteins from the interstitial space. Extravasated plasma proteins increase the colloid osmotic pressure of the interstitium, which in turn tends to draw even more water out of the vascular space and into the interstitial space. When the rate of plasma flowing into the interstitium exceeds the lymphatic system’s ability and capacity to remove these proteins, the result is interstitial edema (see Chapter 11).

Large molecules located in the interstitial tissues cannot readily diffuse across the capillary endothelium of blood vessels and enter the intravascular space. An extravasated plasma protein molecule reenters the intravascular space by first entering, then being transported by, lymphatic vessels. Edema fluid resulting from tissue trauma and inflammation has a high content of large plasma protein molecules. If the lymphatic vessels have been impaired by trauma, the proteinaceous edema fluid cannot easily return to the intravascular space.

Thus edema fluid in most traumatized tissues is functionally isolated from the intravascular fluid volume. It is also physically isolated from most of the body’s interstitial space. In essence, therefore, the edema fluid in traumatized and inflamed tissues is functionally a third compartment that is distinct and isolated from the intravascular space and the peripheral interstitial space.

The greater the volume of liposuction-induced tissue damage (greater the number of areas suctioned or greater the volume of fat aspirated), the greater is the potential for problems with ECFV homeostasis.

Tumescent Vasoconstriction

Beta-adrenergic agonists such as epinephrine cause arteriolar and capillary vasoconstriction. In adipose tissue, extremely dilute tumescent epinephrine (1 mg/L or less) produces profound vasoconstriction. This tumescent vasoconstriction not only produces hemostasis and greatly delays systemic lidocaine absorption, but also minimizes extravasation and “third spacing” of intracellular water.

Hydrostatic Vasocompression. The trauma of liposuction disrupts blood vessels, causing hemorrhage into treated areas and release of inflammatory mediators. The combined physical and biochemical insult to vascular endothelium increases capillary permeability to plasma proteins. The free flow of plasma proteins into the interstitium equalizes the intravascular and extravascular colloid osmotic pressure. With equilibrated colloid osmotic pressure, the hydrostatic pressure gradient determines the direction of transcapillary fluid exchange. Capillaries and venules remain patent only when the intravascular blood pressure exceeds the interstitial pressure. Tumescent infiltration elevates interstitial hydrostatic pressure above capillary blood pressure.

Tumescent hydrostatic pressure causes a net flow of water from the interstitial space into the intravascular space. At the periphery of a globular mass of tumescent adipose tissue, where vasoconstriction is less than complete, the elevated tumescent hydrostatic pressure produces a net intravascular absorption of crystalloid. After absorption into the systemic circulation, the tumescent solvent is redistributed throughout the ECFV, including the interstitial fluid volume. In essence, the tumescent liposuction patient is somewhat overhydrated. This is substantiated by the observation that the postoperative urine specific gravity is typically decreased compared with the preoperative urine.

Tumescent hydrostatic pressure prevents third spacing of intravascular fluid. In effect, tumescence provides a net increase in intravascular volume and eliminates the need for perioperative IV crystalloid infusions.

Hemostatic Effects. Tumescent vasoconstriction is the net effect of tumescent hydrostatic vasocompression and beta-adrenergic vasoconstriction. Tumescence is unique in simultaneously providing arteriolar, capillary, and venular vasoconstriction. Tumescent arteriolar vasoconstriction is mediated by epinephrine and shrinks arterioles and capillaries. Tumescent venular vasocompression is mediated by hydrostatic pressure and collapses capillaries, venules, and small veins. In essence, tumescent vasoconstriction shuts off the vascular supply of the infiltrated adipose tissue. The combination of no blood flowing from the upstream capillary bed and tumescent hydrostatic pressure causes even the larger veins within tumescent fat to collapse.

The net effect of tumescent vasoconstriction is an unprecedented type of hemostasis that not only conserves red blood cells, but also preempts massive shifts of extracellular water out of the intravascular space into the interstitial space.

The tumescent vasoconstrictive effects are well balanced. Too little tumescent vasoconstrictive effect would increase surgical hemorrhage, increase the local inflammation, and increase postoperative healing time; it would also increase the risk of hypovolemia, the need for IV crystalloid replacement, and thus the risk of iatrogenic pulmonary edema. Too much (excessively prolonged) vasoconstriction would cause local tissue necrosis. Only the adipocytes’ meager oxygen requirement prevents anoxic necrosis.

Careful, deliberate tumescent infiltration maximizes the hemostatic effect. Rapid, haphazard infiltration provides less complete local anesthesia and vasoconstriction.

Tumescent vasoconstriction is responsible for (1) isolation of tumescent lidocaine from the systemic circulation and (2) pharmacokinetic behavior (one-compartment model) of the tumescent technique.

Intravenous Fluid Overload

The tumescent technique for local anesthesia and IV fluid infusion is a potentially dangerous combination. Again, IV fluids are relatively contraindicated with tumescent liposuction. Unawareness of the fluid kinetics (rate of intravascular absorption) of the tumescent anesthetic solution from the subcutaneous compartment can lead to fluid overload.

Former liposuction techniques with general anesthesia required large volumes of perioperative IV fluids. Loss of intravascular fluid because of third spacing was one of the greatest risks. Management of these liposuction patients included infusion of significant volumes of IV fluids, plasma expanders, and autologous blood transfusions. For example, for every liter of aspirate, 1 to 2 L of IV fluids was infused.

After adopting the superwet technique, some clinicians have continued to inundate patients with IV fluids. Infusion of significant IV fluid volumes into normovolemic patients who just underwent tumescent liposuction can result in dangerous IV fluid overload and pulmonary edema.

Pulmonary Edema

The classic findings on physical examination in the setting of pulmonary edema include basilar rales, jugular venous distension, orthopnea, and frothy pink sputum. To prevent pulmonary edema with tumescent liposuction, the surgeon should not use IV fluids.

The etiology of pulmonary edema is similar to that of edema throughout the body. With simultaneous IV fluid overload and acute cardiovascular stress, however, the onset of pulmonary edema can be extremely rapid and fatal. The distance separating the capillary blood from the alveolar air sac is so short, 0.5 μm, and the volume of the pulmonary interstitial space so small, 200 ml or less, that any fluid leaking from the pulmonary capillary will rapidly fill the alveoli.

Types and Causes

Many different types of injury and physical stress to lung tissue can result in pulmonary edema. The different causes of pulmonary edema can be classified in several ways (Box 9-1).

Intravascular fluid overload from excessive IV crystalloid infusion precipitates a high–capillary pressure pulmonary edema, the most common iatrogenic form of pulmonary edema in a liposuction patient. It is one of the most common causes of liposuction-related mortality. Any condition that predisposes to systemic fluid overload, such as chronic cardiac, hepatic, or renal insufficiency, will predispose to perioperative high–capillary pressure pulmonary edema.

Cardiogenic pulmonary edema is the result of left-sided heart failure from cardiac valvular insufficiency, idiopathic or drug-induced dysrhythmia, acute myocardial infarction, or atherosclerotic cardiovascular disease. As the direct result of a relative IV fluid overload, cardiogenic pulmonary edema can also occur during liposuction surgery. An unexplained, acute-onset pulmonary edema in an otherwise healthy young patient should raise the suspicion of cardiogenic pulmonary edema.

Despite up to 7 years of surgical training, few surgeons have the clinical experience to diagnose and manage this condition. The surgeon, not the anesthesiologist, is responsible for screening patients for relevant predisposing conditions and, when appropriate, obtaining preoperative clearance from a specialist in internal medicine. Although most liposuction patients are healthy and have no significant surgical risk factors, the surgeon must always be alert for potential problems. Surgeons must realize their limitations and seek medical consultation as appropriate to assist in the preoperative evaluation of some patients.

Inflammation-mediated pulmonary edema, or adult respiratory distress syndrome (ARDS), may be viewed as a form of low–capillary pressure pulmonary edema. In the liposuction patient, especially with general anesthesia, ARDS can be associated with drug reactions, sepsis, gastric aspiration, fat embolism, transfusion reaction, or massive blood transfusion. Other causes of ARDS are burn-inhalation injury and acute pancreatitis.

In an otherwise healthy patient, IV fluid overload, cardiac dysrhythmia (drug induced or otherwise), and acute left ventricular failure can produce abrupt pulmonary edema, with frothy pink sputum, dyspnea, panic, and sudden death. The combination of IV fluid overload and acute bupivacaine toxicity (intractable ventricular fibrillation) is a risk of the superwet liposuction technique.

Pulmonary edema has two stages. The first stage, interstitial pulmonary edema, involves edema of the pulmonary interstitial space. Within certain limits, the pulmonary lymphatics can accommodate a gradually increased interstitial fluid load by increasing lymph flow and thus can compensate for interstitial edema. When the rate of interstitial fluid production exceeds the capacity of the pulmonary lymphatics, the result is the second stage, alveolar pulmonary edema. Fluid crosses the capillary endothelium, then the interstitial collagen, and finally the alveolar epithelium, filling the alveoli with fluid. Alveolar edema prevents pulmonary gas exchange and causes local hypoxia.


The prevention of pulmonary edema resulting from IV fluid overload is the most basic aspect of applied physiology. In a healthy patient who is already somewhat overhydrated by tumescent fluids, infusion of excessive IV fluids poses a substantial risk of fluid overloading and pulmonary edema. Surgeons continue this practice apparently because they do not appreciate the rate and extent of systemic absorption of subcutaneous crystalloid (NS, LR) after tumescent infiltration.

Among cosmetic surgeons there is widespread failure to recognize that (1) safety requires biostatistical validation and (2) safety can never be proved by one anecdotal report. On the other hand, a single sentinel case report can establish the dangers inherent in a surgical procedure. The fact that one healthy liposuction patient survived a 15-L dose of parenteral fluids (IV plus tumescent fluids) is not sufficient proof that such a high dose generally is safe in all patients. The risk of such a high dose was demonstrated when an 80-kg (176-pound) male patient developed pulmonary edema after liposuction using the superwet technique. He had been given 7900 ml of subcutaneous fluid and 2200 ml of IV fluids during liposuction of 1150 ml of supranatant fat.8

The volume of isotonic crystalloid infiltrated in the subcutaneous space with tumescent technique more than compensates for the trauma of liposuction. With tumescent liposuction, urine specific gravity is typically greater before than after surgery, indicating that the intravascular space is not volume depleted. With true tumescent liposuction the patient is alert and fully conversant and can drink fluids at will. No need exists for IV fluid supplementation. A patient who requires IV fluids after tumescent liposuction indicates either too much liposuction or too little tumescent anesthesia.

To my knowledge, pulmonary edema has never been associated with liposuction using the true tumescent technique.

Pulmonary Lymphatic System

The pulmonary lymphatic system is an important compensatory mechanism of maintaining pulmonary interstitial fluid homeostasis. The distal pulmonary lymphatic capillaries meander just below the basement membrane of the alveolar epithelium. Lymphatic capillaries coalesce proximally to form small canaliculi that course through the lung tissue parallel and adjacent to arterioles and bronchioles; larger lymphatic vessels subsequently follow the path of pulmonary arteries and bronchi into the large, collecting hilar trunk vessels. Chest radiographs identify pulmonary interstitial edema by the classic butterfly pattern of hilar fullness.

The kinetics of fluid exchange between the pulmonary vasculature and interstitial space seem to obey Starling’s law. Under normal conditions the net effect of lymphatic drainage, hydrostatic pressures, and colloid osmotic pressures on the diffusion of water into and out of capillaries is creation of a pulmonary interstitial fluid pressure that is slightly negative relative to atmospheric pressure. Healthy persons have a small pulmonary lymph flow of about 20 ml/hr. Anything that elevates the pulmonary interstitial pressure into the positive range will precipitate sudden interstitial edema and flooding of the alveoli with free fluid.

In patients with chronic conditions, the lung lymphatics have a tremendous capacity to augment lymph flow gradually and prevent pulmonary edema. In acute left ventricular insufficiency, however, the pulmonary lymphatics are quickly overwhelmed, precipitating acute alveolar pulmonary edema.

Associated Conditions

Hypoxic and Acidotic Vasoconstriction. A decrease in alveolar, but not arterial, oxygen pressure below 70 mm Hg causes a marked contraction of the vascular smooth muscle in the walls of small pulmonary arterioles. This contraction elevates pulmonary arteriolar pressure. At very low alveolar oxygen tension the local blood flow may be abolished.

Low pulmonary arterial blood pH (acidosis) causes vasoconstriction. This effect is augmented by alveolar hypoxia.

Hypoxia at high altitude may cause generalized pulmonary vasoconstriction, a large rise in pulmonary arterial pressure, and acute pulmonary edema with cough and frothy pink sputum. This situation is typically associated with inadequate acclimatization and extreme exertion, such as hiking, jogging, mountain climbing, or skiing at high altitude.

Acute Heart Failure. Heart failure consists of low cardiac output, high pulmonary venous pressure, or both. The early stage of heart failure is typically first manifested as shortness of breath on exertion. In advanced heart failure, symptoms can occur at rest. Left ventricular failure causes increased left atrial pressure, which in turn causes increased pulmonary venous pressure. When pulmonary venous pressure is sufficiently high, it causes pulmonary interstitial edema and eventually pulmonary alveolar edema.

The pulmonary alveolar epithelium is fragile and has minimal tensile strength. The alveolar epithelial membranes rupture, and pink fluid pours into the alveolar space when the interstitial fluid volumes increases by 100 ml, which represents more than 50% of the normal interstitial fluid volume. Even 1 mm Hg of positive pressure in the interstitial fluid space relative to atmospheric pressure may cause immediate rupture of the alveolar epithelium.9

A sufficiently abrupt and large increase in pulmonary capillary pressure can forcibly pull apart the delicate gap junction between adjacent endothelial cells. The pulmonary capillaries actually leak very dilute blood into the alveoli through rents in the pulmonary capillary endothelium. Trapped alveolar air and the exudation of blood-tinged fluid leaking from pulmonary capillaries combine to produce pathognomonic frothy pink sputum and dyspnea.

Abrupt Cardiac Decompensation. The most common cause of pulmonary edema in healthy liposuction patients is IV fluid overload. The additional insult from drug-induced cardiac dysrhythmias greatly increases the risk of alveolar pulmonary edema. Rapid systemic absorption of bupivacaine and epinephrine-induced tachycardia have produced ventricular fibrillation with frothy pink sputum and sudden death in at least one liposuction patient. The general anesthetics propofol, halothane, isoflurane, and enflurane are all associated with a significant risk of cardiac dysrhythmias. Mixing excessive IV fluids with general anesthesia is a high-risk recipe for iatrogenic edema.

Mitral Valve Disease. As many as 7% of women have some mitral valve prolapse. Most cases are subclinical and undiagnosed. The more severe forms of mitral valve disease have a high probability of causing pulmonary edema. Both mitral valve regurgitation and mitral stenosis cause excessive left atrial pressure, a marked predisposition to elevate pulmonary venous pressure, and thus edema. Mean left atrial pressure greater than 30 mm Hg can be rapidly fatal. With subacute or chronic elevation of left atrial pressure, the pulmonary lymphatics can greatly increase lymph drainage and compensate for atrial pressures up to 40 mm Hg.

Physiologic compensation for elevated left atrial pressure maintains cardiac output by increasing blood volume. With increased blood volume, however, the functional cardiac reserve decreases. Any abrupt fluid overload may easily precipitate acute pulmonary edema. Liposuction surgeons must be aware of their patients’ preoperative left atrial pressure. They must know the risk of an acute IV fluid overload in a patient who already has excess intravascular fluids from subcutaneous infiltration of tumescent anesthesia.

In humans the normal pulmonary capillary pressure is 7 mm Hg, and plasma osmotic pressure is 28 mm Hg. Canine studies have shown that pulmonary edema appears abruptly as soon as the pulmonary capillary pressure exceeds the plasma colloid osmotic pressure. Extending this finding to humans, a safety factor of 21 mm Hg seems to protect against pulmonary edema. When the pulmonary capillary pressure abruptly exceeds 40 to 50 mm Hg, however, fulminant and rapidly fatal pulmonary edema can ensue.

Lethal Cycle

The volume of IV fluid necessary to precipitate acute pulmonary edema is predictable by multifactorial, probabilistic dose-response function. In other words, the volume that might correspond to a median lethal dose (LD50) of IV fluids should be determinable. Similarly, there is a dose of IV fluids that should produce fatal pulmonary edema in 1:1000 patients. Unfortunately, this threshold dose for toxicity is unknown. Because IV fluids are not necessary with the true tumescent technique, it is safer simply to avoid IV fluid infusions.

The patients most susceptible to acute pulmonary edema will likely have multiple predisposing factors, including mitral valve disease (mitral stenosis or regurgitation), drug interactions causing dysrhythmias or acute cardiac decompensation, preexisting cardiopulmonary vascular disease, metabolic or respiratory acidosis, metabolic effects of surgical trauma (e.g., inflammatory mediators), and fat emboli.

The interaction between excessive IV fluids and systemic anesthetic drugs may be the most common predisposing factor to acute liposuction-related pulmonary edema. As emphasized earlier, administration of large IV fluid doses to patients already fluid overloaded from the tumescent infiltration is dangerous. Anesthesiologists should be familiar with the fluid physiology of tumescent anesthesia to prevent serious problems.

Swan-Ganz Studies. Although some anesthesiologists have proposed it to study the intravascular fluid status of tumescent liposuction patients, Swan-Ganz catheterization is too dangerous to be used merely to determine the maximum safe volume of IV fluids. In Orange County, California, for example, four deaths within 6 years resulted from faulty Swan-Ganz catheter placement in patients with cardiac disease.10 Since many more liposuction surgeries are performed than Swan-Ganz catheterizations, the risk of catheter placement is much greater than that of liposuction.


The tumescent liposuction of less than 4 L of supranatant fat and less than 3% of body weight does not require IV fluid supplementation. By the time the surgeon has done so much liposuction that the patient requires IV fluids, the amount of liposuction is excessive, by definition. With true tumescent liposuction, no rationale exists for giving IV fluid supplementation.


  1. Rohrich RJ, Beran SJ, Fodor PB: The role of subcutaneous infiltration in suction-assisted lipoplasty: a review, Plast Reconstr Surg 99:514-526, 1997.
  2. Hauser CJ et al: Oxygen transport responses to colloids and crystalloids in critically ill surgical patients, Surg Gynecol Obstet 150:811-816, 1980.
  3. Klein JA: Tumescent technique for local anesthesia improves safety in large volume liposuction, Plast Reconstr Surg 92: 1085-1098, 1993.
  4. Klein JA: The tumescent technique, Dermatol Clin 8:425, 1990.
  5. Collins JV et al: Some aspects of pulmonary function after rapid saline infusion in healthy subjects, Clin Sci Mol Med 45:407-410, 1973.
  6. Virgilio RW et al: Colloid vs crystalloid resuscitation: is one better? Surgery 85:129-139, 1979.
  7. Hahn RG, Svensén C: Plasma dilution and the rate of infusion of Ringer’s solution, Br J Anaesth 79:64-67, 1997.
  8. Gilliland MD, Coates N: Tumescent liposuction complicated by pulmonary edema, Plast Reconstr Surg 99:215-219, 1997.
  9. Guyton AC, Hall JE: Textbook of medical physiology, Philadelphia, 1996, Saunders.
  10. Orange County Coroner’s Office: Cases 87-02972, 88-0348-EL, 91-05743, and 92-06995.
BOX 9-1 Etiology of Pulmonary Edema
High Capillary Pressure
Iatrogenic (extrinsic)
      Excessive IV crystalloid infusion
       Peritoneal or bladder irrigation
Left-sided heart failure (intrinsic)
       Cardiac valvular insufficiency
       Atherosclerotic cardiovascular disease
       Acute myocardial infarction
Inflammation mediated (Adult Respiratory Distress Syndrome)
Drug reaction
Gastric aspiration
Fat embolism
Transfusion reaction
Massive blood transfusion
Burn-inhalation injury
Acute pancreatitis
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