The Tumescent Technique By Jeffrey A. Klein MD
Extracellular postliposuction edema occurs when excessive fluid fills the extracellular space postoperatively. The two factors responsible for extracellular edema are impaired lymphatic drainage and excessive capillary filtration. Lymphedema is distinct from venous capillary edema,1 and the treatments for these conditions also differ.
Maximum postliposuction edema occurs when egress of subcutaneous fluid is prevented (1) by trapping the maximum amount of bloody fluid within the subcutaneous space and (2) by simultaneously blocking all lymphatic drainage. This situation is produced by closing incisions with sutures, then applying a high degree of external compression to collapse lymphatic capillaries.
In contrast, open drainage with bimodal compression minimizes postliposuction edema. Open drainage refers to expedited drainage of blood-tinged anesthetic solution through incisions not closed by sutures. Bimodal compression refers to two sequentially applied degrees of postoperative compression: (1) relatively high-grade compression that accelerates the drainage through open incisions and (2) low-grade compression, employed after drainage has ceased, that is mild enough not to collapse the lymphatic capillaries but adequate to increase interstitial hydrostatic pressure.
Lymphatic Function and Lymphedema
To facilitate optimal healing after liposuction, the surgeon must have a thorough understanding of the pathophysiology of edema and the relevant vocabulary. The body fluids are solutions consisting of water as the solvent and two types of solutes, crystalloids and colloids (Box 11-1).
Impaired Lymphatic Drainage
The surgical effect of liposuction on the lymphatics is unique in two respects. First, liposuction disrupts or destroys most lymphatic capillaries within the targeted adipose tissue. Second, lymphatic damage from liposuction is not permanent; lymphatic capillaries regenerate within a few weeks after being torn asunder by a liposuction cannula. In contrast, lymphatic damage is permanent after surgical lymph node dissection.
Damaged lymphatics are not able to transport excess interstitial fluid back to the blood. Lymphatic insufficiency can cause severe swelling and edema. The persistence of extravasated plasma proteins increases the interstitial fluid osmotic pressure and draws even more fluid out of the capillaries.
The lymphatics are the safety valve that prevents severe edema. The lymphatic system is critical to the homeostasis of interstitial fluid protein concentration, interstitial fluid volume, and interstitial fluid pressure. The lymphatic system controls and compensates for interstitial fluid overflow by returning excess interstitial fluid and protein to the circulation.
Under normal circumstances, 2 to 3 L of lymph fluid containing large molecules is removed each day from the interstitial space and returned to the blood by way of the lymphatics. The lymph fluid that is derived from interstitial fluid has a protein content of about 20 g/L. The removal of protein from the interstitial space is essential; without functioning lymphatics, death would occur in 1 or 2 days.
Excessive Capillary Filtration
Excessive capillary filtration, or fluid shift from the intravascular to the interstitial space, is influenced by (1) increased capillary permeability, (2) decreased plasma colloid osmotic pressure, and (3) increased capillary hydrostatic pressure.
Increased capillary permeability occurs after liposuction as a result of trauma, ischemia, and associated inflammatory mediators (e.g., prostaglandins, histamines). Massive trauma to subcutaneous hematic capillaries allows the leakage of large molecules out of intravascular spaces and into interstitial spaces. The resulting relative increase in interstitial osmotic pressure escalates the osmolar edema.
Decreased plasma colloid osmotic pressure occurs after liposuction as a result of (1) loss of plasma protein through ruptured capillaries, (2) consumption of hemostatic procoagulant proteins, (3) iatrogenic hemodilution with unnecessary intravenous (IV) fluid crystalloids, and (4) possible hemorrhage.
Increased capillary hydrostatic pressure occurs after liposuction as a result of general anesthesia and secondary immobilization of limbs, with loss of sympathetic vascular tone. Acute renal failure, as seen in patients with excessive blood loss before the advent of tumescent liposuction, causes kidney retention of salt and water.
Other causes of increased capillary filtration must be included in the differential diagnosis of edema (Box 11-2). Causes of increased capillary permeability include bacterial infections and vitamin C deficiency. Causes of decreased plasma protein and plasma colloid osmotic pressure include proteinuria, liver disease, and serious malnutrition. Causes of increased capillary pressure include excessive salt retention by the kidneys, as in chronic renal failure and mineralocorticoid excess (Cushing syndrome); high venous pressure, as in heart failure, muscle paralysis, and failure of venous valves; and decreased arteriolar resistance, as from hyperthermia or vasodilator drugs.
Lymphedema is edema caused by inadequate lymphatic function resulting from agenesis, destruction, or obstruction of lymph vessels or lymph nodes. These causes include primary lymphedema from developmental dysgenesis (impaired development, idiopathic obliteration of the lymphatics) and secondary lymphedema from acquired physical destruction (surgery, radiation, infection) or obstruction (malignancy, parasitic infection). Postliposuction lymphedema is unique in that it usually resolves spontaneously with time, typically within 2 to 6 months. The more common causes of lymphedema are chronic and usually not self-limited.
On a molecular level, lymphedema is the result of a failure of the lymphatics to remove large-molecular-weight proteins from the interstitial space. Whereas both hematic and lymphatic capillaries reabsorb interstitial water, the lymphatic capillaries are the only route for absorbing proteins from interstitial tissue. No other route is available for the removal of excessive interstitial fluid proteins. The excess proteins simply accumulate indefinitely, along with a proportionate increase in osmotically attracted interstitial water.
The lymphatic capillaries throughout the adipose tissue undergo damage from cannulas. Lymph capillary injury is an inevitable consequence of liposuction, but the extent and the duration of liposuction lymphedema can be significantly reduced by rational postoperative care. Early and aggressive efforts to expel as much blood-tinged anesthetic fluid as possible are immediately beneficial. Once the drainage fluid is allowed to become trapped within interstitial microloculations, the edema becomes persistent, resolving only when the injured lymphatic capillaries regenerate.
Pitting Versus Nonpitting Edema. The acute lymphedema that occurs soon after liposuction demonstrates pitting on firm digital pressure. The lymphedema of recent onset, especially in a young patient, may be associated with pitting edema. After years of accumulated interstitial deposition of protein, however, chronic lymphedema gradually becomes a nonpitting edema.
In general, pitting edema is usually associated with venous capillary edema caused by excessive capillary filtration of intravascular water. Pitting edema is present when a firm, continuous pressure of a finger pressing on the affected skin causes a distinct temporary depression that can last for many minutes. Chronic lymphedema of the skin and subcutaneous tissue has the clinical appearance of a brawny, coarse, nonpitting edema. Chronic lymphedema causes an accentuation of adnexal pores and hair follicle ostia, giving the overlying skin an orange peel (peau d’orange) appearance.
Treatment. The best therapeutic approach to lymphedema is a vigorous effort at prevention. The open drainage and bimodal compression technique will prevent most of the edema that might otherwise follow tumescent liposuction. Even with this technique, however, some postliposuction edema occurs and may require weeks or months to resolve.
Treatment of lymphedema not associated with liposuction is less than satisfactory. In mild cases of primary lymphedema, treatment is high elevation of the affected limb, with simultaneous elastic support, and intermittent pneumatic compression. With secondary lymphedema, treatment is usually symptomatic.
Proteins and other large molecules are too large to be absorbed into the blood directly across capillary membranes. Lymphatic capillaries have large gaps between adjacent endothelial cells that permit passage of large-molecular-weight substances. Lymphatic endothelial cell edges slightly overlap each other, forming minute unidirectional endothelial valves into the lymphatic capillary lumen. In addition, some lymphatic capillary endothelial cells overlap to a much greater degree and form internal bivalvular flaps that act as one-way valves inside the lymphatic capillary. This valve structure inhibits retrograde lymph flow (Figure 11-1).
Microscopic Structure. The wall of a terminal lymphatic capillary has an interior layer formed by a single, thin endothelial cell and an external, widely fenestrated basal lamina. In many places, wide gaps exist between adjacent endothelial cells. These holes in the lymphatic capillaries facilitate the uptake of macromolecules: proteins, bacteria, blood cells, and tumor cells.2 Blood capillaries, with continuous basement membranes and relatively tight intracellular junctions, resist absorption of large molecules.
Anchoring fibrils connect the lymphatic endothelial cells to the surrounding collagenous connective tissue.3 These anchoring fibrils reinforce the valvular function of individual lymphatic endothelial cell edges. The anchoring fibrils on the upstream edge of the lymphatic capillaries tend to spread the cell’s edge and facilitate the entry of interstitial fluid into the lymphatic capillary.
Effects of Edema and Compression. An important distinction exists between (1) the effects of increased interstitial pressure caused by edematous fluid overload and (2) the effects of external compression that elevates interstitial hydrostatic pressure (Figure 11-2).
In the first situation, expansion of the swollen interstitial tissue causes the inside diameter of the lymphatic capillary to dilate. Edema causes each point within the tissue compartment to move farther apart from every other point; this includes the lymphatic endothelial cells. In effect, as the collagenous infrastructure of the interstitial tissue expands, the anchoring fibrils tug on the lymphatic epithelial cells and expand the inside diameter of the lymphatic capillaries. The expanded inside diameter of the lymphatic capillary facilitates homeostatsis by increasing lymph flow, which tends to reduce the edema. With progressively more edema, however, the anchoring fibrils literally pull on the individual lymphatic endothelial cells to such a degree that the capillaries no longer function as a tubular channel. The lymphatic capillary becomes nonfunctional.
In the second situation, external compression squeezes the interstitial tissue and can compress the capillary lumen. This constriction limits the flow of lymph and ultimately impairs the lymphatic capillary’s ability to reduce edema.
Lymphatic Pump Mechanism. The rate of lymph flow is determined by the lymphatic pump mechanism and interstitial fluid pressure. The one-way lymphatic capillary valves allow a degree of lymphatic pumping when lymphatic capillaries are compressed intermittently by an external force, such as large muscles of a limb, body movements, arterial pulsation, and external massage.
When larger lymphatic vessels become stretched with lymph fluid, the smooth muscle in the wall of the vessels contracts automatically, forcing the lymph fluid through the proximal valve and into the next segment of the lymphatic vessel. As this newly filled segment of lymphatic vessel is stretched with fluid, its intrinsic smooth muscles contract, advancing the fluid into the next segment. This sequential segmental lymphatic contraction is the basis for the lymphatic pumping mechanism, which generates the negative interstitial fluid pressure.
For the liposuction patient, excessive external pressure from compressive postoperative garments may be counterproductive. Continuous compression from a high-compression garment may cause the delicate lymphatic capillaries to collapse, impede lymph flow, and effectively block lymphatic drainage.
Interstitial Fluid Pressure. The normal interstitial fluid pressure is subatmospheric and ranges from –6 to 0 mm Hg (relative to atmospheric pressure). Experimental measurements in dogs show that the rate of lymph flow varies as a function of interstitial fluid pressure.4 Minimal lymph flow occurs below –6 mm Hg. Between –6 and 0 mm Hg the rate of lymph flow increases exponentially. Lymph flow reaches a maximum of 1 or 2 mm Hg. The rate of flow at 0 mm Hg is 20 times greater than at –6 mm Hg.
When interstitial pressure exceeds 1 or 2 mm Hg, the lymph flow rate reaches a plateau. Lymph flow fails to increase with higher interstitial fluid pressures, probably because of excessive tissue pressure compressing the outside area of larger lymphatic vessels, thereby impeding lymph flow. Therefore a high-compression postoperative garment is unlikely to increase the rate of lymph flow after liposuction.
The clinical laboratory measurement of serum osmolality requires that a serum sample be frozen as soon as possible after it is obtained. A long delay in freezing the sample exposes the serum proteins to temperature-dependent proteolysis. By effectively multiplying the number of solute particles in solution, proteolysis amplifies the osmolality of a sample.
The trauma from tumescent liposuction allows plasma proteins to leak out of injured capillaries and into the subcutaneous wound space. Once a protein molecule has entered the subcutaneous wound space, it can only reenter the blood by way of lymphatic absorption. Between adjacent capillary endothelial cells are intercellular clefts or pores about 6 to 7 nm in width, slightly smaller than the diameter of an albumin molecule. The size of a plasma protein molecule determines the probability that it will diffuse through a gap between capillary endothelial cells. Gaps in the capillary wall are generally too small to permit the reentry by diffusion of extravasated plasma proteins back into the intravascular space.
Fresh wound fluid has an osmolality of approximately 10 mOsmol greater than serum. This osmotic pressure gradient tends to draw water from intravascular space, across the capillary wall, and into the wound space. Incubating residual blood-tinged tumescent fluid at body temperature increases the osmolality of fluid over time. This exacerbates postliposuction edema by an osmotic amplification by incubation.
The rate at which water-soluble molecules diffuse through capillary membrane is 80 times as great as the rate at which water molecules flow linearly along the capillary. Thus the water of interstitial fluid and that of plasma are rapidly interchanged. Iatrogenic hemodilution by infusion of IV crystalloid fluids increases intravascular hydrostatic pressure and thus augments edema.
The degree to which external compression influences the intravascular uptake of water after tumescent liposuction is unknown. Opposing the osmotic gradient with applied external compression is the same as with augmented interstitial hydrostatic pressure. External compression counteracts the effects of intravascular hydrostatic pressure but hinders the lymphatic uptake of wound fluid that contains protein molecules.
Study: Fluid Incubation. The difference between serum osmolality and osmolality of liposuction aspirate was studied in eight patients. The mean serum osmolality was 294.6 mOsm/L (range 290 to 297). The mean osmolality of an immediate sample of infranatant blood-tinged anesthetic solution was 307.5 mOsm/L (range 300 to 313). The mean osmolality of a 24-hour incubated (37° C) sample of infranatant was 311.5 mOsm/L (range 306 to 319).
Thus the difference is (307.5 – 294.6) 12.9 mOsm/L between a patient’s serum osmolality and the residual blood-tinged tumescent anesthetic solution that remains within the subcutaneous tunnels of suctioned fat. Assuming that serum osmolality is unchanged, the theoretic gradient between serum and the incubated drainage fluid entrapped within a subcutaneous wound for 24 hours is (311.5 – 294.6) 16.9 mOsm/L. The incubation of entrapped drainage fluid augments the osmotic gradient between the intravascular space and the subcutaneous space. Closing incisions with sutures and preventing the drainage of blood-tinged anesthetic solution therefore amplify the liposuction edema.
Thighs and Abdomen
Postliposuction edema can be particularly common in certain situations. For example, circumferential liposuction of the thigh can theoretically cause prolonged postoperative edema by precipitating a vicious cycle and temporarily obliterating a significant portion of lymphatic drainage from the lower limb. This liposuction-induced edema produces a mild compartment syndrome with local hematic capillary ischemia, decreasing delivery of oxygenated blood, augmenting anaerobic metabolism, and increasing capillary permeability. This increased capillary permeability produces still more edema.
The hematic capillary edema further compresses the lymphatic capillaries and inhibits the lymphatic clearance of proteinaceous edema fluid. Postoperative swelling is ultimately prolonged unnecessarily for many weeks.
The abdomen tends to require more time than other areas for resolution of postliposuction edema. When the entire abdomen is treated by tumescent liposuction, a significant volume of drainage must be accommodated by the drainage ports along the inferior abdominal margin. Premature closure of slit incisions on the abdomen will entrap a considerable volume of blood-tinged anesthetic solution. The result is prolonged lower abdominal swelling and tenderness. Placing punch excisions or adits along the lower abdomen tends to facilitate more complete drainage.
Amplified Liposuction Edema Syndrome
Every liposuction patient has some degree of postoperative edema as the result of leakage of intravascular plasma proteins from traumatized capillaries, along with some liposuction-induced impairment of subcutaneous lymphatic function. This can be minimized by using postoperative care that includes open drainage and bimodal compression.
Excessive liposuction may be associated with massive postoperative edema, referred to as amplified liposuction edema (ALE). A combination of factors predisposes to this dangerous type of edema. In its mild form, ALE is generally localized to the areas treated by liposuction. In progressive degrees this massive edema can spread to areas distant from the site of tissue trauma, resulting in massive weight gain and systemic complications such as acute renal failure and effusions (pleural, peritoneal, pericardial). In extreme cases, patients can have fatal pulmonary edema and end-stage central nervous system edema.
Therefore ALE is a type of multifactorial edema that can increase progressively. This generalized edema is most likely to occur after extensive or excessive liposuction that overwhelms compensatory homeostatic mechanisms.
Lymphatic Impairment. Massive lymphatic dysfunction is caused by (1) liposuction cannula–induced lymphatic obliteration, (2) lymphatic system overload with excessive, highly osmotic interstitial fluid drainage, and (3) lymphatic vessel occlusion by excessive external compression.
As discussed, lymphatic impairment is the most significant cause of edema. The lymphatic system acts as the physiologic safety valve that protects against edema. When challenged by impending edema, the lymphatics compensate and increase lymph flow by 10-fold to 50-fold. The sudden onset of a multifactorial edema and the simultaneous loss of effective compensatory lymphatic function after liposuction can result in an unprecedented degree of edema.
Fluid Leak. Overwhelming plasma protein leakage from surgically ruptured capillaries can result from massive liposuction trauma. Normal hemostasis of ruptured capillaries involves the formation of a primary platelet plug and secondary fibrin deposition. The body’s supply of platelets and fibrinogen is finite, however, and can be exhausted by massive trauma of capillaries. An insufficient hemostatic plug permits ongoing leakage of both plasma and red blood cells.
This traumatic thrombocytopenia and hypoprothrombinemia can lead to a subacute consumptive coagulopathy. Because of insufficient plugging of ruptured capillaries, significant quantities of osmotically active molecules ooze into the subcutaneous space. After extensive liposuction, inflammatory proteins, tissue fragments, cellular debris, plasma, and erythrocytes all contribute to increased oncotic pressure within the subcutaneous wound and interstitial space. The ultimate result is a massive, osmotically mediated, subcutaneous edema.
Sutures. Sutured incisions prevent the drainage of the blood-tinged anesthetic solution and entrap a massive accumulation of highly osmotic, subcutaneous edema fluid. Closing all incisions with sutures is one way of managing the copious drainage of blood-tinged anesthetic solution. Although closing incisions with sutures does simplify postoperative care, it dramatically worsens and prolongs postliposuction edema.
Inflammatory Mediators. Trapped within the edema fluid, mediating substances ultimately exacerbate postliposuction edema. The blood-tinged anesthetic solution contains erythrocytes and other inflammatory mediators, which promote increased capillary permeability and plasma protein leakage.
Proteolysis. Temperature-dependent proteolysis of plasma proteins and the proteinaceous inflammatory debris causes progressive increases of the osmolality of the trapped edema fluid. Incubation of wound drainage at 37° C (98.6° F) within the subcutaneous space promotes the temperature-dependent cleavage of extravasated plasma proteins, which amplifies the postliposuction edema.
Hemodilution. Iatrogenic hemodilution from IV crystalloids (physiologic saline or lactated Ringer’s solution) further promotes edema by the following:
- Providing an abundant supply of water, which diffuses specifically into the traumatized tissue as a result of elevated oncotic pressure in wound tissue from extravasated plasma proteins
- Diluting the intravascular protein concentration, thereby diminishing the intravascular-extravascular oncotic pressure gradient
- Providing a surfeit of intravascular isotonic solution, 80% of which will redistribute into the interstitial space throughout the entire body, including the liposuctioned tissue
Prevention: Case Studies
A surgeon may unknowingly cause ALE syndrome. As mentioned, postliposuction care may even promote edema (1) by closing all incisions with sutures, thereby trapping the high osmotic drainage in the subcutaneous wound space, and (2) by applying a highly compressive garment that collapses any remaining functional lymphatic capillaries and prevents lymphatic transport of the protein-laden edema fluid.
The risk of causing ALE syndrome is minimized by (1) avoiding excessive liposuction, (2) using open drainage and bimodal compression, and (3) not giving IV fluids. Case Reports 11-1 and 11-2 further illustrate ALE risk factors and preventive measures.
Not “Third Spacing”
ALE and tumescent infiltration are not analogous to the phenomenon of posttraumatic “third spacing” of sequestered fluid in the extracellular space, a well-recognized consequence of tissue trauma (see Chapter 9). Traumatic injury to an extremity results in the mobilization of fluids and electrolytes to the area of injury. Third spacing after nonthermal traumatic injury occurs immediately and is maximal by 5 to 6 hours.5 ALE is maximal 24 to 72 hours after surgery.
Tumescent infiltration of physiologic saline and dilute epinephrine is not analogous to third-space sequestration of fluid. The constituent solutes of the third-space fluid are in dynamic equilibrium with the functional or exchangeable extracellular fluid. For example, in the third-space phenomenon of a pleural effusion, the concentration of electrolytes or drugs is in equilibrium with their concentration in nearby extracellular fluid.
In contrast, the profound vasoconstriction of the tumescent technique precludes rapid chemical transfer and equilibrium of lidocaine and epinephrine between tumescent and surrounding nontumescent tissues. This chemical isolation, along with slow diffusion of drugs out of the tumescent tissue, is the basis for the therapeutic success of the tumescent technique.
- Majino G, Joris I: Cells, tissues, and disease: principles of general anesthesia, Cambridge, Mass, 1994, Blackwell.
- Odland GF: Structure of skin. In Goldsmith LA, editor: Physiology, biochemistry, and molecular biology of the skin, ed 2, New York, 1991, Oxford University Press.
- O’Driscoll CM: Anatomy and physiology of the lymphatics. In Charman WN, Stella VJ, editors: Lymphatic transport of drugs, Boca Raton, Fla, 1992, CRC Press.
- Guyton AC, Hall JE: The microcirculation and the lymphatic system: capillary fluid exchange, interstitial fluid, and lymph flow. In Textbook of medical physiology, ed 9, Philadelphia, 1996, Saunders.
- Gann DS, Foster AH: Endocrine and metabolic responses to injury. In Schwartz SI, Shires GT, Spencer FC, editors: Principles of surgery, ed 6, New York, 1994, McGraw-Hill.
Figure 11-1 Lymphatic capillary structure permits one-way passage of high-molecular-weight substances through gaps in basement membrane, between lymphatic endothelial cells (open junction flap valves, FV), and into lumen of lymphatic capillary. One-way valves (bileaflet valves, BV) within lymphatic capillary are formed by specialized, overlapping endothelial cells located along terminal lymphatic capillaries. Pressure-sensitive smooth muscles (SM) encircle collecting lymphatic capillaries; when a collecting capillary becomes sufficiently distended with lymph, smooth muscles contract, forcing lymph to travel proximally through one-way valves. Anchoring filaments (AF) provide attachments between lymphatic capillary endothelial cells and collagenous connective tissue matrix of interstitial space. With interstitial edema, anchoring filaments pull outward on lymphatic endothelial cells, increasing inside diameter of lymphatics and thereby facilitating and increasing rate of lymph flow to compensate for edema.
Figure 11-2 Three cross-sectional views of a lymphatic capillary within subcutaneous fat of thigh represent distinct degrees of interstitial edema that might occur in tumescent liposuction patient. A, Under normal circumstances, subcutaneous lymphatic capillaries help maintain interstitial fluid homeostasis by transporting lymphatic fluid at same rate as it is produced. Without excessive interstitial fluid or edema, lymphatic capillaries are neither engorged nor compressed. B, Because of anchoring fibrils that connect lymphatic capillary endothelial cells to interstitial collagen matrix, internal diameter of lymphatic capillaries expands as tumescent infiltration expands subcutaneous interstitial volume and increases interstitial pressure. C, Postoperative compression garment augments subcutaneous interstitial pressure and compresses both hematic and lymphatic capillaries. During first 48 hours, hematic capillary compression increases hemostasis and decreases bruising. After 48 hours, lymphatic capillary compression promotes lymphostasis and increases edema.
|CASE REPORT 11-1 Excessive Liposuction and Progressive Edema|
|A 39-year-old healthy, athletic female weighing 46 kg (102 pounds) had liposuction of the abdomen, hips, waist, back, and thighs under general anesthesia using tumescent technique for hemostasis. Five liters of fluid and fat was aspirated with 3-mm and 4-mm cannulas. Total volume of supranatant fat and total dose of lidocaine were not documented. For the first 48 hours the patient was in moderate discomfort but ambulated regularly, wearing a tight postoperative compressive garment that covered the torso and lower extremities.|
|On the third postoperative day the patient noted onset of swelling, which progressed to significant pitting edema of the lower extremities and fingers. For the next 2 days, despite treatment with furosemide (40 mg by mouth twice daily), urine output was minimal. By the fifth postoperative day the edema was severe, and the patient was given a single oral dose of furosemide (120 mg), and urine output was more than 3 L over the following 8 hours. Her subsequent course was unremarkable, with no evidence of anemia at any time.|
|Discussion. Too much fat removed by liposuction, too many areas treated by liposuction, closing incisions with sutures, and excessive compression all contribute to ALE. In this patient the use of furosemide proved helpful in treating the oliguria and suggests the possibility of transient renal insufficiency. The preventive approach would have been to do less liposuction, treat fewer areas on a single day, and allow the incision to remain open.|
|CASE REPORT 11-2 ALE Syndrome: Obesity, Foam, Other Factors|
|A 49-year-old obese female weighing 96 kg (211 pounds) had liposuction of the abdomen, circumferential thighs, back, flanks, buttocks, knees, and arms using tumescent technique for hemostasis plus a mastopexy, all under general anesthesia. Preoperative hematocrit was 39.2%. The volume of tumescent anesthesia was 8400 ml. Intraoperative IV fluids consisted of 2600 ml of crystalloid and 2000 ml of colloid (Plasmalite). The volume of aspirated fluid and fat was 14,680 ml, using 3-mm and 4-mm cannulas. After the 10-hour surgery, all liposuction incisions were closed with sutures, and Reston foam was applied to the treated areas. A compression garment was applied to the torso and lower extremities. Reston foam, tape, and Coban dressings were applied to the arms.|
|On the first postoperative day the patient ambulated slowly. On the second postoperative day, however, the patient could not bend her legs because of lower extremity edema. Later the same day, approximately 48 hours after surgery, edema had progressed; swollen fingers prevented her gripping the hand of a friend. When the compression garment was cut off in an attempt to relieve pain, large blisters were noted along the margins of the Reston foam. By the third postoperative day the patient was so swollen that she could not arise from the couch. In an attempt to go to the bathroom, she fell and could not get up, and was forced to defecate on the floor.|
|On the fourth postoperative day the Reston foam was partially removed, causing extreme pain; multiple denuded bullae were apparent, and the patient reported a low-grade fever. The next day the swelling had begun to lessen, but orthostatic dizziness and lightheadedness persisted. On the sixth postoperative day the patient was instructed to soak off the remaining Reston foam, clean deepithelialized skin wounds with hydrogen peroxide, and apply Silvadene cream. On the seventh day the patient telephoned to report a temperature of 102° F (39° C), and ciprofloxacin (250 mg three times daily) was prescribed.|
|From the fifteenth to twentieth postoperative days she was hospitalized for treatment of cellulitis of the left thigh and leg. Cultures were positive for Pseudomonas and Escherichia coli. The patient reported that several days before her admission, her weight was 116 kg (256 pounds), or 20 kg greater than her weight just before surgery. Several days after admission, a hospital nutrition assessment report noted a weight of 105.5 kg (232 pounds), or 9 kg above her preoperative weight.|
|Discussion. This case demonstrates ALE syndrome resulting from excessive volume of liposuction, too many areas treated, incisions closed with sutures, and excessive compression. It also shows risk factors associated with use of Reston foam and hydrogen peroxide.|
|The most common cause of cutaneous bullae after liposuction is excessive superficial liposuction that injures the subdermal vasculature. Rasping the underside of the dermis will produce an epidermal bulla and prolonged dyschromia. Inattention to the delicate subdermal vascular plexus and aggressive scraping of fat from the undersurface of the dermis will produce some degree of dermal injury, which can include full-thickness dermal necrosis. Denuded traumatized dermis is a likely medium for infectious cellulitis and necrotizing fasciitis. Occluding an ischemic wound with Reston foam increases the risks of infection.|
|Reston foam can cause an intense irritant, traumatic, or allergic contact dermatitis; a bullous reaction can result in a persistent, disfiguring, postinflammatory hyperpigmentation. Although the foam attenuates the appearance of bruising, it does not improve the postoperative recovery, reduce pain or tenderness, or shorten the healing process. No evidence suggests that the ultimate aesthetic results of liposuction are improved by the application of this foam. More importantly, Reston foam prevents the patient from showering daily, which also may predispose to wound infections. The foam obscures the visual examination of the skin and may delay the diagnosis of a cutaneous infection.|
|BOX 11-1 Physiology of Solutions: Definitions|
|crystalloid: Substance capable of being separated from a solution in the form of crystals; distinct from a colloid. Crystalloids in solution can pass easily through semipermeable membranes. Most important physiologic crystalloids are the electrolytes Na+, K+, Cl–, and|
|colloid: Substance characterized by little or no tendency to diffuse through animal membranes or vegetable parchment. Colloids do not readily crystallize, have appearance of glue, and are relatively inert chemically but not very stable. Proteins and large, organic, hydrophilic molecules are examples of colloids. Most important physiologic colloid molecule is albumin.|
|osmosis: Tendency of fluids, separated by porous septa or membrane, to diffuse and pass through the membrane and mix with each other.|
|osmotic pressure: Excess pressure that must be applied to a solution to prevent entry of pure solvent when they are separated by a semipermeable membrane, or excess pressure that develops in the solution when osmosis is allowed to occur in such circumstances. Solutions that have identical osmotic pressures are isotonic solutions. Numeric unit is the osmol, as in osmols (Osm) or milliosmols (mOsm) per liter.|
|oncotic pressure: Osmotic pressure exerted by a colloid, especially plasma proteins. Starling demonstrated that colloids in a liquid solution or suspension exert a small osmotic pressure. This oncotic pressure fluctuates widely, however, because colloidal molecules or aggregates called micellae vary considerably.|
|mole: Unit of measurement that specifies the number of objects as a multiple of Avogadro’s number (6.023 × 1023). A mole of any particular substance has a mass expressed in grams that is numerically the same as its molecular or atomic weight. For example, a mole of carbon 12 contains 6.023 × 1023 atoms and weighs 12 grams. If each molecule of a solute ionizes into two ions, each of which is osmotically active, 1 mol of solute equals 2 osmols.|
|molarity (M): Number of moles of solute per liter of solution.|
|osmolarity: Number of moles of osmotically effective, dissolved particles per liter of solution.|
|The molarity of a given solution varies in general with temperature. Experiments show that osmotic pressure (π) of a solution is a function of its molarity: π = rMT, where r is the gas law constant, M is the molarity of the solution (i.e., number of moles of solute per liter of solution), and T is Kelvin temperature.|
|molality (m): Number of moles of solute per kilogram of solvent.|
|osmolality: Number of moles of osmotically effective, dissolved particles per kilogram of solvent.|
|It is easy to prepare a solution of given molality by accurate weighing procedures. When one mole of any substance is dissolved in a kilogram of water, the solution produced freezes at –1.850° C. From this, osmolality of a sample of serum or tumescent fluid can be determined. Normal subjects have an initial serum osmolality between 273 and 293 mOsm/kg of water.|
|Osmolarity determines the osmotic pressure of a solution. Osmolality is easily measured by freezing point depression. When solubility is very small, molarity and molality of the solution are approximately the same.|
|BOX 11-2 Postliposuction Edema of Lower Extremity: Differential Diagnosis|
|Excessive Capillary Filtration|
|A. Increased capillary hydrostatic pressure caused by increased venous pressure|
|1. Congestive heart failure (CHF)|
|2. Prolonged dependency|
|3. Valvular venous insufficiency|
|4. Arteriovenous fistula|
|5. Venous obstruction|
|a. Extrinsic: constricting band, tumor|
|b. Intrinsic: thrombosis, mass|
|B. Increased capillary permeability|
|1. Inflammation: bacterial toxins, allergic reactions|
|2. Physical injury: trauma, burns, freezing, radiation|
|4. Physiologic stimuli|
|a. Exogenous poisons or drugs|
|b. Endogenous electrolyte abnormalities|
|C. Decreased plasma colloid osmotic pressure in capillary; decreased reabsorption of interstitial fluid|
|1. Hemodilution with excess IV fluids|
|2. Protein-losing disease nephropathy, gastrointestinal enteropathy|
|3. Protein loss from skin burn|
|4. Malnutrition with hypoproteinemia|
|5. Hemorrhagic plasma protein loss|
|6. Hypoproteinemia of cirrhosis|
|D. Increased osmotic pressure in interstitial fluid|
|1. Excessive IV saline|
|2. Lymphatic obstruction with accumulation of proteins|
|3. Increased capillary permeability, allowing protein leak|
|4. Salt retention response to stress, hypertension, CHF, or renal disease|
|A. Primary: agenesis/dysgenesis|
|1. Impaired development|
|2. Destroyed lymphatics|
|B. Secondary: lymphatic obstruction or insufficiency|