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The Tumescent Technique By Jeffrey A. Klein MD



Chapter 14:

Perioperative Bleeding Disorders

Surgical blood loss was the greatest danger of the first liposuction techniques. Because of blood loss, any liposuction aspirate of more than 1500 to 2000 ml was indication for an autologous blood transfusion. For example, among 108 patients who had large-volume suction lipectomy under general anesthesia with no tumescent vasoconstriction, 30% to 45% of the aspirate volume was blood. This patient population required 227 units of autologous blood and 2 units of heterologous blood for transfusion.1

The tumescent technique for liposuction has eliminated most of the risks of surgical bleeding previously associated with liposuction. However, unusual causes of blood loss with tumescent liposuction remain. Undiagnosed inherited bleeding disorders, such as von Willebrand’s disease or hemophilia, can also cause unexpected bleeding. Common over-the-counter drugs can impair normal coagulation and cause significant bleeding problems even with the tumescent technique.

The tumescent technique, first presented in 1986 and published in January 1987, allows liposuction with virtually no blood loss. The tumescent technique was ignored by many liposuction surgeons until 1993, however, when it was published in the plastic surgery literature for the first time. Thus surgical bleeding remained a significant problem for liposuction well into the 1990s, when the most common indication for autologous blood transfusion in Beverly Hills, California, was liposuction. The slow assimilation of a dermatologic surgical technique by plastic surgeons is revealing regarding information exchange between cosmetic surgical specialists.

The original description of tumescent liposuction reported on 22 patients with a mean volume of yellow (bloodless) supranatant fat of 915 ml. The report emphasized that all patients had been treated using local anesthesia instead of general anesthesia. This was also the first published report of the remarkable hemostasis associated with the tumescent technique. The mean volume of infranatant blood-tinged anesthetic solution was 252 ml and contained less than 1.5% packed red blood cell (RBC) volume. Assuming whole blood contains a 40% RBC volume, a simple calculation revealed an average of 10.25 ml of whole blood was aspirated per liter of supranatant fat.2 Therefore most patients lost more blood with the preoperative laboratory evaluation than during the entire liposuction procedure.

Liposuction surgeons, even those who use the tumescent technique, must be aware of the continued dangers of unanticipated surgical and postoperative bleeding.

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a form of systemic bleeding characterized by a depletion of clotting factors and associated with few if any intravascular thrombi. Common causes of DIC include shock, massive tissue trauma, hemorrhage with hemodilution, crush injuries, burns, sepsis, hypothermia, obstetric complications, and transfusion reactions. Excessive liposuction using the superwet technique can also cause DIC. To my knowledge, DIC has not occurred with tumescent liposuction totally by local anesthesia.

In healthy patients the procoagulant and anticoagulant systems maintain a well-balanced state of intravascular homeostasis, with neither system predominating. When multiple factors favor a shift of these biochemical reactions toward coagulation, however, the intravascular consumption of coagulation factors can proceed unchecked. In extreme cases, DIC develops. DIC has been reported in association with general anesthesia, hemodilution, trauma, and hypothermia, all of which are sequelae of excessive liposuction together with infusion of excessive IV fluids.

The clinical diagnosis of DIC is notoriously difficult and is rarely suggested simply by the patient’s appearance. The clinical diagnosis of DIC is usually first suspected with an unexplained abrupt deterioration of the patient’s condition in a clinical setting known to be frequently associated with DIC. A suspected diagnosis of DIC can be confirmed by laboratory tests that show reduced fibrinogen, elevated fibrin degradation products, and a greatly decreased platelet count. Unless DIC is suspected and confirmed with specific laboratory tests, the diagnosis is usually not made while the patient is alive.


Hemodilution can predispose to DIC. The natural homeostatic control of intravascular blood coagulation involves a continuous, delicate, well-balanced interaction between procoagulant and anticoagulant factors.

Hemodilution has been noted to induce a hypercoagulable state.3,4 In vitro a 30% hemodilution with saline significantly increases coagulability.5 Hemodilution may produce abnormal hemostasis before any compromise of tissue oxygen delivery.6 Hemodilution associated with intravenous (IV) lactated Ringer’s solution or normal saline during surgery may predispose to deep venous thrombosis.7

The mechanisms by which hemodilution predisposes to hypercoagulability are not well understood. Hemodilution may disturb the ratio of thrombin to antithrombin III.8 Some preliminary evidence indicates that antithrombin III is decreased to a greater extent after hemodilution than is predicted by calculating the effect of hemodilution alone.9-9b

Hemodilution decreases the concentration of several other anticoagulant factors, thereby inducing acquired forms of protein C deficiency and protein S deficiency. Both deficiencies favor the procoagulant process and contribute to an intravascular consumption of coagulation factors (see Chapter 10).

A hemorrhage is typically followed by hemodilution as interstitial fluid is recruited from the interstitial space into the intravascular space. Similarly, hemorrhage would also be expected to result in homeostatic coagulation. Thus, from a cause-and-effect or teleologic perspective, it is reasonable to associate hemodilution and hypercoagulability.10 If hemodilution is associated with the conversion of prothrombin to thrombin, homeostasis would require that antithrombin be consumed by a thrombin-antithrombin interaction. A relative deficiency in antithrombin would then favor intravascular coagulation.

Tumescent Hemodilution. The infusion of large volumes of crystalloids delivered by both IV infusion and tumescent hypodermoclysis can cause systemic fluid overload and contribute to iatrogenic DIC. In general, if the surgeon anticipates the need for IV fluids with tumescent liposuction, the anticipated volume of liposuction is probably excessive. Prophylactic infusion of IV crystalloids is contraindicated with tumescent liposuction.

Again, as emphasized throughout, the tumescent technique eliminates the need for supplemental IV fluids. When the tumescent technique is used for liposuction, the routine use of IV fluid supplementation is contraindicated.

Tumescent infiltration causes hemodilution with or without subsequent liposuction. A 75-kg (165-pound) female received a total of 5.25 L of physiologic saline in the subcutaneous space by the tumescent technique on two occasions, receiving 35 mg/kg lidocaine each time.11 On the first occasion no liposuction was done; 2 weeks later liposuction produced 1550 ml of supranatant fat. On each occasion the tumescent infiltration of 5.25 L of saline produced significant hemodilution, which was maximal 12 to 24 hours after infiltration. Without liposuction the hematocrit decreased from 35.3 to 32.6 ml/dl; after liposuction it decreased from 36.2 to 32.0 ml/dl. The patient had no evidence of an intravascular fluid deficit, with or without liposuction. On both occasions the tumescent technique produced a postoperative decrease in urine specific gravity and resulted in cumulative urine volumes greater than 70 ml/hr, both of which are evidence of hemodilution.

Liposuction Trauma

Increasing degrees of liposuction trauma produce increasing areas of exposed endothelial surfaces, which activates a greater proportion of circulating platelets and induces progressive intravascular coagulation. In animal studies, increasing amounts of trauma are directly correlated with increasing degrees of thrombosis.12 It is reasonable to assume that the greater the area of the body’s subcutaneous tissue traumatized by liposuction, the greater the amount of intravascular coagulation factors consumed. In addition, increasing surgical trauma induces increased systemic inflammation, which in turn decreases the concentration of circulating free protein S. Acquired or genetic protein S deficiency is a well-established cause of a procoagulant state and thromboembolism (see Chapter 10).


The continuous homeostatic balance between intravascular procoagulation and anticoagulation is a temperature-dependent biochemical process. Hypothermia disturbs this balance and can lead to consumption of coagulation factors. Hypothermia produces marked prolongation of the bleeding time.13

Thrombosis in multiple organs is a common postmortem finding associated with hypothermia. Hypothermia in experimental dogs induces DIC with consumption of multiple clotting factors, and treatment with heparin prevents the decrease in fibrinogen.14 Hypothermia causes DIC in the newborn.15,16 Hypothermia in adults has been reported to cause DIC and pancreatis,17 as well as DIC and thrombocytopenia.18

Both general anesthesia and heavy IV sedation frequently produce mild to moderate perioperative hypothermia as the result of pharmacologic inhibition of thermoregulation and exposure of the patient to the cool operating room environment.

The hypothermia associated with the general anesthesia used with the superwet technique for liposuction can precipitate DIC. Undetected hypothermia is also common during regional, spinal, and epidural anesthesia because core temperature is rarely monitored and patients usually do not feel cold.19

Superwet Technique

The superwet technique for liposuction is characterized by the following:

  1. General anesthesia
  2. Subcutaneous infiltration containing dilute epinephrine without lidocaine
  3. Suboptimal volume of subcutaneous infiltration
  4. Compensation for the suboptimal subcutaneous infiltration by infusing large volume of IV fluids
  5. Compensation for not using tumescent lidocaine by postoperative infiltration of bupivacaine

Recall that, by definition, the tumescent technique for liposuction precludes doing such large volumes of liposuction that the patient requires IV fluids and general anesthesia. Tumescent liposuction totally by local anesthesia specifically employs serial liposuction procedures rather than a single, huge-volume liposuction procedure. Whereas tumescent liposuction avoids DIC by avoiding excessive liposuction, the superwet technique can precipitate DIC through excessive or huge-volume liposuction or even megaliposuction.

Liposuction surgery has a profound effect on the body’s hemostatic mechanism. In particular, superwet liposuction by systemic anesthesia with IV fluid infusion, extensive trauma, and secondary hypothermia can produce DIC. Early liposuction, especially the dry and wet techniques, effectively opened the intravascular space and allowed its contents to flood the subcutaneous wound. The blood loss was great and highly visible.

The hemorrhagic effects of excessive tumescent liposuction are much more subtle. Even with the profound vasoconstriction of the tumescent technique, the disruption of huge numbers of capillaries exposes subendothelial surfaces and tissue thromboplastin to platelets and blood coagulation factors. This exposure precipitates the degranulation and aggregation of a significant proportion of the circulating platelets. With any liposuction, tissue damage simultaneously activates the coagulation, complement, fibrinolytic, and kinin systems. Excessive liposuction may induce a hypercoagulable state.

Underreporting. The association between excessive liposuction and DIC is underreported. The lack of reported cases of DIC with liposuction is not proof that liposuction deaths are not associated with DIC. At least two cases of DIC have resulted from the combination of huge-volume liposuction, general anesthesia, hypothermia, and IV fluid infusion (Case Report 14-1; see also Case Report 13-1). DIC may even be one of the most common causes of death associated with liposuction under general anesthesia.

Originally, liposuction surgery was limited by visible blood loss. The tumescent technique has eliminated the grossly hemorrhagic liposuction aspirate. The combination of general anesthesia and tumescent infiltration, however, has fostered a cavalier attitude toward the risks of overaggressive liposuction. No obvious threshold exists to limit the amount of liposuction. Several new hemorrhagic postoperative syndromes are the direct result of excessive liposuction. Yellow supernatant fat and delayed DIC with massive subcutaneous bleeding may result from excessive liposuction by the superwet technique.

Information and analysis of cosmetic surgical deaths should be shared so that surgeons can learn from others’ mistakes. Every cosmetic surgical death is unexpected, and an iatrogenic death is particularly disturbing because it was the result of an elective procedure.

Occult Hemorrhage

The fat removed by tumescent liposuction is a bloodless yellow, and a delayed occult hemorrhage can occur from a platelet and prothrombin deficiency. Because of the hemodilution, the hemorrhagic bleeding may be mistaken for normal tumescent anesthetic drainage. With massive hemorrhage, patients with postliposuction DIC and hemorrhage may appear pale. Pallor may be the initial clinical indication of a potentially life-threatening anemia.

The most reasonable solution to this problem is prevention, as follows:

  1. Limit total volume of supranatant fat that is aspirated to less than 3 to 4 L.
  2. Limit the total body surface area treated by liposuction to approximately 20%.
  3. Use tumescent anesthetic solution at body temperature.
  4. Avoid excessive IV fluid infusion.

Predisposing Disorders

A number of inherited and acquired disorders can predispose to excessive surgical bleeding. Tumescent infiltration cannot be expected to eliminate all risks of perioperative bleeding. Avoiding such dangers requires a knowledge of potential problems.

von Willebrand’s Disease

von Willebrand’s disease (vWD) is the most common inherited bleeding disorder, with a prevalence of 1 in 800 to 1000 persons. The acquired forms of vWD are less common than the inherited forms. Usually autosomal dominant, it is a heterogeneous disease, but all syndromes share common features.

Patients who have vWD are missing the plasma glycoprotein von Willebrand factor (vWF). vWF is a disulfide-linked, high-molecular-weight multimer present in plasma, platelets, and vascular subendothelium. vWF is necessary for platelet adhesion to subendothelial collagen. vWF also serves as a plasma binding protein that carries factor VIII; thus there is diminished factor VIII:C (procoagulant) activity associated with vWD.

Patients with mild vWD are asymptomatic, except with surgery or trauma, and may have laboratory values that fluctuate between normal and abnormal over time; for example, the bleeding time may be normal or prolonged on any given occasion. Patients with severe vWD may have spontaneous epistaxis and mucosal (oral, gastrointestinal, genitourinary) bleeding.

Typical laboratory profiles show (1) prolonged bleeding time, (2) low plasma vWF concentration, (3) low ristocetin activity (diminished platelet aggregation in response to ristocetin), and (4) low factor VIII activity.

Treatment for vWF includes cryoprecipitate transfusion or an infusion of 1-desamino-8-d-arginine vasopressin (desmopressin, DDAVP). Transfusion with cryoprecipitate, which is rich in vWF, carries a risk of infection from blood-borne pathogens. DDAVP infusion increases vWF concentration in patients with mild vWD. Response to DDAVP is variable, and prophylactic treatment before surgery requires preoperative testing to confirm the benefits of DDAVP.

Acquired vWD is caused either by antibodies that inhibit vWF function or by tumors that selectively adsorb vWF onto their surface (e.g., lymphoid tumors, Waldenström’s macroglobulinemia, Wilms’ tumor).


Hemophilia A, the classic hemophilia, is a sex-linked recessive disorder, caused by a deficiency in factor VIII:C, the coagulation portion of the factor VIII complex. England’s Queen Victoria was a carrier, and the disease affects approximately one in every 5000 to 10,000 males in the United States. Individuals with severe, moderate, or mild hemophilia have 1% or less, 1% to 5%, or 5% or greater, respectively, of normal factor VIII:C activity in their blood.

Hemophilia B, clinically indistinct from hemophilia A, is also a sex-linked recessive disorder. It causes 15% of all hemophilias and has a factor IX defect.

Patients with mild hemophilia may not be detected until they experience surgery or trauma, whereas severe hemophilia is usually manifested by severe bleeding in infancy. Typical laboratory findings for hemophilia show extremely prolonged partial thromboplastin time (PTT), with normal prothrombin time (PT) and platelet count.

Mild hemophilia is the most dangerous type of hemophilia that a liposuction surgeon can encounter. Patients with severe hemophilia are unlikely to seek liposuction. A patient with mild, previously occult hemophilia, however, may slip by a surgeon who does not require preoperative PT and PTT. Occult hemophilia and liposuction can be a life-threatening combination. Bleeding that begins on the first postoperative day is characteristic of thrombocytopenia and mild occult hemophilia.

Vitamin K Deficiency

Vitamin K deficiency can predispose to prolonged bleeding and attendant surgical complications. Phylloquinone (phytonadione), or vitamin K1, is a yellow fat-soluble oil that is present in green leafy vegetables and is important in blood clotting. To some extent, phylloquinones are absorbed intact from the intestines, and they have some vitamin K activity. Most of the ingested phylloquinone is altered by intestinal bacteria, which remove the side chain to produce menadione. After menadione is absorbed, a new side chain is constructed to create menaquinone, the principal form of vitamin K found in animals.

Vitamin K2, which is formed by some bacteria, differs from phylloquinone only in the substituent in the 3 position of the naphthoquinone ring.

Vitamin K is an important cofactor for enzymes that effect posttranslational (postribosomal) gamma (γ-) carboxylation of glutamic acid in proteins. This γ-carboxylation, which is essential for the biologic activity of many proteins, occurs in hepatocytes and is mediated by hepatic microsomal enzyme systems. The resulting γ-carboxyglutamic acid residue is secreted by hepatocytes into the blood. Liver disease may impair vitamin K metabolism.

Clotting factors II, VII, IX, and X, and the coagulation inhibitors (anticoagulant) proteins C and S are vitamin K–dependent proteins. Warfarin (Coumadin) is an anticoagulant drug that competes with vitamin K and inhibits γ-carboxylation of the precursor to prothrombin and causes hypoprothrombinemia. Salicylates such as aspirin can cause hypoprothrombinemia, which can be inhibited by vitamin K.

In normal circumstances, 80% of dietary vitamin K is absorbed from the small bowel. Vitamin K deficiency can occur in association with intestinal malabsorption of fat. In patients who have a limited dietary intake of vitamin K, long-term treatment with oral antibiotics may eliminate intestinal bacteria as a source for vitamin K and may precipitate a vitamin K deficiency. Obstructive jaundice or biliary fistulas may decrease vitamin K absorption and may lead to hypoprothrombinemia.

Patients who drink too much alcohol and do not eat enough green leafy vegatables may have clinically significant vitamin K deficiency. This situation is probably not rare, and therefore it is reasonable to prescribe 2 weeks of vitamin K supplementation to all liposuction patients before surgery.

Phytonadione (Mephyton, USP vitamin K1) is available in 5-mg tablets. In normal animals and humans who are not vitamin K deficient, phytonadione is devoid of any pharmacologic activity.

No evidence indicates that vitamin K predisposes patients to thromboembolism. On the contrary, vitamin K deficiency can produce an acquired form of deficiency in protein C and protein S, which in turn can predispose to thromboembolism. Large amounts of vitamin K can block the effects of oral anticoagulants and, when given to pregnant women, can cause jaundice in the newborn.

Normal and Impaired Hemostasis

Normal hemostasis can be divided into two stages. The first stage is platelet plug formation, which is initiated within seconds of a vascular injury that exposes subendothelial tissue. The second stage is activation of the plasma coagulation cascade, which results in fibrin formation. These two processes are closely interlinked, and one can stimulate and accelerate the other.

Platelet plug formation involves three important phases: platelet adhesion, platelet granule release, and platelet aggregation. Platelet plug formation can be impaired by various aspirin-like drugs. Plasma coagulation depends on normal vitamin K metabolism and the presence of normal circulating proteins, which are part of the coagulation process that produces fibrin.

Nonsteroidal Antiinflammatory Drugs

A number of commonly prescribed drugs and nonprescription drugs can predispose to surgical bleeding. The most common of these, the nonsteroidal antiinflammatory drugs (NSAIDs), are widely available without prescription (Box 14-1).

Patients must be warned to avoid these drugs before surgery. Liposuction surgeons must understand that patients often take NSAIDs as a reflexive response to any discomfort. Any patient is at risk of taking an aspirin or NSAID before surgery despite repeated warnings. Patients may so embarrassed about having forgotten the warnings that they deny taking an NSAID and place themselves and the surgeon at risk of excessive surgical bleeding.

Aspirin and other NSAIDs impair the hemostatic function of platelets.

Cyclooxygenase. Cyclooxygenase exists in two isozyme forms in mammalian cells. Both forms of cyclooxygenase activity are involved in the synthesis of prostaglandins, prostacyclins, and thromboxanes. Human platelets contain cyclooxygenase type 1 (COX-1), whereas blood vessels, synovial cells, bone marrow, and other tissues contain cyclooxygenase type 2 (COX-2).

COX-1 is a platelet-derived enzyme that catalyzes the production of arachidonic aid, the cyclic endoperoxide precursor of thromboxane A2 (TXA2). When platelets are appropriately stimulated, they produce TXA2, which induces platelet aggregation and vasoconstriction. Vascular TXA2 production plays an important role in the maintenance of hemostasis.20 Different NSAIDs have different degrees of pharmacologic selectivity for COX-1 and COX-2.21

Antiplatelet drugs such as aspirin and other NSAIDs are used in clinical medicine to prevent thromboembolic complications of cardiovascular diseases. Aspirin is an approximately 150-fold to 200-fold more potent inhibitor of the constitutive isoform of the platelet enzyme (COX-1) than the inducible isoform (COX-2), which is triggered by the actions of cytokines, inflammatory stimuli, and some growth factors. This explains the different dosage requirements of aspirin as an antithrombotic agent (COX-1) and an antiinflammatory drug (COX-2).

Aspirin Effects. The most common cause of unexpected bleeding during liposuction is an aspirin-induced, nonreversible defect in platelet function. Aspirin inhibits platelet cyclooxygenase and prevents the production of TXA2 and thromboxane B2, the stable metabolite of TXA2. Aspirin covalently acetylates the functionally important amino acid residue serine 529 near the active site of cyclooxygenase. This prevents the access of the substrate (arachidonic aid) to the catalytic site of the enzyme at tyrosine 385 and results in an irreversible inhibition of platelet-dependent thromboxane formation.22 Other NSAIDs bind to platelets in a reversible manner, and much of the cyclooxygenase inhibition dissipates 4 to 5 days after administration.

Platelets, fragments of megakaryocytes, are not complete cells and are incapable of synthesizing new proteins. Therefore aspirin is permanently bound to platelet cyclooxygenase and inactivates cyclooxygenase for the life span of the platelet (half-life of 7 days). As little as 80 mg of aspirin can produce prolongation of skin bleeding time and cause dangerous perioperative bleeding. An alternate-day regimen of 100-mg aspirin produces functional platelet inhibition.23

Aspirin and NSAIDs are taken more often than is generally appreciated. Among patients who undergo unanticipated surgery, as many as 50% may have biochemical evidence of recent aspirin ingestion.24 If a patient admits to having ingested aspirin less than 7 days or ibuprofen less 4 days before surgery, the surgeon must consider rescheduling the surgery. The surgical staff must maintain a friendly, nonjudgmental attitude toward patients to encourage them to admit having taken an aspirin or NSAID. Rescheduling a surgery is inconvenient for all concerned, but it is even more inconvenient when an ashamed patient denies taking aspirin.

Patients should be advised to avoid aspirin (e.g., Anacin, Bufferin) or any medications that contain aspirin for 7 to 10 days before surgery. Similarly, NSAIDs, such as ibuprofen (e.g., Advil, Motrin, Nuprin), naproxen (e.g., Aleve), or any medications that contain these drugs, should be avoided for 4 to 7 days before surgery. These drugs promote significant bleeding during liposuction surgery.

To prevent unintentional ingestion of aspirin, NSAIDs, or aspirin-like substances, patients should be told to check the labels on all medications, including over-the-counter drugs. Similarly, patients should be advised to remove any products containing aspirin from their medical supplies. Inadvertently taking aspirin-containing oral pain medications can precipitate immediate intraoperative bleeding or delayed bleeding on postoperative days 2 to 7, especially in patients who have a platelet disorder or hemostatic defect.

Prospective patients should be asked if they are taking aspirin, aspirin-like drugs, antiarthritis medications, or blood-thinning anticoagulants.

Vitamin E

Vitamin E is a mixture of organic alcohols known as tocopherols, which are yellow oily liquids remarkably stable to heat. Vitamin E is any or all of a group of closely related fat-soluble compounds that occur in plant oils and are antioxidants essential in the diets of many animals and probably of humans.

Vitamin E supplementation has been shown to reduce platelet adhesion significantly.25 Clinically, at doses of 400 international units (IU), vitamin E can cause noticeably increased bleeding during tumescent liposuction. The relatively low dose of vitamin E in multivitamin tablets does not seem to cause any unusual surgical bleeding. Similarly, the amount of vitamin E contained in a healthy diet has not been found to inhibit platelet aggregation greatly in vivo.26

Of the eight naturally occurring tocopherols that possess vitamin E activity, alpha-tocopherol is the most widely distributed in foods and the most biologically active. Vitamin E probably acts as an antioxidant rather than a cofactor for enzyme-mediated biochemical reactions. Diets containing large amounts of polyunsaturated fatty acids increase the need for vitamin E. Newborns have 20% of the maternal levels, and maternal milk (but not cow’s milk) provides infants with adequate amounts of vitamin E.

Red Wine

Red wine, but not white wine, contains a relatively high concentration of polyphenols and has been shown to reduce aggregation of platelets significantly. Red wines greatly inhibit the synthesis of TXA2, and its metabolite thromboxane B2, whereas white wines have little effect on the mediators of platelet aggregation.27

Alcohol can also have an inhibitory effect on platelet function. Ingesting alcohol, especially red wine, should be discontinued at least 4 to 5 days before surgery.28

Dietary Supplementation

Some dietary supplements may predispose to perioperative bleeding. Garlic powder, garlic tablets, and raw garlic are widely used as health food supplements. Allicin, a heatsensitive component of garlic, inhibits platelet aggregation. Dietary garlic used as a condiment probably has no adverse effect on surgical bleeding. Garlic supplementation in the form of high-dose garlic powder or garlic extract, however, is associated with an increased risk of perioperative bleeding.29

Ginkgo Biloba, widely used in Europe, is derived from a tall tree native to China and Japan. It is a potent competitive inhibitor of platelet activating factor (PAF) that displaces PAF from its binding sites.

Willow bark, derived from the white willow tree (Salix species), contains the precursor to acetylsalicylic acid (aspirin) and has therapeutic and platelet effects that are similar to those of NSAIDs.

Tanacetum (Chrysanthemum) parthenium (feverfew) is used to treat headaches, arthritis, and allergies. It is thought to inhibit the synthesis of arachidonic acid, a precursor of prostaglandins. In a manner similar to the effects of NSAIDs, feverfew impedes platelet aggregation.


The potential for serious bleeding disorders in cosmetic surgical patients is different from that of traditional therapeutic surgery. The surgeon must always be alert to the prospective patient who, motivated by an intense desire to be rid of unsightly fat deposits, may deny having a potential for excessive bleeding. Because of this real possibility, the cosmetic surgeon needs to know when to suspect a patient’s veracity. All prospective liposuction patients should be suspected of having a hemorrhagic diathesis until proved otherwise. Appropriate preoperative laboratory tests should be done.


  1. Courtiss EH, Choucair RJ, Donelan MB: Large-volume suction lipectomy: an analysis of 108 patients, Plast Reconstr Surg 89:1068-1082, 1992.
  2. Klein JA. The tumescent technique for liposuction surgery, Am J Cosmetic Surg 4:263-267, 1987.
  3. Rutmann TG, James MFM, Viljoen JF: Haemodilution induces a hypercoagulable state, Br J Anaesth 76:412-414, 1996.
  4. Ng KF, Lo JW: The development of hypercoagulability state, as measured by thromboelastography, associated with intraoperative surgical blood loss, Anesth Intensive Care 24:20-25, 1996.
  5. Egli GA, Zollinger A, Seifert B, et al: Effect of progressive haemodilution with hydroxyethyl starch, gelatin, and albumin in blood coagulation, Br J Anaesth 78:684-689, 1997.
  6. McLoughlin TM et al: Profound normovolemic hemodilution: hemostatic effects in patients and in a porcine model, Anesth Analg 83:459-465, 1996.
  7. Janvrin SB, Davies G, Greenhalgh RM: Postoperative deep vein thrombosis caused by intravenous fluids during surgery, Br J Surg 67:690-693, 1980.
  8. Monkhouse FC: Relationship between anti-thrombin and thrombin levels in plasma and serum, Am J Physiol 197:984-988, 1959.
  9. Rutmann TG, James MFM: Pro-coagulant effect of in vitro haemodilution is not inhibited by aspirin, Br J Anaesth 83: 330-332, 1999.9a.       Rutmann TG, James MFM, Aronson I: In vivo investigation into the effects of haemodilution with hydroxyethyl starch (200/0.5) and normal saline on coagulation, Br J Anaesth 80:612-616, 1998.9b.       Rutmann TG, James MFM, Viljoen JF: Haemodilution induces a hypercoagulable state, Br J Anaesth 76:412-414, 1996.
  10. Fletcher JE, Heard CMB: Possible mechanism to explain increased coagulability of blood after haemodilution, Br J Anaesth 78:478, 1997.
  11. Klein JA: Tumescent technique for local anesthesia improves the safety of large-volume liposuction, Plast Reconstr Surg 92:1085-1098, 1993.
  12. Borgstrom S, Gelin LE, Zederfeldt B: The formation of vein thrombi following tissue injury: an experimental study in rabbits, Acta Chir Scand Suppl 247:1-14, 1951.
  13. Michelson AD, Barnard MR, Khuri SF, et al: The effects of aspirin and hypothermia on platelet function in vivo, Br J Haematol 104:64-68, 1999.
  14. Johannson BW, Nilsson IM: The effect of heparin and є-aminocaproic acid on the coagulation in hypothermic dogs, Acta Physiol Scand 60:267-277, 1964.
  15. Chadd MA, Gray OP: Hypothermia and coagulation defects in the newborn, Arch Dis Child 47:818-821, 1972.
  16. Cohen IJ: Cold injury in early infancy: relationship between mortality and disseminated intravascular coagulation, Isr J Med Sci 13:405-409, 1977.
  17. Mahood JM, Evans A: Accidental hypothermia, disseminated intravascular coagulation and pancreatitis, NZ Med J 87:283-284, 1978.
  18. Easterbrook PH, Davis HP: Thrombocytopenia in hypothermia: a common but poorly recognized complication, Br Med J 291:23, 1985.
  19. Sessler DI: Mild perioperative hypothermia, N Engl J Med 336:1730-1737, 1997.
  20. Fuse I, Ootsuka T, Hattori A, et al: Vascular thromboxane formation in hemostasis mechanism: correlation between bleeding time and vascular TXB2 in a patient with congenital platelet cyclo-oxygenase deficiency, Int J Hematol 63:317-324, 1996.
  21. Kawai S, Nishida S, Kato M, et al: Comparison of cyclooxygenase-1 and -2 inhibitory activities of various nonsteroidal anti-inflammatory drugs using human platelets and synovial cells, Eur J Pharmacol 347:87-94, 1998.
  22. Schror K: Aspirin and platelets: the antiplatelet action of aspirin and its role in thrombosis treatment and prophylaxis, Semin Thromb Hemost 23:349-356, 1997.
  23. Ridker PM, Hennekens CH, Tofler GH, et al: Anti-platelet effects of 100 mg alternate day oral aspirin: a randomized, double-blind, placebo-controlled trial of regular and enteric coated formulations in men and women, J Cardiovasc Risk 3:209-212, 1996.
  24. Ferris VA, Swanson E: Aspirin usage and perioperative blood loss in patients undergoing unexpected operations, Surg Gynecol Obstet 156:439-442, 1983.
  25. Jandak J, Steiner M, Richardson PD: Reduction of platelet adhesiveness by vitamin E supplementation in humans, Thromb Res 49:393-404, 1988.
  26. Steiner M: Influence of vitamin E on platelet function in humans, J Am Coll Nutr 10:466-473, 1991.
  27. Pace-Asciak CR, Rounova O, Hahn SE, et al: Wines and grape juices as modulators of platelet aggregation in healthy human subjects, Clin Chim Acta 246:163-182, 1996.
  28. Wolfort FG, Pan D, Gee J: Alcohol and preoperative management, Plast Reconstr Surg 98:1306-1309, 1996.
  29. Petry JJ: Garlic and postoperative bleeding, Plast Reconstr Surg 96:483-484, 1995 (letter).
CASE REPORT 14-1 Superwet Disseminated Intravascular Coagulation and Death
A 46-year-old white female had a preoperative weight of 68.2 kg (150 pounds) and was taking Synthroid, Premarin, and Claritin. Her surgery lasted 10½ hours and included liposuction, blepharoplasty, minor facelift, endoscopic brow-lift procedure, laser surgery to face, and fat transfer to buttock. Total aspirate removed by “tumescent” liposuction was 10.9 L, and total urine output was 775 ml.
Over the course of the surgery the patient received a tumescent subcutaneous infiltration of “14 to 15 liters of warmed xylocaine, epinephrine, Ringer’s lactate Solution.” No written orders specified the lidocaine dose, but according to the county coroner’s forensic toxicologist, the total dosage of lidocaine was 95 mg/kg. In addition, the anesthesiologist gave 18,800 ml of LR plus 1000 ml of Hespan.
About 2½ hours after surgery, paramedics took patient to local hospital, where she was described as grossly edematous and bleeding from sutured incision sites. Laboratory values were platelet count, 20,000/mm3; hemoglobin, 2.1; hematocrit, 6.8; and with agonal electrocardiographic rhythm. The patient received 8 units of whole blood and 6 L of physiologic saline in the emergency room, where she died.
At autopsy the patient weighed 82.7 kg (182 pounds), an increase of 14.5 kg, most of which is attributable to excessive IV fluids.
Discussion. Significant postoperative anemia and thrombocytopenia are diagnostic of DIC associated with hemodilution, general anesthesia, and excessive trauma. Diagnosis of DIC was not considered until after the patient’s death. Serial surgeries would have been safer.


BOX 14-1 Common Trade and Generic Drugs Available in the United States That Can Cause Perioperative Bleeding
Advil Cephalgesic Empirin Indomethacin Oruvail Sine-Off
Alcohol Cheracol Caps Emprazil Ketoprofen Oxybutazone Sodium thiosalicylate
Aleve Children’s aspirin Endodan Ketorolac Oxyphenbutazone Soma Compound
Alka-Seltzer Choline salicylate Excedrin Lortab ASA Oxaprozin Sulindac
Amigesic Clinoril Feldene Magan Pamprin Synalgos DC
Anacin Congesprin Fenoprofen Magnesium salicylate Pepto-Bismol Tanacetum
Anaprox Cope Feverfew Meclofenamate Percodan (Chrysanthemum)
Anaproxin Coricidin Fiorinal Meclofen Persantine parthenium
Ansaid Corticosteroids Flurbiprofen Medipren Phenaphen Tolectin
APC Coumadin 4-way cold tablets Mefenamic Phenylbutazone Tolmetin
Argesic-SA Darvon ASA Froben Menadol Piroxicam Toradol
Arthra-G Darvon Compound Garlic capsules Midol Ponstel Trandate
Arthrapan Daypro Gelpirin Mobidin Prednisone Trendar
A.S.A. Depakote Genpril Mono-Gesic Quagesic Trental
Ascodeen Dexamethasone Genprin Motrin Relafen Trigesic
Ascriptin Diclofenac Ginko Biloba Nabumetone Rexolate Trilisate
Aspergum Dipyridamole Goody’s Body Pain Nalfon Robaxisal Tusal
Aspirin Disalcid Halfprin Naprosyn Roxiprin Vanquish
Baby aspirin Divalproex Haltran Naproxen Rufen Vitamin E
Bayer Doan’s Pills Ibuprin Norgesic Saleto Voltaren
BC Powder Dolobid Ibuprofen Norwich Extra-Strength Salflex Warfarin
Brufen Dristan Ibuprohm Nuprin Salsalate Willow bark
Bufferin Easprin Indameth Ocufen Salsitab Zactrin
Butazolidin Ecotrin Indocin Orudis Sine-Aid Zorprin
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