skip to Main Content
949-248-1632 x1204 Email Michele

The Tumescent Technique By Jeffrey A. Klein MD



Chapter 13:
Hypothermia and Cryoanesthesia

Some surgeons seem to believe that “coldness” improves the quality of local anesthesia. For example, some incorporate chilled saline (less than 4° C [25° F]) in a modification of the tumescent technique, presumably to improve hemostasis or local anesthesia. In fact, warm tumescent anesthetic solution (37° C [98.6° F]) provides complete local anesthesia1 and profound hemostasis and is more comfortable for the patient.2-4

Hypothermia and cryoanesthesia are unnecessary and present significant dangers to the liposuction patient. Employing “coldness” in tumescent liposuction is seldom justified.


Hypothermia, a medical emergency, occurs when the core or central body temperature is 35° C (95° F) or lower.5 Below 30° C (86° F), refractory ventricular fibrillation may occur. Loss of consciousness usually occurs below 26.6° C (80° F). Coma and areflexia occur below 25° C (77° F). Hypothermia has potent toxic effects on coagulation of blood and hemodynamics, with excessive oxygen consumption.6

Hypothermia is associated with potentially fatal cardiac dysrhythmias.7-9 Relatively mild degrees of hypothermia, as when a naked patient under general anesthesia is exposed to cold operating room temperatures, have been shown to predispose patients to sepsis.10 Hypothermia has been associated with increased surgical bleeding.11 Hypothermia also may decrease the rate of hepatic lidocaine metabolic transformation by impairing enzymatic activity.

Lactic acidosis is typically associated with hypothermia. Increased hemoglobin-oxygen affinity (dissociation curve shifted to the left) and decreased tissue perfusion cause hypoxemia. Some patients show serum amylase elevation, and pancreatitis may be noted at autopsy.

Hypothermia may delay healing, increase the risk of surgical wound infections, and prolong hospitalization.10 Mild hypothermia associated with anesthesia lowers guinea pig resistance to infection by Escherichia coli12 and Staphylococcus aureus.13 Mild perioperative hypothermia (approximately 2° C below the normal core body temperature) is a common result of anesthetic-induced impairment of thermoregulation, exposure to cold, and altered distribution of body heat. Mild core hypothermia can directly impair immune function, such as granulocyte chemotaxis and phagocytosis, macrophage motility, and antibody production.14 Intraoperative hypothermia during surgery under general anesthesia can be avoided by actively warming the patient.15

Cardiac Effects

When body temperature is less than 34° C (93.2° F), intracardiac conduction velocity decreases. This is manifested on the electrocardiogram (ECG) by prolonged PR and QT intervals, widened QRS complex, T-wave changes, and characteristic J waves (Osborne waves) at the QRS complex–ST segment junction. Atrial fibrillation is common.

Hypothermia increases sympathetic arterial tone, left and right ventricular afterload, heart rate, stroke volume, cardiac output, and blood pressure, which increases myocardial oxygen consumption. Ultimately, this may decrease cardiac output.16 Shivering also increases metabolism, oxygen consumption, and cardiac work.

Patients who arrive in the intensive care unit with temperatures less than 35° C (95° F) have a significantly higher incidence of postoperative myocardial ischemia (36% versus 13%) than normothermic patients.17 Furthermore, despite similar perioperative risk factors, hypothermic patients have a higher rate of postoperative angina (18% versus 1.5%).

Adverse cardiac events are the major cause of morbidity and mortality after noncardiac surgery. In patients undergoing noncardiac surgery, early postoperative myocardial ischemia is an important correlate of adverse cardiac outcomes.18 Mild hypothermia (33° C [91.4° F]) can attenuate nitroglycerin-induced vasodilation.19

General Anesthesia

Mild perioperative hypothermia is a common sequela of general anesthesia and heavy intravenous (IV) sedation because of the pharmacologic inhibition of thermoregulation and the patient’s exposure to the cool environment. Undetected hypothermia is also common during regional, spinal, and epidural anesthesia because core temperature is rarely monitored and because patients usually do not feel cold.20,21

Anesthesiologists play an important role in monitoring a patient’s body temperature and maintaining normothermia (37° C).22

Impaired Coagulation

Hypothermia has been associated with increased surgical bleeding.11 Although focal hypothermia causes local vasoconstriction, the systemic effects of hypothermia may cause a serious bleeding diathesis.23 Hypothermia impairs enzymatic activation of coagulation factors, accentuates fibrinolysis, and may cause disseminated intravascular coagulation (DIC)24 (Case Report 13-1). Decreased body temperature is associated with increased activity of heparin-like factor Xa inhibitor, which is not neutralized by protamine.25,26 Hypothermia causes reversible platelet sequestration in the spleen.27

Patients with essential (mixed) cryoimmunoglobulinemia of immunoglobulins G and M (IgG, IgM) and those with monoclonal cryoglobulinemia may be more susceptible to intravascular thrombi formation.


Cryoanesthesia is the process of lowering tissue temperature and thus inducing a degree of cutaneous insensitivity. Cryoanesthesia predisposes to hypothermia. Deliberate cryoanesthesia for liposuction is produced by subcutaneous infiltration with a chilled anesthetic solution or by direct application of ice to a patient’s skin. Using a chilled tumescent solution or packing the patient in ice has no significant benefit.

Infiltrating with chilled saline and tumescent anesthetic solution has been promoted, but no comparative studies have documented any advantage.

Chilled anesthetic solution is unnecessary, is potentially dangerous, and should not be used as part of the tumescent technique. The subcutaneous infiltration with a tumescent anesthetic solution at or slightly less than 37° C produces sufficient clinical vasoconstriction.

Occasionally, cryoanesthesia is associated with morbidity. Cryoanesthesia causes shaking chills and significant patient discomfort that usually necessitates ancillary IV sedation. Hypothermia can result from the parenteral infiltration of large volumes of chilled (4° C [39.2° F]) liquids, such as chilled tumescent anesthetic solution.

Most surgeons who use cryoanesthesia for liposuction do not monitor core body temperature. Monitoring core temperature during cryoanesthesia, however, is just as important as monitoring oxygen saturation during administration of drugs that depress respiration.


Deaths have occurred associated with using chilled anesthetic solution for cryoanesthesia during liposuction. Cryoanesthesia may be a reasonable adjunct to piercing the ear, but it is contraindicated for liposuction.

Two major reasons exist not to use cryoanesthesia. First, patients are more comfortable when the tumescent solution is approximately 37° C. With the true tumescent technique, the anesthetic solution is heated 37° to 39° C (98.6° to 102.2° F) in a blanket warmer before infiltration. Second, warmed tumescent solution provides such profound vasoconstriction and such exquisite hemostasis that using a dangerous additional treatment modality such as cryoanesthesia is unnecessary.

The ethical use of cryoanesthesia requires full, written, informed patient consent that includes all the risks and alternatives to cryoanesthesia.

Cold Compresses and Dermal Necrosis

Some surgeons believe cryoanesthesia for liposuction is safe and effective. I believe that the prolonged application of ice to the skin of a liposuction patient is contraindicated. Some surgeons have covered their patients in ice packs or plastic blankets containing frozen gel in an attempt to achieve subcutaneous vasoconstriction and minimal surgical anesthesia. Postoperative ice compresses are advocated for reduction of swelling and inflammation. Additionally, conventional tumescent anesthesia with lidocaine and epinephrine has been “augmented” by chilling the solution to below 4° C before infiltration into the patient’s subcutaneous fatty tissues.

Prolonged cutaneous contact with ice or prolonged immersion in ice water results in full-thickness necrosis.28 In frozen tissue, ice crystal formation and development of strong salt solutions disrupt cell membranes. Significant cold injuries lead to vascular stasis and a fulminating inflammatory vascular reaction, resulting in tissue damage similar to that produced by burns.5

It is now well known that treating snakebite by immersion of an affected limb in ice water can result in massive tissue slough, often necessitating amputation.29-31 Because of unnecessary damage to healthy tissue, experts agree that cryotherapy should never be used to treat snakebite.32

The pathologic sequela of frostbite is primarily the result of irreparable damage to blood vessels. The vasculature of frozen dermis and subcutaneous tissue becomes occluded by agglutinated cells and thrombi, and blood flow ceases. In this setting, tissue damage is aggravated by trauma and other factors that compress tissue and decrease blood flow.

Because patients do well without application of cold compresses, the risk of cryotrauma is unnecessary. The idea that cold compresses will “decrease inflammation” is an inappropriate, potentially dangerous application of unsubstantiated clinical dogma. Cold compresses are unlikely to decrease inflammation directly by inhibiting the generation of inflammatory mediators (e.g., prostaglandins) on a molecular level. At best, cold compresses will decrease extravasation of blood into traumatized tissues. If the skin and subcutaneous tissues are already vasoconstricted, cold compresses offer little incremental benefit.

Excessive use of cold compresses postoperatively may have disastrous consequences for liposuction patients. Any factor that injures or compromises the subdermal vascular plexus may predispose skin to unexpected injury. Superficial liposuction, profound localized pharmacologic vasoconstriction, or an endogenous cryoglobulinemia may result in severe skin necrosis.

Cold compresses are usually innocuous, but patients may not understand or follow instructions for postoperative care. For example, one liposuction patient with unrecognized cryoglobulinemia applied ice packs under an elastic support garment, resulting in full-thickness necrosis of the affected skin.


Cryoglobulins are cold-insoluble serum proteins or protein complexes that undergo reversible precipitation at low temperatures. Many connective tissue, autoimmune, infectious, and neoplastic diseases are associated with cryoglobulinemia.33 Several unrelated proteins, such as fibrinogen and immune complexes, are cryoprecipitable under certain conditions. Cryoimmunoglobulins and immunocomplexes are clinically the most important.

Cryoglobulins may consist of monoclonal proteins, as seen in multiple myeloma, Waldenström’s macroglobulinemia, or occasionally in other lymphoproliferative disorders.34 Mixed immunoglobulin complexes usually consist of IgM, which precipitates at lower temperatures (cryoprecipitate) and is directed against normal endogenous IgG, as in connective tissue diseases, autoimmune diseases, infectious diseases, and neoplastic diseases.

Cryoglobulinemia. The term essential mixed cryoglobulinemia applies when no underlying disease can be identified in association with the cryoglobulinemia. One of the causes of typical cutaneous hypersensitivity vasculitis (leukocytoclastic lymphocytic cutaneous vasculitis) is essential mixed cryoglobulinemia.

Cryoglobulinemia can be pathogenic in a number of vasculitic syndromes. When immune complexes containing IgG and IgM precipitate into vascular lumina, the classic complement pathway is activated, and tissue-specific pathology can ensue. Biopsy of a skin lesion shows precipitates of the cryoglobulin within dermal vessels.

The most common symptoms of cryoglobulinemia result from exposure to low environmental temperatures, inducing cryoprecipitation within the capillaries of the skin, which in turn impairs cutaneous blood flow.35 Cold exposure can lead to exacerbations of the disease, which often presents as ulceration and necrosis, hemorrhagic infarcts of skin, purpura, Raynaud’s phenomenon, cold urticaria, or livedo reticularis.


  1. Klein JA: Tumescent technique for local anesthesia improves safety in large volume liposuction, Plast Reconstr Surg 92: 1085-1098, 1993.
  2. Mader TM, Playe JL, Garb JL: Reducing the pain of local anesthetic infiltration: warming and buffering have a synergistic effect, Ann Emerg Med 23:550-554, 1994.
  3. Kaplan B, Moy RL: Comparison of room temperature and warmed local anesthetic solution for tumescent liposuction, Dermatol Surg 22:707-709, 1996.
  4. Bainbridge LC: Comparison of room temperature and body temperature local anesthetic solutions, Br J Plast Surg 44: 147-148, 1991.
  5. Petersdorf RG: Hypothermia and hyperthermia. In Wilson JD, Braunwald E, Isselbacher KJ, et al, editors: Harrison’s Principles of internal medicine, ed 12, New York, 1991, McGraw-Hill.
  6. Gallagher EG, Pearson DT: Ultrasonic identification of sources of gaseous microemboli during open heart surgery, Thorax 28:295-305, 1973.
  7. Lloyd EL, Mitchell B: Factors affecting the onset of ventricular fibrillation in hypothermia, Lancet 2:1294, 1974.
  8. Towne WD, Geiss WP, Yanes HO, Rahimtoola SH: Intractable ventricular fibrillation associated with profound accidental hypothermia: successful treatment with partial cardiopulmonary bypass, N Engl J Med 287:1135, 1972.
  9. Frank SM, Fleisher LA, Breslow MJ, et al: Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events, JAMA 277:1127-1134, 1997.
  10. Kurz A, Sessler DI, Lenhardt R, Study of Wound Infection and Temperature Group: Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization, N Engl J Med 334:1209-1215, 1996.
  11. Schmied H, Kurz A, Sessler DI, et al: Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty, Lancet 347:289-292, 1996.
  12. Hohn DC, McCay RD, Halliday B, Hunt TK: The effect of O2 tension on microbial function of leukocytes in wound and in vitro, Surg Forum 27:18-20, 1976.
  13. Mader JT, Brown GL, Guckian JC, et al: A mechanism for the amelioration by hyperbaric oxygen of experimental staphylococcal osteomyelitis in rabbits, J Infect Dis 142:915-922, 1980.
  14. van Oss CJ, Absolom DR, Moore LL, et al: Effects of temperature on the chemotaxis, phagocytic engulfment, digestion, and O2 consumption of human polymorphonuclear leukocytes, J Reticuloendothelial Soc 27:561-565, 1980.
  15. Kurz A, Kurz M, Poeschl G, et al: Forced-air warming maintains intraoperative normothermia better than circulating water mattresses, Anesth Analg 77:89-95, 1993.
  16. Nussmeier NA, Mills AM: Complications related to cardiopulmonary bypass. In Benumof JL, Saidman L, editors: Anesthesia and perioperative complications, St Louis, 1992, Mosby.
  17. Frank SM, Beattie C, Christopherson R, et al: Unintentional hypothermia is associated with postoperative myocardial ischemia: the Perioperative Ischemia Randomized Anesthesia Trial Study Group, Anesthesiology 78:468-476, 1993.
  18. Mangano DT, Browner WS, Hollenberg M, et al: Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing non-cardiac surgery, N Engl J Med 323:1781-1788, 1990.
  19. Kawaguchi M, Ishimura N, Kurehara K, et al: Mild hypothermia can attenuate nitroglycerin-induced vasodilation of pial arterioles in the cat, Anesth Analg 86:546-551, 1998.
  20. Sessler DI: Mild perioperative hypothermia, N Engl J Med 336:1730-1737, 1997.
  21. Frank SM, Nguyen JM, Garcia CM, Barnes RA: Temperature monitoring practices during regional anesthesia, Anesth Analg 88:373-377, 1999.
  22. Watson D, Laurenson IF, Nimmo AF: Letter to editor, N Engl J Med 338:685, 1998.
  23. Rosenberg H, Horrow JC: Causes and consequences of hypothermia and hyperthermia. In Benumof JL, Saidman L, editors: Anesthesia and perioperative complications, St Louis, 1992, Mosby.
  24. Yoshiara H, Yamamoto T, Mihara H: Changes in coagulation and fibrinolysis occurring in dogs during hypothermia, Thrombosis Res 37:503-512, 1985.
  25. Paul J, Cornillon B, Baguet J, et al: In vivo release of a heparin-like factor in dogs during profound hypothermia, J Thorac Cardiovasc Surg 82:45-48, 1981.
  26. Cornillon B, Mazzorana M, Dureau G, et al: Characterization of a heparin-like factor in dogs during profound hypothermia, Eur J Clin Invest 18:460-464, 1988.
  27. Hessell EA, Schmer G, Dillard DH: Platelet kinetics during deep hypothermia, J Surg Res 28:23-24, 1980.
  28. Arnold RE: Treatment of rattlesnake bites. In Tu AT, editor: Rattlesnake venoms, their actions and treatment, New York, 1982, Dekker.
  29. Bennett JE, Brelsford HG, Lewis SR, Blocker TG: Distal extremity necrosis after snake bite, Plast Reconstr Surg 28: 385-393, 1961.
  30. Lockhart WE: Pitfalls in rattlesnake bite, Texas Med J 66:42-52, 1971.
  31. Mcullough NC, Gennaro JF: Treatment of venomous snake bite in the United States, Clin Toxicol 3:483-500, 1970.
  32. Clark RW: Cryotherapy and corticosteroids in the treatment of rattlesnake bite, Milit Med 136:42-44, 1971.
  33. Foerster J: Cryoglobulins and cryoglobulinemia. In Lee GR, Bithell TC, Foerster J, et al: Wintrobe’s Clinical hematology, ed 9, Philadelphia, 1993, Lea & Febiger.
  34. Bolognia J, Braverman IM: Skin manifestations of internal disease. In Wilson JD, Braunwald E, Isselbacher KJ, et al, editors: Harrison’s Principles of internal medicine, ed 12, New York, 1991, McGraw-Hill.
  35. Brouet JC et al: Biological and clinical significance of cryoglobulins, Am J Med 57:775, 1974.
CASE REPORT 13-1 Hypothermia, Superwet Technique, and Death
A 43-year-old female had liposuction of multiple areas in an outpatient setting. Anesthesia consisted of IV midazolam (Versed, 15 mg), IV methohexital (Brevital) with several liters of a chilled solution of “tumescent” local anesthesia, and 4 L of IV fluids. During recovery the patient became severely hypotensive. After 15 minutes of cardiopulmonary resuscitation (CPR), paramedics arrived to find the patient apneic, pulseless, and asystolic.
At the hospital the emergency room (ER) physician noted pink, frothy sputum through the endotracheal tube, bleeding from the nose, and sutured surgical sites. The rectal (core) temperature was 33.5° F (about 1° C). After CPR for 10 minutes, she recovered spontaneous pulse and blood pressure. Treatment of ventricular fibrillation included lidocaine.
Laboratory values included hematocrit, 8.1 ml/dl; hemoglobin, 2.8 g/dl; platelets, 84,000/mm3; prothrombin time (PT), 25 seconds; and partial thromboplastin time (PTT), 144 seconds. Vigorous CPR included 4 units whole blood, 5 units fresh-frozen plasma to correct coagulopathy, and 1.5 L crystalloid used for drug delivery. No Foley catheter was used, despite administration of IV furosemide (Lasix, 100 mg). Even with hemodialysis in the ER in an effort to remove excess fluid (pulmonary edema, no urine output), the patient died. Causes of death listed by ER physician included pulmonary edema (fluid overload), hypothermia, DIC, coma, hypotension, renal failure, and metabolic acidosis.
Discussion. This case illustrates several unnecessary, severe physiologic insults. Cryoanesthesia and IV general anesthesia contributed to significant hypothermia; excessive IV fluid produced pulmonary edema and hemodilution. All these insults resulted in superwet DIC (see Chapter 9). Hypothermia is well known to cause DIC, cardiac dysrhythmias, and surgical infections.
Chilled saline is contraindicated for tumescent liposuction. Using cryoanesthesia requires continuous monitoring of core body temperature. No scientific data or published reports support the use of cryoanesthesia for liposuction. Any IV fluid supplementation is contraindicated with tumescent liposuction if it exceeds the absolute minimum volume.
Bretylium might be preferred to lidocaine for the initial treatment of ventricular dysrhythmias in the patient with potential local anesthetic toxicity. Although the plasma lidocaine concentration resulting from the tumescent anesthesia was probably not near the threshold for toxicity in this case, additional IV lidocaine to treat ventricular fibrillation might not be my first choice.
Back To Top