Hydrotherapy-mechanisms and indications

Pharmac. Ther. Vol. 20, pp. 79 to 93, 1983 Printed in Great Britain.

0163-7258/83/010079-15507.50/0

Specialist Subject Editors: E. SCHONBAUMand P. LOMAX

HYDROTHERAPY--MECHANISMS AND INDICATIONS P. FRANCHIMONT*,J. JUCHMESt and J. LECOMTEt *Service de Physioth&apie, H~pital de Balvidre and ~fInstitut de Physiologie, Universitd de Liege, Belgium

1. INTRODUCTION According to many authors, e.g. Wyman (1944), Coulter and Piersol (1950), Licht (1963), hydrotherapy refers to the external application of water, hot or cold, in any form, for the treatment of disease. Water may be applied locally or to the whole body by immersion. Balneotherapy, or general hydrotherapy, refers to the latter form of bathing. Water has been used for therapeutic purpose since earliest recorded times. Wyman (1944) and K~iz~k (1963) gave short and excellent historical reviews of hydrotherapy. Both emphasize mystical aspects of its primitive indications, such as purification of body and soul, elimination of evils or bad humors, and so on. Since these times hydrotherapy has been embodied in mysterious attributes, both 'fantastic and absurd' (Wyman, 1944), which have led to extensive indications for use of external water far beyond its therapeutic value. Ancient French and German medical writings are particularly rich in clinical descriptions of diseases to be considered as 'cured' at reputed thermal centers, e.g. Kowarschik (1957); 'Therapeutique Thermale et Climatique' (1972). On the other hand, the rational basis of hydrotherapy and balneotherapy needs to be clearly defined in order to understand how they can be applied to the nonspecific treatment of some diseases. The purpose of this review is to recount the main physical properties of water related to its medical applications, i.e. heat transfer through the skin, Archimides forces, hydrostatic pressure acting as a counter-pressure on the body, with special reference to the changes in caloric balance. These properties are described in full detail in the volume devoted to hydrotherapy, edited by Licht and Kamenetz (1963). See also Duffield (1969). In general, hydrotherapy is based on these physical properties of water, acting from outside the body mainly during the time of its application. The underlying cause of the disease being treated is not affected, so hydrotherapy must be considered as an adjunct, as a palliative measure facilitating the activity of other remedies or spontaneous healing. 1.1. OUTLINEOF REVIEW The subject has been approached as follows, Section 2 is devoted to the local thermic effects of water acting through the skin: localized hyperthermia or hypothermia. Section 3 will consider systemic aspects of whole body immersion in hot and cold water: general hyperthermia or hypothermia. Section 4 deals with clinical indications. According to Stitt (1979), hyperthermia is considered as a rise in body temperature resulting from failure of peripheral heat dissipating mechanisms or impairment of central thermoregulatory mechanisms, produced by external interventions. The definition notably applies to the rise in core temperature of humans observed after general application of hot water. According to Blair (1964) and Hirvonen (1979), hypothermia means lowering of body temperature below 35°C; it is observed after immersion in cold water. Local hypothermia refers to a situation where the temperature of a tissue or organ falls below its normal range measured at the thermal optimum; local hyperthermia, to the converse. 79

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Changes in metabolic rate, in enzymatic kinetics and in cell activity are direct consequences of changes beyond the physiological range of tissue temperature. These changes, frequently expressed in terms of the temperature coefficient, Q10, or in terms of the 'energy of activation' obtained from the equation of Arrhenius, are not considered in this review (see Rose, 1967). 2. LOCAL HYDROTHERAPY Local hydrotherapy depends mainly on thermic effects induced through the skin by the application of hot or cold water. The skin and the subcutaneous tissues are to be considered as a heat insulator for the body core and as an effective 'radiator' system due to the flow of blood, the most efficient mechanism of transfer of heat from the body core to the tegument. Water has a specific heat several thousand times as great as that of air so that each unit portion of water adjacent to the skin can absorb far greater quantities of heat than can air when the temperature of water is below that of blood and skin, thus provoking a fall in temperature of the adjacent tissues. On the contrary, when the temperature of the external water is above that of the skin and blood, heat is transferred to the adjacent tissues, with a rise in local temperature. These notions are discussed in textbooks of medical physiology (see e.g. Guyton, 1981). They represent the physical basis of local hydrotherapy.

2.1. LOCALHYPERTHERMIA

2.1.1. Some Methods Local hyperthermia of the skin and of the subcutaneous tissues can be induced either by conduction (local hot baths of the arm and leg, application of various materials containing hot water, blankets, wrappings, small peloid packs), by convection or by conversion. In the latter case, local heating is obtained by transfer of energy, either electrical (high frequency currents, diathermy, short waves), electromagnetic (microwaves) or vibration (ultra-sounds) and its transformation into heat within the tissues. In general the shorter the wave length of electric or electromagnetic radiations, the more deeply the caloric action will be effective (see Glaser, 1944, 1950, 1960, and Licht and Kamenetz, 1965, for technical data and physical principles involved). Only heating by conduction is to be considered in hydrotherapy. 2.1.2. Effects of Heatin 9 by Conduction Through the Skin Skin and the adipose tissue beneath it are poor conductors and act as heat insulators. In contrast, the tolerance of the cutaneous tissues for high temperature is relatively good. Pain arises when the skin temperature is raised above 42°C, as polymodal nociceptors are stimulated (for a review see Besson et al., 1982). A device kept at 50°C can be applied for 20 min without blister formation (Williamson and Scholtz, 1949). Therapeutic application of warm water is limited by these two factors, i.e. temperature around 40°C on the skin for a duration of 30 min, if burns are to be prevented. The temperature of the skin in close contact with an external heat source is increased in proportion to the intensity of heating achieved 'in situ'. However when temperature equilibrium is not attained between subcutaneous tissues and the external hot body, heating leads to the opening of subdermal arterioles, venules and arterio-venous shunts (Clara, 1939). This is followed by a fall in their resistances to flow and by an increase in local blood supply (for reviews, see Downey and Darling, 1971; Grayson and Kuhn, 1979). As the blood is warmed under the hot body, this increase in blood flow facilitates distant heat diffusion and increases the ability of the skin to tolerate high temperatures. In other respects, the local increase in temperature, which is maximal over the epidermis under the hotbody, diminishes towards the subcutaneous tissues and underlying muscu-

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lar aponevroses, mostly as a result of heat transfer due to circulatory changes. Thus, following the application of a container filled with water at 56°C, the outside fixed at 50°C, one must wait about 30 min in order to obtain a clearcut and lasting increase in the temperature of the deep muscles and joints, from 34.5°C to 37.6°C (Bierman and Licht, 1952). According to Fischer and Solomon (1965), many factors are involved in the establishment of the final temperature gradient after immersing a limb in a water bath, particularly changes in vasomotor tone. This holds true also for the temperature of the knee joints, as measured by Cobbold and Lewis (1956). Heating of the skin and of the immediate underlying areas for therapeutic purposes leads to at least two types of phenomena: (1) those immediately related to the hyperthermia itself; and (2) those which depend on the stimulation of warm-receptors. This explains the specific sensations and the metameric spinal reflexes. Thermoregulatory responses involving the temperature regulating areas of the hypothalamus are also to be considered as well as inhibition of tonic cold receptor activity. 2.1.2.1. Effects directly related to hyperthermia Direct arteriolar dilation is observed which is proportional to the degree of heating, the most superficial vasodilation leading to erythema. This is followed by an increase in blood flow. A direct increase in the metabolism of the heated tissues following the Qlo law is provoked. Such metabolic demand induces an increased oxygen consumption and a related production of an excess of vasodilator metabolites (Abramson et al., 1958). Local direct heat vasodilation is potentiated by these substances (Fischer and Solomon, 1965). So hyperthermia per se induces vasodilation by two mechanisms: the first is a physical action on the smooth muscles of the vascular walls; the second an autoregulating mechanism linked with aerobic metabolic demand. The clearance of radiolabeled sodium can be used as a quantitative measure of these changes in the local circulation (Harris, 1960, 1963). Enzymatic activities are also increased in connection with the Qlo law, notable is synovial collagenase (Harris and McCroskery, 1974; Castor and Yarow, 1976; Feibel and Fast, 1976). 2.1.2.2. Effects due to neural mechanisms--thermoreceptors and thermoregulatory centers When the skin temperature remains below 40°C warm receptors are stimulated leading to warm and hot sensations and accommodation occurs. Above 42°C, nociceptors are stimulated causing pain sensation. No accommodation is Observed when heating is prolonged. Thermal nociceptors are sensitized by preceding mechanical trauma (Besson et al., 1982). Stimulation of the warm thermoceptors leads to an inhibition of the tonic activity of the ?-neurons in the anterior horn of the spinal cord segments where the warm sensitive afferents are distributed. The inhibition of ?-neurons relaxes the neuromuscular stretch receptors. This leads to a decrease in the corresponding striated muscle tone. This hypotonia is reinforced by inhibition of the descending reticular pathways by the hypothalamic thermoregulatory centers (Euler and Soederberg, 1956). When systemic blood temperature is increased by local warming of large skin areas, an activation of systemic thermolytic processes sets in, which produces vasodilation and sweating in distal extremities (consensual changes). Vasodilation is facilitated by the simultaneous suppression of tonic afferent stimuli from peripheral cold receptors which reflexly maintain the sympathetic adrenergic vasomotor tone. Grayson and Kuhn (1979) emphasize that the distribution of sympathetically mediated vasomotor tone is not uniform in the skin. It is limited to the distal extremities; dilation of their vessels is an excellent sign of heat loss and an index of the efficacy of warm hydrotherapy. VasodilaJ.P.T. 20/I--F

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tion is due to an inhibition of adrenergic mechanisms modulated by noradrenaline release. Sweating is related to a sympathetic cholinergic mechanism. Activation of the sweat glands is followed by the release of kallikrein. Bradykinin is then formed which is a potent vasodilator of the proximal subcutaneous vessels (Fox and Hilton, 1958). In summary, cutaneous vasodilation due to therapeutic local hyperthermia is a complex phenomenon involving direct physical influences, reflex release of sympathetic vasomotor tone and kinin formation. When a fall in systemic vascular resistance is provoked by marked cutaneous vasodilation and when a sufficient loss of plasma water occurs due to sweating, vasoconstriction is observed in the splanchnic area and the renal circulation, as a result of systemic sympathetic homeostatic activation (Rowell, 1974). 2.1.3. Pathophysiological Consequences Consequences of local skin heating below the cutaneous nociceptor threshold have been summarized by Stillwell (1965). Some of the consequences appear to be beneficial, analgesia, release of spasticity, antiinflammatory activity. Others are deleterious and may lead to tissue destruction. Application to the surrounding skin of a device causing an increase in temperature of the deep tissues of 3-4°C is particularly useful in some painful diseased joints and muscles affected by spasm, contracture or retraction. This heat increase results in analgesia and relaxation. These are explained by the increased blood flow, which carries away pain stimulating substances formed at the site of the lesion by anaerobic processes, by the increase in aerobic metabolism and by inactivation of various long-reflex loops provoking and sustaining painful muscular contractures. Some trophic effects of heating on diseased muscles are also observed, due to locally increased blood flow and to better aerobic metabolism. Local application of heat is sometimes useful in acute inflammatory lesions. One observes analgesia, exudate disappearance by increased resorption, increased phagocytosis, increased extensibility of connective structures, and, in arthritis, reduction in viscosity of the synovial fluid. Some suppurative processes are accelerated. On the contrary, application of heating devices on inflamed sites are harmful when hyperthermia leads to an increase in exudate formation and stimulation of lysosomal and collagenolytic enzymes (Harris and McCroskery, 1974) leading to tissue destruction and release of toxic substances. Furthermore, thermal vasodilation can induce spreading of toxic materials released 'in situ' and extend inflammatory processes. Likewise, before local hyperthermia is used, one must be certain that those areas where aerobic metabolism is supposed to increase are sufficiently vascularized. In case of relative ischemia, increased metabolism induces anaerobic processes which sometimes provoke necrosis.

2.2. LOCAL HYPOTHERMIA 2.2.1. Some Methods Application of compresses and ice-packs as local cold arm and leg baths cool the corresponding areas, by accelerating heat transfer from the subcutaneous tissues (see Licht and Kamenetz, 1965). 2.2.2. Effects of Cooling by Conduction Through the Skin An ice-pack is well tolerated by the healthy skin for 15-30 min. Its temperature tends to equilibrate with that of the underlying skin. Subcutaneous regions are also cooled, but to a lesser degree. Fischer and Solomon (1961) have published schemes of temperature changes in subcutaneous tissues and in deep muscles, in relationship to caloric gradients and duration of cold applications. As the gradient increases, the time to establish the

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same degree of cooling is shorter. Under 15°C, nociceptors are stimulated and pain is provoked (Besson et al., 1982). Therapeutic application of cold is limited by the nociception but this tends to disappear as cooling is going on. Cooling of the skin and of the immediately underlying areas leads to at least two phenomena: (a) those which are in direct relationship to the local cooling; (b) those which depend on the stimulation of cold receptors leading to specific sensation, to local reflexes or to activation of long pathways involving the temperature regulating areas of the hypothalamus. 2.2.2.1. Local cooling Cooling the skin induces a direct decrease in the caliber of arterioles and venules which is proportional to the drop in temperature. Local blood flow is reduced and cooled skin areas are pale. Local metabolic rate is reduced, according to the Q10 law. Reduction of blood flow and oxygen supply leads to anaerobic processes with the production of vasodilator metabolites which accumulate in situ. Histamine is also released by direct damage to subcutaneous mast cells, causing cold urticaria in some individuals (Soter and Wasserman, 1980). Once a sufficient concentration of these vasodilators is reached cold constriction is interrupted by the development of a reactive hyperemia. The skin, at first pale, becomes red as blood flow is re-established, then returns to pale, and so on. This is the 'hunting reaction', first described by Lewis (1930). Redness of the skin is also sometimes observed in the first minutes of cooling due to vascular paralysis coupled with a temporary arrest of blood flow. Viscosity of the blood increases when temperature falls, provoking intrinsic resistance elevation in the cooled areas. This explains the arrest of the blood flow and the development of frost-bite lesions. Direct cooling of a striated muscle reduces its performance, contraction and relaxation times are increased (Turtle, 1941). Manual dexterity is reduced (Fox, 1961). Nerve conduction fails at low temperatures, explaining cold analgesia and accommodation to cooling devices (Besson et al., 1982). 2.2.2.2. Neural mechanism Specific cold sensations depend on cold thermoreceptor stimulation. Pain arises at temperatures lower than 15°C by excitation of polymodal nociceptors. With cold application for long periods pain finally disappears when nerve conduction is blocked. Pain intensity and duration are subject to individual variation (Besson et al., 1982). Afferent pathways from cold receptors reflexly stimulate the anterior horn 7-neurons of the spinal segment, with an increase in the tonic activity of the corresponding striated muscles (Euler and Soederberg, 1956). Reflex vasoconstriction is also observed in some individuals leading to systemic hypertension. This is the basis for the cold pressor test, first introduced by Hines and Brown (1933). Thermogenic systems such as shivering and cutaneous vasoconstriction are also stimulated by cold afferents. Finally, cutaneous vasoconstriction due to therapeutic local hypothermia depends on complex phenomena: (a) direct physical effects on vascular smooth muscle, and (b) reflex sympathetic activation by segmental afferents and by the descending loop from the thermoregulatory centers.

2.2.3. Pathophysiological Consequences In general, local cooling relieves pain and relaxes muscular spasticity (Light, 1965). Superficial or deep areas of acute inflammation, some skin injuries and skeletal muscle contractures which are associated with pain of anaerobic origin are alleviated by local cold application. The metabolic slow-down lowers the production of endogenous factors

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maintaining inflammation, the spread of which is also reduced by diminution of local blood flow. Likewise, arteriolar vasoconstriction creates conditions favorable to the resorption of exudates and the reduction of painful focal and perifocal tissue tension. Finally, cold anesthesia of nonmyelinated C fibers blocks the conduction of pain causing potentials. This results in the disappearance of certain muscular spasms, particularly those linked with muscular anaerobic acidosis. Spasms are also reduced when cooling slows down the discharge frequency of the muscle spindles (Eldred et al., 1960). 3. GENERAL HYDROTHERAPY OR BALNEOTHERAPY When the whole body is introduced into a water bath where the caloric balance becomes either positive or negative by conduction, systemic hyper- or hypothermia can be produced with related metabolic and physiological changes. Such states are also affected by central thermoregulatory responses following stimulation of cutaneous thermoreceptors or from modification of the temperature of blood perfusing the hypothalamus. In air, only these thermal effects are observed, e.g. in a sauna. In water baths, physiological consequences of Archimedes force and hydrostatic pressure are also to be taken into account when considering the medical applications of balneotherapy.

3.1. GENERALHYPERTHERMIA

3.1.1. Some Methods Methods for producing general hyperthermia by conduction are numerous and many books and treatises have been devoted to the topic. Notably see "Handbook of Physical Medicine and Rehabilitation" (1960) and volumes II and VII of the "Physical Medicine Library Collections" (E. Licht, Publ. 1963 and 1965). A short account will be given of some of the methods directly related to balneotherapy. 3.1.1.1. Warm, moist air (60-80°C), water saturated (sauna) Exposure to such a warm and moist atmosphere for 30min consistently elevates central temperature. 3.1.1.2. Dry heatin9 devices A simple heating mattress, similar to that used domestically, can be used to create some degree of hyperthermia (Page, 1981). The body can also be heated by more complex devices where water is circulated at 45°C. In this manner one can achieve hyperthermia up to 41.5°C in an anesthetized subject. This can be maintained for several hours under close monitoring (Kim et al., 1979). 3.1.1.3. Hot water bath This is one of the simplest ways to cause general hyperthermia; a plain water bath is used above 34-35°C, which is the neutral temperature for a water environment. The intensity and the rate of shift in heat flow depend on the positive temperature gradient between the water and the surface of the immersed body. Heating the skin above 40°C is painful in most patients. 3.1.1.4. Hot peloid baths (fan9o) Addition of a peloid to a water bath results in an increase in its viscosity and thereby reduces convection currents which normally occur when the temperature of the bath is raised. Only a small sheet of water, in contact with the skin, serves for heat transfer to

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the core. This creates a situation where the immersed subject experiences a clearcut sensation of warmth as a result of the activation of cutaneous thermoreceptors without having to undergo the discomfort of generalized hyperthermia; heat transfer is slowed down as a result of the presence of the suspended mineral or vegetable material. Physical laws of heat transfer in a peloid bath are very complicated--stability, density, deepness of the pool are variables (Prat and Brozek, 1963).

3.1.2. Physiological Effects of Induced Hyperthermia 3.1.2.1. Warm, moist air (60-80°C), water saturated. Under such circumstances the entire skin surface is maintained in air at an elevated temperature. A caloric gain is induced. Processes of thermolysis set in, notably cutaneous vasodilation and sweating. However, cutaneous vasodilation is ineffective due to the ambient temperature whilst the water saturation impedes any heat loss by sweating. Body temperature sometimes increases from 37.6 to 40°C, according to the sauna conditions (Eisalo, 1963; Damato et al., 1968). Metabolic rate is increased. A decrease of plasma volume, systemic arterial hypotension and stimulation of the sympathetic efferents of the visceral cardiovascular system are observed. Blood noradrenaline levels are increased (Hussi et al., 1977) which explain the tachycardia and the palpitations. Cardiac output is elevated. There is also adrenocortical stimulation; both gluco- and mineralocorticosteroids are produced in excess (Kosunen et al., 1976). Cutaneous vasodilation is due to suppression of adrenergic vasomotor tone and is similar to that obtained by local sympathectomy (Grayson and Kuehn, 1979). Blood flow is incresed in the subcutaneous tissues whose temperature is high. This is the most likely explanation for cold immunity as experienced after a sauna bath. This explanation also holds true for the tolerance to carbon dioxide baths. 3.1.2.2 Dry heatin 9 devices Anesthetized subjects placed in dry heating devices develop hyperthermia with subsequent activation of thermolytic processes and corresponding cardiovascular adaptative reactions (Rowell, 1974). Cardiac output is increased as a result of sympathetic stimulation, blood catecholamine and cortisol levels are both increased (Kim et al., 1979). 3.1.2.3 Hot water baths In a water bath at an indifferent temperature (34°C), the forces of Archimedes operate, as well as the hydrostatic pressure on the skin which is proportional to the height of water measured from the surface (Knebel, 1960; Duffield, 1969; Gauer, 1975). (a) Water exerts a vertical force on the body (principle of Archimedes) directed upwards and equal to the weight of the water volume corresponding to the immersed parts of the body; this force opposes gravity. As for the immersed parts of the body, antigravity skeletal muscle tone is inhibited; stresses on bones and intra-articular structures are decreased. As a result, general metabolism is lower (Knebel, 1960). Locally, nutrition of cartilages is improved (Duffield, 1969). (b) Hydrostatic pressure exerted through the skin empties the venous reservoirs of the dependant parts of the body and facilitates the reabsorption of interstitial fluid (Kaiser et al., 1969; Khosla and DuBois, 1979). As a result, the intrathoracic venous reservoirs are repleted. This facilitates cardiac filling and increases cardiac output (Arborelius et al., 1972). A slight increase in systemic arterial pressure ensues which inhibits sympathetic tone (McGoodall et al., 1964). Bradycardia, a fall in peripheral resistance, a reduction in the secretion of renin and consequently of aldosterone are observed (Epstein, 1976; Epstein and Saruta, 1971; Epstein et al., 1980). ADH liberation is blocked; this is the Gauer-Henry reflex (Gauer et al., 1970; Epstein et al., 1975).

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(c} In a water bath at a temperature greater than 35°C (36-40"C) heat transfer occurs from the water to the body, depending on the temperature difference. The subject is thus submitted not only to the physical forces described above but also to a positive change in caloric balance. He gradually becomes hyperthermic (Bazett and Haldane, 192l). Cutaneous vasodilation, resulting from direct vasodilation on the one hand and from an inhibition of sympathetic vasomotor tone on the other, leads to heating of the blood circulating under the skin. Furthermore, evaporation of the produced sweat is impossible within the bath. So central temperature rises and tends to become equal to that of the water. As a result, above core temperatures of 38.5°C, the subject experiences sensations of restraint and discomfort, a very disagreeable sense of weakness and suffocation, palpitations due to tachycardia resulting from sympathetic activation and parasympathetic inhibition. Arterial pressure falls progressively due to thermolytic cutaneous vasodilation and to reduction of plasma volume due to the ineffective sweating. Splanchnic and renal vessels are constricted due to regulatory sympathetic control. Hyperreninemia, hyperaldosteronemia and hypercortisolemia occur (Rowell, 1974). The bath has to be interrupted when the core temperature is around 40°C since some subjects will enter a state of cardiovascular collapse and syncope. 3.1.2.4 Hot peloid bath Following immersion in a therapeutic peloid bath maintained at 40°C, the superficial skin temperature is generally fixed at 38°C while the body reaches this temperature more slowly (in 60 min) due to limitations of caloric transfer. Cutaneous thermoreceptors are activated. So thermolytic processes occur as well as the segmental processes described in Section 2. Archimedes forces and hydrostatic pressure also operate. Discomfort is minimized as the general hyperthermia is limited (Hattori, 1963). 3.1.3. Pathophysiological Consequences The pathophysiological effects of general hyperthermia differ according to the techniques used. Effects of immersion as such and those of heating must be distinguished. From a general point of view, immersion in plain water reduces the forces of gravity leading to disappearance of reflex spasm and muscular tension, with better muscular activity. It improves articular nutrition as a result of the weight reduction. Plasma filtration is reduced and the resorption of excess interstitial fluid is accelerated, with disappearance of edema. Disease articulations are less painful. Certain movements are facilitated when Archimedes forces lighten the weight of the limbs to be moved, so motor reeducation is facilitated (Duffield, 1969). 3.1.3.1 In water at temperatures 9reater than 35°C Beneficial effects of immersion in water at these temperatures are limited as bathing causes cardiovascular effects which are sometimes intolerable. Meanwhile muscular relaxation is increased by hyperthermia. 3.1.3.2 Immersion in peloid baths This is characterized by pleasant sensations due to heating of the skin, a decrease in skeletal muscle tone, disappearance of muscle contractures and resorption of edema. Likewise, cardiac rhythm is close to normal as sympathetic stimulation is minimal. Arterial pressure falls slightly. Beneficial consequences of peloid baths are of several kinds: general sedation; muscular relaxation; reduction in skeletal muscle spasms, facilitated by loss of postural tone and articular constraints; disappearance of the functional block of joints immobilized by pain; easier mobilization and reeducation. By comparison with immersion in plain water, use of peloid baths has a marked

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advantage, maintaining for a longer period the patient in an elevated temperature environment without risk of hyperthermia. Carbon dioxide-saturated baths may be used to enhance the sensation of warmth at a lower temperature (33°C). Their characteristics are described in Appendix A (see also Section 4.1.3.1).

3.2. GENERAL HYPOTHERMIA 3.2.1. Some Methods According to Blair (1964) many methods can be used to obtain hypothermia. Heat regulating control must be first depressed before creating an external cold environment or cooling the blood. Two basic methods are used: (1) surface-contact cooling (surface immersion; ice-bath; blankets), and (2)blood stream cooling (extracorporeal cooling; bypass cooling). Cold balneotherapy belongs to the first type. 3.2.2. Physiological Effects of General Cooling In normal awake man lowering of internal temperature provoked by prolonged immersion in cold water below 20°C stimulates thermogenic processes, cutaneous vasoconstriction and shivering occur. Sympathetic nervous activity is stimulated (Johnson et al., 1977). Energy reserves are rapidly exhausted, the lowering of temperature leading to paralysis of central neuronal activity, with coma and death (Hayward et al., 1976). Death may be anticipated if the subject is anesthetized before establishing hypothermia. In such a case, thermogenic adaptative responses are suppressed. During hypothermia conducted under anesthesia systemic metabolism is markedly diminished; ventilation is slowed. Respiratory movements cease below 28°C and artificial respiration is required. Bradycardia and systemic hypotension are observed. Cardiac output is reduced. According to Blair (1964), the brain is the critical organ in any evaluation of hypothermia, and must be monitored during the whole procedure of cooling and rewarming. Spontaneous electro-cortical activity disappears at 18-20°C. Reflex responses disappear, first cortical, lastly bulbar. Endocrine systems are generally depressed in hypothermia. Death may result from ventricular fibrillation or from acidosis and hypoxia, usually below 28°C. 3.2.3. Pathophysiological Consequences Cooling an awake normal subject to 34 + 2°C increases general metabolism by shivering. Mobilization of energy stores is observed. Cardiovascular reserves are stimulated cardiac output and total peripheral resistance are increased. Cardiac failure may Occur.

Cooling an anesthetized subject to 30 + 2°C lowers general metabolism and reduces cardiovascular activity. The physiology of hypothermia is discussed in detail by Blair (1964). The pharmacology of drugs used to induce hypothermia is described by Laborit (1979) as well as the consequences of what is called artificial hibernation (Laborit and Huguenard, 1953). 4. CLINICAL INDICATIONS Hydrotherapy and balneotherapy have been advocated as an adjunct for the treatment of numerous diseases, psychic disorders and sequelae of injuries. In modern psychiatry, the use of cold showers and cold bald baths is disappearing. In internal medicine, external applications of mineral or thermal waters as 'anticongestive' treatments, by inhalation, aerosolization or colonic drainage, are obsolete. External applications of cold or warm water through the skin are now mainly used as inexpensive

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adjunct manoeuvres in some osteo-articular affections at noninflammatory stages, immersion being also useful in rehabilitation. The pathophysiological effects of hydrotherapy having been described, some clinical applications will now be presented. But many difficulties arise when collecting data establishing the efficacy of hydrotherapy in clinical practice. It has been used traditionally for a long time and reappraisal of its value is quite impossible by the usual double blind studies. |t is worth repeating that, in applying hydrotherapy, the cause of the disease is not affected. Symptomatic results only are to be expected.

4.1. INDICATIONS ACCORDING TO THE MODE OF HYDROTHERAPY 4.1.1. Local Hyperthermia Induced Through the Skin Local application of hot blankets, devices containing hot peloids, hot showers, etc. are limited to diseased areas which are easily accessible, i.e. painful joints and muscles of the legs, arms and spine, sometimes associated with nerve irritation. When these disorders are in a nonprogressive state (mainly degenerative or arthritic processes) local heat reduces pain and relieves muscular spasms and contractures. Mobilization is facilitated. Also in rheumatoid arthritis, superficial heating (heating pad, paraffin bath) provides analgesia for active inflamed joints and relaxes muscle spindles prior to stretching a contracture (Gerber, 1981). Daily heat therapy is a useful adjunct to the therapy of rheumatoid arthritis (Mainardi et al., 1979). In case of muscular atrophy due to poliomyelitis, nerve interruption or immobilization, direct vasodilation with heating stimulates trophicity. Localized superficial hyperthermia of a greater degree and for longer duration is used in the treatment of certain cutaneous malignancies (melanomas, lymphomas, Kaposi's sarcomas) either alone in repeated applications or in association with radiotherapy or chemotherapy. The aim of such therapy is to increase the vulnerability of the tissues by metabolic Qlo effects. The aerobic hyperactivity exhausts the energy stores necessary for mitosis (Bhuyan, 1979; Malkinson, 1980).

4.1.2. Local Hypothermia Induced Through the Skin Local cooling restricted to some acute inflammatory processes, either superficial or more deeply situated, is used to prevent further development, i.e. abcess, appendicitis, arthritis, etc, awaiting more specific treatment or surgery. Analgesic, vasoconstrictive and antispasmodic effects of cold are also used in the treatment of joint or bone injuries. Osteoarthritis of the knee is a common indication (Clarke et al., 1974). Massage of the skin with an ice-block vasoconstricts first the blood vessels, then leads to the appearance of a marked reactive hyperemia. This prevents bed sores in the elderly. Certain surgical procedures on limbs are preceded by cooling of the region to be operated upon, this is particularly the case for large joints. Vasoconstriction is then an adjunct for the prevention of bleeding. Both hyper- and hypothermia can be induced in deeper tissues through perfusion techniques. Their uses are considered in more detail in Appendix B.

4.1.3. General Balneotherapy Immersion is used in the majority of the cases to aid the kinesthetist to move muscles and joints in various spa treatments. It seems then more appropriate to speak of underwater mobilization than hydrotherapy. Some effects of heating or cooling the whole body by immersion are meanwhile useful in rare cases.

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4.1.3.1. Underwater mobilization. Underwater or whirlpool mobilization--active or passive--is indicated when the force of muscle contraction is impaired by degeneration, by neuro- or myelopathy, by sequels of trauma and joint diseases or by atrophy after prolonged immobilization (e.g. after fractures). This physical treatment is indicated in rehabilitation after injuries, following orthopedic surgery, rehabilitation of degenerative arthropathy, especially low back pain, whether or not complicated by sciatica. Treatment of scoliosis is also an indication for underwater mobilization. Plain water at 35°C is generally used. When muscle spasms or contractures are present with pain and functional restriction of joints movement, some benefit is obtained in a warm water or peloid bath, between 39-40°C, the temperature being adapted to the peloid, its dilution, and to the particular disease. Details on the procedures to be followed for the correct use of peloids will be found in Hatori (1963) and in Lehman et al. (1974). Carbon dioxide baths (see Appendix A) are used at 33°C to relieve pain and contractures. According to Knebel (1960) and Ott (1963) they are specially useful in the treatment of borderline systemic hypertension. Lowering of the systolic pressure by 3-5 cmHg has been observed; this can be explained by psychosomatic influences in patients suffering cardiac erethism of emotional origin. 4.1.3.1. Temperature changes (a) In hypothermic states, immersion in a hot water bath (38°C) and wrapping the entire entire body in warm blankets are both used in some hypothermic states, e.g. comatose patients found in a cold room or acute intoxication by ethyl alcohol etc. Rewarming must be cautious with fluid balance being restored. Application of external heat is necessary when hypothermia is deep (22-25°C). Warm water (40-42°C) is generally used, the warming rate being fixed around 0.5-1°C per hour. Rapid warming is sometimes followed by a secondary fall in the core temperature due to mobilization of cold blood arrested in the skin (Hirvonen, 1979). Advantages of direct core rewarming are also discussed by Hirvonen (1979). (b) Hyperthermic effects. Intense and prolonged hyperthermic effects obtained with the aid of heating devices have been used for the cure of psoriasis, of dermatoses with marked cellular proliferation, either benign or malignant, melanomas, Kaposi sarcomas and cutaneous lymphomas. Generalized hyperthermia favors the disappearance of certain malignancies with metastases by a direct inhibitory effect of heat on the process of cellular multiplication. A similar degree of hyperthermia is moreover often used during administration of antimitotic drugs. The effects of hyperthermia on the immune system are described in Appendix C. (c) Sauna. In spite of a vast literature, no specific effects can be ascribed to the sauna. No properly controlled studies are currently available (see Fritzsche and Fritzsche, 1980). (d) In hyperthermic states. Patients in a state of pathological hyperthermia or fever who poorly tolerate the corresponding metabolic and cardiovascular demands (e.g. malignant hyperpyrexia) may benefit from immersion in a cold water bath usually 2-3°C below body temperature. Use of cold wrapping or ice-packs leads to the same result--a reduction in a relatively short time of the risks inherent in persistance of elevated body temperature (Denborough, 1979). 4.1,4. Artificial Hibernation When cooling a normal awake man, thermogenic processes set in--shivering and metabolic demands rapidly exhaust body energy stores leading to serious impairment. This can be avoided when the patient to be cooled is first anesthetized. Thermoregulatory systems are simultaneously depressed; shivering does not appear and a fall in central

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temperature occurs. This method has been developed by Laborit as a method for treating disorders and casualties where the necessity to deal with metabolic needs threatens survival. Such artificial hibernation is indicated in the induction of certain surgical procedures. As an example, prior to certain surgical procedures on the heart, once anesthesia has been achieved, the patient can be cooled by immersion in a cold bath or by use of a peri-corporeal device. Working in a low temperature atmosphere will prolong the duration of the initial hypothermia (for a review, see Laborit, 1979). 4.2. INDICATIONS ACCORDING TO THE PATHOLOGICAL PROCESSES

Few pathological processes benefit from hydrotherapy, local or general: (1) Osteo-articular diseases in a nonevolutive state, mainly when pain arises, from muscular spasms, from periarticular edema or from gravitational compression. (2) Muscle spasms. (3) Muscular atrophy and impairment of contraction. (4) Localized and superficial inflammation: skin, subcutaneous tissues, joints, abdominal cavity. Insect bites. (5) Malignant tumours (superficial and localized). (6) General sedation in psychiatric disorders or anxious states, notably with cardiovascular erethism. (7) Toxic hyperthermia. (8) Accidental hypothermia. (9) In association with general anaesthesia, cardiac or bone surgery, treatment of malignancies; accidental metabolic disorders with energy supply depletion. As hydrotherapy is acting as a palliative treatment during the time of its application, treatments are repeated according to the severity of the disease. In most cases, alleviation of pain remains the criterion for deciding whether cold or heat will be preferred. As cartilage degradation is accelerated by deep heating of joints, cold seems more appropriate in the active states of arthritis (Feibel and Fast, 1976). 4.3. CONTRAINDICATIONS AND DANGERS

Hyperthermia and hypothermia may be harmful per se. When used in the restricted field of hydrotherapy, heating a focal inflammation can spread toxic products or accelerate enzymatic local destruction; heating an area when circulation is impaired can induce necrosis. Bathing a patient suffering from cardiac failure may cause lung edema. Paroxysmal systemic hypertension is observed in cold water. Thermic stress may cause loss of consciousness or convulsions in the elderly. But, in general, few accidents are described which are directly related to hydrotherapy, which appears relatively safe.

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BLIGH,J. (1959) Aspects of thermoregulatory physiology pertinent to hyperthermic treatment of cancer. Cancer Res. 39: 2307-2312. BUHRING, M., BOK-W6LWER, L. and KRIPPNER, H. (1982) Peripheral T lymphocytopenia under exogenous thermal stress, Cancer Res. 42: 2794-2797. CASTOR, C. and YARON, M. (1976) Connective tissue activation: VIII, The effects of temperature studied "in ritro". Arch. phys. Med. Rehabil. 57: 5-12. CLARA,M. (1939) Die Arterio-veniisen Anastomosen. BARTH (Ed.) Leipzig. CLARKE, G., WILLIS, L., STENNER, L. and NICHOLS, J. (1974) Evaluation of physiotherapy in the treatment of osteoarthrosis of the knee. Rheum. Rehabil. 13: 190-196. COBBOLD, A. F. and LEWIS, O. J. (1956) Blood flow to the knee joint of the dog. Effect of heating, cooling and adrenaline. J. Physiol. (Lond.) 132: 379-383. COULTER, J. and PIERSOL, S. (1950) Hydrotherapy. In: Handbook of Physical Medicine and Rehabilitation (lst Edtn), pp. 172-194. Blakiston, Philadelphia. DAMATO, A., LAU, S., STEIN, E., HAFT, J., KOSOWSK1, B. and COHEN, S. (1968) Cardiovascular response to acute thermal (hot dry environment) in unacclimatized subjects. Am. Heart J. 76: 769-774. DENBOROUGH, M. (1979) Malignant Hyperpyrexia. In: Body Temperature, pp. 551-559, LOMAX P. and SCHONBAUME. (eds). M. Dekker, New York. DIJI, A. and GREENFIELD, A. (1960)The local effect of carbon dioxide on human blood vessels. Am. Heart J. 60: 907-914. DOUGLAS, M., PARKS, L. and BEBIN, J. (1981) Sudden myelopathy secondary to therapeutic total-body hyperthermia. New Engl. J. Med. 304: 583-585. DOWNEY, J. and DARLING, R. (1971) Physiological Basis of Rehabilitation Medicine. W. B. Saunders, Philadelphia. DUFFIELD, M. (1969) Exercise in water. Bailli6re, Tindall and Cassell, London. EISALO A. (1963) Sauna. In: Medical Hydrology, pp. 291-299, LICHT S. and KAMENETZH. (eds). E. Licht, New Haven (Corm). ELDRED E., SCHNETZLEIN, H., LINDSLEY, D. and BUCHWALD, J, (1960) The effect of cooling on mammalian muscle spindle. Expl Neurol. 2: 144-152. EPSTEIN M. (1976) Cardiovascular and renal effects of heat-out water immersion in man. Circulation Res. 39: 619-628. EPSTEIN, M., DE NUNZIO, A. and RAMACHANDRAN,M. (1980) Characterization of renal response to prolonged immersion in normal man. J. app. Physiol. 49: 184-188. EPSTEIN. M., PINS, D. and MILLER, M. (1975) Suppression of ADH during water immersion in normal man. J. app. Physiol. 38, 1038-1044. EPSTEIN. M. and SARUTA,T. (197l) Effect of water immersion on renin-aldosterone and renal sodium handling in normal man. J. app. Physiol. 31: 368-374. EULER,C. (yon) and SODERBERG,U. (1956) The relation between gamma motor activity and the electroencephalogram. Experientia 12: 278-279. FEIBEL, A. and FAST, A. (1976) Deep heating of joints: A reconsideration. Arch. phys. Med. Rehabil. 57: 513516. FISCHER, E. and SOLOMON, S. 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(1944, 1950, 1960) Medical Physics. (1944, vol. 1: 1950, vol. II; 1960, vol. III). Year Book Publ., Chicago, Illinois. GOLLWITZER-MEIER, K. (1938) Zur Frage der Wirkung des Kohlens~iuerebades auf die Herzenergetik. Balneolore 5: 434-445. GRAYSON, J. and KUEHN, L. A. (1979) Heat transfer and heat loss. In: Body Temperature, pp. 71-87, LOMAX, P. and SCH6NBAUM, E. (eds). M. Dekker, New York. GUYTON, A. (1981) Textbook of Medical Physiology. W. B. Saunders, Philadelphia. HARRIS, R. (1960). Effect of short wave diathermy on radio-sodium clearance from the knee joint in the normal and in rheumatoid arthritis. 3rd International Congress of Physical Medicine, p. 241. Session on Arthritis, Aug. 23, Washington D.C. HARRIS, R. (1963) The effect of various forms of physical therapy on radio-sodium clearance from the normal and arthritic knee joint. A. phys. Med. 7: 1-14. HARRIS, E. JR. and MCCROSKERY, P. (1974) The influence of temperature and febril stability on degradation of cartilage collagen by rheumatoid synovial collagenase. New Engl. J. Med. 290: 1-6. HATTORI, I. (1963) Pelotherapy. In: Medical Hydrology, pp. 273-290, LICTH S. and KAMENETZH. (eds). E. Licht, New Haven (Conn,). HAYWARD, J. S., ECKERSON, J. D. and COLLIS, M. L. (1975) Thermal balance and surviVal time prediction of man in cold water. Can. J. Physiol. Pharmac. 53: 21-32. HERON, I. and BERG, K. (1978) The actions of interferon are potentiated at elevated temperature. Nature 274: 508-510.

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HINES, E. A. and BROWN, C. E. (1933) A standard test for measuring the variability of blood pressure. Ann. intern. Med. 7:209 217. HIRVONEN, J. (1979) Accidental Hypothermia. In: Body Temperature, pp. 561 585, LOMAXP. and SCH/JNBAUME. (eds). M. Dekker, New York. HussI, E., SONCK, T., Poso, H., REMES,J., EISALO,A. and JANNE, J. (1977) Plasma catecholamines in a Finnish sauna. Ann. clin. Res. 9: 301-304. JOHNSON, D. G., HAYWARD, J. S., JACOBS, T. P., COLLIS, M. L., ECKERSON,J. D. and WILLIAMS, R. H. (1977) Plasma norepinephrine responses of man in cold water. J. app. Physiol. 43, 216~220. KAISER, D., LINKENBACH,H. J. and GAUER, O. H. (1969) Changes of plasma volume in man during immersion in a thermoindifferent water bath. Pfluegers Arch. yes. Physiol. 308: 16(~173. KHOSLA, S. S. and DuBolS, A. B. (1979) Fluid shifts during initial phase of immersion diuresis in man. J. app. Physiol. 46: 703-708. KIM, J. H. and HAHN, E. W. (1979) Clinical and biological studies of localized hyperthermia. Cancer Res. 39: 2258-2261. KIM, Y. D., LAKE, C. R., LEES, D. E., SCHUETTE, W, H., BULL, J. M., WEISE, V. and KOPIN, I. J. (1979) Hemodynamic and plasma catecholamines responses to hyperthermic cancer therapy in humans. Am. J. Physiol. 237: H570-H574. KNEBEL, R. (1960) Wirkung und Indikation der B~iderbehandlung bei Herzkranken. In: Handbook der Inneren Medizin, pp. 653-705.4 ° Aufl. Band IX/1. Springer Verlag, Berlin. KOSUNEN, K. J., PAKARINEN, A. J., KUOPPASALMI,K. and ADLERCREUTZ, H. (1976) Plasma renin activity, angiotensin II, and aldosterone during intense heat stress. Int. J. app. Physiol. 41 : 323-329. KOWARSCHIK,J. (1977) Physikalische Therapie. 2nd Edtn. Springer Verlag, Wien. KRI~EK, V. (1963) History of Balneotherapy. In: Medical Hydrology, pp. 131-159, Vol. VII of Physical Medicine Library. LICHT, S. and KAMENETZ,H. (eds). E. Licht, New Haven (Conn.). LABORIT, H. M. (1979) Clinical Hypothermia. 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E. Licht, New Haven (Conn.). ROSE, A. H. (1967) Thermobiolog). Academic Press, London. ROWELL, L. B. (1974) Human cardiovascular adjustments to exercise and thermal stress. Physiol. Rev. 54: 75-159. SCHMIDT, K. L., OTT, V. R., ROCHER, J. and SCHALLER,H. (1979) Heat, cold and inflammation. Zelschr(/~jiir Rheurnatologie 38:391 403. SCH~NDEWOLF, G. and WEIGMANN,R. (1952} Uber die Wirkung des Kohlendioxyds auf die Thermoreceptoren der Haut. Klin. Wschr 30: 547-550. SHAH, S. A. and D1CKSON, J. A. (1978) Effect of hyperthermia on the immuno-competence of V X Z tumorbearing rabbits. Cancer Res. 38:3523 3531. SHAH, S. A. and D1CKSON,J. A. (1979)Effect of hyperthermia on the immune response of normal rabbit. Cancer Res. 39: 3518-3522. SOTER, N. and WASSERMAN,S. (1980) Physical urticaria -angioedema. J. Allergy 66: 359-365. STEHLIN, J. S., GIOVANELLA, B. C., DE IPOLYI, P. D., MUENZ, L. R. and ANDERSON, R. F. (1975) Results of hyperthermic perfusion for melanoma of the extremities. Surgery 140: 338-348. STILLWELL, K. (1965) General principles of thermotherapy. In: Therapeutic Heat and Cold, pp. 232-265, LICHT, S. and KAMENETZ,H. (eds). E. Licht, New Haven (Conn.). STITT, J. T. (1979) Fever versus hyperthermia. Fedn Proc. 38:39 43. STORM, F. K., HARRISON, W. H., ELLIOTT, R. S. and MORTON, D. L. (1979) Normal tissue and solid tumour effects of hyperthermia in animal models and in clinical trials. Cancer Res. 39:2245 2251. TUTTLE, W. W. (1941) The effects of decreased temperature on the activity of intact muscle. J. lab. clin. Med. 16: 1913 1917.

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WILLIAMSON,C. and SCHOLTZ,J. R. (1949) Time-temperature relationship in thermal blister formation. J. invest. Dermatol. 12: 41-53. WYMAN, J. (1944) Hydrotherapy. In: Medical Physics. vol. I, pp. 619 622, GLASER, O. (ed). Year Book Publ. Chicago (Illinois). APPENDIX A A.I. CHARACTERISTICSOF CARBONDIOXIDEBATHS Replacement of the water of the bath by a saline solution saturated with carbon dioxide at normal barometric pressure is well tolerated down to 33°C; at this temperature, some 2°C below the optimum for water, neither abnormal sensations of cold nor shivering but a feeling of well-being occur (Gollwittzer-Meier, 1968). Carbon dioxide is absorbed through the skin at the rate of mMol.min- Lm -2 (Lecomte et al., 1976). Skin vessels are directly dilated by CO2 (CO2 erythema) (Diji and Greenfield, 1960). The vasodilation increases local blood flow and skin temperature, leading to stimulation of warm receptors with a feeling .of warmth (Schindewolf and Weigmann, 1952). Meanwhile, loss of heat occurs from the body to the water inducing hypothermia. Sympathetic depression, as linked with immersion, is also observed. Systemic arterial hypotension is sometimes described (see Knebel, 1960). APPENDIX B B.1. DEEP LOCALTHERMALEFFECTS Local hydrotherapy is limited to the skin and the underlying tissues. Warm and cold saline perfusions by extracorporeal circulation are used to extend the use of hypothermia and hyperthermia to the deeper tissues and to limit their effects to localized diseased areas. These procedures are no longer 'hydrotherapy' but their pathophysiological consequences are similar. General anesthesia is required for their application. B.l.1. Hyperthermia As a result of numerous clinical observations showing that episodes of hyperthermia or fever are followed by a marked slowing of the growth of certain malignant tumors and, at times, by the appearance of necrotic areas within them, local heating using extracorporeal circulation has been applied with the aim of arresting the growth of certain localized malignancies. Providing that the corresponding blood vessels are technically accessible, extracorporeal perfusion with saline solutions at a temperature between 41.5-42.5°C is followed by a subtantial temperature increase for several hours in the organ. The general anesthesia impairs thermoregulatory processes. As an adjunct, perfusion fluid can be at lower oxygen tensions and other therapeutic agents may be incorporated (Bligh, 1959). The maximum temperature change is at the arteriolar side of the circuit, at the level of the endothelium. Metabolism is greatly increased in hyperthermic regions and blood vessels are maximally dilated. As neoplastic cells are less resistent to heat then are healthy ones (Stehlin et al., 1975), hyperthermia, with or without hypoxia, exhibits antimitotic properties. By using hyperthermic perfusion one can raise the temperature of a deep tumor in such a way that the survival of the neoplasic cells is impaired, either directly via its own circulation or indirectly via neighboring tissues (Storm et al., 1979; Kim and Hahn, 1979). The risks of these high temperature perfusions essentially are those due to lesions of the vascular endothelium from local excessive heating combined with other treatments, thrombosis and necrosis may follow reestablishment of the normal circulation (Douglas et al., 1981). B.1.2. Hypothermia Perfusions with low temperature refrigerated saline (5-10°C) have been used for extracorporeal perfusion of some body segments or organs. The lowering of metabolism due to cooling is used for certain surgical procedures (Laborit and Huguenard, 1953; Blair, 1964; Laborit, 1979). APPENDIX C C.1. HYPERTHERMIAAND IMMUNOREACTIVITY Hyperthermia can lead to functional changes in the immune system. Experimentally, in the rabbit and rat, generalized hyperthermia reduces humoral immunity, stimulates (following a small elevation in body temperature) or decreases (with more marked elevations in temperature) cellular immunity, increases phagocytosis and activates leucocyte interferon (Shah and Dickson, 1978, 1979; Heron and Berg, 1978). These characteristics could be responsible for the antiinflammatory effect produced by local or general heating in experimental chronic inflammatory processes such as polyarthritis induced by adjuvant, the granulomatous reaction to cotton pellets and the cutaneous reaction to tuberculin (Schmidt et al., 1979). In healthy man, immersion in a hot bath leading to a rectal temperature of 38.5°C, provokes a significant reduction in T lymphocytes without any related changes in blood cortisol levels (Buhring et al., 1982). In patients with visceral neoplasia general or local heating of the tumor stimulates cutaneous cellular immune reactions and lymphoblastic transformation.