Thermoregulation

Thermoregulation-physiology, anaesthetic effects, hypothermia,hyperthermia and fever, malignant hyperthermia,temperature monitoring,guidelines

1. THERMOREGULATION PRESENTOR :- DR. KANIKA CHAUDHARY 1

2. 2 OVERVIEW INTRODUCTION CORE TEMPERATURE AND SKIN TEMPERATURE HEAT PRODUCTION AND HEAT LOSS NORMAL THERMOREGULATION CHANGES IN GENERAL ANESTHESIA CHANGES IN REGIONAL ANESTHESIA EFFECTS OF HYPOTHERMIA CONSEQUENCES OF MILD INTRAOP HYPOTHERMIA INDUCTION OF MILD HYPOTHERMIA DELIBERATE SEVERE HYPOTHERMIA MAINTAINING INTRAOP HYPOTHERMIA HYPERTHERMIA & FEVER MALIGNANT HYPERTHERMIA TEMPERATURE MONITORING GUIDELINES

3. INTRODUCTION Humans are homeothermic and require a nearly constant internal body temperature for maintaining normal physiological functions. The homeostatic mechanisms for regulating body temperature represents the thermoregulatory system . Body temperature is controlled by balancing heat production against heat loss. The thermoregulatory system usually maintains core body temperature with in 0. 2° C of normal , which is about 37° C in humans . 3

4. CORE TEMPERATURE AND SKIN TEMPERATURE The temperature of the deep tissues of the body — the “core” of the body—remains very constant, within ± 0.6°C No single core temperature can be considered normal. Range:- 36.5–37.5°C . Core temperature gradually decreases with age Core temperature measurements (e.g. tympanic membrane, pulmonary artery, distal esophagus, and nasopharynx ) are used to monitor intraoperative hypothermia,prevent overheating, and facilitate detection of malignant hyperthermia The core thermal component is composed of highly perfused tissues whose temperature is uniform and high compared with the rest of the body 4

5. The skin temperature, in contrast to the core temperature, rises and falls with the temperature of the surroundings. Body temperature shows circadian rhythm , highest in the afternoon or in the evening and least at 5:00 A.M in the morning and vary by 0.5 to 1 °C. Rectal temperature is 0.5°C more than core temperature. In children, body temperature is 0.5°C higher. Non-pregnant women in their reproductive phase of life show 0.5°C higher body temperature in the luteal phase of menstrual cycle. 5

6. 6 How body temperature is controlled? When the rate of heat production in the body is greater than the rate at which heat is being lost, heat builds up in the body and the body temperature rises. Conversely, when heat loss is greater, both body heat and body temperature decrease . Body temperature is controlled by balancing heat production against heat loss.

7. 7 HEAT PRODUCTION B asal rate of metabolism of all the cells of the body extra rate of metabolism caused by muscle activity, including muscle contractions caused by shivering extra metabolism caused by the effect of thyroxine (and, to a less extent, other hormones, such as growth hormone and testosterone) on the cells extra metabolism caused by the effect of epinephrine, norepinephrine, and sympathetic stimulation on the cells extra metabolism caused by increased chemical activity in the cells themselves, especially when the cell temperature increases extra metabolism needed for digestion, absorption, and storage of food

8. 8 HEAT LOSS Most of the heat produced in the body is generated in the deep organs, especially in the liver, brain, and heart, and in the skeletal muscles during exercise. Then this heat is transferred from the deeper organs and tissues to the skin, where it is lost to the air and other surroundings. The rate at which heat is lost is determined by two factors: how rapidly heat can be conducted from where it is produced in the body core to the skin how rapidly heat can then be transferred from the skin to the surroundings

9. 9 How heat is lost from the skin surface? RADIATION A t normal room temperature, about 60 percent of total heat loss is by radiation Loss of heat by radiation means loss in the form of infrared heat rays, a type of electromagnetic wave The human body radiates heat rays in all directions. Heat rays are also being radiated from the walls of rooms and other objects toward the body.

10. 10 2. CONDUCTION A bout 3 percent, are normally lost from the body by direct conduction from the surface of the body to solid objects, such as a chair or a bed Loss of heat by conduction to air is 15 percent

11. 11 3. CONVECTION The removal of heat from the body by convection air currents is commonly called heat loss by convection. Actually, the heat must first be conducted to the air and then carried away by the convection air currents A bout 15 percent of total heat loss occurs by conduction to the air and then by air convection away from the body

12. 12 4. EVAPORATION When water evaporates from the body surface, 0.58 Calorie of heat is lost for each gram of water that evaporates. Even when a person is not sweating, water still evaporates insensibly from the skin and lungs at a rate of about 600 to 700 ml/day. This causes continual heat loss at a rate of 16 to 19 Calories per hour

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14. 14 NORMAL THERMOREGULATION Thermoregulation is similar to other physiologic control systems in that the brain uses negative and positive feedback to minimize perturbations from preset, “normal” values The processing of thermoregulatory information occurs in three phases:- Afferent thermal sensing Central regulation Efferent responses

15. AFFERENT SENSING 15 Cold receptors A δ fibres Warm receptors C fibres Anterior spinothalamic tract Hypothalamus

16. 16 CENTRAL REGULATION Temperature is regulated by central structures (primarily the hypothalamus) that compare integrated thermal inputs from the skin surface, and deep tissues with threshold temperatures for each thermoregulatory response. Although integrated by hypothalamus, most thermal information is “preprocessed” in the spinal cord and other parts of the CNS The preoptic nuclei in the hypothalamus contains temperature sensitive neurons(cold and heat sensitive neurons). Preoptic nucleus of anterior hypothalamus integrates input from peripheral and central thermoreceptors. Approximately 80% of this thermal input is derived from core body temperature. There is evidence however that some thermoregulatory functions occur at the level of the spinal cord not involving the hypothalamus. The interthreshold range (core temperatures not triggering autonomic thermoregulatory responses) is 0.2 degree centigrade. This range is bounded by the sweating threshold at its upper end and by vasoconstriction at the lower end.

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19. EFFECTOR RESPONSE 19

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21. 21 TEMPERATURE DECREASING MECHANISM:- When body is too HOT

22. nerves Less heat generated More water covers the skin. More evaporation and hence heat loss Skin arteries dilate More blood to the skin. Heat loss by More radiation & conduction Muscles of skin arteriole walls relax Sweat glands increase secretion Muscles reduce activity Core body temperature >37°C Hypothalamus Thermoreceptors 22

23. RESPONSE TO HEAT Hypothalamic mechanism: there is vasodilatation and sweating starts when temperature exceeds 37.1˚ C. Behavioural adjustment: Bathing in cold shower. Circulation of air by fan Voluntary muscular activities diminish and muscle tone is reduced. 23

24. RESPONSE TO HEAT SWEATING: Is mediated by post-ganglionic cholinergic fibres which is an active process where body can dissipate heat in an environment, exceeding core temperature . 0.58 kcal dissipated per gram of evaporated sweat Threshold for sweating is temperature>37˚ C   24

25. RESPONSE TO HEAT VASODILATION Caused by inhibition of sympathetic centers in the posterior hypothalamus that causes vasoconstriction Is an active process mediated by Nitric oxide. Has a similar threshold but lower gain when compared to sweating . 25

26. 26 TEMPERATURE INCREASING MECHANISM:- When body is too COLD

27. More heat generated Less water covers the skin. Less evaporation Skin arteries constrict Less blood to the skin. Less radiation & conduction of heat Muscles of skin arteriole walls constrict Sweat glands decrease secretion Muscles shivering Core body temperature <37°C Thermoreceptors Hypothalamus 27

28. RESPONSE TO COLD 1. Cutaneous vasoconstriction: Most consistently used autonomic effector response. Threshold for vasoconstriction is 36.5˚C Caused by stimulation of posterior hypothalmic sympathetic centers First response to a decrease in core temperature below the normal range(36.5-37.0 ˚C) 28

29. RESPONSE TO COLD 2. Shivering: it is involuntary oscillatory, unsynchronised muscular contractions. Threshold for shivering is 36 to 36.2 ˚C When the environmental temperature is 23˚C (critical temperature), shivering begins and increases heat production by 50 to 100%. Shivering does not occur in infants and not fully effective in children until they are seven years old. 29

30. RESPONSE TO COLD 3. Piloerection: this leads to standing up of the body hair due to posterior hypothalamus stimulation. In between the erect hair, considerable amount of air is trapped and helps to preserve body temperature. 4. Adipose tissue lipolysis : cause heat generation. 30

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32. 32 Non shivering thermogenesis N onshivering thermogenesis, produce heat in response to cold stress. This type of thermogenesis is stimulated by sympathetic nervous system activation, which releases norepinephrine and epinephrine, which in turn increase metabolic activity and heat generation. B rown fat, sympathetic nervous stimulation causes liberation of large amounts of heat. This type of fat contains large numbers of mitochondria and many small globules of fat instead of one large fat globule. In these cells, the process of oxidative phosphorylation in the mitochondria is mainly "uncoupled." When the cells are stimulated by the sympathetic nerves, the mitochondria produce a large amount of heat but almost no ATP, so almost all the released oxidative energy immediately becomes heat. .

33. THERMOREGULATION IN PAEDIATRICS Loss of heat in neonates is much greater due to following reasons large surface area to body mass ratio (term neonate 1 and adult 0.4) Greater thermal conductance (less subcutaneous fat) Greater evaporative heat loss (less keratin content)

34. THERMOREGULATION IN PAEDIATRICS Infants are especially vulnerable to hypothermia because of the large ratio of body surface area to weight, the thinness of the skin, and a limited ability to cope with cold stress. Cold stress causes increased oxygen consumption and a metabolic acidosis, particularly in preterm infants because of even thinner skin and limited fat stores The head comprises of 20% surface area and shows highest regional heat flux. hence covering of head is very important

35. Prevention: Heat loss by radiation is decreased by use of double shelled isolates during transport. Heat loss by conduction is reduced by placing baby on a warming mattress and warming the OT room. Heat loss through convection is minimized by keeping the infant in an incubator, covered by blankets and by covering head. Heat lost through evaporation is lessened by humidification of inspired gases, use of plastic wrap to decrease water loss through skin.

36. 36 THERMOREGULATION DURING GENERAL ANESTHESIA Anesthetic- induced normal autonomic thermoregulatory impairment has a specific form: warm-response thresholds are elevated slightly cold-response thresholds are markedly reduced The inter- threshold range is increased from its normal values near 0.2° C to approximately 2° C to 4° C

37. 37 Interthreshold range is distance between first cold response(vasoconstriction) and the first warm response(sweating); temperature with in this range will not elicit autonomic thermoregulatory compensation During GA, the thresholds for vasoconstriction and non-shivering thermogenesis are shifted down to 34.5°C and thresholds for vasodilation and sweating increased to 1°C . Interthreshold range thus increases from 0.2°C to 4°C

38. 38 RESPONSE THRESHOLD Propofol , alfentanil , and dexmedetomidine all produce a slight, linear increase in the sweating threshold combined with a marked and linear decrease in the vasoconstriction and shivering thresholds . Isoflurane and desflurane also slightly increase the sweating threshold; however, they decrease the cold-response thresholds non- linearly. The volatile anesthetics inhibit vasoconstriction and shivering less than propofol at low concentrations, but more than propofol at typical anesthetic doses. In all cases (except after meperidine and nefopam administration), vasoconstriction and shivering decrease synchronously and maintain their normal approximate 1° C difference.

39. 39 The combination of increased sweating thresholds and reduced vasoconstriction thresholds increases the inter threshold range approximately 20-fold, from its normal value near 0.2° C to approximately 2° C to 4° C. Temperatures within this range do not trigger thermoregulatory defenses; by definition , patients are poikilothermic within this temperature range

40. 40 Isoflurane, desflurane , enflurane , halothane, and the combination of nitrous oxide and fentanyl decrease the vasoconstriction threshold 2° C to 4° C from its normal value near approximately 37° C. The dose dependence is nonlinear (i.e., greater concentrations produce disproportionate threshold reductions). The shivering thresholds decrease synchronously. In contrast, these drugs increase the sweating threshold only slightly Clonidine synchronously decreases cold-response thresholds, while slightly increasing the sweating threshold. Nitrous oxide decreases the vasoconstriction and shivering thresholds less than equipotent concentrations of volatile anesthetics. In contrast, midazolam only slightly impairs thermoregulatory control T he vasoconstriction threshold is approximately 1° C less in patients 60 to 80 years old than in those between 30 and 50 years old

41. 41 INADVERTANT HYPOTHERMIA DURING GENERAL ANESTHESIA Hypothermia= core body temperature<36 ˚C Mild:- 35 ˚C -32.2 ˚C Moderate:- 32.2 ˚ C - 28 ˚ C Severe:- <28 ˚ C Inadvertent hypothermia during anesthesia is the most common perioperative thermal disturbance. Hypothermia results from a combination of anesthetic-impaired thermoregulation and exposure to a cold operating room environment. Common in patients at extremes of age, and in those undergoing abdominal surgeries or procedures of long duration

42. CAUSES OF INTRA-OP HYPOTHERMIA OT temperature of <21˚C Administration of cold blood or IV fluids Prolonged surgery. Intraabdominal surgery or intrathoracic surgery due to exposure to large viscera, body cavities. Use of repeated large volumes of irrigating fluids. Direct effect of anaesthetic drugs  

43. 43 Patterns of intraoperative hypothermia

44. 44 General anaesthesia typically results in mild core hypothermia (1–3°C). Phase 1 is a rapid reduction in core temperature of 1.0–1.5°C within the first 30–45 min. This is attributable to vasodilatation and other effects of general anaesthesia . Vasodilatation inhibits normal tonic vasoconstriction resulting in a core-to-peripheral temperature gradient and redistribution of body heat from core to peripheral tissues. Phase 2 is a more gradual, linear reduction in core temperature of a further 1°C over the next 2–3 h of anaesthesia . This is due to heat loss by radiation, convection and evaporation exceeding heat gain which is determined by the metabolic rate. Phase 3 is a ‘plateau’ phase where heat loss is matched by metabolic heat production. This occurs when anaesthetised patients become sufficiently hypothermic to reach the altered threshold for vasoconstriction which restricts the core-to- peripheral heat gradient.

45. 45 HYPOTHERMIA DURING REGIONAL ANESTHESIA Epidural and spinal anesthesia each decrease the thresholds triggering vasoconstriction and shivering (above the level of the block) approximately 0.6° C The vasoconstriction and shivering thresholds are decreased during regional anesthesia, suggesting an alteration in central, rather than peripheral control. The mechanism by which peripheral administration of local anesthesia impairs centrally mediated thermoregulation may involve alteration of afferent thermal input from the legs Regional anesthesia blocks all thermal input from blocked regions, which in the typical case is primarily cold information. The brain may then interpret decreased cold information as relative leg warming. This appears to be an unconscious process because perceived temperature does not increase. Leg warming proportionately reduces the vasoconstriction and shivering thresholds. Consistent with this theory, a leg skin temperature near 38° C is required to produce the reduction in cold-response thresholds in an unanesthetized subject that is produced by regional anesthesia. Furthermore, reduction in the thresholds is proportional to the number of spinal segments blocked

46. 46 Core hypothermia during regional anesthesia may not trigger a perception of cold. The reason is that thermal perception (behavioral regulation) is largely determined by skin temperature, rather than core temperature. Because redistribution during spinal or epidural anaesthesia is usually confined to the lower half of the body, the initial core hypothermia is not as pronounced as in general anaesthesia (approximately 0.5°C). Subsequent hypothermia results simply from heat loss exceeding metabolic heat production. Unlike patients given general anesthesia, however, core temperature does not necessarily plateau after several hours of surgery. Because the legs constitute the bulk of the peripheral thermal compartment, an effective plateau cannot develop without vasoconstriction in the legs and the resulting decrease in cutaneous heat loss and constraint of metabolic heat to the core

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49. 49 CONSEQUENCES OF MILD INTRAOP HYPOTHERMIA BENEFITS:- Substantial protection against cerebral ischemia and hypoxia is provided by just 1° C to 3° C of hypothermia. Protection initially was thought to result from the approximate 8%/°C linear reduction in tissue metabolic rate. Other actions (e.g., decreased release of excitatory amino acids ) also explain the protective action of hypothermia . Rapid induction of hypothermia is thus becoming routine for patients after recovery from cardiac arrest. The other situation in which therapeutic hypothermia appears beneficial is in asphyxiated neonates The potential protection afforded by mild hypothermia is so great that reduced core temperature (i.e., ≈34° C) is sometimes used during neurosurgery and other procedures in which tissue ischemia can be anticipated

50. 50 Hypothermic protection against ischemia may extend to other organs. For example, mild hypothermia markedly reduced infarct size in experimental studies. Acute malignant hyperthermia is more difficult to trigger in mildly hypothermic than in those kept normothermic . Furthermore, once triggered, the syndrome is less severe. Various data suggest that active warming should be avoided in patients known to be susceptible to malignant hyperthermia; instead, these patients should be allowed to become slightly hypothermic during surgery

51. 51 ADVERSE EFFECTS OF HYPOTHERMIA:- 1.Wound infection:- the most common serious complication, due to Impaired immune function decreased cutaneous blood flow decreases wound oxygen delivery decreased synthesis of collagen 2.REVERSIBLE COAGULOPATHY Hypothermia reduces platelet function and decreases the activation of the coagulation cascade H ypothermia directly impairs enzymes of the coagulation cascade. This is not apparent during routine coagulation screening because the tests are performed at 37° C Increases blood loss and the need for allogenic transfusion during elective primary hip arthroplasty

52. 52 3.PROLONGED RECOVERY Mild hypothermia decreases the metabolism of most drugs Propofol ---during constant infusion, plasma conc. is 30% greater than normal with a 3 ℃ fall in temperature Atracurium ---a 3 ℃ reduction in core temp. increase the duration of muscle relaxation by 60 percent 4.DRUG METABOLISM Prolongation of NDMR : – vecuronium > atracurium Reduction in MAC for volatile anaesthetics Hypothermia increases the solubility of volatile anaesthetics

53. 53 5.SHIVERING The best thermoregulatory response to counteract a decrease in body temperature is through shivering. A 2 fold increase in metabolic heat production can be sustained over increased durations. Uncomfortable, psychologically distressing May exacerbate wound pain, increase intracranial and intraocular pressure 6.OTHERS Altered mental status. DIC Hypoglycemia Decrease renal perfusion. Respiratory depression Increased pulmonary vascular resistance

54. 54 Postanesthetic shivering The incidence of postoperative shivering-like tremor reportedly is approximately 40%, but it now appears to be less as more patients are kept normothermic and opioids are administered more frequently and in larger doses than in the past Shivering is an involuntary, oscillatory muscular activity that augments metabolic heat production upto 600% above basal level. Shivering occurs in approximately 40% of unwarmed patients who are recovering from general anaesthesia and in about 50% of patients with a core temperature of 35.5 degree centigrade and in 90% of patients with a core temperature of 34.5 degree centigrade The tonic pattern consistently demonstrated the waxing-and-waning pattern of four to eight cycles/ minute that characterizes normal shivering and apparently it is a simple thermoregulatory response to intra- operative hypothermia

55. 55 Although the precise etiology of shivering remains unknown, the cause may be anesthetic-induced disinhibition of normal descending control over spinal reflexes Consequences of postanesthetic shivering:- Increased oxygen consumption and carbon dioxide production . Catecholamine release and Sympathetic stimulation . Increased CO and HR and BP Increased intraocular pressure, increased intracranial pressure . Patient discomfort.

56. 56 Prevention : Intra-operative use of forced air warming device Heating and humidifying inspired gases Warmed I.V. fluids Covering the skin with surgical drape OT room temperature increased to 25˚C

57. 57 Treatment : Pethidine more effective in the treatment of postoperative shivering than other opioids Tramadol 50mg IV Clonidine 75 μg IV Ketanserine 10mg IV Physostigmine 0.04mg/kg IV Magnesium sulphate 30mg/kg IV

58. 58 INDUCTION OF MILD HYPOTHERMIA Hypothermia is occasionally used during neurosurgery or acute myocardial infarction. Target core temperatures are 32° C to 34° C, and it is thought to be important to reach the target temperature quickly Administration of refrigerated intravenous fluids also is effective and reduces mean body temperature 0.5° C/L Forced-air cooling is easy to implement, but it is relatively slow, taking approximately 2.5 hours to cool neurosurgical patients to 33° C Newer circulating-water systems include garment-like covers or “energy exchange pads” that cover far more skin surface and transfer large amounts of heat and are fairly effective

59. 59 The best way to induce therapeutic hypothermia rapidly is probably endovascular cooling. These systems consist of a heat-exchanging catheter, usually inserted into the inferior vena cava via the femoral artery, and a servo- controller. They can decrease core temperatures at rates approaching 4° C/hour Pharmacologically, the best method so far identified is the combination of buspirone and meperidine, drugs that synergistically reduce the shivering threshold to approximately 34° C without provoking excessive sedation or respiratory toxicity.

60. 60 DELIBERATE SEVERE INTRAOP HYPOTHERMIA Severe hypothermia may be induced deliberately to confer protection against tissue ischemia, specifically during cardiac surgery and, occasionally, neurosurgery. Drugs such as barbiturates and volatile anesthetics provide considerably less protection than even mild hypothermia C ardiac surgery is increasingly performed at either “tepid” temperatures (i.e., 33° C) or normothermia . O utcomes of bypass surgery , whether on or off pump, are improved by maintaining normothermia or near normothermia . Deep hypothermia (i.e., 18° C) remains routine for cases of intentional circulatory arrest.

61. 61 ORGAN FUNCTION Hypothermia decreases whole-body metabolic rate by approximately 8%/° C, to approximately half the normal rate at 28° C. Whole-body oxygen demand diminishes, and oxygen consumption in tissues that have higher than normal metabolic rates, such as the brain, is especially reduced . Low metabolic rates allow aerobic metabolism to continue during periods of compromised oxygen supply; toxic waste production declines in proportion to the metabolic rate. This decreased metabolic rate certainly contributes to the observed protection against tissue ischemia, other effects of hypothermia, including “membrane stabilization” and decreased release of toxic metabolites and excitatory amino acids, appear to be most important. Cerebral blood flow also decreases in proportion to metabolic rate during hypothermia because of an autoregulatory increase in cerebrovascular resistance.

62. 62 Cerebral function is well maintained until core temperatures reach approximately 33° C, but consciousness is lost at temperatures lower than 28° C Primitive reflexes such as gag, pupillary constriction, and monosynaptic spinal reflexes remain intact until approximately 25° C Hypothermic effects on the heart include a decrease in heart rate, increased contractility, and well-maintained stroke volume. Cardiac output and blood pressure both decrease . At temperatures lower than 28° C, sinoatrial pacing becomes erratic, and ventricular irritability increases. Fibrillation usually occurs between 25° C and 30° C, and electrical defibrillation is usually ineffective at these temperatures. Because coronary artery blood flow decreases in proportion to cardiac work, hypothermia per se does not cause myocardial ischemia.

63. 63 Hypothermia decreases blood flow to the kidneys by increasing renovascular resistance. Respiratory strength is diminished at core temperatures less than 33° C, but the ventilatory CO2 response is minimally affected . Hepatic blood flow and function also decrease, thus significantly inhibiting metabolism of some drugs

64. MAINTAINING INTRA-OP HYPOTHERMIA Prevention and treatment of mild peri -operative hypothermia There are 3 basic strategies Minimizing redistribution of heat Cutaneous warming during anaesthesia Internal warming 64

65. 65 Minimizing redistribution of heat The initial 0.5° C to 1.5° C reduction in core temperature is diffcult to prevent because it results from redistribution of heat from the central thermal compartment to cooler peripheral tissues .Although redistribution is diffcult to treat,but it can be prevented This may be achieved by: pre-operative warming of peripheral tissue pre-operative pharmacological vasodilatation

66. 66 1.Pre-operative warming of peripheral tissue This reduces the normal core-to-peripheral temperature gradient so that induction of anaesthesia does not result in the sudden core hypothermia seen in Phase 1. However, to be effective , this would require subjecting patients to over 1 h of exposure to a source of radiated heat pre-operatively 2. Pre-operative pharmacological vasodilatation This facilitates core-to-peripheral redistribution of heat before anaesthesia ; it does not compromise core temperature because patients are not anaesthetised and their thermoregulatory responses are intact. Oral nifedipine , taken pre-operatively, has been shown to reduce effectively the extent of the initial redistribution hypothermia by 50%.

67. 67 Cutaneous warming during anaesthesia 1.Passive insulation A single layer of any insulator ( e.g . space blanket) reduces cutaneous heat loss by approximately 30% because it traps a layer of still air between it and the skin. Adding further layers of passive insulation does little or nothing to preserve core temperature. 2.Active warming Active warming systems maintain normothermia much more effectively than passive insulation. -electrically powered air heater fan - circulating water mattress - active warming by resistive heating blankets

68. 68 1.Fluid warming Fluids should be warmed to body temperature prior to infusion . The administration of one litre of fluid at room temperature decreases core temperature by 0.25°C. Warm fluids should be used when large amounts of fluid or blood replacement are anticipated. 2.Airway humidification Airway heating and humidification are more effective in infants and children than in adults. Hygroscopic condenser humidifiers and heat-and-moisture exchanging filters (“ artificial noses”) retain substantial amounts of moisture and heat within the respiratory system INTERNAL WARMING

69. 69 3.Invasive internal warming techniques Cardiopulmonary bypass transfers heat at a rate and magnitude not seen in any other situation. Peritoneal dialysis is also very effective but neither technique is relevant to mild peri - operative hypothermia. 4.Amino acid infusion Amino acid infusion during anaesthesia increases metabolic rate and patients are less hypothermic compared with those given the same volume of crystalloid. This technique has not gained wide-spread acceptance because of doubts about the effect on cardiac outcome of increased metabolic rate during anaesthesia .

70. 70 HYPERTHERMIA AND FEVER Hyperthermia is a generic term simply indicating a core body temperature exceeding normal values. Hyperthermia:- hypothalamic set point is normal but peripheral mechanisms are unable to maintain body temperature that matches the set point Fever occurs when the hypothalamic set point is increased by the action of circulating pyrogenic cytokines, causing intact peripheral mechanism to conserve and generate heat until the body temperature increases to elevated set point In general, patients with fever and increasing core temperature have constricted fingertips whereas those with other types of hyperthermia are vasodilated.

71. 71 Causes of perioperative hyperthermia:- dehydration, fever, premedication with anticholinergic drugs, excessive surgical draping, malignant hyperthermia, thyroid storm, neuroleptic syndrome, septicaemia , excessive heat delivery from the radiant warmers Treatment of hyperthermia depends on the etiology, with the critical distinction being between fever and the other causes of hyperthermia. Treatment of hyperthermia should be directed at prompting heat dissipation and terminating excessive heat production ( e.g dantrolene for malignant hyperthermia) Treatment of fever should be directed at identification and eradication of pyrogens and lowering the thermoregulatory set point with antipyretic drugs such as aspirin, acetaminophen and cyclooxygenase inhibitors  

72. 72 MALIGNANT HYPERTHERMIA Malignant hyperthermia(MH) is a pharmacogenetic clinical syndrome that, in its classic form, occurs during anesthesia with a volatile halogenated alkane such as halothane and/or the administration of the depolarizing muscle relaxant succinylcholine. MH, first described by Denborough and Lovell in 1960, is an inherited clinical syndrome characterized by elevated core temperature, tachycardia, tachypnea, hypercarbia, muscle rigidity and rhabdomyolysis, acidosis and hyperkalemia The incidence of fulminant MH was reported to be 1 case per 62,000 anesthetics adminis - tered when triggering agents were not used, but the number of suspected cases was 1 case per 4500 anesthetics administered when triggering agents were administered

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74. 74 Excitation-contraction coupling

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76. 76 Pathophysiology of malignant hyperthermia The most common genetic defect is a defective calcium channel “RYR1” located in the membrane of the sarcoplasmic reticulum of skeletal muscle. More than 70% of MH cases are linked to the RYR1 located on chromosome 19. Less than 2% are related to mutations in the gene coding for dihydropyridine receptor(DHPR) known as CACNA1s The MH syndrome results from an abnormal and uncontrolled elevation of intracellular calcium levels in skeletal muscle. During an MH episode, the mutated RYR1 calcium channel is remained in an open position , leading to an uncontrolled release of calcium with elevation of intracytoplasmic calcium levels and continous muscle activation as well as ATP breakdown. ATP breakdown during this process aggravates heat production further.

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78. 78 Acute management for MH is as follows:- Discontinue all anesthetic agents and hyperventilate with 100% O2 with a fresh flow to at least 10 L/min. With increased aerobic metabolism, normal ventilation must increase. However, CO2 production is also increased because of neutralization of fixed acid by bicarbonate; hyperventilation removes this additional CO2. Reconstitute dantrolene in sterile water (not saline), and administer rapidly (2.5 mg/kg intravenously [IV] to a total dose of 10 mg/kg IV) every 5 to 10 minutes until the initial symptoms subside. Administer bicarbonate (1 to 4 mEq /kg IV) to correct the metabolic acidosis with frequent monitoring of blood gases and pH.

79. 79 4.Control fever by administering iced fluids, cooling the body surface, cooling body cavities with sterile iced fluids, and, if necessary, using a heat exchanger with a pump oxygenator. Cooling should be halted when the temperature approaches 38° C to prevent inadvertent hypothermia. 5.Monitor urinary output, and establish diuresis if urine output is inadequate. Administer bicarbonate to alkalinize urine to protect the kidney from myoglobinuria - induced renal failure. 6.Blood gases, electrolytes, CK, temperature, arrhythmia, muscle tone, and urinary output guide further therapy. Hyperkalemia should be treated with bicarbonate, glucose, and insulin. Effective doses of dantrolene to reverse MH are the most effective way to lower serum potassium levels. In severe cases, calcium chloride or calcium gluconate may be used. 7.Analyze coagulation studies (e.g., international normalized ratio [INR], platelet count, prothrombin time, fibrinogen , fibrin split degradation products).

80. 80 The clinical course will determine further therapy , dantrolene should probably be repeated at least every 10 to 15 hours, since its half-life is at least 10 hours .The total dose of dantrolene that can be used is up to 30 mg/kg . Follow the initial dosing regimen with a dose of 1 mg/kg IV or 2 mg/kg orally four times daily for 3 days. Treatment is extended to 3 days to prevent recurrences . The most common side effect of dantrolene is muscle weakness, particularly grip strength, which usually resolves in 2–4 days after the drug is discontinued

81. 81 Dantrolene is packaged in 20-mg in 70ml vial with sodium hydroxide for a pH of 9.5 (otherwise, it will not dissolve) and 3 g of mannitol, which converts the hypotonic solution to isotonic .. Dantrolene must be reconstituted in sterile water rather than salt solutions or it will precipitate. Warming the sterile water to 40°C immediately prior to mixing can speed up the process and also help drawing the drug in a syringe because the solution is fairly viscous. In 2009, a newer, rapid soluble dantrolene ( Ryanodex ) is a nanocrystalline dantrone sodium suspension(DSS) that allow for a much larger dose of 250mg to be dispensed in a vial that requires only 5ml of sterile water to dissolve it in solution. It reconstitutes in approximately 20 seconds, which is significantly faster than the older version

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83. 83 TEMPERATURE MONITORING INDICATIONS FOR TEMPERATURE MONITORING :- The monitoring guidelines of the American Society of Anesthesiologists state that “Every patient receiving anesthesia shall have temperature monitored when clinically significant changes in body temperature are intended, anticipated or suspected.” Temperature monitoring should be performed whenever large volumes of cold blood and/or intravenous fluids are administered, when the patient is deliberately cooled and/or warmed, for pediatric surgery of substantial duration, and in hypothermic or pyrexial patients or those with a suspected or known temperature regulatory problem such as malignant hyperthermia . Major surgical procedures, especially those involving body cavities, should be considered a strong indication for temperature monitoring.

84. 84 MEASURING DEVICES:- A.Thermistor :- A thermistor is composed of a metal (i.e., manganese, nickel, cobalt, iron, or zinc) oxide sintered into a wire or fused into a rod or bead Measure temperature change by changing electrical resistance. Resistance of the metal oxide increases as the temperature decreases and vice versa so the resistance can be converted to a temperature Advantages of thermistors include small size, rapid response time, continuous readings , and sensitivity to small changes in temperature. They are inexpensive . Probes can be interchangeable and disposable.

85. 85 B.Thermocouple :- A thermocouple consists of an electrical circuit that has two dissimilar metals welded together at their ends . One of the two metal junctions remains at a constant temperature. The other is exposed to the area being measured , producing a voltage difference that is measured and converted to a temperature reading. Advantages of thermocouples include accuracy, small size, rapid response time, continuous readings, stability, and probe interchangeability. The materials are inexpensive, so the probes can be made disposable.

86. C.Liquid crystal probes :- They change colour as a function of temperature, used for measuring skin temperature. use the thermal optic transmission qualities of crystals . Advantages: Commercial kits are available. Ease of application Continuous information output Simplicity in screening for MH Disadvantages: need for subjective observer interpretation and the inability to interface with a recording system. They are less accurate than other devices. Extreme ambient temperature, humidity, and air movement can cause inaccuracy.

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88. D.Infrared sensors:- Detect electromagnetic heat radiation from the body. Used to measure tympanic membrane temperature. Advantage: Response time is <5 seconds Very good index of core temperature Disposable thin plastic film cover reduces risk of infection Disadvantage: Probe must be accurately placed aimed at the tympanic membrane. Only intermittent spot checks can be made Bleeding can occur from around tympanic membrane Trauma to the tympanic membrane

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90. SITES FOR MONITORING CENTRAL/ CORE Oesophageal Pulmonary artery Tympanic membrane Nasopharynx

91. SITES FOR MONITORING PERIPHERAL: Oral Axilla Skin OTHERS: Rectum Bladder

92. CORE TEMPERATURE MONITORING Oesophageal : probe is placed 20cm below from pharyngo-esophageal junction, which shows accurate core-temperature because of closer proximity with heart and descending aorta. Pulmonary artery : temperature probes can be incorporated into the pulmonary artery (Swan- Ganz ) catheters. Electrical safety standards have to be met with respect to leakage currents.

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94. CORE TEMPERATURE MONITORING Tympanic Membrane : it approximates brain temperature better than any other tissue. The blood supply to tympanic membrane is by internal carotid artery which also supplies hypothalamus. Nasopharynx : The temperature is in close approximation with brain temperature. the danger of causing epistaxis is a consideration especially in patients who are on anticoagulants.

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96. CORE TEMPERATURE MONITORING Jugular Bulb : done by inserting 5 French Swan- Ganz catheter into jugular bulb. Gold standard in cardiac bypass surgery. Spinal subarachnoid space : in neurosurgical and cardiovascular procedures. Intrathecal temperature with a thermocouple incorporated catheter in subarachnoid space.

97. PERIPHERAL MONITORING Oral : The location of temperature probe is sublingual on either side of frenulum , affected by cold and hot food, mouth breathing, crying. Axilla : 1˚C lower than core temperature . Skin : it is not a reliable index of core temperature because the degree of vasoconstriction or vasodilatation can significantly affect the measurements obtained.

98. Bladder : It is reliable index of core temperature, during steady state. But drawback is that it is dependant on the urine output . Rectum : It is an adequate indicator of core temperature, during steady state. But drawback is that it seldom reflects the actual core temperature in anaesthetised patient when temperature changes are relatively rapid.

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100. 100 GUIDELINES Thermal management guidelines as proposed by “Outcome Research Consortium” Core body temperature should be measured or reliably estimated in most patients given general anesthesia for more than 30 minutes . 2) Temperature should also be measured or reliably estimated during regional anesthesia when changes in body temperature are intended, anticipated, or suspected . 3) Unless hypothermia is specifically indicated (e.g., for protection against ischemia), efforts should be made to maintain intra-operative core temperature >36°C.

101. 101 According to ASA Standards, “every patient receiving anesthesia shall have temperature monitored when clinically significant changes in body temperature are intended, anticipated or suspected”. For office-based sedation, regional anesthesia, or general anesthesia, the ASA also requires that "the body temperature of pediatric patient shall be measured continuously .

102. 102 Temperature monitoring should always be directed toward the core temperature. — Preventive measures should be instituted against inadvertent hypothermia . In adult patients who are at risk for malignant hyperthermia or who are under general anesthesia for a period exceeding 30 minutes, temperature should be monitored . Ambient temperature should be kept between 21 degrees C and 24 degrees C for adults; and between 21 degrees C and 26 degrees C for children, with a relative humidity level of 40-60 percent . Warming of infusion fluids to 38 degrees C is always recommended in children. In adults, the use of this preventive measure should be assessed on a case-by-case basis . Italian society of Anesthesiologists recommends:-

103. 103 Active external warming systems are always recommended. — The forced-air warming system is always recommended for use in children by reason of its proven effectiveness, even under conditions of reduced usable surface . In adults, the use of a forced-air warming system should be considered when the intervention will last longer than 30 minutes or when the core body temperature falls below 36 degrees C . The patient should never be discharged from the recovery room until normothermia is restored, or if signs of hypothermia are present.

104. 104 In 2007, American college of cardiology and American heart association published a guidelines for care of patients undergoing non-cardiac surgery. They recommended that “Maintenance of body temperature in a normothermic range is recommended for most procedures other than during periods in which mild hypothermia is intended to provide organ protection ( e.g , during high aortic cross-clamping )”

105. 105 SUMMARY General anesthetics decrease the thresholds (triggering core temperatures) for vasoconstriction and shivering by 2° C to 3° C . Anesthetic-induced impairment of thermoregulatory control, combined with a cool operating room environment, makes most patients hypothermic. The major initial cause of hypothermia in most patients is core-to-peripheral redistribution of body heat. Neuraxial anesthesia impairs both central and peripheral thermoregulatory control and is associated with substantial hypothermia . Body temperature should be monitored in patients having surgery lasting more than 30 minutes, and core temperature should be maintained at 36° C or higher whenever possible. Forced-air warming currently offers the best combination of high efficacy, low cost and remarkable safety Malignant hyperthermia (MH) is an anesthetic-related disorder of increased skeletal muscle metabolism. It is an inherited condition in an autosomal dominant pattern. Dantrolene significantly attenuates myoplasmic calcium (Ca2+) concentrations and thereby allows restoration of normal metabolism, with a reversal of the signs of metabolic stimulation

106. 106 REFERENCES:- Miller’s Anesthesia 8 th edition & 6 th edition Guyton and Hall textbook of Medical Physiology 12 th edition Wylie and Churchill-Davidson's A Practice of Anesthesia 7 th edition Yao & Artusio’s Anesthesiology, 8 th edition Morgan and Mikhail's Clinical Anesthesiology, 5 th edition Stoelting pharmacology and physiology, south asia edition, 5 th edition Understanding Anesthesia Equipment( Dorsch and Dorsch ), 5 th edition Harrison’s principle of internal medicine, 19 th edition David A Kirkbride , Donal J Buggy; Thermoregulation and mild peri ‐operative hypothermia,  BJA CEPD Reviews , Volume 3, Issue 1, 1 February 2003, Pages 24–28 Luthra A, Dube SK, Kumar S, Goyal K. Intraoperative hyperthermia: Can surgery itself be a cause?. Indian J Anaesth 2016;60:515-7 Bhattacharya PK, Bhattacharya L, Jain RK, Agrarwal RC. Post anaesthesia shivering (PAS): A review. Indian J Anaesth . 2003;47(2): 88–93 http:// www.or.org/temp_monitoring.htm ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

107. 107 THANK YOU