Temperature regulation disorders

The Effects of Temperature and its dysregulation on health and in disease. Includes Heat stroke, Malignant Hyperthermia, Neuroleptic malignant syndrome as well as Hypothermia and Frost bite

1. TEMPERATURE REGULATION DISORDERS

2. Introduction Body temperature -controlled by the hypothalamus. Neurons in the preoptic anterior hypothalamus and the posterior hypothalamus Receive two kinds of signals: from peripheral nerves and the other from the temperature of the blood bathing the region . Maintain the core temperature between 36.5 & 37.5°C, despite environmental variations

3. Introduction T he mean oral temperature is 36.8° ± 0.4°C (98.2° ± 0.7°F ) with low levels at 6 a.m. and higher levels at 4–6 p.m. The maximum normal oral temperature is 37.2°C (98.9°F) at 6 a.m. and 37.7°C (99.9°F ) at 4 p.m.; define the 99th percentile for healthy individuals . In light of these studies, an am temperature of > 37.2°C ( > 98.9°F) or a pm temperature of > 37.7°C ( > 99.9°F) defines a fever . Variations in oral, rectal and tympanic membrane temperature are observed

4. FEVER Fever is an elevation of body temperature that exceeds the normal daily variation and occurs in conjunction with an increase in the hypothalamic set point A fever of >41.5°C (>106.7°F) is called hyperpyrexia . Hyperpyrexia can develop in patients with severe infections but most commonly occurs in patients with CNS hemorrhages. Infectious causes rarely cause temperatures to go above 41.1 °C

5. HYPERTHERMIA

6. HYPERTHERMIA Most patients with elevated body temperature have fever, there are circumstances in which elevated temperature represents not fever but hyperthermia Hyperthermia is characterized by an uncontrolled increase in body temperature that exceeds the body’s ability to lose heat. does not involve pyrogenic molecules 2 mechanisms – Exogenous heat exposure & Endogenous heat production

7. HYPERTHERMIA Causes of Hyperthermia

8. HYPERTHERMIA – Heat Stroke Exertional heat stroke – typically exercising at elevated ambient temperatures and/or humidity. In a dry environment and at maximal efficiency , sweating can dissipate ~600 kcal/h, requiring the production of >1 L of sweat. Dehydration or common medications may precipitate exertional heat stroke. Heat stroke Exertional Non-exertional

9. HYPERTHERMIA – Heat Stroke Non-exertional heat stroke - typically occurs in either very young or elderly individuals, particularly during heat waves. The elderly, the bedridden, pts on anticholinergic/ antiparkinsonian /diuretics individuals confined to poorly ventilated and non-air-conditioned environments are most susceptible. Heat stroke Exertional Non-exertional

10. Heat Stroke vs Heat Exhaustion Exhaustion

11. HYPERTHERMIA – Drug induced Drug-induced hyperthermia may be caused by Monoamine oxidase inhibitors ( MAOIs) Tricyclic antidepressants Amphetamines Illicit use of phencyclidine (PCP), lysergic acid diethylamide (LSD), methylene- dioxy -methamphetamine (MDMA , “ecstasy”), crystal methamphetamine and cocaine .

12. HYPERTHERMIA – The neuroleptic malignant syndrome Occurs in the setting of the use of neuroleptic agents (0.02 % to 3% among patients taking them) antipsychotic phenothiazines , haloperidol, prochlorperazine , metoclopramide OR The withdrawal of dopaminergic drugs (characterized by “lead-pipe” rigidity , extrapyramidal side effects , autonomic dysregulation, and hyperthermia) Caused by the inhibition of central dopamine receptor in the hypothalamus Resulting in increased heat generation and decreased heat dissipation

13. HYPERTHERMIA – The neuroleptic malignant syndrome The four defining features that characterize NMS are: Motor symptoms Altered mental status Hyperthermia Autonomic instability Lab findings: Creatine Kinase is typically more than 1,000 IU/L and can be as high as 100,000 IU/L Elevated LDH Leukocytosis

14. HYPERTHERMIA – The neuroleptic malignant syndrome Differential Diagnosis Central nervous system infection (meningitis/encephalitis) Heat stroke Delirium tremens Parkinsonism Seizures Acute porphyria Septic shock Tetanus Strychnine toxicity Pheochromocytoma

15. HYPERTHERMIA – The serotonin syndrome Seen with selective serotonin uptake inhibitors (SSRIs), MAOIs, and other serotonergic medications. Has many features that overlap with those of the neuroleptic malignant syndrome (including hyperthermia ) diarrhea, tremor, and myoclonus – distinguish it from NMS

16. HYPERTHERMIA – Malignant Hyperthermia A life threatening reaction that is most often triggered by the use of anesthetics (mostly inhalational) Desflurane • Enflurane • Halothane • Isoflurane • Methoxyflurane • Sevoflurane Succinyl choline – non inhalational Nitrous Oxide – no malignant hyperthemia increased cytosol Ca 2+ concentrations  Increased muscle contracture, hypermetabolism & ATP hydrolysis by myosin  causes hyperthermia hyperthermia is usually not the initial presenting sign

17. HYPERTHERMIA – Other causes

18. HYPERTHERMIA – Evaluation It is important to distinguish between fever and hyperthermia Hyperthermia can be rapidly fatal and does not respond to antipyretics Hyperthermia is diagnosed on the basis of the events immediately preceding the elevation of core temperature However, a full workup for fever is mandated in cases where history is suggestive of an infection.

19. TREATING HYPERTHERMIA A high core temperature in a patient with an appropriate history along with appropriate clinical findings suggests hyperthermia . Physical cooling with sponging , fans , cooling blankets , and even ice baths should be initiated immediately in conjunction with the administration of IV fluids If sufficient cooling is not achieved by external means, internal cooling can be achieved by gastric or peritoneal lavage with iced saline . Hemodialysis or even cardiopulmonary bypass with cooling of blood may be performed – in extreme cases

20. TREATING HYPERTHERMIA In NMS - Supportive medical care, specific pharmacotherapy and electroconvulsive therapy Intensive monitoring and supportive treatment need admission to the intensive care unit Discontinue neuroleptic agent or precipitating drug Maintain cardiorespiratory stability. Mechanical ventilation, antiarrhythmic agents Maintain euvolemic state using intravenous (IV) fluids If CK is very elevated, high volume IV fluids and urine alkalinization with IV sodium bicarbonate [Na(HCO3)] may help to prevent renal failure from rhabdomyolysis. Lower the temperature using cooling blankets, ice cold water, gastric lavage and ice packets in axilla and cold sponging. Lower BP, if markedly elevated (Clonidine) LMWH for DVT prevention Use benzodiazepines (clonazepam or lorazepam) to control agitation if necessary

21. TREATING HYPERTHERMIA

22. TREATING HYPERTHERMIA Malignant hyperthermia should be treated immediately with cessation of anesthesia and IV administration of dantrolene sodium . The recommended dose of dantrolene is 1–2.5 mg/kg iv q6 h for at least 24–48 h—until oral dantrolene can be administered May even be useful in the hyperthermia of the serotonin syndrome and thyrotoxicosis Induction of muscle paralysis with curare and pancuronium may be attempted as well.

23. HYPOTHERMIA

24. HYPOTHERMIA Hypothermia occurs when there is an unintentional drop in the body’s core temperature below 35°C (95°F ) Many of the compensatory physiologic mechanisms that conserve heat begin to fail . Primary accidental hypothermia is a result of the direct exposure of a previously healthy individual to the cold. Secondary hypothermia is a complication of a serious systemic disorder  mortality rate is much higher

25. HYPOTHERMIA

26. HYPOTHERMIA Heat loss occurs through five mechanisms: Radiation (55–65% of heat loss) Conduction (10–15% of heat loss but much greater in cold water) convection (increased in the wind) Respiration Evaporation (which are affected by the ambient temperature and the relative humidity ) The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system Prolonged exposure to cold also stimulates the thyroid axis, leading to an increased metabolic rate

27. HYPOTHERMIA Risk factors

28. HYPOTHERMIA Risk factors

29. HYPOTHERMIA Mild  35°C (95°F )– 32.2°C (90°F ) Moderate  <32.2°C (90°F )– 28°C (82.4°F ) Severe  < 28°C (82.4°F)

30. HYPOTHERMIA Mild Hypothermia

31. HYPOTHERMIA Moderate Hypothermia

32. HYPOTHERMIA Severe Hypothermia

33. HYPOTHERMIA - Treatment Hypothermia is confirmed by measuring the core temperature Preferably at two sites. Rectal probes should be placed to a depth of 15 cm and not adjacent to cold feces. A simultaneous esophageal probe should be placed 24 cm below the larynx

34. HYPOTHERMIA - Treatment After a diagnosis of hypothermia is established, cardiac monitoring should be instituted + attempts to limit further heat loss . If the patient is in ventricular fibrillation, one defibrillation is attempted  if failed, rewarm to >30 °C and shock again Supplemental oxygenation is always warranted Ryle’s tube and Foley’s catheter Dehydration is common and most patients benefit from a bolus of Normal (RL not preferred due to liver’s inability to metabolize lactate)

35. HYPOTHERMIA - Treatment REWARMING STRATEGIES Passive external rewarming simply involves covering and insulating the patient in a warm environment. With the head also covered , the rate of rewarming is usually 0.5° to 2°C /h. Ideal for previously healthy patients who develop acute, mild primary accidental hypothermia . The patient must have sufficient glycogen to support endogenous thermogenesis. Application of heat directly to the extremities of patients should be avoided as it can induce peripheral vasodilation and precipitate core temperature “ afterdrop ,” a response characterized by a continual decline in the core temperature after removal of the patient from the cold. Truncal heat application reduces the risk of afterdrop .

36. HYPOTHERMIA - Treatment REWARMING STRATEGIES Active rewarming is necessary in severe hypothermia 2 types Active external rewarming Active core rewarming Active external rewarming is best accomplished with forced-air heating blankets. Other options include devices that circulate water through external heat exchange pads, radiant heat sources, and hot packs . Electric blankets are avoided  burns

37. HYPOTHERMIA - Treatment REWARMING STRATEGIES A ctive core rewarming Airway rewarming with heated humidified oxygen 40 °– 45°C via mask or endotracheal tube . it eliminates respiratory heat loss and adds 1°–2°C (34°–36°F) to the overall rewarming rate . Crystalloids should be heated to 40°– 42°C, but the quantity of heat provided is significant only during massive volume resuscitation . The most efficient method for heating and delivering fluid or blood is with a countercurrent in-line heat exchanger. Heated irrigation of the gastrointestinal tract or bladder transfers minimal heat because of the limited available surface area . Hemodialysis is especially useful for patients with electrolyte abnormalities, rhabdomyolysis, or toxin ingestions.

38. HYPOTHERMIA - Treatment Achieving a mean arterial pressure of at least 60 mmHg should be an early objective. If the hypotension does not respond to crystalloid/colloid infusion and rewarming, low-dose dopamine (2–5 μg /kg per min) support should be considered. Perfusion of the vasoconstricted cardiovascular system also may be improved with low-dose IV nitroglycerin . Bad Prognostic indicators are: intravascular thrombosis (fibrinogen <50) cell lysis (K>10) ammonia (>250)

39. HYPOTHERMIA - Prevention The importance of layered clothing and headgear, adequate shelter, increased caloric intake, and the avoidance of ethanol should be emphasized…

40. FROSTBITE

41. Introduction Peripheral cold injuries include both freezing and nonfreezing injuries to tissue F reezes quickly – metallic/volatile substances Occurs when the tissue temperature drops below 0°C ( 32°F) Ice crystal formation subsequently distorts and destroys the cellular architecture.

42. Pathophysiological changes Damaged vascular endothelium Microvascular thrombosis Stasis Dermal ischemia Increased tissue pressures Edema Superficial necrosis Ischemia Thrombosis

43. Clinical presentation Initial presentation of frostbite can be deceptively benign Sensory deficiency affecting light touch, pain, and temperature perception Clumsy or “chunk of wood” sensation in the extremity Deep frostbitten tissue can appear waxy, mottled, yellow, or violaceous-white

44. Classification Frostbite Superficial (Non freezing peripheral) Deep Chilblain (dry) Immersion foot (wet) No tissue loss Anaesthesia Erythema Hemorrhagic vesicles Sub cuticular , muscular or osseous tissue damage