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
 The 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:
1. Motor symptoms
2. Altered mental status
3. Hyperthermia
4. 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
1. Central nervous system infection (meningitis/encephalitis)
2. Heat stroke
3. Delirium tremens
4. Parkinsonism
5. Seizures
6. Acute porphyria
7. Septic shock
8. Tetanus
9. Strychnine toxicity
10. 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 Ca2+ 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:
1. Radiation (55–65% of heat loss)
2. Conduction (10–15% of heat loss but much greater in cold water)
3. convection (increased in the wind)
4. Respiration
5. 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.
1. Rectal probes should be placed to a depth of 15 cm and not
adjacent to cold feces.
2. 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
A. 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
B. 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
Active 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:
1. intravascular thrombosis (fibrinogen <50)
2. cell lysis (K>10)
3. 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
 Freezes 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 necrosisIschemiaThrombosis

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