Download - Temperature regulation disorders
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TEMPERATURE REGULATION DISORDERS
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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
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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
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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
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HYPERTHERMIA
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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
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HYPERTHERMIA
Causes of Hyperthermia
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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 ExertionalNon-exertional
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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 ExertionalNon-exertional
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Heat Stroke vs Heat Exhaustion
Exhaustion
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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.
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HYPERTHERMIA – The neurolepticmalignant syndrome
Occurs in the setting of the use of neuroleptic agents (0.02% to 3% among patients taking them) antipsychotic phenothiazines, haloperidol, prochlorperazine,
metoclopramideOR
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
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HYPERTHERMIA – The neurolepticmalignant syndrome
The four defining features that characterize NMS are: 1. Motor symptoms 2. Altered mental status 3. Hyperthermia4. 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
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HYPERTHERMIA – The neurolepticmalignant syndrome
Differential Diagnosis1. Central nervous system infection (meningitis/encephalitis) 2. Heat stroke 3. Delirium tremens4. Parkinsonism5. Seizures 6. Acute porphyria 7. Septic shock 8. Tetanus 9. Strychnine toxicity 10.Pheochromocytoma
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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
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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
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HYPERTHERMIA – Other causes
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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.
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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
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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
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TREATING HYPERTHERMIA
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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.
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HYPOTHERMIA
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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 disordermortality rate is much higher
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HYPOTHERMIA
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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. Respiration5. 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
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HYPOTHERMIA
Risk factors
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HYPOTHERMIA
Risk factors
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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)
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HYPOTHERMIA
Mild Hypothermia
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HYPOTHERMIA
Moderate Hypothermia
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HYPOTHERMIA
Severe Hypothermia
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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
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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)
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HYPOTHERMIA - Treatment
REWARMING STRATEGIESA. 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.
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HYPOTHERMIA - Treatment
REWARMING STRATEGIESB. 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
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HYPOTHERMIA - Treatment
REWARMING STRATEGIESActive 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.
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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)
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HYPOTHERMIA - Prevention
The importance of layered clothing and headgear, adequate shelter, increased
caloric intake, and the avoidance of ethanol should be emphasized…
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FROSTBITE
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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.
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Pathophysiological changes
Damaged vascular
endothelium
Microvascular thrombosis
Stasis
Dermal ischemia
Increased tissue pressures Edema
Superficial necrosisIschemia Thrombosis
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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
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Classification
Frostbite
Superficial (Non freezing peripheral)
Deep
Chilblain (dry)
Immersion foot (wet)
No tissue loss
Anaesthesia
Erythema Hemorrhagic
vesiclesSub cuticular, muscular
or osseous tissue damage