temperature regulation disorders

TEMPERATURE REGULATION DISORDERS

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

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

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

HYPERTHERMIA

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

HYPERTHERMIA

Causes of Hyperthermia

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

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

Heat Stroke vs Heat Exhaustion

Exhaustion

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.

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

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

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

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

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

HYPERTHERMIA – Other causes

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.

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

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

TREATING HYPERTHERMIA

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.

HYPOTHERMIA

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

HYPOTHERMIA

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

HYPOTHERMIA

Risk factors

HYPOTHERMIA

Risk factors

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)

HYPOTHERMIA

Mild Hypothermia

HYPOTHERMIA

Moderate Hypothermia

HYPOTHERMIA

Severe Hypothermia

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

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)

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.

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

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.

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)

HYPOTHERMIA - Prevention

The importance of layered clothing and headgear, adequate shelter, increased

caloric intake, and the avoidance of ethanol should be emphasized…

FROSTBITE

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.

Pathophysiological changes

Damaged vascular

endothelium

Microvascular thrombosis

Stasis

Dermal ischemia

Increased tissue pressures Edema

Superficial necrosisIschemia Thrombosis

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

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