Downloaded 108 times
![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](https://image.slidesharecdn.com/temperatureregulationdisorders-160507100055/85/Temperature-regulation-disorders-20-320.jpg)
Uploaded byAneesh Bhandary
Temperature regulation disorders
The document discusses temperature regulation disorders, including fever, hyperthermia, and hypothermia. It explains the physiological mechanisms behind these conditions, their causes, clinical presentations, and treatment strategies. Additionally, it covers complications like drug-induced hyperthermia and frostbite, highlighting preventive measures and approaches for managing severe cases.
More Related Content
Similar to Temperature regulation disorders
Temperature regulation disorders
- 1.
- 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 meanoral 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 isan 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.
- 6. HYPERTHERMIA Most patientswith 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.
- 8. HYPERTHERMIA – HeatStroke 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 – HeatStroke 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 vsHeat Exhaustion Exhaustion
- 11. HYPERTHERMIA – Druginduced 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 – Theneuroleptic 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 – Theneuroleptic 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 – Theneuroleptic 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 – Theserotonin 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 – Othercauses
- 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 Ahigh 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 InNMS - 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.
- 22. TREATING HYPERTHERMIA Malignanthyperthermia 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.
- 24. HYPOTHERMIA Hypothermia occurswhen 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
- 25.
- 26. HYPOTHERMIA Heat lossoccurs 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.
- 28.
- 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.
- 31.
- 32.
- 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 REWARMINGSTRATEGIES 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 REWARMINGSTRATEGIES 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 REWARMINGSTRATEGIES 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 Theimportance of layered clothing and headgear, adequate shelter, increased caloric intake, and the avoidance of ethanol should be emphasized…
- 40.
- 41. Introduction Peripheral coldinjuries 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 Dermalischemia Increased tissue pressures Edema Superficial necrosisIschemiaThrombosis
- 43. Clinical presentation Initialpresentation 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) Immersionfoot (wet) No tissue loss Anaesthesia Erythema Hemorrhagic vesicles Sub cuticular, muscular or osseous tissue damage