Transcript Hypothermia
Hypothermia Amy Gutman MD [email protected] Overview • Definitions • Historical Review & Epidemiology • Etiology & Pathophysiology • Evaluation & Management Historically WWI cold deaths >500,000 (civilian + military) 218BC Hannibal loses 50% troops crossing Alps 350/12,000 Napolean army survive Russian retreat. Those rapidly rewarmed died > slowly re-warmed 218 BC 1812 1778 Hippocrates suggests rolling patient in cow dung WWII 1st human trials for active re-warming 1915 1845-55 1940s 1950s 1980s-Current Crimean war hypothermia deaths > 50,000 10% Korean War deaths secondary to cold Valley Forge winter decimates Washington’s troops 1980s treatments include AV , VV, cardiac bypass Epidemiology ~ High Risk Groups •Urban: ETOH, drugs, psych, homeless •Rural: Outdoorsmen, sportsmen, work-related •Geography: Occurrence higher in Northern climates (duh) Mortality higher in Southern climates •Gender: Men>Women •Age: Very young, very old Definitions •Hypothermia Core temperature <35C (95F) •Timeframe Acute <6 hours; Chronic >6 hours •Classification Mild 32-35C/ 89.6-95F Moderate 28-32C/ 82.4-89.6F Severe <28C/ <82.4F •Categories Accidental, Intentional Mild Hypothermia Core Temp Characteristics 37.6 99.6 Normal rectal temp 37 98.6 Normal oral temp 35 95 Maximum shivering thermogenesis 34 93.2 Clumsiness, requires respiratory stimulation 33 91.4 Ataxia, apathy Moderate Core Temp Characteristics 30 89.6 Stupor 25% decreased metabolism 31 87.8 Shivering stops 30 86 Atrial arrhythmias 33% decreased metabolism 28 82.4 VF with any stimuli 50% decreased metabolism Severe Core Temp Characteristics 27 80.6 Reflexes & pain response lost 25 77 Pulmonary edema 23 71.6 Maximal VF risk 22 68 Cannot defibrillate 19 66.2 EEG & cardiac activity lost (asystole) 16 60.8 Lowest adult survival 15 59.2 Lowest infant survival 9 48.2 Lowest therapeutic hypothermia survival Hypothermia Pathophysiology Temperature & Wind Chill Just as heat + humidity increase heat’s impact, cold + wind combine to increase cold effects Combined effect of cold + wind = Wind Chill Factor USFA recommends initiating rehab operations when wind chill <10ºF (-12º C) Homeostasis ~ Temperature Regulation Basal heat production – Increased w/ muscle activity – Limited glycogen & muscle fatigue limit heat production Shivering thermogenesis – BMR & O2 consumption increased 2-3X Hypothalamus – Similar to “Flight or Fight” response Basal Heat Decreased Heat Production Endocrine Disorders Metabolic Disorders CNS Depression Malnutrition Immobility Very Young Elderly Increased Heat Loss Environmental exposure Exfoliative skin diseases Vasodilatation ETOH Hypoglycemia Drugs (ETOH, benzos) Sepsis CNS Disorders Hypothermia & Drug Effects Impaired Vasoconstriction Impaired Vasodilation CCBs Phosphodiesterase Inhibitors (i.e. Viagra) Benzodiazepines Barbituates TCAs Organophosphates Heroin Lithium Clonidine Acetaminophen Atropine Anesthesia Heat Loss • Loss Rate: • Diff b/w body & environment temps • More “insulation” = slower cooling • • Evaporation: • Skin, respiration, wet clothing • Conduction: • Direct contact with colder objects • Convection : • Air motion across body surfaces • Radiation (65%): • All exposed surfaces Hypothermia Evaluation History •Who How many, Gender, Ages PMH/ Social History? •What Hypothermia vs frostbite? Acute, Chronic, Accidental, Iatrogenic •Where Snow / Immersion / Ground •Why/How Cardiac arrest on lake + immersion + hypothermia? Drinking and fell asleep outside? •When Time of exposure Time from exposure to discovery Time from discovery to ED Exam Basics Variable presentation with range of symptoms from mild, nonspecific complaints to unresponsiveness If unresponsive, may appear pulseless, with fixed / dilated pupils Pulse often bradycardic, with unpalpable radial pulse Extremities rigid (resembling rigor mortis), cyanotic or edematous Specific Exam Findings The patient is not dead until they are WARM & DEAD! •Vitals Check pulse for 3 mins if “pulseless” •HEENT Tongue swells •Pulm CHF & pneumonia •GI/ GU No BS, + incontinence •MS/ Skin Fractures, frostbite, mucus membrane injury •Heme Coagulopathy, hemorrhage •Neuro AMS •CV Often unpalpable pulse Osborn waves Osborne Waves Osborn Waves DDX ~ When Cold is a Symptom, Not the Cause Sepsis Endocrine Toxic Metabolic Traumatic CNS (CVA) Cardiac Arrest Coma Narcotic Abuse Severe Shock Treatment Basics Gentle handling to avoid inducing VF Remove wet clothing Keep covered, but DO NOT massage cold extremities (increases skin dilation & decreases shivering) Keep ambulance warm Warm blankets, but NO heat packs to neck, pits, groin Warm & humidify oxygen Establish IV / IO, check glucose, give narcan Confirm pulselessness for 3+ minutes prior to CPR Treatment ~ Rewarming Strategies Passive Rewarming – >30C/ 86F – Remove wet clothing – Dry / warm environment produces “endogenous thermogenesis” Active Rewarming (<30C/86F) •Airway: 40-45C humidification •IVF: 40-42C •Blankets, Bair Hugger •Cool Stuff At The Hospital •Pleural & Peritoneal Irrigation •Hemodialysis •Continuous AV-VV Blood Exchange •Cardiac Bypass Non-Invasive Core Rewarming Products: – Benechill – Res-Q-Air Ht 1000 Provides both heated 108°F (42°C) and humidified oxygen or air should be administered Inhalation rewarming is simple, non-invasive treatment suitable for prehospital & hospital active core rewarming Rewarming Afterdrop •Acidosis + hypotension + increased metabolic rate lead to sudden cardiac death •Peripheral vasodilation exchanges cold for warm core blood causing uneven surface / core rewarming & increasing mortality •Avoid by using multiple rewarming techniques with close monitoring 2.4 Hypothermia & Cold Emergencies ~ Assessment & Treatment Priorities Scene safety, BSI Gentle handling to avoid arrhythmias; no pt exertion, limit oral intake Open airway, O2 as indicated, consider C-spine injuries Check hemodynamic status with serial assessment of LOC, ABCs, Vitals, ECG / monitor strip SAMPLE history Remove wet clothing; limit heat loss using blankets / mylar wrap *Place heat source at neck, armpits, flanks, groin Do not massage extremities Rapid transport w/ wo ALS *Per Dr G…NO, NO, NO!!! Can cause afterdrop & lethal arrythmias 2.4 Basic Procedures Determine hemodynamic status; assess pulse & RR for a period of 60 secs* If cardiopulmonary arrest initiate CPR using AED Use warm / humidified O2 Contact Medical Control & notify receiving If possible & necessary, activate ALS. Do not delay rapid transport If SBP <100 treat for shock *3 mins is national standard 2.4 ALS Procedures Manage airway using warm / humidified O2 IV NS KVO; If SBP <100 give 250cc IVF, titrate to hemodynamic status Apply monitor, obtain ECG Manage specific medical emergencies per appropriate protocol (i.e. hypoglycemia, CVA, arrhythmias) Administer Naloxone if suspected narcotic OD Contact Medical Control & receiving hospital Rapid Transport 2.4 Frostbite Hypothermia protocol Avoid trauma to injured areas Apply dry dressings, splint prn, avoid pressure / constriction Do not allow patient to use injured part(s) Do not rapid prehospital rewarming of affected area Keep frozen part from direct contact with heat source Pulseless, Apneic Pt Management Compressions 20% effective w/ moderate hypothermia Heart only needs 2-3 bpm at extreme hypothermia Apply cardiac monitor: – VF or VT, defibrillate at 200J – Bretylium 5-10 mg/kg – No lidocaine or procainamide (pro-arrythymia) Begin CPR / ACLS protocols – Less emphasis on advanced airway if effective BVM ventilation with heated O2 Rapid transport, if possible to a hospital with cardiac bypass capabilities Leave The Cold & Dead Alone! Research shows worse outcomes in hypothermic patients with “premature” CPR Hypothermia induction is considered standard of care for patients post cardiac arrest It is difficult to stand back & do “nothing”, but in many cases, this is the best treatment When Hypothermia Is Beneficial Hypothermia & Trauma •If trauma ISS >25 + core temp <77 deg = 100% mortality •Heat production decreases causing coagulopathy •However hypothermia protective if induced pre-shock, as decreased metabolism causes “hibernation state” •This is especially true for head injured patients •So if pt “not quite dead” they may have increased survival Hypothermia after Cardiac Arrest Study Group: Mild Therapeutic Hypothermia Improves Neurologic Outcome after Cardiac Arrest Cardiac arrest with cerebral ischemia generally leads to severe neurologic deficits. Group studied if mild hypothermia increases rate of neurologic recovery after VF resuscitation 75/136 pts in hypothermia group had good neurologic outcomes compared with 54/137 in normothermic group. Mortality at 6 mo 41% in hypothermic compared with 55% in normothermic group Conclusions: In pts successfully resuscitated after VF cardiac arrest, therapeutic hypothermia increased rate of a positive neurologic outcome & reduced mortality Unconscious adult pts with spontaneous circulation after OOHCA should be cooled to 32- 34°C for 1224 hrs if VF initial rhythm Cooling may be beneficial for other rhythms or inhospital cardiac arrest (not proven yet) Common Hypothermia “Failures” •Not considering hypothermia if AMS •Not considering causes of secondary hypothermia •Not recognizing treating arrhythmias often ineffective •Not realizing rough handling precipitates arrhythmias •Not continuing resuscitation until core temp >32C •Not volume resuscitating •Not monitoring for afterdrop Summary Early recognition & treatment Broaden differential diagnosis Gentle handling of patients Prolonged (or no) CPR may be necessary Do not assume AMS due to hypothermia Patient not dead until WARM & DEAD! Questions? [email protected] / www.TEAEMS.com www.usmra.com AHA Cardiopulmonary Resuscitation 2010 Update (Cardiology Journal) Medscape.com ~ “Hypothermia” Pubmed.com ~ “Hypothermia”