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”