hypothermia, frostbite and heat illness
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HYPOTHERMIA, FROSTBITE AND HEAT ILLNESS . Mark Bromley PGY3. Outline. Heat Stroke Hypothermia Frostbite. HEAT STROKE. Case. 68 M is brought into the ED for decreased LOC Found in bed in his apartment Freezer door was left open PMHx: CAD, CHF, DMII Meds: - PowerPoint PPT PresentationTRANSCRIPT
HYPOTHERMIA, FROSTBITE AND HEAT ILLNESS Mark Bromley PGY3
Outline Heat Stroke Hypothermia Frostbite
HEAT STROKE
Case 68 M is brought into the ED for decreased LOC Found in bed in his apartment Freezer door was left open
PMHx: CAD, CHF, DMII
Meds: Metoprolol, Altace, Lipitor, ASA, NTG Patch, Gluconorm
OE: 42oC HR: 65 GCS:3
What are this patients HS risk factors?What other diagnoses are you concerned about?How would you like to manage?
Perspective Disease of the young and the old
Outdoor laborers Athletes, children, and the elderly
Proportional to climate US
20 cases per 100,000 people 240 deaths annually #1 cause of death among US soldiers in the 1st gulf war
Heat wave in 2003 (France) caused 14,802 deaths
Life-threatening emergency needing immediate treatment
Heat Generation
Thermoregulation
Respiration
TerminologyHeat wave
Three or more consecutive days during which the air temperature is >32.2°CHeat stress
Perceived discomfort and physiological strain associated with exposure to a hot environment, especially during physical workHyperthermia
A rise in body temperature above the hypothalamic set point when heat-dissipating mechanisms are impaired (by drugs or disease) or overwhelmed by external (environmental or induced) or internal (metabolic) heatHeat exhaustion
Mild-to-moderate illness due to water or salt depletion that results from exposure to high environmental heat or strenuous physical exercise; signs and symptoms include intense thirst, weakness, discomfort, anxiety, dizziness, fainting, and headache; core temperature may be normal, below normal, or slightly elevated (>37°C but <40°C)Heat stroke
Severe illness characterized by a core temperature >40°C and central nervous system abnormalities such as delirium, convulsions, or coma resulting from exposure to environmental heat (classic heat stroke) or strenuous physical exercise (exertional heat stroke)Multiorgan-dysfunction syndrome
Continuum of changes that occur in more than one organ system after an insult such as trauma, sepsis, or heat stroke
Progression of Disease
Perceived discomfort and physiological strain
A rise in body temperature above the hypothalamic set point
Mild-to-moderate illness due to water or salt depletion
Severe illness characterized by a core temp >40°C and CNS abnormalities
Changes in more than one organ system
Symptomatic
SickHot InsideHot Outside
Clinical and Metabolic Manifestations Hyperthermia CNS Dysfunction
Tachycardia, Hyperventilation (CO2 < 20) Respiratory Alkalosis / Metabolic Acidosis Hypophosphatemia / Hypokalemia Rhabdomyolysis (↑PO4, ↑K, ↓Ca) MODS
encephalopathy, rhabdomyolysis, acute renal failure, acute respiratory distress syndrome, myocardial injury, hepatocellular injury, intestinal ischemia or infarction, pancreatic injury, and hemorrhagic complications, DIC, with pronounced thrombocytopenia
Exertional vs ClassicExertional Classic Healthy Predisposing factors/medications Younger Older Exercise Sedentary Sporadic Heat wave occurrence Diaphoresis Anhidrosis Hypoglycemia Normoglycemia DIC Mild coagulopathy Rhabdomyolysis Mild CPK elevation Acute renal failure Oliguria Marked Lactic acidosis Mild acidosis Hypocalcemia Normocalcemia
Case 68 M is brought into the ED for decreased LOC Found in bed in his apartment Freezer door was left open
PMHx: CAD, CHF, DMII
Meds: Metoprolol, Altace, Lipitor, ASA, NTG Patch, Gluconorm
OE: 42oC HR: 65
What are this patients HS risk factors?What other diagnoses are you worried about?How would you like to manage?
Case 37 F presents altered and hot Post-op Day 1
PMHx: Graves
OE: 135 39oC 143/62 (widened pulse pressure) Moist skin Loose stools
Case 45-year-old man who had been outside mowing grass. EMS later found him unresponsive, and he arrived at the
emergency department with a GCS of 3
OE: His skin was warm and dry Rectal temperature 42.2°C HR:170/min. Pupils are 7mm and
reactive.
Urine tox screen was positive for cocaine and marijuana
He was admitted to the ICU, and rhabdomyolysis developed. He recovered with supportive care and was discharged 1 week
later.
What are his risk factors?Why is he dry?
Case 67 F with dementia Increased confusion and agitation, requiring
haloperidol 1mg at bedtime for ~5 months Agitated in the ED Found on the roof of her building
Progressively became minimally responsive, rigid, and incontinent, with a temp of 40.5oC
Case 58 M with Hyperthermia Feeling unwell for the past 48h Shaking Chills – Altered
OE: 40oC 120 75/52 25 Flushed/warm peripherally
Classic Heat Stroke (non-exertional)
Results from exposure to high temperature Unable to compensate
Thoughts?Approach? Consider:
Alternate Diagnoses Hepatic Transaminase elevations may be useful Treating presumptively (sepsis)
Case 42 F collapsed just shy of the finish line It was her first marathon, and a hot day.
But according to her friend she had been keeping “pretty well hydrated.”
Brought to the ED via EMS confused Tonic-clonic in the trauma bay
Risk Factors?Concerns?Management?
Exertional Heat Stroke
Results from strenuous exercise Typically young healthy people
(athletes/workers)
Thoughts? Consider:
Hydration Hyponatremia
Treatment Cooling
Active cutaneous vasodilation ↑ temperature gradient b/w skin and environment (conduction) ↑ gradient of water-vapor pressure b/w skin and environment
(evaporation) ↑ velocity of air adjacent to the skin (convection) How would you like to do it?
Evaporation / Convection Cool water or wet sheets applied to the
skin Fan Spritz or Mist
This rarely causes shivering
Conduction
†Internal cooling, which has been investigated in animals, is infrequently used in humans. Gastric or peritoneal lavage with ice water may cause water intoxication.
Cold water immersion has been linked with asystolic arrestsUsed by the military without incidentMay be more significant in “classic” heat stroke (14% mortality study of 28 patients with CHS)
Rectal lavage
ConductionThis may cause shivering
How can you stop it? If the pt is shivering:
Vigorous massage spray with tepid water (40°C) expose to hot moving air (45°C)…either at the same time as cooling methods
are applied or in an alternating fashion
Case A buddy recently back from visiting out east,
tells us it was way hotter than anything we’ve experienced here.
According to the Canadian Weather Services the average temperature was exactly the same.
“Yeah but it was a wet hot! It was way hotter!”
What do you think?Does humidity make a difference?
Case 68 M with Heat Stroke You continue to cool His BP falls to 68/40
How would you like to manage?
Resuscitation
Fever vs Hyperthermia Fever does not cause primary pathologic
or physiologic damage Fever does not require therapeutic
intervention…unless the patient has limited physiologic
reserve
Infectious agents / Toxins / Mediators of inflammation(Pyrogens)
stimulateMonocytes / Macrophages / Endothelial cells / Other cell types
releasePyrogenic cytokines - IL- 1, TNF, IL- 6, IFNs
stimulateAnterior hypothalamus (Mediated by PGE2)
results inElevated thermoregulatory set point
leads toIncreased Heat conservation
(Vasoconstriction/ behaviour changes)Increased Heat production
(involuntary muscular contractions) result in
F E V E R
(Antipyretics/ NSAIDs act here)
Decreasing the Set Point Antipyretics
Not useful in true Heat Shock May be useful in mixed presentations (ie.
Sepsis/Heatshock)
Prevention Acclimatize yourself to heat Schedule outdoor activities during cooler times ↓ level of physical activity Drink additional fluids Consume salty foods ↑ amount of time spent in air-conditioning Automobiles should be locked, and children
should never be left unattended in an automobile during hot weather
AcclimatizationSuccessive exposures over weeks… Enhanced CV performance Activation of Renin-Angiotensin-Aldosterone
Axis Salt conservation by sweat glands Increased capacity to secrete sweat Expansion of plasma volume Increase in GFR Increase in ability to resist rhabdomyolysis
HYPOTHERMIA
Case 48 F presents with decreased LOC Found outside by police talking strangely to
passers-by Complaining about her bulky coat Undressing despite the cold
What is your approach? Differential Diagnosis? Why is this lady at risk? How is she losing heat?
Pathophysiology Evaporation
Vaporization of water through both insensible loss and sweat
Radiation Emission of infrared electromagnetic energy
Conduction Direct transfer of heat to an adjacent, cooler
object Convection
Direct transfer of heat to convective air currents
PathophysiologyCell membrane dysfunction
Efflux of intracellular fluid
Enzymatic dysfunction
Electrolyte imbalances
CaseOE: 48 10 110/62 34oC CNS Depression (GCS 5) – No focal findings Reflexes globally reduced Not shivering But she feels cold!
What would you like to do?
Assessment Thermometer
Need a “low” reading thermometer Oral temps influenced by respiration Tympanic temps unreliable
Rectal Probe “Core” temp Altered if adjacent to cold/frozen stool
Esophageal Probe Next to the Aorta
Bladder Probe
CaseOE: Repeat temperature via rectal probe =
28oC
What’s going on Doctor? Is Hypothermia a diagnosis? How would you classify?
Clasification Mild: 32-35oC
tachypnea, tachycardia, ataxia, dysarthria, impaired judgement, shivering, “cold diuresis”
Moderate: 28-32oC decreased heart rate, hypoventilation, CNS
depression, hyporeflexia, decreased renal blood flow, loss of shivering, paradoxical undressing, AFIB, junctional bradycardias
Severe: <28oC pulmonary edema, oliguria, areflexia, coma,
hypotension, bradycardia, ventricular arrhythmias, asystole
Differential Diagnosis
Differential Diagnosis
Why is this patient hypothermic?
CaseWhat investigations would you like to
order?
Investigations C/S (hypoglycemia) CBC, Lytes, INR/PTT ABG EKG
Anything else you’d like?
Coagulopathy Clotting factors are temperature
dependant…they don’t work when they’re cold
Coags are performed in the lab at 37°C...thus, clinical coagulopathy → “N” INR
and PTT
ABG Lactate Metabolic screen
pH, pCO2, pO2 Gas tension and H+ decline with the
temperature Use uncorrected values
EKG
•Rhythm abnormalities•AFIB/Sinus Bradycardia
•Intervals•PR/QRS/QTc prolonged
•Osborn J waves
CaseHow would you like to manage this
patient?
Management Passive External Rewarming
remove wet clothing blankets
Active External Rewarming warmed humidified O2 forced air warming systems
Active Internal Rewarming warmed IV fluids (42oC) pleural/peritoneal/bladder irrigation Extracorporeal (dialysis/bypass/continuous
venous)
Case You begin Initially by covering the
patient in warmed blankets while someone set’s up the Bair Hugger.
Patient goes into VFIB
How would you like to proceed?
Modifications of BLS for Hypothermia If not in cardiac arrest,
warm the patient Handle the victim gently for all procedures Physical manipulation may precipitate VF
If in cardiac arrest, Assess pulse/respirations for 30-45s (may be
difficult) Bag with warmed O2 If shockable (ie. VF) shock once them resume CPR
defer further attempts till warm
“Hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation. Drug metabolism is reduced.”
Modifications of ACLS for Hypothermia Intubation
ventilation with warm, humidified oxygen isolate the airway to reduce the likelihood of aspiration
Difibrilation try initial shock if unsuccessful, defer until core temperature > 30°C
IV meds may accumulate to toxic levels (decreased metabolism) < 30°C hold > 30°C give at increased intervals
Re-warming as discussed above
Volume patients who have been hypothermic for 45-60 min are likely to require volume
because the vascular space expands with vasodilation
Routine use of steroids, barbiturates, and antibiotics has not been shown to increase survival or decrease post-resuscitation damage.
Severe hypothermia is often preceded by other disorders (eg, drug overdose, alcohol use, or trauma). The clinician must look for and treat these underlying conditions while simultaneously treating the hypothermia.
CaseInitial shock converts briefly to sinus then
pt becomes asystolicContinue CPR for 30 minutes with no ROS
When do you stop?
Withholding and Cessation of Resuscitative Efforts In the field
resuscitation may be withheld if the victim has obvious lethal injuries or if the body is frozen so that nose and mouth are blocked by ice and chest compression is impossible
“you’re not dead until you’re warm and dead” hypothermia may exert a protective effect on the brain and organs
if the hypothermia develops rapidly in victims of cardiac arrest. it may be impossible to distinguish 1o from 2o hypothermia
stabilize the patient with CPR basic maneuvers to limit heat loss rewarming interventions
Once the patient is in the hospital, physicians should use their clinical judgment to decide when resuscitative efforts should cease in a victim of hypothermic arrest.
FROSTBITE
Case
16-year-old male attempted to "get high" by inhaling airbrush propellant which contained a fluorinated hydrocarbon
The patient lost consciousness and upon waking his lips and tongue were frozen
His main complaints on presentation were dyspnoea and pain in the oral/peri-oral areas
Case
OE: 159/94 101 24 37.1oC Alert and Appropriate Severe edema of the tongue and lips, with
blisters on the lips and frozen saliva in the oral cavity
What else would you like to know? Initial management/approach?
Case 4 hours after presentation develops
acute respiratory distress Nasally intubated – stabilized
- admitted (ICU) Endoscopy showed 1st and 2nd degree burns
of the larynx with vocal cord involvement and 1st degree burns of the trachea, main stem bronchi, and esophagus.
The oral cavity had 2nd and 3rd degree burns which required debridement
Pathophysiology
Classification
Classification
Classification1st Degree:
Central pallor and anesthesia of the skin Surrounding edema
2nd Degree: Blisters containing clear/milky fluid Surrounding edema/erythema
3rd Degree: Deeper injury Hemorrhagic blisters progressing to black eschar
4th Degree: Injury extends to muscle/bone Involves complete tissue necrosis
Who is at risk for frostbite?
Behavioural Physiologic
Risk Factors Increased Conductive Heat Loss
Contact with metal or water Increased Convective Heat Loss
Exposure to wind Alcohol
Behavioural Changes Vasodilation
Smoking Hx of Frostbite African Americans / Women Ice Packs (iatrogenic)
Diagnosis Clinical
Numbness (sensory deficit) Distal extremeties
Plain Radiographs Coincidental fractures Soft tissue swelling
Technetium (Tc)-99 scintigraphy Predicts long-term tissue viability Allows early debridement
MRI/MRA Predicts tissue variability Visualize occluded vessels – demarcate ischemic tissue
Management?
TreatmentPrehospital Transport the patient to a warm environment Remove wet clothing Insulate affected areas Avoid walking on frostbitten feet
...Don`t re-warm if there is a possibility of re-freezing use of stoves (tissue is insensate) use friction
TreatmentHospital Re-warming
Immerse affected area in water bath (40-42oC) 30 min – tissue is purple and soft Analgesia - opiods
Analgesia Dressing
Bulky dressing to decrease oedema Splint to prevent contractures
Tetanus (consider) Rehydration
Cold diuresis – increases blood viscosity and sludging
Thrombolysis
Design: Single institution retrospective review of clinical outcomes and resource use.
Setting: Burn unit of a tertiary academic referral center. Patients: 2001-2006, patients with severe frostbite admitted within 48 hours of
injury underwent digital angiography and treatment with intra-arterial tPA if abnormal perfusion was demonstrated. These patients were compared with those treated from 1995 to 2006 who did not receive tPA.
Interventions: tPA vs traditional management of frostbite injury. Main Outcome Measures: Number and type of surgery were recorded, along
with amputations of digits (fingers or toes) and more proximal (ray, transmetatarsal, or below-knee) amputations. Resource utilization including length of stay, total costs, cost per involved digit, and cost per saved digit were analyzed.
Results: 32 patients with digital involvement (hands, 19%; feet, 62%; both, 19%) were identified. 7 patients received tPA, 6 within 24 h of injury. The incidence of digital amputation in patients who did not receive tPA was 41%. In those patients who received tPA within 24 hours of injury, the incidence of amputation was reduced to 10% (P.05).
Conclusions: tPA improved tissue perfusion and reduced amputations when administered within 24 hours of injury. This modality represents the first clinically significant advancement in the treatment of frostbite in more than 25 years.
Treatment of experimental frostbite with pentoxifylline and
aloe vera cream OBJECTIVE: To compare the therapeutic effects of systemic
pentoxifylline and topical aloe vera cream in the treatment of frostbite.
DESIGN: The frostbitten ears of 10 New Zealand white rabbits were assigned to one of four treatment groups: untreated controls, those treated with aloe vera cream, those treated with pentoxifylline, and those treated with aloe vera cream and pentoxifylline.
MAIN OUTCOME MEASURES: Tissue survival was calculated as the percent of total frostbite area that remained after 2
weeks. RESULTS: The control group had a 6% tissue survival. Tissue
survival was notably improved with pentoxifylline (20%), better with aloe vera cream (24%), and the best with the combination therapy (30%).
CONCLUSION: Pentoxifylline is as effective as aloe vera cream in improving tissue survival after frostbite injury.
Arch Otolaryngol Head Neck Surg 1995; 121:678
Miller MB, Koltai PJ
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