Hypothermia, Frostbite and heat illness

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Transcript Hypothermia, Frostbite and heat illness

HYPOTHERMIA, FROSTBITE
AND HEAT ILLNESS
Mark Bromley PGY3
Outline

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Heat Stroke
Hypothermia
Frostbite
HEAT STROKE
Case

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
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

42oC HR: 65 GCS:3
OE:
What are this patients HS risk factors?
What other diagnoses are you concerned about?
How would you like to manage?
Perspective
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
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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
Muscle
Contraction
(shivering - exercise)
Liver
Environmental
(metabolic inefficiency)
Heat
Production
Thermoregulation
Behavioural
Cardiac Output
Intact Sweat
glands
Vasodilatation
Change Environment
Appropriate
Clothing
Cooling Strategies
Shunts warm blood
to the surface
Sweat Production
Evaporation
Respiration
Terminology
Heat wave

Three or more consecutive days during which the air temperature is >32.2°C
Heat stress

Perceived discomfort and physiological strain associated with exposure to a hot environment, especially
during physical work
Hyperthermia

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) heat
Heat 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
Mild-to-moderate illness due to water or salt depletion
Perceived discomfort and physiological strain
Changes in more than one organ system
Heat Stress
Hot Outside
Hyperthermia
Hot Inside
Heat
Exhaustion
Heat Stroke
Symptomatic
Sick
MODS
A rise in body temperature above the hypothalamic set point
Severe illness characterized by a core temp >40°C and CNS abnormalities
Clinical and Metabolic Manifestations
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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 Classic
Exertional
Healthy
Younger
Exercise
Sporadic
Diaphoresis
Hypoglycemia
DIC
Rhabdomyolysis
Acute renal failure
Lactic acidosis
Hypocalcemia
Classic
Predisposing factors/medications
Older
Sedentary
Heat wave occurrence
Anhidrosis
Normoglycemia
Mild coagulopathy
Mild CPK elevation
Oliguria Marked
Mild acidosis
Normocalcemia
Case
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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

42oC HR: 65
OE:
What are this patients HS risk factors?
What other diagnoses are you worried about?
How would you like to manage?
Case
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
37 F presents altered and hot
Post-op Day 1
PMHx:
 Graves
OE:
o
 135 39 C 143/62 (widened pulse pressure)
 Moist skin
 Loose stools
Case
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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
What are his risk factors?
OE:
Why is he dry?
 His skin was warm and dry
 Rectal temperature 42.2°C HR:170/min. Pupils are 7mm and reactive.
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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.
Case
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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
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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
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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
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Cooling
Core
Skin
Environment

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)
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
How would you like to do it?
Evaporation / Convection
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Cool water or wet sheets applied to the skin
Fan
Spritz or Mist

This rarely causes shivering
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Conduction
Rectal lavage
Cold water immersion has been linked with asystolic arrests
Used by the military without incident
May be more significant in “classic” heat stroke
(14% mortality study of 28 patients with CHS)

†Internal cooling, which has been investigated in animals, is infrequently used in humans. Gastric or peritoneal
lavage with ice water may cause water intoxication.
Conduction
This may cause shivering
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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
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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
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How would you like to manage?
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Resuscitation
Fever vs Hyperthermia
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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)
stimulate
Monocytes / Macrophages / Endothelial cells / Other cell types
release
Pyrogenic cytokines - IL- 1, TNF, IL- 6, IFNs
stimulate
Anterior hypothalamus (Mediated by PGE2)
results in
(Antipyretics/ NSAIDs act here)
Elevated thermoregulatory set point
leads to
Increased Heat conservation
(Vasoconstriction/ behaviour changes)
Increased Heat production
(involuntary muscular contractions)
result in
FEVER
Decreasing the Set Point

Antipyretics
 Not
useful in true Heat Shock
 May be useful in mixed presentations (ie. Sepsis/Heatshock)
Prevention
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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
Acclimatization
Successive 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
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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
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Evaporation
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Vaporization of water through both insensible loss and sweat
Radiation
 Emission

Conduction
 Direct

of infrared electromagnetic energy
transfer of heat to an adjacent, cooler object
Convection
 Direct
transfer of heat to convective air currents
Pathophysiology
Cell membrane dysfunction
Efflux of intracellular fluid
Enzymatic dysfunction
Electrolyte imbalances
Case
OE:
 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
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Rectal Probe

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“Core” temp
Altered if adjacent to cold/frozen stool
Esophageal Probe


Need a “low” reading thermometer
Oral temps influenced by respiration
Tympanic temps unreliable
Next to the Aorta
Bladder Probe
Case
OE:
 Repeat temperature via rectal probe = 28oC
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What’s going on Doctor?
Is Hypothermia a diagnosis?
How would you classify?
Clasification

Mild: 32-35oC

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Moderate: 28-32oC
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tachypnea, tachycardia, ataxia, dysarthria, impaired
judgement, shivering, “cold diuresis”
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
Increased Heat
Loss
Impaired
Regulation
Skin Disorders
Induced
Vasodilation
Environmental
Exposure
Iatrogenic
Peripheral
Burns
Psoriasis
Exfoliative
dermatitis
Drugs
Alcohol
Toxins
Cold infusion
Emergenct
deliveries
Bypass
CRRT
Spinal Cord
Neuropathy
Diabetes
Decreased Heat
Production
Other
Endocrine
Sepsis
Pancreatitis
Carcinomatosis
Uremia
Trauma
Vascular
Insufficiency
Hypopituitary
Hypoadrenal
Hypothyroid
Insufficient Fuel
NeuroMuscular
Insufficiency
Hypoglycemia
Malnutrition
Extremes of
Age
Impaired
Shivering
Inactivity
Central
CVA
SAH
Parkinsonism
Hypothalamic
dysfunction
MS
Anorexia
Drugs
Increased Heat Loss
Skin Disorders
Induced
Vasodilatation
Burns
Psoriasis
Exfoliative
dermatitis
Drugs
Alcohol
Toxins
Environmental
Exposure
Iatrogenic
Cold infusion
Emergent deliveries
Bypass
CRRT
Impaired Regulation
Peripheral
Central
Spinal Cord
Neuropathy
Diabetes
CVA
SAH
Parkinsonism
Hypothalamic
MS
Anorexia
Drugs
Decreased Heat
Production
Endocrine
Hypopituitary
Hypoadrenal
Hypothyroid
Insufficient Fuel
NeuroMuscular
Insufficiency
Hypoglycemia
Malnutrition
Extremes of Age
Impaired
Shivering
Inactivity
Other
Sepsis
Pancreatitis
Carcinomatosis
Uremia
Trauma
Vascular
Insufficiency
Differential Diagnosis
Increased Heat
Loss
Impaired
Regulation
Skin Disorders
Induced
Vasodilation
Environmental
Exposure
Iatrogenic
Peripheral
Burns
Psoriasis
Exfoliative
dermatitis
Drugs
Alcohol
Toxins
Cold infusion
Emergenct
deliveries
Bypass
CRRT
Why is this patient hypothermic?
Spinal Cord
Neuropathy
Diabetes
Decreased Heat
Production
Other
Sepsis
Pancreatitis
Carcinomatosis
Uremia
Trauma
Vascular
Insufficiency
Central
Endocrine
Insufficient Fuel
NeuroMuscular
Insufficiency
Hypopituitary
Hypoadrenal
Hypothyroid
Hypoglycemia
Malnutrition
Extremes of
Age
Impaired
Shivering
Inactivity
CVA
SAH
Parkinsonism
Hypothalamic
dysfunction
MS
Anorexia
Drugs
Case
What investigations would you like to order?
Investigations

C/S (hypoglycemia)
CBC, Lytes, INR/PTT
ABG
EKG

Anything else you’d like?

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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
Case
How 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
IV fluids (42oC)
 pleural/peritoneal/bladder irrigation
 Extracorporeal (dialysis/bypass/continuous venous)
 warmed
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
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
Difibrilation

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

may accumulate to toxic levels (decreased metabolism)
< 30°C hold
> 30°C give at increased intervals
Re-warming


try initial shock
if unsuccessful, defer until core temperature > 30°C
IV meds


ventilation with warm, humidified oxygen
isolate the airway to reduce the likelihood of aspiration
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 postresuscitation 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.
Case
Initial shock converts briefly to sinus then pt becomes
asystolic
Continue 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
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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)
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
 Endoscopy
Pathophysiology
Ice Crystal
Formation
(intra/extra
cellular)
Lysis of cell
membranes
Inflammatory
Response
Stasis/Coagulation
Tissue
Ischemia/Necrosis
Classification
Classification
Classification
1st 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

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Who is at risk for frostbite?
Behavioural
Physiologic
Risk Factors

Increased Conductive Heat Loss

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Increased Convective Heat Loss
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Exposure to wind
Alcohol


Contact with metal or water
Behavioural Changes
Vasodilation
Smoking
Hx of Frostbite
African Americans / Women
Ice Packs (iatrogenic)
Diagnosis

Clinical



Plain Radiographs



Coincidental fractures
Soft tissue swelling
Technetium (Tc)-99 scintigraphy



Numbness (sensory deficit)
Distal extremeties
Predicts long-term tissue viability
Allows early debridement
MRI/MRA


Predicts tissue variability
Visualize occluded vessels – demarcate ischemic tissue

Management?
Treatment
Prehospital
 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
Treatment
Hospital
 Re-warming





Analgesia
Dressing




Bulky dressing to decrease oedema
Splint to prevent contractures
Tetanus (consider)
Rehydration


Immerse affected area in water bath (40-42oC)
30 min – tissue is purple and soft
Analgesia - opiods
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
Miller MB, Koltai PJ
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



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
Thank you