EXTREMES OF TEMPERATURES
– Heat generation
– Heat loss
– Heat conservation
• Normal core body temp- 37±0.5ᴼC
• Failure of body’s normal thermal regulatory
mechanism to produce sufficient heat in cold
environment. Core temp. falls below 35ᴼC .
• Increase metabolism
Hypothermia is common in
• Very young children
• Elderly people
• Addison’s disease
• Hepatic failure
• Exposure to extreme cold climates
EFFECTS OF SYSTEMIC HYPOTHERMIA
• Decreased respiratory drive
• Decreased O2 consumption
• Decreased central and peripheral nerve
• Decreased GI motility
• Decreased myocardial repolarization
• Decreased coagulation cascade
Clinical features of hypothermia
• Core temp of body 32ᴼ-35ᴼC
• Tachypnea, tachycardia, hypertension and
• Impaired coordination and apathy
• At temp 32-28ᴼ- shivering stops
• Bradycardia, pupils dilate, reflexes slow,
confusion and lethargy
• Death in hypothermia is due to ventricular
• Initiation of rewarming
• Rectal temp should be measured
• Monitoring of vitals, cardiac rhythm, blood
• Treat hypoxia
• Treat fluid and electrolyte imbalance
• Control arrhythmias
HYPOTHERMIA OF THE EXTREMITIES
• TRENCH FOOT
• FROST BITE
• Cold-induced injuries to the extremities (ie, frostnip,
chilblain, trench foot, and frostbite) range from mild to
• Cold exposure of the extremities produces immediate
localized vasoconstriction followed by generalized
• When the skin temperature falls to 25°C, tissue
demand for oxygen is greater than what is supplied by
the slowed circulation: the area becomes cyanotic.
• At 15°C, tissue damage occurs due to marked
reduction in tissue metabolism and
• This gives a deceptive pink, well-oxygenated
appearance to the skin.
• Tissue damage may result from ischemia and
intravascular thromboses, endothelial damage, or
by actual freezing.
• Freezing (frostbite) may occur when the skin
temperature drops below −4 to −10°C
• Frostnip is a mild temporary form of cold-induced
• The involved area has local paresthesias that
completely resolve with passive external
• Chilblains or erythema pernio are inflammatory
skin changes caused by exposure to cold without
actual freezing of the tissues.
• These skin lesions may be red or purple papular
lesions, which are painful or ,with burning or
• Immersion foot (or hand) TRENCH FOOT is caused by
prolonged immersion in cool or cold water or mud,
usually < 10°C.
• cold and anesthesia of the affected area.
• follows with hot sensation, intense burning, and
• part becomes pale or cyanotic with diminished
pulsations due to vasospasm
• blistering, swelling, redness, ecchymoses,
• necrosis, peripheral nerve injury, or gangrene
• Frostbite is injury from tissue freezing and formation of ice
crystals in the tissue particularly the extremities.
• The tissues become anesthetised.
• Tissue is initially pale and doughy to touch.
• Later becomes hard and insensitive to pain.
• Gangrene may form.
• Rewarming in warm water
• Protecting the injured tissue
• Avoid infection
• Surgical treatment may be reqd. to remove dead tissue
• Heat syncope or sudden collapse may result in
• volume depletion and cutaneous vasodilation
• with consequent systemic and cerebral
• history of prolonged vigorous physical activity or
prolonged standing in a hot humid environment.
• Typically, the skin is cool and moist, the pulse is
weak, and the systolic blood pressure is low
• t/t –rest in recumbent position
• Water and electrolyte rehydration
• Characterized by painful muscle cramps
(painful skeletal ms contractions)following
vigorous exercise in hot weather.
• No increase in core temperature.
• The patient is alert with normal vitals
• Due to extracellular Na+ depletion following
electrolytes loss due to persistent sweating.
• Responds rapidly to salt replacement.
• Occurs when the core temp. increases between 37ᴼC-40ᴼC
following vigorous physical activity in hot environment and
• It is characterized by dehydration, sodium depletion.
• increased pulse, and moist skin. nausea, vomiting,
• malaise, myalgias, hyperventilation, thirst, and weakness.
• CNS symptoms include headache, dizziness, fatigue,
• removal of the pt. from hot environment
• Cold sponging
• Fluid replacement saline or isotonic glucose saline
• life-threatening medical emergency
• Characterized by core temp. >40ᴼC and cerebral dysfunction .
• Loss of heat regulatory mechanism.
• Symptoms include all those seen in heat exhaustion with
additional symptoms of dizziness, weakness, confusion, delirium,
blurred vision, convulsions, collapse, and unconsiousness
• Skin will be hot
• No sweating
• Treatment is aimed at rapidly reducing the
core temperature (within 1 hour) while
supporting circulatory and organ system
function to prevent irreversible tissue damage
• Oral or intravenous fluid administration.
• Cold sponging
• Metabolic abnormalities and cardiac
arrythmias should be treated
• Drowning describes submersion resulting in asphyxia and death.
• Following inhalation of water
hypoxemia + pulmonary oedema
• Absorption of large amount of water(hypotonic ) fluid leads
• Near drowning describes a submersion event leading to injury.
Submersion injury may result in
aspiration,laryngospasm,hypoxemia, and acidemia
• “Wet” drowning is due to aspiration of fluid or foreign material.
• “Dry” drowning is due to laryngospasm or airway obstruction
• The first requirement of rescue is immediate
basic life support and CPR.
• Patient must also be assessed for
hypothermia, hypoglycemia, concurrent
injuries, and medical conditions.
• Clinical manifestations are hypoxemia,
pulmonary edema, and hypoventilation
• Arterial blood gas - Pao2 is usually decreased;
Paco2 may be increased; pH is decreased.
• blood sugar must be checked rapidly.
• kidney function,
• electrolytes, urinalysis,
• blood count,
• coagulation studies,
• A. First Aid
• immediate CPR. - Ventilation, oxygenation, and
• Hypothermia and associated trauma, especially brain
and cervical spine injury, should always be suspected.
• Patient must be assessed for hypoglycemia, metabolic
acidosis, and concurrent medical conditions.
• Rescuer should not attempt to drain water from the
victim’s lungs. The “Heimlich maneuver”
(subdiaphragmatic pressure) should be used only if
foreign material airway obstruction is suspected.
• Oxygen should be administered immediately at
the highest available concentration.
• Oxygen saturation should be maintained at 90%
• Endotracheal intubation and mechanical
• Hypotension is treated with vasopressors
• Pulmonary oedema- diuretics
• Metabolic acidosis –by proper ventilation and
• Hypothermia should be corrected
HIGH ALTITUDE ILLNESS
• As altitude increases, there is a decrease in both barometric
pressure and oxygen partial pressure leading to hypoxia.
• Acclimatization occurs as a physiologic response to the rise in
altitude and increasing hypoxia.
• Acclimatisation to hypoxaemia at high altitude results in increased
erythropoiesis, haemoconcentration, and hyperventilation
• Physiologic changes include increases in alveolar ventilation and
oxygen extraction by the tissues and increased hemoglobin level
and oxygen binding
• Ascent to altitudes up to 2500 m or travel in a pressurised aircraft
cabin is harmless to healthy people.
• Above 2500 m high-altitude illnesses may occur in previously
healthy people, and above 3500 m these become common.
ACUTE MOUNTAIN SICKNESS
• Characterized by neurologic and pulmonary symptoms.
• Characterized by headache with N,V, dizziness, fatigue
• Facial pallor, dyspnea and cyanosis
• Later - vertigo, tinnitus, visual disturbances
• Occurs in 6-24 hrs. of ascent.
• M/M – Rest, analgesic and Acetazolamide
(acetazolamide acts by inhibiting carbonic anhydrase
enzyme causing metabolic acidosis and thus increasing
• Prevention – slow ascent and acclimatization
High altitude cerebral edema
• Extension of CNS symptoms of acute mountain
• Over >3500 m due to loss of acclimatization
• Altered consciousness and ataxic gait
• Confusion, Behavioral changes, Hallucinations
• Seizures, ff by obtundation,and coma
M/M –immediate descent
- steroids (dexamethasone)
- diuretics( mannitol)
High altitude pulm edema
• High-altitude pulmonary edema is a serious
complication of hypoxia induced pulmonary
• The hallmark is markedly elevated pulmonary artery
pressure followed by pulmonary edema. It usually
occurs at levels above 3000 meters
• Early symptoms may appear within 6–36 hours after
arrival at a high-altitude area.
• These include persistent dry cough, shortness of
breath, headache, fatigue, dyspnea at rest, and chest
• Later, wheezing, orthopnea ,and hemoptysis may occur
as pulmonary edema worsens
• Physical findings include tachycardia, mild fever,
tachypnea, cyanosis, prolonged respiration, and rales
• The patient may become confused or comatose
• The patient must rest in the semi-Fowler position
(head raised), and
• 100% oxygen must be administered.
• Immediate descent is essential.
• Nifedepin to reduce the pulmonary arterial pressure
DYSBARISM & DECOMPRESSION
• Dysbarism and decompression sickness are
physiologic problems that result from altitude
changes and the environmental pressure effects
on gases in the body during underwater descent
and ascent, particularly when scuba diving is
followed closely by air travel or hiking to high
• As a diver descends, the gases in the body
compress; gases dissolve in blood and tissues.
During the ascent, gases in the body expand.
• Dysbarism results from gas compression or
expansion in parts of the body that have limited
• results in pneumomediastinum, pneumothorax,
and rupture of the pulmonary vein causing
arterial gas embolism
• gastric rupture, bowel obstruction or perforation,
• Less serious conditions can also occur such as ear
squeeze, sinus squeeze, headache, tooth
• Decompression sickness occurs when the
ascent is too rapid and gas bubbles form and
cause damage depending on their location
(eg, coronary, pulmonary, spinal or cerebral
blood vessels, joints, soft tissue).
• The range of clinical manifestations varies depending on
the location of the gas bubble formation or the
compressibility of gases in the body.
• Symptom onset may be immediate, within minutes or
hours (in the majority), or present up to 36 hours later.
• Decompression sickness symptoms include pain in the
• skin pruritus or burning , or rashes;
• labyrinthine decompression sickness characterized by
• pulmonary decompression sickness causing inspiratory
pain, cough, and respiratory distress
• arterial gas embolism (cerebral or pulmonary)
• Decompression sickness must be considered if
symptoms are temporally related to recent diving
or altitude or pressure changes within the past 48
• Immediate consultation with a diving medicine or
hyperbaric oxygen specialist is indicated
• Continuous administration of 100% oxygen is
indicated and beneficial for all patients.
• Aspirin may be given for pain. Opioids should be
used very cautiously,
• Damage from radiation is determined by the
source, type, quantity, duration, bodily location,
and susceptibility and accumulation of exposures
of the person.
• Radiation exposure from medical diagnostic
imaging has dramatically risen over the past few
decades; medical imaging radiation dosing needs
to be standardized and regulated in order to
minimize necessary radiation exposure
• Radiation occurs from both nonionizing and
ionizing radiation sources.
• Nonionizing radiation is low energy, resulting in
injuries related to local thermal damage (ie,
microwave, ultraviolet, visible light and
• Ionizing radiation is high energy, causing bodily
damage in several ways (ie, cellular disruption,
DNA damage, and mutations).
• Ionizing radiation is either electromagnetic (ie, x-
rays and gamma rays) or particulate (ie, alpha or
beta particles, neutrons, and protons
• X rays, CT Scan, MRI and Radiotherapy
• The energy absorbed by a unit mass of a
tissue is the radiation dose.
• This is measured in grays (Gy) and is useful to
assess the high dose exposure.
• Effective dose to cause damage to a particular
tissue is measured in sieverts (Sv). This is
useful to assess chronic low dose exposure.
• Effect depends on the dose and tissue
• Radiation exposure results in early and
• Early effects involve damage of the rapidly
dividing cells (ie, the mucosa, skin, and bone
• This may be manifested as nausea, vomiting,
and decreased lymphocyte count over hours
to days after exposure.
• Delayed effects include malignancy,
reproduction abnormalities, liver, kidney, and
central nervous system and immune system
A. Injury to Superficial Structures
• Acute radiation exposure to the skin and
mucous membranes may cause erythema,
destruction of fingernails,
• Chronic damage includes skin scarring,
atrophy, and xerostomia. Radiation effects on
the eyes include cataracts, dry eye syndrome,
B. Injury to Deep Structures
• Hematopoietic system radiation exposure causes
injury to the bone marrow that may vary from
transient decreases to complete destruction of
• Hematopoietic effects consisting of anemia,
thrombocytopenia, and bone marrow
• Bone marrow failure is the main cause of death
within the first few months following exposure to
• Nervous system structures are sensitive to radiation.
• The brain and spinal cord are much more sensitive
than the peripheral nerves.
• cardiovascular system effects of ionizing radiation
result in damage to the heart and coronary arteries.
• Delayed effects from radiation include obliterative
endarteritis; coronary artery disease; pericarditis with
effusion; or constrictive pericarditis,
• Pulmonary system cause pneumonitis or
• Gastrointestinal system radiation results in mucositis
and mucosal edema within hours or days after
• Symptoms include odynophagia, anorexia, nausea,
vomiting, dehydration, and weakness. Delayed effects
include hepatitis, liver dysfunction, and intestinal
• The stomach and colon are the gastrointestinal organs
most at risk for cancer.
• Urogenital system radiation effects are dose-
• Endocrine system organs are relatively resistant to low
or moderate doses of radiation. The thyroid gland is
the endocrine gland at highest risk for cancer induction
from internal radiation exposure.
C. Systemic Reaction (Acute Radiation Syndrome)
• Acute radiation syndrome is due to an exposure
to high doses of ionizing radiation over a brief
• The symptom onset is within hours to days
depending on the dose.
• Symptoms include anorexia, nausea, vomiting,
weakness, exhaustion, and lassitude.
• Dehydration, anemia, and infection may follow
• Treatment is focused on decontamination,
• Symptomatic relief, supportive care, and
• Adequate hydration
• Marrow transplantation for marrow aplasia
• Chelating agents