lOMoARcPSD|27929433
PATHOPHYSIOLOGY
SUMMARIZED ALL
TOPICS
, lOMoARcPSD|27929433
1. Environmental Extremes - Extremes of Temperature, Atmospheric Pressure
THERMAL INJURIES
- Both excess heat and excess cold are important causes of injury.
Thermal Burns:
The clinical significance of burns depends on the following important factors:
- Depth of the burn
- Percentage of body surface involved
- Possible presence of internal injuries from inhalation of hot and toxic fumes
Promptness and efficacy of therapy, especially fluid and electrolyte management and prevention or control
of wound infections
- Full-thickness burn = total destruction of the epidermis and dermis, with loss of the dermal
appendages that would have provided cells for epithelial regeneration.
o 3rd + 4th degree burns in this category
- Partial-thickness burns = deeper portions of the dermal appendages are spared.
o Includes 1st burns (epithelial) and 2nd burns (both epidermis and superficial dermis)
Any burn exceeding 50% of the total body surface, whether superficial or deep, is grave and potentially
fatal.
- Burns of >20 % of the body surface = rapid shift of body fluid into the interstitial compartments, both
at the burn site and systematically - result in hypovolemic shock.
- Mechanisms include:
o increase in local interstitial osmotic pressure (from release of osmotically active constituents
of dying cells)
o Both neurogenic and mediator-induced increases in vascular permeability.
- Because protein from the blood is lost into interstitial tissue, generalized edema, including
pulmonary edema, may become severe if fluids used for volume replacement are not osmotically
active.
Another important consideration = is degree of injury to the airways and lungs.
- Inhalation injury may result from inhalation of toxic components in smoke.
- Water-soluble gases (chlorine, sulfur oxides, ammonia) may react with water to form acids of alkalis
o In upper airways, to produce inflammation and swelling = partial or complete airway
obstruction.
- Lipid-soluble gases (nitrous oxide and products of burning plastics) - deeper airways = producing
pneumonitis.
- Unlike shock, which develops within hours, pulmonary manifestations may not develop for 24 to 28
hours.
Complications:
- Secondary burn infection = important complication in all burn patients who have lost epidermis.
- Organ system failure resulting from burn sepsis
- The burn site - ideal for growth of microorganisms;
o The serum and debris provide nutrients, and the burn injury compromises blood flow,
blocking effective inflammatory responses.
o Pseudomonas aeruginosa (most common) but antibiotic-resistant strains of other common
hospital-acquired bacteria, i.e. S. aureus, and fungi (Candida species) may also be involved.
o Furthermore, cellular and humoral defenses against infections are compromised, and both
lymphocyte and phagocyte functions are impaired.
- Pneumonia or septic shock with renal failure and the acute respiratory distress syndrome are the
most common serious sequelae.
Another important pathophysiologic effect of burns is the development of a hypermetabolic state with
excess heat loss and an increased need for nutritional support.
- It is estimated that when more than 40% of the body surface is burned, the resting metabolic rate
may approach twice normal.
- The consequence is breakdown of tissue, which may result is loss of essential protein stores,
reaching lethal proportions comparable to starvation within several weeks.
.
, lOMoARcPSD|27929433
- Thus, it is essential to keep the patient’s room temperature elevated to reduce body heat loss and
to implement appropriate nutritional supplementation.
HYPERTHERMIA
Prolonged exposure to elevated ambient temperatures can result in heat cramps, heat exhaustion,
and heat stroke.
- Heat cramps result loss of electrolytes through sweating.
- Cramping of voluntary muscles, usually in association with vigorous exercise -
Heat-dissipating mechanisms are able to maintain normal core body temperature.
Heat exhaustion is probably the most common heat syndrome.
- Its onset is sudden, with prostration and collapse
o It results from a failure of the cardiovascular system to compensate for hypovolemia
, secondary to water depletion.
- After a period of collapse, which is usually brief, equilibrium is spontaneously re-established.
Heat stroke is associated with high ambient temperatures and high humidity.
- Thermoregulatory mechanisms fail, sweating ceases, and core body temperature rises
. - Body temperatures of 112 to 113 F have been recorded in some terminal cases.
- Clinically, a rectal temperature of 106F or higher is considered a grave prognostic sign, and
the mortality rate for such patients exceeds 50%.
- The underlying mechanism is marked generalized peripheral vasodilation with peripheral pooling
of blood and a decreased effective circulating blood volume.
- Necrosis of the muscles and myocardium may occur.
- Arrhythmias , disseminated intravascular coagulation , and other systemic effects are common.
- Elderly persons, individuals undergoing intense physical stress (including young athletes and
military recruits), and persons with cardiovascular disease are prime candidates for heat stroke.
HYPOTHERMIA
Prolonged exposure to low ambient temperature leads to hypothermia, a condition seen all too frequently
in homeless persons.
- Lowering of body temperature is hastened by high humidity in cold, wet clothing and dilation
of superficial blood vessels are a result of the ingestion of alcohol.
- At about 90 F, loss of consciousness occur, followed by bradycardia and atrial fibrillation at
lower core temperatures.
Local Reactions. Chilling or freezing of cells and tissues causes injury in two ways.
- Direct effects are probably mediated by physical dislocations within cells and high salt
concentrations incident to the crystallization of the intracellular and extracellular water
.
- Indirect effects are exerted by circulatory changes.
o Depending on the rate at which the temperature drops and the duration of the drop,
slowly developing chilling may induce vasoconstriction and increased permeability,
leading to edematous changes.
- Alternatively , with sudden sharp drops in temperature that are persistent , the vasoconstriction and
increased viscosity of the blood in local area may cause ischemic injury and degenerative
changes in peripheral nerves.
- In this situation, only after the temperature begin to return toward normal do the vascular injury
and increased permeability with exudation become evident.
- However, during the period of ischemia, hypoxic changes and infarction of the affected tissue
may develop (e.g., gangrene of toes or feed).
INJURIES RELATED TO CHANGES IN ATMOSPHERIC PRESSURE
Depending on the direction of change (decrease or increase) in atmospheric pressure, its rate
of development, and the magnitude of change, four syndromes can be produced:
- High altitude
illness - Blast injury
- Air or gas embolism
- Decompression disease – also known as caisson disease – which is sometimes referred to
as barotrauma
, lOMoARcPSD|27929433
High-Altitude Illness.
- Encountered in mountain climbers in the rarefied atmosphere encountered at altitudes above 4000
m.
- The lowered oxygen tension produces progressive mental obtundation and may be accompanied by
poorly understood increased capillary permeability with systemic and, in particular, pulmonary
edema.
Blast Injury.
- Implies increase in pressure either in the atmosphere (air blast) or in water (immersion blast).
- With air blast, the compression wave impinges on the side toward the explosion and so may
collapse the thorax or violently compress the abdomen, with rupture of internal organs.
- The pressure wave may enter the airways and damage the alveoli.
- The following wave of decreased pressure, with its sudden expansion of the abdomen and thorax,
may rupture the intestines or lungs.
- In immersion blast, the pressure is supplied to the body from all sides, including injuries similar to
those of air blast.
Air or Gas Embolism.
- Complication of scuba diving, mechanical positive-pressure ventilatory support, the hyperbaric
oxygen therapy and only rarely as a manifestation of decompression disease.
- Common to all these settings is an abnormal increase in intra-alveolar air or gas pressure
- Leading to tearing of tissue with entrance of air into interstitium and small blood vessels.
- Pulmonary, mediastinal, and subcutaneous emphysema may result, and in some instances,
o Combination of numerous small air or gas emboli that gain access to the arterial circulation
may lead acutely to stroke-like syndromes or a myocardial ischemic episode.
o Either the neurologic or the myocardial embolism may cause sudden death.
Decompression (Caisson) Disease.
- Encountered in deep-sea divers and underwater workers who spent long periods in caissons or
tunnels, under increased atmospheric pressure.
- The injury, encountered with too rapid decompression, is a function of Henry’ law, which is essence
states that the solubility of a gas in a liquid (e.g., blood) is proportional to the partial pressure of the
gas in the environment.
- As the underwater depth and consequent atmospheric pressure increase, larger and larger amounts
of oxygen and accompanying gases (nitrogen and helium) dissolve in the blood and tissue fluids.
- Once the ascent begins (decompression), the dissolved gases come out of solution and form
minute bubbles in the bloodstream and tissues.
- Joining of these bubbles produces even larger masses capable of becoming significant emboli in
the bloodstream.
- The oxygen bubbles are soluble in blood and tissues and so re-dissolve.
o The nitrogen and helium dissolve only slowly.
- Periarticular bubbles produce the bends. Bubbles formed within the lung or gaseous emboli give
rise to respiratory difficulties, with severe substernal pain referred to as the chokes.
- Various central nervous system manifestations may appear, ranging from headache and visual
disturbances to behavioral disorientation.
- Involvement of the inner ear may produce vertigo and the staggers.
- All these manifestations may appear within hours of the too rapid ascent, but skeletal manifestations
– caisson disease of bone – may sometimes appear days later.
- This takes the form of foci of aseptic necrosis, typically of femoral and humeral heads, and
medullary foci, particularly in the lower femur and upper tibia, attributed to embolic occlusion of the
vascular supply.
ELECTRICAL INJURIES
- Passage of electric current may be without effect or cause sudden death by disruption of neural
regulatory impulses, producing:
o cardiac arrest
o thermal injury to organs interposed in the pathway of the current.
.
PATHOPHYSIOLOGY
SUMMARIZED ALL
TOPICS
, lOMoARcPSD|27929433
1. Environmental Extremes - Extremes of Temperature, Atmospheric Pressure
THERMAL INJURIES
- Both excess heat and excess cold are important causes of injury.
Thermal Burns:
The clinical significance of burns depends on the following important factors:
- Depth of the burn
- Percentage of body surface involved
- Possible presence of internal injuries from inhalation of hot and toxic fumes
Promptness and efficacy of therapy, especially fluid and electrolyte management and prevention or control
of wound infections
- Full-thickness burn = total destruction of the epidermis and dermis, with loss of the dermal
appendages that would have provided cells for epithelial regeneration.
o 3rd + 4th degree burns in this category
- Partial-thickness burns = deeper portions of the dermal appendages are spared.
o Includes 1st burns (epithelial) and 2nd burns (both epidermis and superficial dermis)
Any burn exceeding 50% of the total body surface, whether superficial or deep, is grave and potentially
fatal.
- Burns of >20 % of the body surface = rapid shift of body fluid into the interstitial compartments, both
at the burn site and systematically - result in hypovolemic shock.
- Mechanisms include:
o increase in local interstitial osmotic pressure (from release of osmotically active constituents
of dying cells)
o Both neurogenic and mediator-induced increases in vascular permeability.
- Because protein from the blood is lost into interstitial tissue, generalized edema, including
pulmonary edema, may become severe if fluids used for volume replacement are not osmotically
active.
Another important consideration = is degree of injury to the airways and lungs.
- Inhalation injury may result from inhalation of toxic components in smoke.
- Water-soluble gases (chlorine, sulfur oxides, ammonia) may react with water to form acids of alkalis
o In upper airways, to produce inflammation and swelling = partial or complete airway
obstruction.
- Lipid-soluble gases (nitrous oxide and products of burning plastics) - deeper airways = producing
pneumonitis.
- Unlike shock, which develops within hours, pulmonary manifestations may not develop for 24 to 28
hours.
Complications:
- Secondary burn infection = important complication in all burn patients who have lost epidermis.
- Organ system failure resulting from burn sepsis
- The burn site - ideal for growth of microorganisms;
o The serum and debris provide nutrients, and the burn injury compromises blood flow,
blocking effective inflammatory responses.
o Pseudomonas aeruginosa (most common) but antibiotic-resistant strains of other common
hospital-acquired bacteria, i.e. S. aureus, and fungi (Candida species) may also be involved.
o Furthermore, cellular and humoral defenses against infections are compromised, and both
lymphocyte and phagocyte functions are impaired.
- Pneumonia or septic shock with renal failure and the acute respiratory distress syndrome are the
most common serious sequelae.
Another important pathophysiologic effect of burns is the development of a hypermetabolic state with
excess heat loss and an increased need for nutritional support.
- It is estimated that when more than 40% of the body surface is burned, the resting metabolic rate
may approach twice normal.
- The consequence is breakdown of tissue, which may result is loss of essential protein stores,
reaching lethal proportions comparable to starvation within several weeks.
.
, lOMoARcPSD|27929433
- Thus, it is essential to keep the patient’s room temperature elevated to reduce body heat loss and
to implement appropriate nutritional supplementation.
HYPERTHERMIA
Prolonged exposure to elevated ambient temperatures can result in heat cramps, heat exhaustion,
and heat stroke.
- Heat cramps result loss of electrolytes through sweating.
- Cramping of voluntary muscles, usually in association with vigorous exercise -
Heat-dissipating mechanisms are able to maintain normal core body temperature.
Heat exhaustion is probably the most common heat syndrome.
- Its onset is sudden, with prostration and collapse
o It results from a failure of the cardiovascular system to compensate for hypovolemia
, secondary to water depletion.
- After a period of collapse, which is usually brief, equilibrium is spontaneously re-established.
Heat stroke is associated with high ambient temperatures and high humidity.
- Thermoregulatory mechanisms fail, sweating ceases, and core body temperature rises
. - Body temperatures of 112 to 113 F have been recorded in some terminal cases.
- Clinically, a rectal temperature of 106F or higher is considered a grave prognostic sign, and
the mortality rate for such patients exceeds 50%.
- The underlying mechanism is marked generalized peripheral vasodilation with peripheral pooling
of blood and a decreased effective circulating blood volume.
- Necrosis of the muscles and myocardium may occur.
- Arrhythmias , disseminated intravascular coagulation , and other systemic effects are common.
- Elderly persons, individuals undergoing intense physical stress (including young athletes and
military recruits), and persons with cardiovascular disease are prime candidates for heat stroke.
HYPOTHERMIA
Prolonged exposure to low ambient temperature leads to hypothermia, a condition seen all too frequently
in homeless persons.
- Lowering of body temperature is hastened by high humidity in cold, wet clothing and dilation
of superficial blood vessels are a result of the ingestion of alcohol.
- At about 90 F, loss of consciousness occur, followed by bradycardia and atrial fibrillation at
lower core temperatures.
Local Reactions. Chilling or freezing of cells and tissues causes injury in two ways.
- Direct effects are probably mediated by physical dislocations within cells and high salt
concentrations incident to the crystallization of the intracellular and extracellular water
.
- Indirect effects are exerted by circulatory changes.
o Depending on the rate at which the temperature drops and the duration of the drop,
slowly developing chilling may induce vasoconstriction and increased permeability,
leading to edematous changes.
- Alternatively , with sudden sharp drops in temperature that are persistent , the vasoconstriction and
increased viscosity of the blood in local area may cause ischemic injury and degenerative
changes in peripheral nerves.
- In this situation, only after the temperature begin to return toward normal do the vascular injury
and increased permeability with exudation become evident.
- However, during the period of ischemia, hypoxic changes and infarction of the affected tissue
may develop (e.g., gangrene of toes or feed).
INJURIES RELATED TO CHANGES IN ATMOSPHERIC PRESSURE
Depending on the direction of change (decrease or increase) in atmospheric pressure, its rate
of development, and the magnitude of change, four syndromes can be produced:
- High altitude
illness - Blast injury
- Air or gas embolism
- Decompression disease – also known as caisson disease – which is sometimes referred to
as barotrauma
, lOMoARcPSD|27929433
High-Altitude Illness.
- Encountered in mountain climbers in the rarefied atmosphere encountered at altitudes above 4000
m.
- The lowered oxygen tension produces progressive mental obtundation and may be accompanied by
poorly understood increased capillary permeability with systemic and, in particular, pulmonary
edema.
Blast Injury.
- Implies increase in pressure either in the atmosphere (air blast) or in water (immersion blast).
- With air blast, the compression wave impinges on the side toward the explosion and so may
collapse the thorax or violently compress the abdomen, with rupture of internal organs.
- The pressure wave may enter the airways and damage the alveoli.
- The following wave of decreased pressure, with its sudden expansion of the abdomen and thorax,
may rupture the intestines or lungs.
- In immersion blast, the pressure is supplied to the body from all sides, including injuries similar to
those of air blast.
Air or Gas Embolism.
- Complication of scuba diving, mechanical positive-pressure ventilatory support, the hyperbaric
oxygen therapy and only rarely as a manifestation of decompression disease.
- Common to all these settings is an abnormal increase in intra-alveolar air or gas pressure
- Leading to tearing of tissue with entrance of air into interstitium and small blood vessels.
- Pulmonary, mediastinal, and subcutaneous emphysema may result, and in some instances,
o Combination of numerous small air or gas emboli that gain access to the arterial circulation
may lead acutely to stroke-like syndromes or a myocardial ischemic episode.
o Either the neurologic or the myocardial embolism may cause sudden death.
Decompression (Caisson) Disease.
- Encountered in deep-sea divers and underwater workers who spent long periods in caissons or
tunnels, under increased atmospheric pressure.
- The injury, encountered with too rapid decompression, is a function of Henry’ law, which is essence
states that the solubility of a gas in a liquid (e.g., blood) is proportional to the partial pressure of the
gas in the environment.
- As the underwater depth and consequent atmospheric pressure increase, larger and larger amounts
of oxygen and accompanying gases (nitrogen and helium) dissolve in the blood and tissue fluids.
- Once the ascent begins (decompression), the dissolved gases come out of solution and form
minute bubbles in the bloodstream and tissues.
- Joining of these bubbles produces even larger masses capable of becoming significant emboli in
the bloodstream.
- The oxygen bubbles are soluble in blood and tissues and so re-dissolve.
o The nitrogen and helium dissolve only slowly.
- Periarticular bubbles produce the bends. Bubbles formed within the lung or gaseous emboli give
rise to respiratory difficulties, with severe substernal pain referred to as the chokes.
- Various central nervous system manifestations may appear, ranging from headache and visual
disturbances to behavioral disorientation.
- Involvement of the inner ear may produce vertigo and the staggers.
- All these manifestations may appear within hours of the too rapid ascent, but skeletal manifestations
– caisson disease of bone – may sometimes appear days later.
- This takes the form of foci of aseptic necrosis, typically of femoral and humeral heads, and
medullary foci, particularly in the lower femur and upper tibia, attributed to embolic occlusion of the
vascular supply.
ELECTRICAL INJURIES
- Passage of electric current may be without effect or cause sudden death by disruption of neural
regulatory impulses, producing:
o cardiac arrest
o thermal injury to organs interposed in the pathway of the current.
.
