Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Burns and Plastic Surgery PPT 1 Burn Pathophysiology Lecture Notes
Describe the Pathophysiology of
Burns
Burns & Plastic Surgery
Introduction
? 66% of burn injuries occur at home
? Fatalities at extremes of age
? Flame and Scald most common cause
? Scald burn victims commonly< 5years
? Survival rate for all burns 94.6%
Burn Classification
Causes
? Flame
? Scald
? Contact
? Chemical
? Electricity
Classification ..
Depth of Burn
1st Degree
? Burns involving only the epidermis.
? Erythematous and very painful but do not
form blisters.
? Sunburns fit this category of superficial,
epidermal injury.
? Within 3?4 days, the dead epidermis sloughs
and is replaced by regenerating keratinocytes.
2nd degree (Superficial dermal burns)
? Extend into the papil ary dermis and characteristical y
form blisters.
? Appearance is pink, wet and hypersensitive to touch.
? Painful as uncovering the wound al ows currents of air
to pass over it.
? These wounds blanch with pressure as the blood flow
to the dermis is increased due to vasodilation.
? Superficial dermal burns usual y heal within 2?3 weeks
without risk of scarring and therefore do not require
operation.
3rd degree (Deep Dermal Burns)
? Extend into the reticular dermis and general y wil take
3 or more weeks to heal.
? They also blister, but the wound surface appears
mottled pink and white
? The patient complains of discomfort and pressure
rather than pain.
? When pressure is applied to the burn, capil aries refil
slowly
? Partial-thickness burns that are predicted not to heal
by 3 weeks should be excised and grafted.
4th Degree (Ful Thickness)
? Ful -thickness burns involve the entire dermis and
extend into subcutaneous tissue.
? Their appearance may be charred, leathery, firm, and
depressed when compared to adjoining normal skin.
? These wounds are insensitive to light touch and
pinprick.
? Non-charred ful -thickness burns can be deceptive as
they may have a mottled appearance
? Must be excised and grafted early
Local Changes in Burn Injury- Jacksons
Zones
Zone of Stasis
? Can survive or go on to coagulative necrosis. The
zone of stasis is
? associated with vascular damage and vessel
leakage.
? Thromboxane A2, and Bradykinin a potent
vasoconstrictor, is present in high
? Local endothelial interactions with neutrophils
mediate some of the local inflammatory
responses associated with the zone of stasis.
? studies demonstrate that blockage of
leukocyte adherence with anti-CD18 or anti-
intercellular adhesion molecules &
monoclonal antibodies improve tissue
perfusion and tissue survival in animal models.
Zone of Hyperemia
? Contains viable tissue
? No risk of necrosis
? Characterized by vasodilation due to effect
from zone of stasis
Systemic Changes in Severe
burns(>40%)
Hypermetabolic Response
Phase 1 of Post Burn Metabolic
phenomenon(Ebb Phase)
? Lasts 48 hours
? Decrease in Cardiac Output/O2 Consumption
? Causes hyperglycemia
Phase 2 ( Flow phase)
? Begins after 48 hours
? Increase in metabolic rate and cardiac output
? Hyperglycemia in spite of raised insulin
? Reaches a plateau in about 5-7 days
? Persists upto 1-3 years
? 10-50 fold increase in corticosteroid and
catacholamine levels
? Results in Protein breakdown in muscles
? Amino Acids ( Alanine ) from protein breakdown
recruited for gluconeogenesis
? Fat breakdown in liver leads to glycerol formation
which is used for gluconeogenesis
? End product of anaerobic respiration in the burn
wound (lactate) sent for gluconeogenesis
? Glucose is delivered to peripheral tissue but
glucose oxidation does not occur
? This in turn raises insulin levels
? Overal effect is loss of lean body mass
10% loss- decreased immune function
20% loss- chronic infections
30% loss- pneumonia & pressure ulcers
40% loss- Can lead to death
? Severe burns cause upto 25% loss
? Increased cotisol also causes transport of
calcium and magnesium from long bones
? Decreased bone mineral density and content
leading to susceptibility to fractures
Immune Dysfunction
? Depressed function of Macrophages,
Neutrophils, T cells and B cells
? Even though G-CSF levels actually increase
after severe burn but bone marrow G-CSF
receptor expression is decreased, which may
in part account for the immunodeficiency seen
in burns
? Release of negative regulators of myeloid
growth decrease Macrophage production
? Neutrophil counts increase after severe burn
but they are dysfunctional
? Altered diapedesis, chemotaxis and
phagocytosis due to loss of CD11b/CD18
? Decreased Respiratory burst due to deficiency
of p47-phox activity
? Poor motility sue to impaired actin mechanics
? Counts begin to fall after 72 hours
? Depressed T helper function
? Polarization from Th1 to Th2 immune response
? IL2 and IFN- responsible for initiation of
phagocytosis and intracellular killing is
decreased
? Increase in IL4 and IL 10 which is mostly
antibody based immunity
? Cytotoxic T lymphocyte activity also decreased
? Administration of IL 10 antibodies and growth
factors decreases the effect of the polarization
of immune response
Inflamation and Odema-Landis Starling
Equation
Mediators involved in edema
formation
? Mast cells in the burned skin release histamine
in large quantities immediately after injury,
which elicits a characteristic response in
venules by increasing intercellular junction
space formation causing increased
permeability
? Serotonin released from aggregated platlets
causes pulmonary vasoconstriction
? Mediators causing Increased permeability
Prostaglandin E2 and I2
Free Oxygen Radicles
Thromboxane A2 & B2
? Leukotrines B4 and D4 cause pulmonary
hypertension
? Angiotensin & Vasopressin responsible for
systemic vasoconstriction and gut ischemia
? In the first 12 hours there is an abrupt
increase in the fluid levels in the burn tissue
? After 24 hour there is a more gradual increase
in fluid content both in burned and non
burned soft tissue
? This gradual 3rd space loss is eventually
responsible for burn shock
? Prompt and adequate fluid resuscitation
improves outcome of the burn patient
? It is imperative to avoid Over ?resuscitation
as well
? This trend of providing fluid in excess of the
Parkland formula has been termed `fluid
creep'
? Complications of fluid creep are
Eye injuries due to elevated orbital pressures
Pulmonary edema
Prolonged mechanical ventilation
Graft failure
Need for fasciotomy of uninjured extremities
Abdominal Compartment Syndrome
? Intra-abdominal pressure (IAP) >30 cmH2O is
defined as intra-abdominal hypertension (IAH).
? ACS is sustained IAH + clinically tense
abdomen combined + ventilation aberrations
due to elevated pulmonary inspiratory
pressures
OR
oliguria despite aggressive fluid resuscitation
Myocardial Dysfunction
? Myocardial contractility is depressed along
with relaxation capacity leading to a stiff
myocardium
? Possible causes for this are
Raised Intracellular calcium levels
Circulating Myocardial depressant factor( not
isolated)
Raised TNF alpha levels
? Even though contractility is depressed , the
cardiac Output may be increased upto 130-
150% for a period of 2 years
? Adrenergic stimulation causes increased heart
rate as well as raised Systemic and Pulmonary
vascular resistance
? Mortality occurs because of cardiac stress in a
setting of myocardial dysfunction
GI System
? Apoptosis of epithelium of Small intestine
mucosa
? Vesiculation of microvilli with breakdown of
actin filaments in the microvilli of small
intestine
? Loss of brush border lipase activity ? loss of
fatty acids
? Poor uptake of Glucose and amino acids from
the lumen
? Increased gut permeability leading to fluid loss
? Vasoconstriction leading to ischemia which
causes bacterial and endotoxin translocation
across the mucosa causing septicemia
? Inverse relation between blood flow and gut
permeability
Lungs
? In large burns there is a pronounced increase
in pulmonary vascular resistance (PVR)
? Both pre and post capilary vasoconstriction
occurs which causes pulmonary odema
? Hypo-protenemia still remains the dominant
cause of pulmonary odema
? In case of inhalational injury factors released
due to injury to bronchial tree and lung
parenchyma occurs
Renal Dysfunction
? Local and Systemic cytokine release causes
decreased renal blood flow which causes Acute
Kidney Injury
? Free Oxygen Radicles can cause direct tubular
damage
? Other factor maybe myoglobinurea fol owing
rhabdomyolysis ( Myoglobin> 1500-3000ng/ml)
? AKI may occur despite adequate fluid
resuscitation by Parkland Formula
? Imperative to identify and diagnose Acute
Kidney Injury so that patient can be shifteds
for renal replacement therapy( Dialysis)
? RIFLE and AKIN criteria developed to aid
diagnosis and plan therapy
? AKIN is modification of RIFLE with only change
that it should be applied within 48 hours of
burn injury
? Even though creatinine is not the ideal
biochemical marker of kidney dysfunction it
still remains the gold standard
? New markers of AKI, such as cystatin-C, have
shown promise as earlier detectors of changes
in GFR
? In order to differentiate pre renal from renal
failure it is important to analyze the following
indices
? Fractional excretion of urea is a more reliable
indicator as it negates the effect of diuretic
use
Change in Membrane Potentials
? Membrane potential in non burned distant
tissues such as skeletal muscles , nerves, Gi
tissues partial y depolarize ( from -90 to -70)
? Cel death can occur at resting potentials of -60
? This change causes action potential dampening
which may be responsible for tissue dysfunction
? This change is brought about increased sodium
conductance
? The factor which leads to this has not yet been
identified but it has a complex and probably
dynamic structure
This post was last modified on 07 April 2022