FISIOLOGI

LUK A
BAK AR
F E P / C E A / P R M / N I O / Z A M / N YO / D E S / C E N
2019
BURN INJURY

Thermal injury results in massive

fluid shifts from the circulating
plasma into the interstitial space of
both burned tissue and (in burns
>20–30% TBSA) unburned tissue,
causing hypovolemia and edema.
 (A) the zone of
coagulation

LOCAL RESPONSE
(B) the zone of stasis
(C) the zone of
hyperemia
LOCAL
RESPONSE
Zone of Coagulation
Necrotic area with cellular
disruption
Irreversible tissue damage

Zone of Stasis
Moderate insult with decreased
tissue perfusion
Can survive or go on to
coagulative necrosis depending
on wound environment

Zone of Hyperemia
Viable tissue, not at risk for
further necrosis
SYSTEMIC
RESPONSE
Inflammatory mediators has
systemic response in > 30
% TBSA burn which alter
the organ function
 Cardiovascular system
 Respiratory system
 Metabolic system
 Immune system
 EBB
Occurs usually in the first 24 hours
It’s initial period of hypofunction manifests as:
• Hypotension
PHASE • Low cardiac output
• Metabolic acidosis
(1ST 24 HOURS • Hypoventilation
AFTER INJURY) • Hyperglycemia
• Low oxygen consumption
• Inability to thermoregulate
Responds to fluid resuscitation
 Characterized by gradual
increases in:
FLOW • Cardiac output
PHASE • Heart rate
• Oxygen consumption
HYPERMETABOLIC
PHASE • Supranormal increases of
temperature
 Hypermetabolic hyperdynamic response peaks in
10-14 days after the injury after which condition
HYPERMETABOLIC slowly recedes to normal as the burn wounds heal
PHASE naturally or surgically closed by applying skin
grafting
INTRAVASCULAR FLUID LEAKING INTO INCREASED SYSTEMIC VASCULAR
THE INTERSTITIAL SPACE RESISTANCE

PLASMA LEAKAGE
CARDIAC VASCULAR
BURN
SHOCK
DEPRESSION RESISTANCE

HUMORAL FACTORS AND

LOSS OF PRELOAD
Injured tissue Increases permeability of entire vascular tree
with loss of water, electrolytes and proteins from the
vascular compartment , severe hemoconcentration occurs

Protein leakage causing hypoproteinemia, increase osmotic

pressure in the interstitial space

Decreased cell membrane potential cause inward shift of

Na+ and H2O cellular swelling EDEMA
In the injured skin, effect maximal 30 min after the burn but
capillary integrity not restored until 8-12 hours after, usually
resolved by 3-5 days

In non-injured tissues, only mild and transient leaks even for

burns >40% BSA
CARDIOVASCULAR
RESPONSE Decreased preload induced by fluid shifts

• Cardiac output normal within 12-18 hours,

with successful resuscitation
• After 24 hours, it may increase up to 2 ½
times the normal and remain elevated until Cardiac Output ↓

several months after the burn is closed

• Increased systemic vascular resistance & organ
Ischemia ( Renal & GI system) Increased systemic vascular resistance
• Hypovolemia
• Systemic catecholamine release
RENAL SYSTEM
RESPONSE
•Decreased cardiac output,
• decreased blood flow

•Stress induced hormones &

mediators (angiotensin,
aldosterone, vasopressin)

•Decreased renal blood flow &

GFR

Oliguria & renal failure

 GI SYSTEM
RESPONSE Occurs within 12
hours of injury

Hipovolemia
Splanchnic perfusion ↓
Mucosal atrophy
Decreased absorption & increased
intestinal permeability
Curling’s ulcer (stress ulcer).
Increased bacterial translocation and
Septicemia
Acute gastric dilatation
which occurs in 2-4 days
 METABOLIC RESPONSE
INFLAMMATORY MEDIATORS HAS SYSTEMIC RESPONSE IN > 30 % TBSA
BURN

1. Histamine 8. CRF (corticotropin

2. PGS releasing factor)
3. Thromboxane 9. Platelet aggregation
factor
4. Kinins
10. Angiotensin 2
5. Serotonin
11. Vasopressin
6. Catecholamines
7. Oxygen free radicals