PATHOPHYSIOLOGY OF CHEMICAL BURN

Risk Factors:
Fire/Combustion Firefighter, Risk Factors: (patient-
Industrial Worker, Occupant of burning based)
structures, Chemical Exposure, Life threatening event
Industrial Worker Incidental pouring of strong
Electrical Exposure Electrician, acid or base
Electrical Power Distribution Worker
Accidents Chemical spilling (strong
Explosion acid) Rule of Nines:
2nd degree burn injury in Head = 9% (front and back)
Impaired
Impaired skin
skin integrity
integrity r/t
r/t the right side of the Chest(front) = 9%
skin
skin and
and tissue
tissue damage
damage head, face and neck, Body in contact with the strong Chest back (right side only) =
secondary
secondary toto major
major left upper extremity and acid 4.5%
chemical
chemical burn
burn 2
nd
2nd degree
degree chest, right ear, with
noted redness over and Major burn >25% body surface area in Arm (left upper extremity front
surrounding the area,
adults and back) = 9%
presence of blisters on Total = 31.5% 2nd degree
the area

Hematology
Disturbed
Disturbed body
body image
image result as of :
r/t
Skin and tissue trauma/disruption Increase capillary
r/t disrupted
disrupted skin
skin and
and WBC=19.86(incr
tissue
tissue membrane
membrane eased), permeability
Risk
Risk for
for
Neutrophils=
0.84(increased) deficient
deficient fluid
fluid
volume
volume r/tr/t
Sodium, water capillary
capillary
SURGICAL Nociceptor Disruption of damage
Open wound and protein shift damage
TREATMENT: s of the cell (resolved)
from IVS to ITS (resolved)
Emergency dermis membrane
Debridement
Site/location:
During admission
Left
at side
the ER:of the
Inflammator head,
>Pain face
ratedandas 10/10, Decrease
Stimulation Increase Hyponatremi
y process neck, left
10 as upper
the highest and circulating
of the concentratio a
extremity
most and painful, blood
thermosen radiating
chest, earthe head n of blood
left on volume up to
sitive pain part, left upper cells
receptors extremity, chest and 50%
Migration back,
Risk for pain
Risk for infection
infection
of
Neutrophils characterized
r/t
r/t loss
loss of
of as Increase Hypovolemia
Sultamicillin 750mg TID neutrophils burning
protective
protective and pinching
releases blood
Clindamycin 300mg BID dermal
pain, barrier
dermal aggravated by
barrier
lipases secondary viscosity
secondary
touch andtoto
movement
including destruction
destruction of
of
Pain >Grimacing and
phospholipase skin
skin and
and tissue
crying tissue
impulse A2(produces >Unable to move
AA from affected or burned
membrane area
 PATHOPHYSIOLOGY OF CHEMICAL BURN

Increase Massive Decrea

myocardial stress, SNS se in
Primary
depressant activation BP
afferent
factor
neuron in
the
peripheral
nerve Adrenal
Cyclooxygena corticoid
se converts hormone
AA to and
Second Prostaglandin catecholami
order ne release
neuron in
the dorsal Release of
horn of the other
spinal cord biochemical
pain Peripheral Tachycardia
mediators vasoconstriction
Pain is
modified PAIN
During
by
assessment(latest) Peripheral
modulation >Pain rated as 8/10,
factors resistance
10 as the highest and
most painful, radiating
Spinothalamic on the head part, left
tract upper extremity, chest Increased
and back, pain
afterload
characterized as
Brain stem burning and pinching
pain, aggravated by
touch and movement
>Grimacing Decreased cardiac
thalamus >presence of output (RESOLVED)
numbness, tingling
and burning pain on
the area
Acute pain r/t
>with complaints of
destruction of
itchiness on the right
Inhibitory
Releaseneurons
Inhibits of WDR neuron skin and tissues
areendogenous
incoming/ as
shortlived Somatic activation = spinal secondary to
they
ascending arepain PAIN sensory
opioids,
Descending ON THE
PAIN cord wind up =
Amplification major chemical
reabsorbed cortex
systeminto
serotonin,
impulse SITE
PERCEPTION NMDA
ofPain
painactivation
persists
signals burn in jury 2nd
nd
the nerves
norepinephrine
 PATHOPHYSIOLOGY OF CHEMICAL BURN

Celecoxib 200mg BID

Tramadol 50mg BID

NMDA
receptors
calcium
channel opens

Pain reaches
the CNS