Professional Documents
Culture Documents
CASE 2
THERMAL BURNS
THERMAL BURNS
Injuries to the skin resulting from
contact with heat, electrical current,
radiation, or chemical agents
Less than 44oC well tolerated
Above 60oC denaturation of
protein
EPIDEMIOLOGY
American Burn Association
500.000 burn injuries, 40.000 admissions
4.000 deaths
Caused by : Fire (46%), scalds (32%), hot
objects (8%), electricity (4%), chemical agents
(3%)
38% >10% TBSA, 10% >30% TBSA
Age 19-44
Location : UE (41%), LE (26%), Head & Neck
(17%)
<5% full thickness
PATHOPHYSIOLOGY
Three concentric zone
Zone of irreversible coagulative necrosis
Zone of ischemia
Zone of hyperemia
PATHOPHYSIOLOGY
Clotting inflammatory cells
recruitment (B2-integrins, CD11b, CD18) cells
marginate to vessel walls (ICAM-1)
release of mediators and cytokines
(cytotoxic reactive oxygen and nitrogen species) lipid
peroxidation accumulation of
leukocytes, RBC, platelet
microthrombi reduce local
perfusion
PATHOPHYSIOLOGY
Inhalation injury
Caused by steam, aldehydes, oxides of sulfur
and nitrogen, PVC, Hydrochloric Acid, CO
Airway edema & de-epithelization of injured
mucosa necrotic lining
pseudomembranous cast airway obstruction
Edema & congestion of pulmonary
parenchyma bronchospasm, inflammation,
destruction decreased lung compliance
microatelectasis progressive hypoxemia
ARDS
CLASSIFICATION
CLASSIFICATION
Percentage of TBSA involved
Rules of nine : 18% front trunk, 18%
back trunk, 18% each LE, 9% each UE,
9% head & neck, 1% perineal
CLASSIFICATION
LUND-BROWDER CHART
1st degree
Fitzpatricks Dermatology in General Medicine 7th Ed
3RD
DEGREE
BURN
INJURY
MANAGEMENT
Prior to ED arrival
Stop burning process, extinguish flame,
chemical injury tap water wash
Protect from additional injury
Adequacy of airway and ventilation intubation
CO poisoning 100% oxygen
Extensive burns IV fluid LR, Parkland Formula
Morphine sulfate 2-4mg IV bolus
Cover burns with clean dressing
Prevent hypotermia
INPATIENT / OUTPATIENT
MANAGEMENT
At Emergency Department (ABC!!)
Airway
Check for upper airway edema fiberoptic
laryngoscopy
Endotracheal intubation or crycothyrotomi if
needed
Escharotomies if needed
Maintain PO2 >92%
Urethral catheter monitor urine output
and eval for rhabdomiolysis and
myoglobinuria
NGT prevent gastric distention
MANAGEMENT
Inhalation Injury
MANAGEMENT
Circulation and Fluid Resuscitation
RESUSCITATION FORMULAS
MANAGEMENT
Local Wound Care
Cleansing with soap + water, removal of
debris and necrotic tissue, TT booster
Cooling : tap water 10o-25o C up to
30mins after injury, avoid hypothermia,
ice/ice water contraindicated
Burn Blisters : Fluid confined by necrotic
skin heal faster less infection, 2nd
degree debridement + intact less
scaring, heal faster
MANAGEMENT
Burn dressing
Open method : antimicrobial topical until
skin is re-epithelialized. Used on exudative
burn. Mostly used silver sulfadiazine and
mafenide acetate. Daily removed
Closed method : moist wound healing
environment heal faster. Mostly used :
Nanocrystalline silver.
At home : washing, apply topicals. Occlusive
should not be opened unless saturated or
malodorous go to ER. If swelling of fever
go to ER
BURN DRESSINGS
MANAGEMENT
Escharotomy
Releasing constriction of burn eschar
with scalpel
Eschar constriction interrupts
arterial outflow pain, loss of
sensation, delayed capilarry refill.
Indication: Doppler Signal & Pulse
oximetry <90%
Avoid to cut underlying vessels and
nerves
MANAGEMENT
Pain Types and Management
3 phases of burn recovery
Emergency / Resuscitative Phase
Healing Phase
Rehabilitative Phase
MANAGEMENT
Non pharmacologic
Cooling, tap water 10o-25oC
Moist occlusive dressing
Pharmacologic
COMPLICATION
COMPLICATION
Streptococcal Cellulitis
HYPERTROPHIC SCAR
BEFORE SURGERY
AFTER SURGERY
BURN PREVENTION
SEPSIS SYNDROMES
DEFINITIONS
Activated Inflammatory cascade
cause the bodyd defenses and
regulatory system become
overwhelmed leading to disruption of
hemeostasis
Systemic Inflammatory Response
Syndrome (SIRS) 2 or more :
tachycardia, tachypnea,
hyperthermia or hypothermia, high
or low WBC count, bandemia.
DEFINITIONS
EPIDEMIOLOGY
In United States :
10th most common
cause of death
571.000 cases of
severe sepsis
Mortality rate 2050%
Incidence
PATHOPHYSIOLOGY
Infection host response
neutrophil and macrophage
mobilization to injury site release
cytokines inflammatory cascade
synthesis is not well regulated
sepsis
Ongoing toxin persistent
inflammatory response mediator
activation cellular hypoxia, tissue
injury, shock, Multi-Organ Failure,
PATHOPHYSIOLOGY
Mediators of Sepsis
Proinflammatory : IL-1, IL8, TNF
Anti-inflammatory IL-10, IL-6 TGF B,
IL-1ra
Growth promoting
PATHOPHYSIOLOGY
Vasopressin release in stress
condition, cause vasoconstriction,
osmoregulation, maintenance of
normovolemia
NO Regulating vascular tone,
platelet adhesion, insulin secretion,
neurotransmission, tissue injurt,
inflammation and cytotoxicity
ORGAN SYSTEM
DYSFUNCTION
Neurologic
Altered mental status and lethargy septic
encephalopathy
Cardiovascular
Myocardial depression : killed organism /
bacteria
Distributive shock : toxic mediators
Early sepsis : Cardiac output , vascular
resistance
Reversible cardiac function usually in 10 days
ORGAN SYSTEM
DYSFUNCTION
Pulmonary
Right-to-left shunting, arterial
hypoxemia, intractable hypoxemia
Sepsis : High catabolic state + airway
resistance ARDS
Gastrointestinal
Ileus hypoperfusion. splanchnic blood
flow.
Aminotransferase + bilirubin
hepatic failure (rare)
ORGAN SYSTEM
DYSFUNCTION
Endocrine
Adrenal insufficiency
IL-1 & IL-6 activate hypothalamicpituitary axis
TNF-A & corticostatin, depressed bloow
flow, depress pituitary function and
secretion
Hematologic
MEDS
SCORE
SOURCE OF INFECTIONS
Respiratory (most common) : cough, fever,
chills, throat and ear pain, pneumonia, etc
GI (2nd most common) : abdominal pain,
Murphy sign, McBurney Sign, etc
Neurologic : meningitis
Genitourinary :Flank pain,dysuria,polyuria,
etc
Musculoskeletal
IV drug abuse, artificial heart valve,
endocarditis
DIAGNOSTIC FEATURES
Hematology
Leukocytosis
Febrile neutropenic admission, isolation,
empirical IV antimicrobial
Bandemiarelease of immature cell from
marrow
Ht >30%, Hb >10g/dL
Acute phase platelet
Low platelet shock
Thrombocytopenia, pTT & aPTT , fibrinogen
, DIC & severe sepsis syndrome
DIAGNOSTIC FEATURES
Chemistry
bicarbonate acidosis & inadequate
perfusion
serum creatinine ARF
Lactate inadequate perfusion, shock
Arterial blood gas detect acid base
disturbance
Metabolic acidosis inadequate perfusion
Bilirubin source from gallbladder
Amilase & Lipase pancreatitis
DIAGNOSTIC FEATURES
Microbiology
Culture from blood, sputum, urine, CSF, tissue
Obtained before/soon after AB administration
Start with empirical therapy
Radiology
Chest pneumonia, ARDS
Bowel perforation free air aunder
diaphragm
Pneumomediastinum esophageal
perforation, mediastinitis
DIAGNOSTIC FEATURES
Ct-Scan diverticulitis, appendicitis,
necrotizing pancreatitis,
microperforation, intra-abdominal
abscess
Head CT septic emboli
Abdominal USG Cholycystitis
Pelvic USG endometritis
Transesophageal USG --> endocaditis
MRI soft tissue
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
Principles
AB therapy
Maintenance of adequate tissue
perfusion
MANAGEMENT
Respiratory Support
Airway protection, intubation,
mechanical ventilatory support if
needed
Cardiovascular support
MANAGEMENT
Drugs : Vasopresin, Norepinephrine,
Dopamine, Phenylephrine, Epinephrine.
Inotropic agents : Dobutamine,
Bicarbonate, AB
Novel Therapies
Activated Protein C
Steroid Therapy
MANAGEMENT
REFERENCES
Marx JA, Hockberger RS, Walls RM,
Adams JG, editors. Rosens
Emergency Medicine Concepts and
Clinical Practice. 7th Ed. Philadelpia :
Mosby Elsevier, 2010
Wolff K, Goldsmith LA, Katz SI,
Gilchrest BA, editors. Fitzpatricks
Dermatology in General Medicine.
7th Ed. New York : McGraw-Hill, 2008