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405090155Emergency medicine Block
problem2
CLASSIFICATION
Definisi
• The burn is a form of tissue damage or loss caused by contact with a heat source such as fire, water, heat, chemicals, electricity and radiation.
Phase to Burn
1. The initial phase, the acute phase, the phase of shock • The main problem revolves around the disruption of the
respiratory tract (eg, inhalation injury) and circulatory disorders (fluid-electrolyte balance, hypovolemic shock) systemic
2. Phase after the shock ends, sub-acute phase • The main problem: Systemic Inflammatory Response
Syndrome (SIRS), Multi-system Organ Dysfunction Syndrome (MODS) and sepsis.
3. Further Phase • Since the closure of the wound - tissue maturation • Problem: The complications of burns: hypertrophic
scars, contractures and other deformities that occur because of the fragility of certain tissues or structures caused by the inflammatory process a great and long lasting.
Classification of Burn Injuries
– Based on the causes • Fire burns • Burns caused by hot water • Burns caused by chemicals (which is a strong acid or
base) • Electrical burns and lightning • Burns due to radiation • Injuries due to very low temperatures (frost bite)
– Based on the depth of tissue damage
Degrees of Burn Injuries
– Degree burns I • Damage limited to the superficial epidermis • Skin dried, giving efloresensi erythema hiperemik • Not found bullae • Pain due to nerve endings of sensory irritation • Healing occurs spontaneously within 5-10 days • For example: the sun burns
• Second degree burns Damage includes epidermis and dermis in part, in the form of an acute inflammatory reaction accompanied by the exudation – Bullae found – Basic red or pale sores are located higher on the
surface of normal skin – Pain due to nerve endings of sensory irritation – Divided into two:
• Divided into two: – Grade II shallow (superficial)
• Damage to the superficial part of the dermis • Apendises skin such as hair follicles, sweat glands,
sebaceous glands are still intact. • Healing occurs spontaneously within 10-14 days.
– Degree II in (deep) • Damage on almost all parts of the dermis • Apendises skin such as hair follicles, sweat glands,
sebaceous glands partially intact • Healing takes longer, depending apendises remaining
skin. • Usually healing occurs in more than 1 month.
• Third degree burns Damage includes the entire thickness of the dermis and deeper layers. – Apendises skin such as hair follicles, sweat glands,
sebaceous glands were damaged. – Not found bullae – Burned skin gray and pale. Dry, lying lower than the
surrounding skin due to the coagulation proteins in the epidermis and dermis layers (skar)
– Not found even pain sensation is lost because the ends of the sensory nerve fibers damage / death.
– Healing takes a long time because there is no spontaneous epithelialization process both from the bottom of the wound, the wound edges and skin apendises.
Degrees 1
Degrees 2
Degrees 3
Degree burns 1 / superficial 2 / dermis 3 Shallow In
About Layer of the epidermis
. Upper dermis
The whole Dermis
The entire layer of skin
Sign Skin color Hiperemik (erythematous) Pale / brown Painful y - Bulla - y - Eskar - y Healing 5-7 days 10-14
days > 1month Old
Scarring - y
CLASSIFICATION Light Moderate Weight Degree 2 - Kids <10% 10-20% 20% /> Degrees of 2-Adults <15% 15-25% 25% />
Degree 3 <2% <10% 10% />
Other - other Hands, face, ears, eyes, legs and genitalia / perineum
Inhalation injury, electrical, other trauma
DISTINCTION DEGREES INTO LB Degree 1 (1 0) Degree 2 (2 0) /
Partial Thickness Burn
Degree 2 (2 0) / Superficial Partial Thickness Bunr)
Degree 3 (3 0) / Deep Partial
Thickness Burn
LOCATION Epidermis The epidermis-third dermis
Almost the entire dermis
The epidermis-dermis-layer that>
the (bone & muscle
Dermal-epidermal JUNCTION
Intact Broken Broken Broken
COLOR or APPEARANCE
Red Sometimes pale-red edematous and exudative;
blisters
• Pink - white • Yellowish
white (thin eskar)
Pale or> OK eskar white,
black, or brown
PAIN (+) (+) (+) (-) TEXTURE Normal Edema (bullae) Thick Leathery
APENDISES SKIN (hair follicles, sweat kel, kel sebaceous)
Intact Intact Some intact Broken
DURATION & EFFECTS recovered
5-7 days without
scarring jar
10-14 days + / - jar of scar
25-60 days + jar thick scar
#
Damage Zone Distribution
– Coagulation zone, the zone of necrosis • Areas of direct damage (protein coagulation) due to the
influence of thermal injury, almost certainly the network is undergoing necrosis some time after contact,
– Static Zone • The area immediately outside / around the zone of coagulation • Vascular endothelial damage occurs with damage to platelets
and leukocytes impaired perfusion (no flow phenomenon) followed by changes in capillary permeability and local inflammatory response
• This process lasts for 12-24 hours post-injury tissue necrosis
– Zone of hyperemia • The area outside the static zone, share the form of
vasodilatation without much reaction involving cellular reactions.
• Depending on the general condition and treatment given, three zones can experience spontaneous healing, or even turned into a second zone of the first zone.
CRITERIA
• (American Burn Association) • 1. Light Burns.
– - Second degree burns <15% – - Second degree burns <10% in children - child – - Third degree burns <2%
• 2. Moderate burns – - Second degree burns 15-25% in adults – - Burns II 10 - 20 at child - child – - Third degree burns <10%
• Burn weight - Burns Grade II 25% or more on person adult - Burns Grade II 20% or more on child - child. - Third degree burns of 10% or more - Burns about hands, face, ears, eyes, legs and
genitalia / perineum. - Burns with injury inhalation, electricity, along with
other trauma.
Area burns Percentage (in percent)
The whole head (front and back) and neck
9
Chest 9
Stomach 9
Upper limb (left and right) 2 x 9
Back and buttocks 2 x 9
Thigh and calf (left and right)
4 x 9
Perineum and genitalia 1
Total 100
Rules Of Nine
RULE OF NINES
RULE OF NINES
Birth 1 year 5 years
10 years
15 years
Adult
½ head 9 ½% 8 ½% 6 ½% 5 ½% 4 ½% 3 ½%
Half thigh 2 ¾% 3 ¼% 4% 4 ¼% 4 ½% 4 ¾%
Half leg 2 ½% 2 ½% 2 ¾% 3%
Rumus Lund and Browder
PATOPHISIOLOGY
SYSTEMIC CHANGES
Pathophysiology
Inflammation and edema
•Mast cells Inflammatory mediators (histamine, bradykinin, vasoactive amines, PG, leukotriene, catecholamines, which complement activated) Arterial and capillary permeability capillary vasodilation ↑ fluid (and protein) leaves the capillaries into the tissue For edema •Platelet serotonin aggregate issued m ↑ pulmonary vascular resistance (right) & mpburuk effect vasokonstriktif various vasoactive amines (# directly); serotonin blockade >cardiac index, pulmonary artery pressure ↓, ↓ O2 consumption after burns •Thromboxane A2 (potent vasoconstrictor) vasoconstriction and platelet aggregation (wound) expansion zone of stasis •Pd microvascular changes cardiopulmonary changes (lost plasma volume, peripheral vascular resistance ↑ m, cardiac outpur <)
Renal •Blood volume and cardic output< renal blood flow and GFR < •Hormones that induce stress and mediators (angiotensin, aldosterone, vasopressin) decreased <renal blood flow oliguria # th / acute tubular necrosis and renal failure
SYSTEMIC CHANGES Pathophysiology
GIT •Mucosal atrophy: apoptosis, vesikulasi microvilli, actin filament network breakdown OK p <flow of blood in circulation splangnikus •Changes in absorption: uptake of glucose and amino acids <, absorption of fatty acids <, brush border lipase activity <; return N 48-72 hours after damage •Intestinal Permeability>: m ↑ apoptosis; pd polyethylene 3350, lactulose, mannitol mperluas burns; intestinal blood flow <(5 hours after burn) •Liver: hypoxemia g3 metabolism, synthesis, and detoksikasi p> [] SGOT and SGPT, alkaline phosphatase, gamma globulim transferase and bilirubin; shock hipometabolisme; circulation back N p> work hepatic (metabolic disorder failed dysfunction >> liver •Stress ulcer / Curling 's OK severe stress ulcer gastric hyperacidity +
HEART •Hypoxia and hypoxemia ischemic myocardium •Ischemia GIT stimulate the release of inflammatory mediators (cytokines, TNF-α), free radicals, and myocardial depressant fk (MDF) OK neutrophile recruitment> mpburuk cardiac work
SYSTEM muscularis •Hypoxia Pmecahan glycoprotein muscle mass urea cycle activation of NO (vasodilator)> tissue damage (muscular system) or condition spsis
IMMUNE SYSTEM •Production of macrophage <(48-72 hours after burn): Elaboration of spontaneous negative regulator dr ptumbuhan myeolid (+ endotoxin and partially th / with G-CSF or inhibition of PGE2) •Neutrophils <(48-72 hours after burn): def p47-Phox activity after stimulation of inflammatory and mechanical keruksan actin motile neutrophil response that bhub •B lymphocytes and T <: polarization IL-2 and INF bdasarkan TH1 cytokine response of THP respond TH2 (IL4 production & -10) •Destruction of CD8 + activity: risk of infection> (fungi and viruses); early burn excision m> cytotoxic T cell activity HIPOMETABOLISME /
INITIAL PHASE •Hypovolemia, TD <cardiac output <, body temperature <, pgunaan O2 <; time: a few minutes up to 48-72 hours post-trauma
HIPERMETABOLISME / PHASE FLOW (Tachycardia, cardiac output>, elevated energy expenditure, consumption of O2>, proteolysis and lipolysis, and the loss of nitrogen by weight)
•Catecholamines: m> availability of glucose via gluconeogenesis and glycogenolysis hepatic = availability as fat via lipolysis of peripheral •Direct: via adrenergic receptor - α and - β (hepatocytes & liposit) •# Direct: jar adrenergic receptor stimulation via endocrine (pancreatic) m> release of glucose •Glucocorticoids: neural stimulation hypothalamua-pituitary-adrenal axis •Glucagon: m> hepatic glucose production and peripheral lipolysis via direct # catecholamine stimulation (receptor α) •Cortisol: induction of insulin resistance •Catecholamines and cortisol, glucagon + m> glucose release that inflamed cells
Change Depth Hypovolaemic Levels of Diuretics
Mechanism Impact Mechanism Impact
Extracellular fluid shift
Vascular interstitial
Hemoconcentration, edema in burns
Interstitial vascular
Hemodilution
Renal function ↓ renal blood flow to
Oliguria ↑ renal blood flow to
Diuresis
Sodium Na + reabsorbed by the kidneys, but the loss of Na + through suspended in fluid exudates and edema.
Sodium deficit Loss of Na + through diuresis (back to normal after 1 week)
Sodium deficit
Potassium levels K + is released as a result of tissue injury tablespoons, krn ↓ excretion decreased renal function
Hiperkalemi K + moves back into the cells, K + wasted through diuresis (started 4-5 days after burn).
Hypokalemia
Change Depth Hypovolaemic Levels of Diuretics
Mechanism Impact Mechanism Impact
Protein content Loss of protein into the tissues due to higher permeability.
Hipoproteinemia Loss of protein catabolism time continuing
Hipoproteinemia
Nitrogen balance Tissue catabolism, loss of protein in the network, the more loss of input.
Negative nitrogen balance
Tissue catabolism, protein loss, immobility.
Negative nitrogen balance
Acid-base balance
increased anaerobic metabolism of acid end products, ↓ renal function, serum bikarbonas loss
Metabolic acidosis.
Loss of sodium bicarbonate through diuresis, hipermetabolisme, increasing the final product
Metabolic acidosis.
Change Depth Hypovolaemic Levels of Diuretics
Mechanism Impact Mechanism Impact
Stress response Occur due to trauma, increased production cortison
Renal blood flow is reduced
Occurs due to the nature and risk of injury longstanding personal psychology.
Stress due to injury
Erythrocyte rupture occurs due to heat
Anemia Does not occur in the first days
Hemoconcentration
Side Gastric ulcers, bleeding, pain
Stimulation of the hypothalamus and central deficits improve cortison number.
Acute intestinal dilatation and paralise.
Increasing the amount of cortisone
Heart MDF 2X ↑ toxic glycoprotein produced by the burned skin.
Cardiac dysfunction
↑ MDF (myocardial depresant factor) up to 26 units, responsible for septic shock
CO decreased
SURVEI PRIMER
A. AIRWAY• The suspicion when the patient inhalation burns experienced
things SBB: – History trapped within space closed – Burn perioral – Reduction awareness including confusion – There signs of respiratory distress – Presence crowded or disappearance sound – Scald on face – Losing eyebrow eye and fur nose – Soot & sign inflammatory acute in oropharynx
• 2 marks if there is sufficient suspicion over the trauma inhalation
B. BREATHING
• respiratory • lay eskar chest wall • kl escharotomy • There is a history of injury to the chest area • kl no sign - a sign of pneumothorax /
hematotoraks pairs chest tube
• Inhalation Burn Injury Treatment – Move victim to place safe – Perform cleaning road breath dr dirt and blood with:
• a. O2 8-10 liters / minute wear hoods • b. within a half-sitting / upright • c. Nebulizer • d.bronkodilator
– Kl there is obstruction: • a. suction mucus • b. endotracheal tube pairs continue with the provision
of O2 – Appraisal early – Give breath artificial if need – Reconciliation
C. CIRCULATION
• See the signs & symptoms of shock • Cl No shock: fluid resuscitation immediately
give crystalloid fluids (Ringer's lactate) • Kl no shock: resuscitation fluids using a liquid
formula imaginable (Baxter / Parkland)
Resusitasi
Cairan intraseluler Cairan Ekstraseluler
40% 15% 5% Dextrose 5%
RLNaCl 0,9%
KoloidProtein plasmaDarah
• ACTION SURGERY – Eskaratomi: make lengthwise
slices that make up eskar free clamping
– Indications: third degree burns around his extremities / body
– Objective: distal circulation due to shrinkage and clamping of eskar (pain, immune to the end - distal end)
– Debridement dispose of dead tissue with tangential excision
Indications Hospitalization A. Grade II burns: Adults> 15% Children> 10% Face, tngan, feet, perineum B. Grade III burns Adults> 2% Child (any degree III) C. Trauma burns with viscera, bones, and the airway
• Advanced Management – Treat wounds (wound washing using running water and soap)
after ABC overcome. – Nutrition is quite (Closing the calorie and negative nitrogen
balance in catabolic phase) – Topical Antibiotics changed 1 times in 1 day with hydrotherapy remove traces of the previous Ab (very dirty wounds / lot crusting / exudate 2-3 times a day)
– Rehabilitation: breathing exercises and movement of muscles and joints.
– broad spectrum systemic antibiotics to prevent infection (pseudomonas aminoglycosides)
– Supplementation of vitamin 10000 per week of vitamin A, vitamin C 500 mg and 500 mg sulfas ferosus
SURVEI SEKUNDER
• Secondary Survey • management
– Principle: lesion closure as soon as possible, prevention of infection, reduce pain, prevention of mechanical trauma to the skin and a vital element in it, and limiting the formation of scar tissue
– Current events: – Alienate the victim from the source of trauma – Extinguish the fire and a hot flush skin with water – Trauma chemicals flush skin with running water – Coagulation widespread destruction cool the burned area
and maintain the cold temperature at first – Submerge the burned part for the first 15 minutes not
recommended in burns> 10% hypothermic cardiac arrest
• Follow-up: • resuscitation ABC note Check the airway airway obstruction • open the airway with airway clearance (suction, etc.), if
necessary trakeostom I / intubation • Give oxygen Attach IV line • fluid resuscitation, give fluids RL (overcome shock) Attach
catheter pot - pot • diuresis monitoring • Insert gastric tube for gastric emptying was paralytic ileus • Insert central venous pressure monitoring blood circulation
monitoring, extensive burns (> 40%)
• Check injuries that occur in all body determine presence inhalation, broad and degree wound grilled
• Therapy fluid wound grilled degree 2/3 with area> 25%, patients no can drinking, stopped when oral input replace Parenteral
• Analgesic morphine / pethidine (IV), IM with impaired circulation hoarding in muscle
• Perform washing wound after circulation stable betadine / nitras Argenti 0.5%
• Give antibiotics topical post washing wound prevent and overcome infections on wound (ointment) 0.5% silver nitrate, 10% mafenide acetate, silver sulfadiazine 1% / gentamicin sulfate Compress nitrate Argenti drabble every 2 hours effective (Silversulfadiazin) bacteriostatic all germs, power translucent enough, not raise resistance, and safe
• Dressing wound kassa roll dried and sterile • Serum anti-tetanus / toxoid ATS 3000 units (adult) and half
(kids)
RESUSITASI
• Handbook of fluid within the electoral process – Colloids be dangerous when given tersendiriutk
resuscitation procedures trauma cases – The albumin ill intended as a form of plasma
expander kasus2 resuscitate critically ill pd, krn shown to increase mortality.
Kristaloid vs Koloid
– Crystalloid: • Isotonic fluid that is safe and effective for cases of hypovolemia • Cool place correspond dng osmolarity of body fluids and fluid
osmotic ill effects cool place • Likely to leave the intravascular (menigisi kompart intersisiel) • 75% and 25% extravascular fluid intravascular fluid • Principle: pd resuscitation kompart extravascular
– Colloid: • Lar dng high molecular weight • Cool place osmotic effect • semipermeabilitas are likely ttp in intravascular • Principle: pd fluid resuscitation aimed kompart intravascular
NaCL 0.9%
– Satu2 bs isotonic fluid that is supplied with blood
– Cause hypernatremia and hyperchloremic metabolic acidosis
Ringer’s Lactate (RL)
• Because physiological isotonic fluids containing electrolyte composition
• lactic acidosis caused ill bases
• SCE converted to bicarbonate in the liver cpt MJD
• Diarrhea NaCl 0.45% (potassium and bicarbonate) – Dehydration (pe ↓
intravascular) dng or without hyponatremia saline or RL
– ≠ Glucose 5% • Hemorrhagic Displacement
dr interstitial into the intravascular intravascular restorsi untuj gol (pe ↓ HT, 72 post-traumatic) – Pe ↓ i Ntra and extras – Colloid and crystalloid
• SIRS Leakage papillae, pe ↓ effective in intravascular fluid edema + (pe ↑ interstitial) – D avoid crystalloid,
colloid give (Hydroxythyl Starch / HSE)
• Burn Instersisiel fluid loss (24 hours I) – Give k ristaloid
Plasma
– 24 hours post trauma interchangeable body tackle any fluid leaks will remain in the intravascular
– Time-out within 24-36 hours after trauma plasma expander supplied interchangeable
– Objective: intravascular fluid deficit dng draw fluid dr intersisiel space (edema)
% Area Burn
Needs plasma (ml) BB pd 70kg
20-40 0-500
40-60 500-1700
60-80 1000-3000
> 80 1500-3500
• Solution hipertronik – In use: 3-6% sodium chloride
(hypertonic saline) – Objective: To draw fluid into
the intravascular space permeability back soon
– ES: demyelinisasi Pontin (pd drops fast)
• Mannitol – Gol: pd intersisiel draw fluid
resuscitation For use RL – Divided evenly within 24
hours – Mannitol 20% improve
perfusion to the renal tubules
lDopamine •Mixture vasodilator and pe ↑ renal blood flow, and cerebral splangnikus •Dose ↑ effect kronotropik me inotropok and ↑ CO
PROGNOSIS & COMPLICATION
Prognosis• Depending on the level and
extent of burns; factors the location of the fire area, age and state of health of the patient
• The higher the extent of burns higher mortality
• Burns to the perineum, armpits, neck, and hands it difficult to maintain prone to contractures
Komplikasi• DEGREES 1 shock due to
fluid loss, acute renal failure, pulmonary edema
• DEGREES 2 SIRS (systemic inflammatory response syndrome) MODS (multiple organ disfunction syndrome) MOF (multiple Ogan failure), infection (pneumonia) and sepsis
• 3 DEGREES hypertrophic scarring and contractures
Electrical BurnsCellular Damage Due To Electrical Current
High vs. Low Tension Injuries
Alternating Current & Direct Current
• High-voltage direct current (DC) :– single muscle spasm often throwing the victim
from the source a shorter duration of exposure but the likelihood of traumatic blunt injury.
• Alternating current (AC):– 3x > dangerous than DC (same voltage)– continuous muscle contraction, or tetany occurs
when the muscle fibers are stimulated at 40-110x/ second
LUKA BAKAR KARENA SENGATAN LISTRIK
• Aliran listrik bolak-balik (AC) merupakan energi dalam jumlah besar, melalui bagian tubuh yg kontak dengan sumber listrik (luka masuk biasanya gosong) dialirkan melalui bagian tubuh yang memiliki resistensi paling rendah (cairan/darah/pembuluh darah) melalui bagian tubuh yg kontak dengan bumi (luka keluar) dialirkan ke bumi ( ground)
• Loncatan energi yg ditimbulkan di udara berubah menjadi api• Kerusakan jaringan bersifat lambat tapi pasti dan tidak dapat
diperkirakan luasnya krn kerusakan p.d. darah ( trombosis, oklusi kapiler ) di sepanjang bagian tubuh yang dialiri listrik.
• Tahanan listrik besar pada tulang, tendo, kulit, rendah pada darah dan saraf
http://www.uic.edu/labs/lightninginjury/treatment.html
Electrical Burns - Acute Care
A - Airway B - Breathing C - Circulation D - Disability E - Expose The Patient
TataLaksana
TataLaksana
Komplikasi
http://www.uic.edu/labs/lightninginjury/treatment.html
SEPSIS
Sepsis
• sepsis is the presence of SIRS plus infection with specific organs based on positive culture results
• is a systemic response to infection by the SIRS plus infection coupled with proven or clinically suspected infection
based on severity of condition
• Sepsis• Severe sepsis, is an infection with no evidence
of organ failure due to hypoperfusion• Septic shock, is severe sepsis with persistent
hypertension after resuscitation given fluids and causes tissue hypoperfusion
Etiology
• Gram-negative bacteria (often)• gram-positive bacteria• Fungi• virus
Patofisiology• involves the interaction between the pathogen infection,
inflammation and pathways coagulation imbalance between proinflammatory cytokines such as (TNF-α), (IL-1β), IL-6 and (IFNγ) & anti-inflammatory cytokines such as IL-1receptor antagonist (IL-1α), IL-4 and IL-10.Overproduction of inflammatory cytokines as a result of the activation of nuclear factor кB (NF-кB) activation of the systemic response SIRS form primarily in the lungs, liver, kidney, intestines and organs others permeability vascular, cardiac function and induces metabolic changes resulting in apoptosis and tissue necrosis, Multiple Organ Failure (MOF), septic shock and death
Sign & simptom
• temperature> 38.3 C or <35.6 C• heart rate> 90 beats / min• The frequency of breathing> 20 beats / min or
PaCO2 <32mmHg• leukocytes> 12,000 cells / mm ³ or <4000
cells / mm ³ or neutrophils> 10%
Treatment
• antimicrobial administration should begin as soon as the blood and other specimens cultured
• culture examination results have not been obtained empiric therapy (effective against gram-negative and gram-positive bacteria)
Indication Empiric therapynot prone to sepsis due to pseudomonas -3rd or 4th generation cephalosporins (eg,
ceftriaxone, cefotaxime)-beta lactam / Betalaktamase inhibitors (eg, ticarcillin-clavulanate, piperacillin- tazobaktam)-carbapenem (eg, imipenem)
if pseudomonas is a pathogen that may be the cause of sepsis
Vancomycin plus 2 of:-cephalosporin with anti-pseudomonal (eg, ceftazidime, sefoperazone)-carbapenem wirh antipseudomonas (eg, imipinem)-beta lactam / betalaktamase inhibitor (eg, ticarcilin-clavulanate, piperacilin-tazobaktam)-fluoroquinolone with anti-pseudomonal good activity (ciprofloxacin)-Monobactam (eg, aztreonam)
Severely ill patient with manifestations of sepsis with unclear etiology
Vankomisin
• culture results have been obtained regimen can be simplified (because often a single antimicrobial can be adequate for the treatment of known pathogens)
