kelompok 9 pemicu 2

8/12/2019 KELOMPOK 9 PEMICU 2

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ANGGOTA KELOMPOK 9 Tutor : dr.Deni Ketua : Pamella Arteliana (405090164) Sekretaris : Ronald Krisbianto Gani (405090223) Penulis : Fendia Riska (405080125)

Anggota : Malik Djamalludin (405080053)

Yunita Widyaningsih (405080004)Meida Astriani (405080062)

Silvina Isditya (405080088)

Thomas Khosasih (405080111)Selvia Shienyanlin Surya (405090098)Thedi Darma Wijaya (405090120)

Priskila Christy (405090252)Monica Sylviana Mayasari (405090259)


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MIND MAPPING

32yoBurn Injury at UE & LE & Face & Nostril BurntTBSA : 63%, suspect inhalation injury

Second Degree Burn Injury + Sepsis

Severe Burn injury

PE & LabTachycardiaTachypneaFeverLeukocytosis

Bullae with pus

High creatinine

SIRS

Assess for Acute Renal Failure

+

+

+


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LEARNING OBJECTIVES

Thermal Burn Sepsis Syndromes


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THERMAL BURNS


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THERMAL BURNS

Injuries to the skin resulting from contact withheat, electrical current, radiation, or chemicalagents

Less than 44 oC well tolerated Above 60 oC denaturation of protein

Rosens Emergency Medicine 7th Ed


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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%)


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BURN ZONES

Burns consist of three geographic zones Zone of coagulation: center of burn; greatest heat

transfer

Zone of stasis: pronounced inflammation andvascular injury; cell survival tenuous

Zone of hyperemia: tissue injury minimal;

expected recovery


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PATHOPHYSIOLOGY

Clotting inflammatory cells recruitment (B2-integrins, CD11b, CD18) cells marginate to vesselwalls (ICAM-1) release of mediators andcytokines (cytotoxic reactive oxygen and nitrogen species) lipid peroxidation accumulation ofleukocytes, RBC, platelet microthrombi

reduce local perfusion



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PATHOPHYSIOLOGY

Damage to the normal epidermal barrier bacterial invasion & external fluid loss ;damaged tissues often become edematous ,further enhancing volume loss . Heat loss canbe significant because thermoregulation ofthe damaged dermis is absent, particularly in

wounds that are exposed.


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BURN DEPTH CLASSIFICATION

Appearance Surface SensationTime toHealing

1st Degree Pink or Red Dry Painful Days

Superficial 2 nd Degree

Pink, clearblisters

Moist Painful 14-21 days

Deep 2 nd Degree

Pink,hemorrhagicblisters, red

Moist Painful Weeks, or mayprogress to 3 rd degree andrequire graft

3rd Degree White, brown Dry, leathery Insensate Requiresexcision

4 th Degree Brown, charred Dry Insensate Requiresexcision


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TOTAL BODY SURFACE AREA


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TOTAL BODY SURFACE AREA

LUND-BROWDER CHART



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BURN SEVERITY CLASSIFICATION

Mild Moderate Severe

Children 10% TBSA

Adult 20% TBSA

Eldery 10% TBSA

All 5% full thickness,high voltage,significant burn toface, eyes, ears,genitalia, or joints,significantassociated trauma

Disposition Outpatient Admission Burn unit


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DIAGNOSIS

Anamnesis History of trauma / exposure

to the heat source (flame, hotwater, hot oil, chemicals,

electricity, radiation) History trapped in a confined

space

History of exposure to a blast

History of falls from a certainheight after exposure to heatsources

Physical examination

Primary Survey : ABC Secondary Survey

Embed also:

1. The degree and extent of burns2. Causes burns3. As well as the problems that exist

at the time of the first inspection,the example problem:

- inhalation injury- Eschar around chest

- shock


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Schwartz's Principles of Surgery


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MANAGEMENT


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MANAGEMENT PRIOR TO ED ARRIVAL

1st priority : stop the burning process &protect the patient from additional injury

Priorities of care : ABC Burns : Covered with a clean dressing &

Cooling Topical antimicrobial agents shouldnt be used in

the prehospital phase of care


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MANAGEMENT AT ED

Upper airway compromised fiberopticlaryngoscopy + endotracheal intubation

Cricothyrotomy : needle/surgical

Airway Management


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MANAGEMENT AT ED

O2 : to maintain an O 2 saturation > 92%

Severe burns : IV access : 2 large-bore IV catheters Urethral catheter : to monitor urine output

Cardiac, O 2 saturation, BP monitoring

General Measures for Moderate to Severe Burns


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MANAGEMENT AT ED

Based on clinical findings :

facial burns singed nasal vibrissae carbonaceous sputum

history of injury within a closed space Signs : wheezing, crepitations, hypoxemia

Recognizing Inhalation Injury


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MANAGEMENT AT ED

Diagnosis : direct visualization

Fiberoptic laryngoscopy & Bronchoscopy Findings : presence of soot, charring, mucosal

inflammation, edema/necrosis

Diagnosis of injury to parenchyma of the lung: xenon ventilation scanning

Recognizing Inhalation Injury


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MANAGEMENT AT ED

Indications for Endotracheal Intubation and Mechanical Ventilation in Burns Patients

Upper airway obstruction Patient obtundation

Inability to handle secretion Muscle fatigue suggested by a low/high RR Hypoxemia despite 100% O 2 Hypoventilation (a PCO 2 >50mmHg & pH < 7.2

The goals of mechanical ventilation : O 2 saturation > 92%

Management of Inhalation Injury

Recommended Initial Ventilator Settings

Tidal Volume 6-8 mL/kg

Respiratory Rate 8-12 in adults ; 12-45 in children

Plateau Pressures < 35cm H 2O

I/E Ratio (inspiratory/exp) 1:1-1:3

Flow Rates 40-100 L/min

PEEP (positive end exp pressure) 8cm H 2O


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MANAGEMENT AT ED

Management of Inhalation Injury

Alveolar lavage : to remove thick secretions &

improve pulmonary toilette Aerosolized N-acetylcysteine +/- aerosolized

heparin : to break down thick mucous

secretions Bronchodilators : patients with wheezing


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MANAGEMENT AT ED

Circulation and Fluid Resuscitation

Small burns : oral fluids

Large burns : IV fluid resuscitation Parkland :

1st 24 hours : LR 4ml/kg/% burn within 1 st 8hr

Next 24 hours : Colloids in amount of 20-60% ofplasma volume; glucose in water added 0.5-1.0ml/kg/hr (adult) & 1 ml/kg/hr (children)


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MANAGEMENT : LOCAL WOUND CARE

All burns are considered contaminated : Cleansing with soap & water Debris & necrotic tissue should be gently

removed

Care of the burn wound requires : oral/IVanalgesic agents

May need : tetanus toxoid booster withtetanus immune globulin


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Cooling of the Burn

Optimal cooling temperature : 10 o-25 oC

pain, progression of tissue necrosis & limit therequirement for skin grafting

Large burns + ice water (1 o-8oC) more

necrosis Large burns + tap water (12 o-18 oC) least

necrosis & fastest healing


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Burn Dressing

The purposes of a burn dressing :

To protect the wound Reduce pain & evaporative heat loss Absorb wound exudate

1st degree burns : topical anesthetic, aloe vera, topical NSAIDs


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Burn Dressing : 2 nd Degree Burns

Open method :

Topical antimicrobials for contaminated largeburns with large amounts of exudate

Close method :

Occlusive dressing to enhance re-epitalization,angiogenesis & reduce pain for superficial 2 nd degree burns with little exudate


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Burn Dressing : 3 rd Degree Burns

Cover the wound with a petrolatum-type dressing

transferred to a burn centerEscharotomy : Indication Doppler signals in the extremity

Pulse oximetry < 90% +/- Doppler signals peak airway pressure/difficulty + ventilation in a

mechanically ventilated burn


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PAIN MANAGEMENT

Non pharmacologic Cooling, tap water 10 o-25 oC Moist occlusive dressing

Pharmacologic Morphine Sulfate (0,05-0,1mg/kg) titrated Acetaminophen (1g adults, 15mg/kg child) /4-6h Ibuprofen (400-800mg adults, 10mg/kg child) / 6-8h

Fentanyl 0,5-1mg/kg Lidocaine Anxyolytics : benzodiazepin (Lorazepam) Others : gabapentin, stimulants, B-Blockers, antidepressants



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NUTRITION

enteral liquid foods RS / commercial formula with viscosityof 1 calorie / mL.

duration of enteral feeding in the bottle should not be> 4hours.

For adults given 45 mL / h, in children 3 years of 10-20 mL / hour.

Enteral nutrition administered via nasogastric tube (for baby& children & for adults 8F 8-14 F).

Droplet velocity using an infusion pump (cyclic). Monitor patients continuously., Especially GI tolerance.


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Micronutrient composition

Carbohydrates 60-65% of total calories / does notexceed 4-5 mg / kg / min.

Protein severe burns : 23-25% of total calories

with calorie ratio: nitrogen = 80:1 / 2.5 to 4 g protein/ kg.

Post-traumatic fat 5-15% of total calories. Omega 3 is recommended in patients with burns

because the omega 3 will compete & inhibitionformation of PGE1 & PGE2 as. Linoleic.


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Micronutrient supplementation

Micronutrients required as coenzyme and cofactorfor the physiological reactions in the cell,macronutrient and energy metabolism.

Vitamin for protein synthesis, wound healing,

enhance immune function and antioxidant. In patients with burns in a state of severe pain and

hipermetabolisme increased vitamin needs. Recommended supplementation increased 500-1000 times

recommended daily allowance (RDA) for vitamins andwater soluble vitamin E, a safe dose for fat soluble vitaminsand vitamin B6 to 10 times the RDA


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Minerals play an important also for woundhealing, immune function, antioxidant, etc..

Zinc to protein metabolism. Selenium-dependent glutathione peroxidase

protect cells from damage by hydrogenperoxide.


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for patients with severe burnsVitamin larut lemak Mikromineral

Beta karoten 10.000 IU Koper 1,5-3 mg

vitamin D 200 IU Mangan 3,5- 5 mg

Vitamin E 400-1000 IU Selenium 100 ug

vitamin K 1 mg Seng 50 mg

Vitamin larut air

Tiamin 10 mgRiboflavin 10 mg

Niacin 200 mg

Asam pantotenat 100 mg

Biotin 5 mgPiridoksin 20 mg

Asam folat 2 mg

Vitamin B12 20 ug

Vitamin C 2000 mg


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COMPLICATION

Risk factors for severe systemic complicationsand mortality include all of the following: Burns of > 40% of BSA Age > 60 yr or < 2 yr Presence of simultaneous major trauma or smoke

inhalation

The most common systemic complications arehypovolemia and infection.


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SYSTEMIC COMPLICATION

Hypovolemia Infection. Most common : streptococci &

staphylococci during the first few days andgram-negative bacteria after 5 to 7 days;however, flora are almost always mixed.


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SYSTEMIC COMPLICATION

Metabolic abnormalities (hypoalbuminemia),Dilutional electrolyte deficiencies(hypomagnesemia, hypophosphatemia, and

hypokalemia), Metabolic acidosis ,Rhabdomyolysis or hemolysis -> acute tubularnecrosis and renal failure.

Hypothermia Ileus is common after extensive burns.


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BURN SHOCK


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LOCAL COMPLICATION

Eschar Scarring and contractures result from

spontaneous healing of deep burns


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SEPSIS SYNDROMES


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DEFINITIONS

Activated Inflammatory cascade cause thebodyd defenses and regulatory systembecome overwhelmed leading to disruption of

hemeostasis Systemic Inflammatory Response Syndrome

(SIRS) 2 or more : tachycardia, tachypnea,

hyperthermia or hypothermia, high or lowWBC count, bandemia.



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DEFINITIONS

Sepsis : SIRS + infection Severe Sepsis : Sepsis + Organ Dysfunction Septic Shock : Severe Sepsis + hypotension

which is not responsive to fluid challange

Approach : PIRO (predisposition, infectionsource, response of host, organ dysfuntion)

Bacteremia is not obligatory in diagnosis ofsepsis



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PREDISPOSING FACTORS

Diabetes mellitus Cirrhosis Leukopenia, especially that associated with

cancer or treatment with cytotoxic drugs;

Invasive devices,ex : ETT, cathethers, drainagetubes, and other foreign materials;

Prior treatment with antibiotics orcorticosteroids.


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EPIDEMIOLOGY

In United States : 10th most common

cause of death

571.000 cases of severesepsis

Mortality rate 20-50% Incidence



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PATHOPHYSIOLOGY

Infection host response neutrophil andmacrophage 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-OrganFailure, death



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PATHOPHYSIOLOGY

Mediators of Sepsis Proinflammatory : IL-1, IL8, TNF Anti-inflammatory IL-10, IL-6 TGF B, IL-1ra Growth promoting

Arachidonat acid pathway peripheraldilation, vasocontriction, leukocyte andplatelet aggregation

PG fever



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PATHOPHYSIOLOGY

Vasopressin release in stress condition,cause vasoconstriction, osmoregulation,maintenance of normovolemia

NO Regulating vascular tone, plateletadhesion, insulin secretion,neurotransmission, tissue injurt, inflammation

and cytotoxicity



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PATHOGENESIS


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Sepsis: Defining a Disease Continuum

A clinical response arisingfrom a nonspecific insult,including 2 of the following: Temperature 38 oC or

36 oC HR 90 beats/min Respirations 20/min WBC count 12,000/mm 3

or4,000/mm 3 or >10%immature neutrophils

SIRS = systemic inflammatory response syndrome.

Bone et al. Chest. 1992;101:1644.

SIRS with a presumed orconfirmed infectiousprocess

Sepsis SIRS Infection/Trauma Severe Sepsis


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Sepsis: Defining a Disease Continuum

Bone et al. Chest. 1992;101:1644; Wheeler and Bernard. N Engl J Med . 1999;340:207.

Sepsis SIRS Infection/Trauma Severe Sepsis

Sepsis with 1 sign of organfailure Cardiovascular (refractory

hypotension) Renal Respiratory Hepatic Hematologic CNS Unexplained metabolic

acidosis

Shock

DIFFERENTIAL DIAGNOSIS


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DIFFERENTIAL DIAGNOSIS



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MANAGEMENT

Principles AB therapy Maintenance of adequate tissue perfusion



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MANAGEMENT

Respiratory Support Airway protection, intubation, mechanical

ventilatory support if needed

Cardiovascular support Initial therapy 2L of isotonic crystalloid Normal Saline/ LR.

Maintain MAP >65mmHg, but 75mmHg in patientith history of severe hypertensive patient



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MANAGEMENT

Drugs : Vasopresin, Norepinephrine, Dopamine,Phenylephrine, Epinephrine.

Inotropic agents : Dobutamine, Bicarbonate, AB

Novel Therapies Activated Protein C Steroid Therapy



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CONCLUSION & SUGGESTION

The patient is suffering from second degreethermal burn and severe sepsis

Perform Primary and Secondary Survey asneeded


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REFERENCES

Marx JA, Hockberger RS, Walls RM, Adams JG,editors. Rosens Emergency MedicineConcepts 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

kelompok 9 pemicu 2

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