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• Burns are injuries to the skin resulting from

contact with heat,electrical current, radiation,


or chemical agents
• Temperatures less than 44° C can generally be
tolerated for prolonged periods without
causing burns.
EPIDEMIOLOGY
• the American Burn Association, 500,000 burn
injuries are treated in medical facilities each year
• The majority of burns occur from :
– fire/flame (46%)
– scalds (32%)
– contact with hot objects (8%)
– electricity (4%)
– chemical agents (3%).
• Most admissions include severe burns of such
vital body areas as the face, hands, and feet
• The most commonly affected body areas :
– the upper extremities (41%),
– lower extremities (26%),
– head and neck (17%).
• Most of the burns were partial-thickness
injuries, and less than 5% were full thickness
Classsification of burns
Thermal Electrical Chemical
• Consisting: flame, • Potential for • Potentially severe
contact, or scald cardiac arrhythmias • Carefully removal
burns and compartement of the toxic
• Highest mortality syndromes with substance and
concurent irrigation with water
rhabdomyolysis min. 30 mins (exc.
• ECG is Concrete powder /
recomended powdered foms of
lye)
PATHOPHYSIOLOGY
• Three concentric zones :
– At the center of the burn is a zone of irreversible
coagulative necrosis that is formed immediately
after injury
– zone of ischemia in which there is a reduction in
the dermal microcirculation
– zone of hyperemia
RULE OF NINE dr Wallace
Superficial

Superficial partial-thickness

Deep partial-thickness

Full-thickness
Very painful, dry, red burns which blanch with pressure. They usually
take 3 to 7 days to heal without scarring. Also known as first-degree
burns. The most common type of first-degree burn is sunburn. First-
degree burns are limited to the epidermis, or upper layers of skin.
Very painful burns sensitive to temperature change and air exposure.
More commonly referred to as second-degree burns. Typically, they
blister and are moist, red, weeping burns which blanch with pressure.
They heal in 7 to 21 days. Scarring is usually confined to changes in skin
pigment.
Blistering or easily unroofed burns which are wet or waxy dry, and are
painful to pressure. Their color may range from patchy, cheesy white to
red, and they do not blanch with pressure. They take over 21 days to
heal and scarring may be severe. It is sometimes difficult to differentiate
these burns from full-thickness burns.
Burns which cause the skin to be waxy white to a charred black
and tend to be painless. Healing is very slow, if at all, and may
require skin grafting. Severe scarring usually occurs.
Burn depth classification

Depth Appearance Surface Sensation Time to healing

1st degree Epidermis Pink or red Dry Painful Days

2nd degree
(partial-thickness)
-Superficial Epidermis + Pink, clear Moist Painful 14-21 days
pars papilare blister

Epidermis +
-Deep pars retikulare Pink, Moist Painful Weeks, or may
hemorrhagic progress to 3rd
blister, red degree, require
graft
3rd degree (full- Epidermis + White, brown Dry Insensate Require excision
thickness) dermis
4th degree Skin, Brown, Dry Insensate Require excision
subcutaneos charred
fat, muscle,
bone
Burn Severity

http://emcrit.org/030-064/056-thermal.burn.htm
Signs and Symptoms
• Inhalation injury:
– Facial burns
– Carbonaceous sputum
– Pharyngeal injection
– Wheezing
– Hoarseness
– Singed nasal hair
History
• Information from emergency medical services
(EMS), family, friends, or witnesses may be
required.
• Medical history, surgical history, medications,
allergies, social history, tetanus immunization
status
• Carbon monoxide poisoning with exposure to
combustion
• Cyanide poisoning from burning wool, silk, nylon,
and polyurethane found in furniture and paper
Physical Exam
• Focus on airway, breathing first, then head-to-toe
secondary survey for concurrent injuries.
• Evaluate face and oropharynx for signs of
inhalation injury.
• Assess need for immobilization of cervical spine.
• Eye examination for corneal burns
• Determine severity of partial- and full-thickness
burns by assessing size and depth of burn:
– Estimate surface area involved
Lab
• For severe burns, obtain CBC, serum
electrolytes, glucose, BUN, creatinine, and
PT/PTT, type and cross-match, pregnancy test
(female)
• Blood gas with carbon monoxide level for
closed space or inhalation exposures
• Cyanide level if suspected
Imaging
• Chest radiograph
• Fiber optic bronchoscopy to assess inhalation
injury
Differential Diagnosis
• Electrical injury
• Chemical injury
• Associated trauma or intoxication
Treatment
Pre Hospital
• Stop the burning process, remove smoldering
clothes/jewelry.
• Establish patent airway; frequent reassessment:
– Intubate early for signs of respiratory distress.
• Initiate early IV fluid therapy.
• Relieve pain.
• Protect the wound with clean sheets.
• Transport to burn center (for major burns) if transport
time shorter than 30 minutes.
• Immobilize spine if decreased sensorium or trauma.
Initial Evaluation
• Airway management
• Evaluation of other injuries
• Estimation of burn size
• Diagnosis of carbon monoxide and cyanide
poisoning
INITIAL TREATMENT – BURN INJURY
MANAGEMENT OF BURNS
• stop the burning process and to protect the
patient from additional injury
– If chemical injury has occurred, immediate and
copious dilution of the chemical agent with tap
water and prompt removal of all involved clothing
are necessary
– If clothing is burning, extinguish the flames with
water or smother the flames with a blanket and
gently remove the involved clothing.
• The suspected inhalation injury or carbon
monoxide intoxication  100% oxygen
delivered by a non-rebreather mask
• Prehospital infusion of intravenous fluid is
beneficial in those patients with extensive
burns (greater than 20% TBSA)
• Wash all burned clothing and skin with cool
water
• Patients may need a tetanus toxoid booster
(dT or aPdT toxoid 0.5 mL IM) with tetanus
immune globulin
Algoritme Management of burns
Cooling of the Burn
• The optimal cooling temperature is around
10° to 25° C
• tap water at 12° to 18° C was used  least
necrosis and fastest healing
• treatment began up to 30 minutes after injury
• Ice and ice water may lead to increased tissue
injury and are contraindicated
Burn Dressings
• protect the wound, to reduce pain, to absorb
wound exudate, and, finally, to reduce vaporative
heat loss
• first-degree burns is not required other than
optional topical anesthetics, aloe vera, and/or
topical (NSAIDs).
• second-degree burns:
– the open method, which consists of topical
antimicrobials
– the closed method, which uses synthetic occlusive
dressings
Dressing
CATEGORY EXAMPLES ADVANTAGES DISADVANTAG
ES
Absorptive
Gauze, Telfa Nonadherent, Requires daily
nonadherent inexpensive dressing
changes
Occlusive
Hydrocolloid Duoderm , Absorbs Opaque, no
Tegasorb exudates, antimicrobial
protective properties
cushioning of
wound
Alginate Seasorb, Absorptive Frequent
Algiderm dressing
changes
Nanocrystallin Acticoat,Aquac Need to keep Need to keep
e silver el Ag dressing dressing
moist moist
Hydrogel Curagel , Rehydrates dry Nonabsorptive
Flexigel Nu- wounds
GeL
Polyurethane Tegaderm , Transparent, Nonabsorptive
foam Opsite inexpensive
Escharotomy
• Releasing the constriction of a burn eschar
with a scalpel or cautery at the bedside
• The procedure is performed by making a
longitudinal incision down to the fat in the
constricting eschar
• Circumferential burn eschar may lead to
neurovascular compromise:
– Monitor pulses; may need Doppler flow probe.
– Elevate burned extremity.
EMERGENCY DEPARTMENT
MANAGEMENT OF BURNS
• Airway Management  Endotracheal intubation
• General Measures for Moderate to Severe Burns
 intravenous access
• Circulation and Fluid Resuscitation  Fluid
resuscitation
• recognizing Inhalation Injury (soot, charring, and
mucosal inflammation, edema, or necrosis) 
endotracheal intubation and mechanical
ventilation
Treatment of the burn wound
• Silver sulfadiazine
• Mafedine acetate
• Silver nitrate
• Nearly healed: bacitracin, neomycin,
polymyxin B
Indications for Endotracheal Intubation and
Mechanical Ventilation
Upper airway obstruction
Inability to handle secretions
Hypoxemia despite 100% O2
Patient obtundation
Muscle fatigue suggested by a high or low respiratory rate

Hypoventilation (a Pco2 > 50 mm Hg and a pH less than


7.2)
Recommended Initial Ventilator Settings
Tidal volume 6–8 mL/kg
Respirator rate :
8–12 in adults
12–45 in children
Plateau pressures <35 cm H2O
I/E ratio 1 : 1–1 : 3
Flow rates 40–100 L/min
Flow rates 40–100 L/min
FORMULA FIRST 24 FORMULA FIRST 24 HOURS FORMULA FIRST 24 HOURS
HOURS NEXT 24 NEXT 24 HOURS NEXT 24 HOURS
HOURS
Parkland LR 4 mL/kg/% burn within first 8 Colloids in amount of 20–
hr 60% of plasma volume;
glucose in water added to
maintain urine output
0.5–1.0 mL/kg/hr in adults
and 1 mL/kg/hr in children
Modified Parkland LR 4 mL/kg/% burn in adults Colloid infusion of 5%
albumin at the amount
(0.3–1 mL/kg/% burn)/16
per hr
Evans Crystalloids in the amount of 1 Crystalloids at 0.5 mL/kg/%
mL/kg/% burn, plus burn, colloids at
colloids at 1 mL/kg/% burn, plus 0.5 mL/kg/% burn, and the
2000 mL glucose same amount of glucose in
in water water as first 24 hr
Brooke LR 1.5 mL/kg/% burn, plus colloids at 0.5 LR 0.5 mL/kg/% burn,
mL/kg/% colloids at 0.25 mL/kg/%
burn, plus 2000 mL glucose in water burn,
and the same amount of
glucose in water as first 24
hr
Modified Modified Brooke LR 2 mL/kg/% burn in the Colloids 0.3–0.5 mL/kg/%
Brooke adult and 3 mL/kg/% burn, glucose in water to
burn in children maintain urine output
Monafo Solution containing 250 mEq Na, 150 mEq Solution titrated with 1/3
lactate, NS according to urine
100 mEq Cl; amount adjusted to urine output
output
Galveston LR at 5000 mL/m2 TBSA burned plus 2000 3750 mL/m2 TBSA burned
mL/m2 plus 1500 mL/m2 TBSA
TBSA, within 8 hr
Electrolyte Solution Colloid D5W
Solution
Isotonic crystalloid formulas
Parkland Lactated Ringer's
formula
4 mL/kg per % TBSA burn
1/ volume during first 8 h postinjury;
2

1/ during next 16 h postinjury


2

Modified Lactated Ringer's


Brooke formula
2.0 mL/kg per % TBSA burn
Haifa formula Lactated Ringer's Fresh-frozen plasma
1 mL/kg per % TBSA burn 1.5 mL/kg per % TBSA
burn
1/ volume during first 8 h postinjury; 1/ volume during first
2 2
8 h postinjury;
1/ during next 16 h postinjury 1/ during next 16 h
2 2
postinjury
Hypertonic formulas
Monafo formula 25 mEq/L NaCl
Volume titrated to UOP 30 mL/h

Warden formula Lactated Ringer's plus 50 mEq NaHCO3 (180 mEq


Na/L) titrated to UOP 30–50 mL/h for 8 h
postinjury

Lactated Ringer's titrated to UOP 30–50 mL/h


beginning 8 h postburn
Colloid formulas
Evans formula 0.9% saline 1 mL/kg per Fresh-frozen plasma 2000 mL
% TBSA burn
1 mL/kg per % TBSA
burn
Brooke formula Lactated Ringer's Fresh-frozen plasma 2000 mL
1.5 mL/kg per % TBSA 0.5 mL/kg per %
burn TBSA burn
Slater formula Lactated Ringer's Fresh-frozen plasma
2000 mL/24 h 75 mL/kg per 24 h
Demling Dextran 40 in 0.9% NaCl Fresh-frozen plasma
formula
2 mL/kg per hour for 8 h 0.5 mL/kg per hour
postinjury; starting 8 h postburn
Lactated Ringer's titrated continued for 18 h
to UOP >30 mL/h for next
18 h postburn
Pharmacologic Therapies
• Minor pain from burns :
– oral acetaminophen (1 g in adults or 15 mg/kg in
children) every 4 to 6 hours
– NSAID such as ibuprofen (400–800 mg in adults or
10 mg/kg in children) every 6 to 8 hours
• Moderate to severe burn :
– Parenteral opioids (such as morphine sulfate 0.05–
0.1 mg/kg) titrated to effect
Nutrition
• The Harris-Benedict equation may be
inaccurate in burns of less than 40% TBSA
• caloric needs = 25 kcal/kg per day + 40 kcal/%
TBSA per day
Nutrition
• Early enteral feeding for patients with burn larger
than 20% TBSA is not only save, but it may help
prevent loss lean body mass
• A commonly used formula in nonburned patients is
the Harris-Benedict equation, but this equation may
be inaccurate in burns of <40%, and in these patients
the Curreri formula may be more appropriate
• 25kcal/kg/day + 40kcal/%TBSA/day
Burn Prevention
Recommendations
Flame burn Check that smoke detectors are
prevention functional
Create an escape plan for the home
and practice with the family
Safety device around fireplace
Matches, lighters in secure place away
from children
Scald Use splash guards on stove
prevention Lower hot water heater maximum
temperature to 49°–54° C
Use thermometer for bath water
Flame burn injuries
• A flammable liquid is involved in most cases
(66%); gasoline is the most common liquid
(63%).
• The high incidence of gasoline burns during
the summer months
• When flammable accelerants are present, the
burning process persists even when the victim
is rolling on the ground
Electrical Burns
Cellular Damage Due To Electrical Current
High vs. Low Tension Injuries
AC & DC
• 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
http://ehs.okstate.edu/modules/electric/Emergency.htm
http://www.uic.edu/labs/lightninginjury/treatment.html
Electrical Burns - Acute Care

A - Airway
B - Breathing
C - Circulation
D - Disability
E - Expose The Patient
http://www.uic.edu/labs/lightninginjury/treatment.html
Lightening Injuries
Patofisiologi
Electrical Burns - Lightening Injuries
• Management
– Primary Survey
– Assess Injury
• History (Other Trauma, Cardiac Arrest)
• Physical Exam (Include Thorough Neurologic Exam)
– Maintain Airway
– Cardiac Monitoring
• ECG On Admission
• Continuous Cardiac Monitor For 24 Hours
Electrical Burns - Lightening Injuries
• Management
– Resuscitation
• Increased Fluid Requirements Due To Underlying
Muscle Damage
• Foley Catheter
• Analyze Urine For Myoglobin
– Maintenance Of Peripheral Circulation
• Frequent Monitoring
• Decompress With Escharotomy Or Fasciotomy
Electrical Burns - Lightening Injuries
• Low Voltage Common
– Usually Minimal Cutaneous Injury
– No Muscle Damage
• Injuries To Oral Commissure
– Look Worse Than They Really Are
– No Immediate Debridement
– Watch For Delayed Bleed With Eschar Separation
Chemical Injuries
• These chemicals, which include acids, alkalis,
and other highly reactive substances
Alkali Burn Acid Burn
Frequently full thickness Usually partial-thickness
injuries injuries
Appear pale Erythema
Basah & kasar erosion

http://www.anatomyatlases.org/firstaid/Burns.shtml
Inhalation injury
• Smoke inhalation caused injury in 2 ways:
– Direct heat injury to the upper airways
– Inhalation of the combustion products intothe lower airways
• Direct injury to the upper airways  airways swelling 
maximal edema in the first 24 to 48 hours after injury 
require short course of endotracheal intubation for airway
protection
• Lower airway injury  combustion products found in smoke,
mos commonly from synthetic substance burned in structural
fires  direct mucosal injury  mucosal sloughing, edema,
reactive broncoconstriction  obstruction of the lower
airways
• Treatment of inhalation injury consist of supportive
care.
– Agressive pulmonary toilet
– Routine use of bronchodilators (eg. Albuterol) are
recomended
• Inhaled nitric oxide may also be useful as a last effort
in burn patients with severe lung injury for whom
other means of ventilatory support has failed
• The use of steroids tradiitionally has been avoided
due to worse outcomes in burn patients
Complication
• Ventilator associated pneumonia
• Abdominal compartement syndrome
• Deep vein thrombosis
• Heparin-induced thrombocytopenia
• Catheter-related bloodstream infections
Rehabilitation
• Patients that are unable to participate due to
mechanical ventilation or other reasons
should have passive range of motion done at
least twice a day
• Patients with foot and extremity burns should
be instructed to walk independently without
the help of crutches to prevent extremity
swelling
Prognosis
• Highest predictive value for mortality:
– Age
– Percent TBSA
– Inhalation injury
– Coexistent trauma
– Pneumonia
Prevention
• Smoke alarm
• Regulation of hot water heater temperatures
Patient Education

• Prevention is the best tool in the management of


burn injuries. Campaigns stressing the use of smoke
detectors and the adoption of laws mandating their
use have decreased the mortality rate from burns
significantly in North America. Additional materials
useful for teaching burn prevention may be obtained
from the American Burn Association.
• The development of flame retardant sleepwear and
the famous program "Stop, Drop, and Roll" have
prevented numerous fire-related injuries.
• Parents should create specific escape plans, discuss
and practice them with their children in case quick
escape from house emergencies is necessary.
• Children should not be allowed to play with lighters or
fireworks.
• EPs should work with their local fire service to develop burn
prevention programs as part of the fire service's fire
prevention strategies.
• Discussions with patients who have sustained burn injuries
should attempt to determine how the injury was sustained
and what steps can be taken to prevent recurrence. As part of
discussions with parents regarding risks in the home, EPs
should ask parents if the water heater is set to 49°C (120°F). If
parents do not know, encourage them to find out and have it
adjusted if necessary. Simple interventions like this can have
significant impact upon the lives of many.
INFEKSI
NOSOKOMIAL

Infeksi yg didptnya di RS, timbul / tjd


sesudah 72jam perawatan pd pasien
rawat inap, tjd pd pasien yg dirawat >
lama dr masa inkubasi suatu peny.
KUMAN PENYEBAB
• Proteus
• E. coli
• Staphylococcus aureus
• Pseudomonas
• Enterococcus faecalis (streptococcus faecalis)
FAKTOR RESIKO
• Usia tua
• Berbaring lama
• Penggunaan obat imunosupresan dan steroid
• Daya tahan m↓ pd luka bakar
• Pasien yg dilakukan prosedur diagnostik invasif
• Infus lama
• Pemasangan kateter yg lama
• IN pd luka operasi
• Byk tjd di tuang rawat itensif
GEJALA DAN TANDA
• Demam
• Napas cepat
• TD rendah,
• Urine output m↓
• Urinary tract infection  sakit ketika BAK dan darah
dlm urin
• Leukosit tinggi
• Radang paru  kesulitan bernapas dan
ketidakmampuan u/ batuk
• Infeksi : bengkak, kemerahan
PENGOBATAN
• Umumnya kuman penyebab IN  sdh resisten thd byk AB.
• AB ϐ laktam, sefalosporin, sefoperazon IM/IV tiap 12jam bs/baik
dipakai walaupun ada g3 ginjal dan neutropenia (<1000/ul)
• ϐ laktam yg msh efektif u/ pseudomonas : mis/ sefoperazon,
seftazidim
• Sblm ada hasil kultur, pengobatan sdh bs dimulai
• 3hr msh demam dan peny progresif  blh di(+)kan vankomisin
• Jk ada kandidiasis sistemik  th/ antifungal (oral/IV)
• Jk e/ kateter  dicabut !!!
• Quinolon  norfloksasin  u/ profilaksis pd pasien neutropenia.
PENGOBATAN u/ Ventilatory Acquired Pneumonia
• Kombinasi AB  sefalosporin generasi III dan
aminoglikosida / aztreonam.

PENCEGAHAN
• Dekontaminasi sal cerna  m↓ insidens pneumonia
nosokomial.
• Dekontaminasi usus
• Membatasi transmisi organisme dari / antar pasien
dgn cara mencuci tgn
• Tindakan asepsis dan antisepsis didlm RS
• AB empiris yg tepat dan memadai  m↓ angka
kematian HAP (hospital acquired pneumonia)
KOMPLIKASI
EKSTRAVASASI Cairan infus masuk ke jar sekitar insersi
(infiltrat) kanul
PENYUMBATA Infus tdk berfungsi tanpa dpt dideteksi
N adanya g3 lain
FLEBITIS Trdpt pembengkakan, kemerahan, dan nyeri
spjg vena
TROMBOSIS Pembengkakan, spjg vena yg mghambat
aliran infus
KOLONISASI Bila sdh dpt dibiakkan MO dr bag kanula yg
KANUL ada dlm PD
SEPTIKEMIA Jk kuman menyebar hematogen dr kanul
SUPURASI Jk tjd bentukan pus disekitar insersi kanul
Systemic Inflammatory
Response Syndrome
(SIRS)
SEPSIS and It’s Disease spectrum
• Various stages of disease
– Bacteremia
– SIRS
– Sepsis syndrome
– Sepsis shock : early and refractory
Definition

• Infection
– Presence of microorganisms in a normally
sterile site.
• Bacteremia
– Cultivatable bacteria in the blood stream.
• Sepsis
– The systemic response to infection.
If associated with proven or clinically
suspected infection, SIRS is called “sepsis”.
American College of Chest Physicians/Society of Critical Care Medicine Consensus
Conference Committee. Crit Care Med. 1992;20:864-874.
SIRS (Systemic
Inflammatory Response Syndrome)

• The systemic response to a wide range of stresses.


– Temperature >38°C (100.4°) or <36°C (96.8°F).
– Heart rate >90 beats/min.
– Respiratory rate >20 breaths/min or
PaCO2 <32 mmHg.
– White blood cells > 12,000 cells/ml or < 4,000
cells/ml or >10% immature (band) forms.
• Note
– Two or more of the following must be present.
– These changes should be represent acute alterations from
baseline in the absence of other known cause for the
abnormalities.
American College of Chest Physicians/Society of Critical Care Medicine Consensus
Conference Committee. Crit Care Med. 1992;20:864-874.
Severe Sepsis

• Sepsis with organ hypoperfusion


one of the followings :
– SBP < 90 mmHg
– Acute mental status change
– PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250)
– Increased lactic acid/acidosis
– Oliguria
– DIC or Platelet < 80,000 /mm3
– Liver enzymes > 2 x normal
American College of Chest Physicians/Society of Critical Care Medicine Consensus
Conference Committee. Crit Care Med. 1992;20:864-874.
MODS
(Multiple Organ Dysfunction Syndrome)
• Sepsis with multiorgan hypoperfusion
Two or more of the followings:
– SBP < 90 mmHg
– Acute mental status change
– PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250)
– Increased lactic acid/acidosis
– Oliguria
– DIC or Platelet < 80,000 /mm3
– Liver enzymes > 2 x normal
American College of Chest Physicians/Society of Critical Care Medicine Consensus
Conference Committee. Crit Care Med. 1992;20:864-874.
Relationship between SIRS and
Sepsis

Bone RC et al, Chest1992;101:164-55.


The Sepsis Continuum
Severe Septic
SIRS Sepsis Sepsis Shock

• A clinical response arising


from a nonspecific insult, SIRS with a Sepsis with Refractory
with 2 of the following: presumed organ failure hypotension
 T >38oC or <36oC or confirmed
 HR >90 beats/min infectious
 RR >20/min process
 WBC >12,000/mm3 or
<4,000/mm3 or >10% SIRS = systemic inflammatory
response syndrome
bands
Chest 1992;101:1644.
Mortality rate in SIRS

Rangel-Frausto, et al. JAMA 273:117-123, 1995.


Pathogenesis of Severe Sepsis
Infection

Microbial Products
(exotoxin/endotoxin)

Cellular Responses
Platelet Coagulation Kinins Cytokines
Activation Activation Oxidases Complement TNF, IL-1, IL-6

Coagulopathy/DIC
Vascular/Organ System Injury

Multi-Organ Failure

Death
Normal Systemic Response to
Infection and Injury (1)
• Leukocytosis Mobilizes neutrophils into the
circulation
• Tachycardia Increases cardiac output, blood flow to
injuried tissue
• Fever Raises core temperature; peripheral
vasoconstriction shunts blood flow to
injuried tissue. Occurs much more
often when infection is the trigger for
systemic responses
Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Normal Systemic Response to
Infection and Injury (2)
• Acute-Phase Responses
– Anti-infective
• Increases synthesis of complement factors, microbe
pattern-recognition molecules(mannose-binding lectin,
LBP, CRP, CD14, Others)
• Sequesters iron (lactoferrin) and zinc (metallothionein)

Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.


Normal Systemic Response to
Infection and Injury (3)
• Anti-inflammatory
– Releases anti-inflammatory neuroendocrine hormones
(cortisol, ACTH, epinephrine, α-MSH)
• Increases synthesis of proteins that help prevent inflammation
within the systemic compartment
• Cytokine antagonists (IL-1Ra, sTNF-Rs)
• Anti-inflammatory mediators (e.g.,IL-4, IL-6, IL-6R, IL-10, IL-13,
TGF-β)
• Protease inhibitors (e.g.,α1-antiprotease)
• Antioxidants (haptoglobin)
– Reprograms circulating leukocytes (epinephrine, cortisol, PGE2,
?other)

Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.


Normal Systemic Response to
Infection and Injury (4)
• Procoagulant
– Walls off infection, prevents systemic spread
• Increases synthesis or release of fibrinogen, PAI-1, C4b
• Decreases synthesis of protein C, anti-thrombin III
• Metabolic
– Preserves euglycemia, mobilizes fatty acids, amino acids
• Epinephrine, cortisol, glucagon, cytokines
• Thermoregulatory
– Inhibits microbial growth
• Fever
Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Risk factors of sepsis

• aggressive oncological chemotherapy and radiation therapy


• use of corticosteroid and immunosuppressive therapies for organ
transplants and inflammatory diseases
• longer lives of patients predisposed to sepsis, the elderly, diabetics,
cancer patients, patients with major organ failure, and with
granulocyopenia.
• Neonates are more likely to develop sepsis (ex. group B Streptococcal
infections).
• increased use of invasive devices such as surgical protheses, inhalation
equipment, and intravenous and urinary catheters.
• indiscriminate use of antimicrobial drugs that create conditions of
overgrowth, colonization, and subsequent infection by aggressive,
antimicrobial-resistant organisms.

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Patients at increased risks of
developing sepsis
• Underlying diseases: neutropenia, solid tumors,
leukemia, dysproteinemias, cirrhosis of the liver,
diabetes, AIDS, serious chronic conditions.
• Surgery or instrumentation: catheters.
• Prior drug therapy: Immuno-suppressive drugs,
especially with broad-spectrum antibiotics.
• Age: males, above 40 y; females, 20-45 y.
• Miscellaneous conditions: childbirth, septic abortion,
trauma and widespread burns, intestinal ulceration.

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Source
(usually an endogenous source of
• intestinal tract infection)
• oropharynx
• instrumentation sites
• contaminated inhalation therapy equipment
• IV fluids.
• Most frequent sites of infection: Lungs, abdomen,
and urinary tract.
• Other sources include the skin/soft tissue and the
CNS.
Angus DC, et al. Crit Care Med 2001, 29:1303-1310.
Diagnosis
• History
– community or nosocomially acquired infection
– immunocompromised patient
– exposure to animals, travel, tick bites, occupational
hazards, alcohol use, seizures, loss of
consciousness, medications
– underlying diseases ; specific infectious agents
– Some clues to a septic event include
• Fever or unexplained signs with malignancy or
instrumentation
• Hypotension
• Oliguria or anuria
• Tachypnea or hyperpnea
• Hypothermia without obvious cause
• Bleeding
Angus DC, et al. Crit Care Med 2001, 29:1303-1310.
Specific Infectious agents

• Splenectomy (traumatic or functional)


• S pneumoniae, H influenzae, N meningitidis
• Neutropenia (<500 neutrophil/ml)
– Gram-negative, including P aeruginosa, gram-positives,
including S aureus
– Fungi, especially Candida species
• Hypogammaglobulinemia (e.g.,CLL)
– S pneumoniae, E coli
• Burns
– MRSA, P aeruginosa, resistant gram-negatives
MacArthur RD, et al. Mosby, 2001:3-10.
Wheeler AP, et al. NEJM 1999;340:207-214.
Chaowagul W, et al. J Infect Dis 1989;159:890-899.
Specific Infectious agents

• Aids
– P aeuginosa (if neutropenic), S aureus, PCP
pneumonia
• Intravascular devices
– S aureus, S epidermidis
• Nosocomial infections
– MRSA, Enterococcus species, resistant gram-
negative, Candida species
• Septic patients in NE of Thailand
– Burkholderia pseudomallei
MacArthur RD, et al. Mosby, 2001:3-10.
Wheeler AP, et al. NEJM 1999;340:207-214.
Chaowagul W, et al. J Infect Dis 1989;159:890-899.
Diagnosis
• Physical Examination
– essential
– In all neutropenic patients and in patients
with as suspected pelvic infection the
physical exam should include rectal, pelvic,
and genital examinations
• perirectal, and/or perineal abscesses
• pelvic inflammatory disease and/or
abscesses, or prostatitis

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Signs and Symptoms

• Nonspecific symptoms of sepsis : not


pathognomonic
– fever
– chills
– constitutional symptoms of fatigue, malaise
– anxiety or confusion
• absent symptoms in serious infections, especially
in elderly individuals

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Complications
• Adult respiratory distress syndrome (ARDS)
• Disseminated Intravascular Coagulation (DIC)
• Acute Renal failure (ARF)
• Intestinal bleeding
• Liver failure
• Central Nervous System dysfunction
• Heart failure
• Death

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Surviving Sepsis Campaign

Guidelines for Management of


Severe Sepsis and Septic Shock

Dellinger RP, et al. Crit Care Med 2004; 32:858-873.


Diagnosis
• Before the initiation of antimicrobial therapy, at least two blood cultures
should be obtained
• At least one drawn percutaneously
• At least one drawn through each vascular access device if inserted
longer than 48 hours
• Other cultures such as urine, cerebrospinal fluid, wounds, respiratory
secretions or other body fluids should be obtained as the clinical situation
dictates
• Other diagnostic studies such as imaging and sampling should be
performed promptly to determine the source and causative organism of
the infection
• may be limited by patient stability
Weinstein MP. Rev Infect Dis 1983;5:35-53
Blot F. J Clin Microbiol 1999; 36: 105-109.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.


Sepsis resuscitation bundle
• Serum lactate measured
• Blood cultures obtained before antibiotics administered
• Improve time to broad-spectrum antibiotics
• In the event of hypotension or lactate > 4 mmol/L (36 mg/dL)
– a. Deliver an initial minimum of 20 mL/kg of crystaloid (or
colloid equivalent)
– b. apply vasopressors for ongoing hypotension
• In the event of persistent hypotension despite fluid resuscitation or
lactate > 4 mmol/L (36 mg/dL)
– a. achieve central venous pressure of > 8 mmHg
– b. achieve central venous oxygen saturation of > 70%

Hurtado FJ. et al. Crit Care Clin;2006; 22:521-9.


Sepsis management bundle

• Fluid resuscitation
• Appropriate cultures prior to antibiotic
administration
• Early targeted antibiotics and source control
• Use of vasopressors/inotropes when fluid
resuscitation optimized

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Sepsis management bundle

• Evaluation for adrenal insufficiency


• Stress dose corticosteroid administration
• Recombinant human activated protein C
(xigris) for severe sepsis
• Low tidal volume mechanical ventilation for
ARDS
• Tight glucose control

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Infection Control

• Appropriate cultures prior to antibiotic


administration
• Early targeted antibiotics and source control

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Early Goal-Directed
Therapy

CVP : central
venous
pressure

MAP : mean
arterial
pressure

ScvO2: central
venous
oxygen
saturation

NEJM 2001;345:1368-77.
Antibiotic use in Sepsis (1)

• The drugs used depends on the source of the sepsis


• Community acquired pneumonia
– third (ceftriaxone) or fourth (cefepime) generation
cephalosporin is given with an aminoglycoside (usually
gentamicin)
• Nosocomial pneumonia
– Cefipime or Imipenem-cilastatin and an aminoglycoside
• Abdominal infection
– Imipenem-cilastatin or Pipercillin-tazobactam and
aminoglycoside

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Antibiotic use in Sepsis (2)

• Nosocomial abdominal infection


– Imipenem-cilastatin and aminoglycoside or Pipercillin-
tazobactam and Amphotericin B
• Skin/soft tissue
– Vancomycin and Imipenem-cilastatin or Piperacillin-
tazobactam
• Nosocomial skin/soft tissue
– Vancomycin and Cefipime
• Urinary tract infection
– Ciprofloxacin and aminoglycoside

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


Antibiotic use in Sepsis (3)

• Nosocomial urinary tract infection:


– Vancomycin and Cefipime
• CNS infection:
– Vancomycin and third generation cephalosporin or
Meropenem
• Nosocomial CNS infection:
– Meropenem and Vancomycin
• Drugs will change depending on the most likely cause of the patient's
sepsis
• Single drug regimens are usually only indicated when the organism
causing sepsis has been identified and antibiotic sensitivity testing

Angus DC, et al. Crit Care Med 2001, 29:1303-1310.


New Drug in Treating Severe
Sepsis
• It is the first agent approved by the FDA
effective in the treatment of severe sepsis
proven to reduce mortality. Activated Protein C
(Xigris) mediates many actions of body
homeostasis. It is a potent agent for the:
– suppression of inflammation
– prevention of microvascular coagulation
– reversal of impaired fibrinolysis
Angus DC, et al. Crit Care Med 2001, 29:1303-1310.
NEJM;355:1699-1723.
Sepsis Cascade
reference
• Rossen. Emergency Medicine
• Environmental Safety Division - University of
Georgia http://www.esd.uga.edu/