Sepsis in Burns

Injuries caused by heat energy is minoris resistentiae loci most common

infectious cause of morbidity and increased mortality is almost universally in
burn patients.
The incidence of sepsis burns influenced by the depth of burns and age of the
patient.
Combined effect of the protein clumps, microbial within lesion and absence of
vascularization prevents delivery of immunologically active cells, humoral
factors and antibiotics.
Immediately after burn gram-positive dominant, end of the 1st week
gram-negative.
Sepsis is one cause of mortality in patients with severe burns.
Infection rarely on partial-thickness burns unless there is negligence in the
handling of 2nd degree burns.
The risk of infection in burns increases if there is an open wound or because of
comorbidities.

Sepsis in Burns
Systemic Inflammatory Response Syndrome (SIRS) and Multi-system
Organ Disfunction syndrome (MODS) is a major cause of mortality in
patients with burns and other trauma patients (81%).
SIRS form of systemic clinical response to various stimuli (such as
trauma, burns, autoimmune reactions, cirrhosis, pancreatitis, etc)
impact of the release of inflammatory mediators (physiological
process of wound healing) influence of several factors turned
excessively and cause damage to organs systemic causing
dysfunction (MODS) and failure (MOF).
There are 5 things that can be activators in SIRS, namely infection,
injury, inflamation, inadequate blood flow and ischemia-reperfusion
injury.

Clinical Criteria for Sepsis (Consensus of the

Society of Critical Care Medicine, 2008)
Common variables:
Fever (> 38.3 C);
Hipothermia (core
temperature <36 C);
Heart rate > 90x / min;
Tachypnea;
Impaired mental status;
Significant edema or
positive fluid balance (>
20 mL /kg within 24 hrs);
Hyperglycemia (plasma
glucose >140mg/dL)
without DM.

Inflammatory variables:
Leukocytosis (WBC>
12,000);
Leukopenia (WBC
<4000);
Normal WBC with> 10%
immature formations;
Plasma CRP > 2 SD
above the normal value;
Plasma procalcitonin> 2
SD above the normal
value.

Sepsis in Burns
Hemodynamic
variables:

Organ dysfunction
variables:

Arterial hypotension
(SBP <90 mmHg);
Arterial blood pressure
an average <70
mmHg;
Or a decline in SBP>
40 mm Hg in adults.

Arterial hypoxemia
(PaO 2 / FIO2 <300);
Acute oliguria (urine
output <0.5 mL / kg
per hour or 45 mmol /
L for at least 2 hours,
with adequate fluid
resuscitation);
The increase in
creatinine> 0.5 mg /
dL;
Abrnormalitas
coagulation (INR> 1.5
or aPTT> 60 s);
Ileus;
Thrombocytopenia
(platelets <100,000);
Hyperbilirubinemia
(total plasma

Tissue perfusion
variables:
Hyperlactataemia (>
the upper limit of
normal laboratory
results);
Decrease in capillary
refill or mottling.

Sepsis in Burns
When obtained evidence that the infection as the cause (of
the blood culture results / bacteremia), then SIRS called
sepsis.
SIRS will always be associated with MODS for MODS is the
end of SIRS.
Basically MODS is a collection of symptoms in the presence
of impaired function in patients with acute organ such that
homeostasis can not be maintained without intervention.
When explored further, SIRS as a continuous process so it is
understandable that the MODS describe the condition more
severe and is the final part of the spectrum of circumstances
that originated from SIRS.

PATOPHYSIOLOGY
Phase 1
Systemic inflammatory response is preceded by a cause, for
example, burns or other severe trauma.
Local damage stimulates the release of proinflammatory
mediators such as cytokines messenger physiological of
the inflammatory response (TNF, IL1, IL6, interferon, CSF,
and others).
Effectors of the cellular inflammatory response is PMN cells,
monocytes, macrophages, and endothelial cells.
Cells to secondary cytokines and inflammatory mediators
such as prostaglandins, leukotrienes, thromboxane, Platelet
Activating Factor (PAF), free radicals, nitric oxide, and
protease.
Endothelial activation and cytokine-rich environment activate
the coagulation cascade local thrombosis reduces blood
loss through injury, but walling off tissue injury isolated

PATOPHYSIOLOGY
Phase 2
Small number of cytokines in circulation increase
local response.
Movement of macrophages, platelets production of
growth factors.
Acute phase response controlled simultaneously by
decreased levels of mediators proinflammatory and
release antagonist endogenous (receptor antagonist IL1
and mediators other anti-inflammatory such as IL4, IL10, IL11, receptor soluble TNF.
Mediators of inflammatory responses to maintain the
initial controlled well by down-regulating cytokine
production and antagonistic effects on cytokines that
have been released lasted until homeostasis is

PATOPHYSIOLOGY
Stage 3
Homeostasis unrestored stage III (SIRS); massive
systemic reaction.
The predominant effect of cytokines turn out to be
destructive.
Circulation flooded inflammatory mediators so that the
integrity of the capillary wall is damaged.
Cytokines penetrated into various organs and cause
damage.
Regional and systemic destructive response increased
peripheral vasodilatation, impaired microvascular
permeability, accelerated microvascular thrombosis,
leukocyte-endothelial cell activation pathological
changes in various organs.
Inflammatory reaction uncontrolled septic shock, DIC,

SIRS, MODS, and SEPSIS

1ST THEORY
SIRS Impaired circulation.
Disturbed bowel tissue perfusion disruption GIT
mucosa bacterial translocation.
Disorders of cerebral circulation -> ensefelopati.
Impaired renal circulation -> Acute Renal Failure.
Impaired peripheral circulation ischemic muscles
increases Nitric Oxide (NO) -> modulator sepsis.
Impaired circulation to the skin and integument
system disorders of the immune system; due to
decreased production of lymphocytes and
decreased barrier function of the skin.

SIRS, MODS, and SEPSIS

2ND THEORY
Release of Lipid Protein Complex (LPC) or
burn toxin of tissue necrosis due to
thermal injury.
LPC has thousands of times over the
toxicity of endotoxin in stimulating the
release of pro-inflammatory mediators;
LPC but the release has nothing to do with
the infection.
Responses were raised initially localized,

SIRS, MODS, and SEPSIS

3RD THEORY
Metabolic system disorder
(hypometabolic in the acute phase,
hypermetabolic in the next phase)
drained all the modalities of the body,
especially immunological system.
Pro-inflammatory mediators released
into the circulation in response to an
injury not only attack foreign substances
or toxins that exist; but also cause

THERAPY
Management of burns aggressive, aimed at preventing the development of SIRS,
MODS, and sepsis.
Early Enteral Nutrition (NED) through a nasogastric tube prevent atrophy of the
intestinal mucosa, prevent and overcome the acute phase hipometabolic, controlling
status hypercatabolism phase flow.
Topical antibiotics burn medication to patients to prevent microbial contamination
of the wound.
Immediate necrotomy and debridement prevent evaporative heat loss that causes
metabolic disorders), barrier against germs and prolonged inflammatory process that
affects the healing process.
Prophylactic systemic antibiotics patterns of nosocomial bacteria in place of
hospitalization.
Symptoms of systemic infection culture of specific pathogen appropriate
antibiotics.
Close monitoring in patients with large burns avoid septic shock.

COMPLICATIONS
Varies depending on the etiology.
Respiratory failure, acute respiratory
distress syndrome (ARDS), nosocomial
pneumonia, kidney failure,
gastrointestinal bleeding and stress
gastritis, anemia, Deep Vein Thrombosis
(DVT), hyperglycemia, and
Disseminated intravascular coagulation
(DIC).

CONCLUSION
Combustio tissue damage or loss caused by contact with a heat source
such as a fire, hot water, electricity, and chemicals.
The burn is a type of trauma with high morbidity and mortality rates that
require a management as well as possible from early phase to late phase.
Systemic Inflammatory Response Syndrome (SIRS) and Multi-system
Organ Disfunction syndrome (MODS) is a major cause of mortality in burn
patients.
Management
development

of
of

burns are more aggressive and aimed at preventing the

SIRS, MODS, and sepsis.

Complications that may occur: respiratory failure, ARDS, nosocomial

pneumonia, kidney failure, gastrointestinal bleeding and stress gastritis,
anemia, DVT, hyperglycemia, and DIC.

REFERRENCES
Bohannon, J., Cui, W., Sherwood, E., Toliver-Kinsky, T. 2010. Dendritic Cell Modification of
Neutrophil Responses to Infection after Burn Injury. J Immunol 185:2847-2853.
Cakir, B., Yegen, BC. 2004. Systemic Responses to Burn Injury. Turk J Med Sci 34:215-226
Damayanti, T., Saputro, ID., 2011. Nilai Uji Diagnostik Prokalsitonin sebagai Deteksi Dini
Sepsis pada Luka Bakar Berat. Journal of Emergency 1(1):13-18.
De Macedo, JLS., Rosa, SC., Castro, C. 2003. Sepsis in burned patients. Revista da
Sociedade Brasileira de Medicina Tropical 36(6):647-652.
Emami, S., Karimi, H., Alijanpour, A. 2015. Epidemiology of burn wound infection and its
antibacterial resistance, burn registry program. Merit Research Journal of Medicine and
Medical Sciences 3(4):135-139.
Farina Jr, JA., Rosique, MJ., Rosique, RG. 2013. Curbing Inflammation in Burn Patients.
International Journal of Inflammation: 1-9.
Mohammed, AA., Muheel, MH., Mujbel, FA. 2014. Microbial drug resistance and potential
immune response by IL7 and IL10 in burn patients with septic and death cases.
International Journal of Advanced Research 2(4):286-292.
Orban, C. 2012. Diagnostic Criteria for Sepsis in Burns Patients. Chirurgia 107(6): 697700.
Shouman, O., Shahin, D., 2009. The Role of Dendritic Cells as a Predictor of Sepsis in
Burnt Patients. J. Plast. Reconstr. Surg 33(2):235-238.