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 REVIEW

CURRENT
OPINION Sepsis - What’s new in 2019?
Mark E. Nunnally and Arpit Patel

Purpose of review
Sepsis-3 guidelines have implications in a deeper understanding of the biopathology of the disease.
Further, the review focuses on timely topics and new literature on fluid resuscitation, the value of steroids in
sepsis, and new therapeutic options such as angiotensin II, vitamin C, and thiamine as well as the
emerging role of procalcitonin (PCT) in managing antibiotics.
Recent findings
Downloaded from https://journals.lww.com/co-anesthesiology by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3pjrohLwRTRF2rT2o7mLKNIbVmuv5oHzxa3v+0rLDldA= on 03/05/2019

Traditional therapies such as type of crystalloid fluid administration and steroid therapy for sepsis are
currently under re-evaluation. Angiotensin II is investigated for reversing vasodilatory shock. The role of
capillary endothelium leak and cellular metabolism can be affected by vitamin C and thiamine levels.
Biomarker level trends, specifically PCT, can aid clinical suspicion of infection.
Summary
Sepsis-3 shifts the focus from a noninfectious inflammatory process and an emphasis on a dysregulated host
response to infection. Hyperchloremic crystalloid resuscitation is associated with poor clinical outcomes.
Steroid administration can reverse shock physiology; however, mortality benefits remain uncertain.
Angiotensin II, vitamin C, and thiamine are novel treatment options that need further validation. PCT assays
can help discern between infectious and noninfectious inflammation.
Keywords
angiotensin II, chloride, sepsis, thiamine, vitamin C

INTRODUCTION for patients in an ICU and a quick SOFA (qSOFA)

There are 1.5 million sepsis cases in the United States score of two or more for patients outside of the ICU,
&

and it is responsible for one out of every three hospital
deaths [1]. The economic impact is estimated at over
$20 billion annually in the United States, and approx-
imately $55 million each day [2]. Septic shock is
associated with mortality as high as 50% [3].
Although easy ‘cures’ are elusive, diagnosis and treat-
ment for sepsis continue to advance. In this review,
we will discuss the implications of the Sepsis-3 criteria
and epidemiologic importance of this concept. Fur-
ther, we will discuss recent data regarding intrave-
nous (IV) fluid administration, the use of steroids,
and new drug therapies including vitamin C, thia-
mine, and angiotensin 2. Although it is unclear
which of these will be practice changing, they raise
important concerns in the management of sepsis.
SEPSIS-3
Sepsis is a diagnosis based on clinical criteria.
Defined as ‘life-threatening organ dysfunction
caused by a dysregulated host response to infection,’
&
[4 ] its objective identification is based on a change
in the [sepsis-associated] Sequential Organ Failure
Assessment (SOFA) score [5] of two points or more
when there is presumed or suspected infection [4 ].
Table 1 specifies the SOFA, qSOFA, and Systemic
Inflammatory Response Syndrome (SIRS) criteria.
These were the basis of a clinical diagnosis of sepsis
since the original ‘Sepsis-1’criteria were established
in 1992 [6]. A subsequent revision established
parameters to support a SIRS response, but retained
SIRS, suggested restraint from using laboratory mea-
surement of various inflammatory markers (aside
from abnormalities of white blood cell count) to
define sepsis, and introduced a framework for eval-
uating sepsis based on predisposition, pathogen,
host response, and organ dysfunction [7]. The
evolution of these criteria and considerations
Department of Anesthesiology, Perioperative Care, and Pain Medicine,
NYU Langone Health, NYU Langone Medical Center, New York, New
York, USA
Correspondence to Mark E. Nunnally, MD, Department of Anesthesiol-
ogy, Perioperative Care, and Pain Medicine, NYU Langone Health, NYU
Langone Medical Center, 550 1st Ave, New York, NY 10016, USA.
Tel: +1 (212) 263 5072; e-mail: Mark.Nunnally@nyulangone.org
Curr Opin Anesthesiol 2019, 32:163–168
DOI:10.1097/ACO.0000000000000707

0952-7907 Copyright ß 2019 Wolters Kluwer Health, Inc. All rights reserved. www.co-anesthesiology.com

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.

 ANALISIS

Efek lain dari trombin prokoagulan mampu
merangsang jalur inflamasi multipel dan lebih
menekan sistem fibrinolitik endogen dengan
mengaktifkan inhibitor fibrinolisis thrombin-
activatable (TAFI).9
Mekanisme kedua melalui aktivasi protein
aktif C yang berkaitan dengan respons
sistemik terhadap infeksi. Protein C adalah
protein endogen yang mempromosikan
fibrinolisis dan menghambat trombosis
dan peradangan, merupakan modulator
penting koagulasi dan peradangan yang
terkait dengan sepsis.8 Kondisi tersebut
memberikan efek antitrombotik dengan
menginaktivasi faktor Va dan VIIIa, membatasi
pembentukan trombin. Penurunan trombin
akan berdampak terhadap proses inflamasi,
prokoagulan, dan antifibrinolitik. Menurut
data in vitro menunjukkan bahwa protein
aktif C memberikan efek antiinflamasi dengan
menghambat produksi sitokin inflamasi
(TNF-α, interleukin-1, dan interleukin-6)
oleh monosit dan membatasi monosit dan
neutrofil pada endothelium yang cedera
dengan mengikat selectin.8,9
Hasil akhir respons jaringan terhadap infeksi
berupa pengembangan luka endovaskuler
difus, trombosis mikrovaskuler, iskemia organ,
disfungsi multiorgan, dan kematian.8
KRITERIA SEPSIS
Skrining awal dan cepat dapat dilakukan di
setiap unit gawat darurat. Kriteria baru sepsis
menggunakan Sequential Organ Failure
Assessment (SOFA).7 SOFA melakukan evaluasi
terhadap fungsi fisiologis, respirasi, koagulasi,
hepatik, sistem saraf pusat, dan ginjal.
Makin tinggi skor SOFA akan meningkatkan
morbiditas dan mortalitas sepsis.7,10

Kriteria simpel menggunakan qSOFA. qSOFA

dinyatakan positif apabila terdapat 2 dari 3
kriteria. Skoring tersebut cepat dan sederhana
serta tidak memerlukan pemeriksaan
laboratorium.7

Syok septik dapat diidentifikasi dengan adanya

klinis sepsis dengan hipotensi menetap.
Kondisi hipotensi membutuhkan tambahan
vasopressor untuk mempertahankan kadar
MAP >65 mmHg dan laktat serum >2 mmol/L
walaupun telah dilakukan resusitasi.7

Kriteria SOFA muncul setelah pembaharuan

definisi dan kriteria sepsis bertujuan untuk
mengurangi morbiditas dan mortalitas sepsis.
Kriteria tahun 1992 menggunakan istilah
Sindrom Respons Inflamasi Sistemik (SIRS).
SIRS terdiri dari kriteria umum yang meliputi
Gambar. Rantai koagulasi dengan dimulainya respons inflamasi, trombosis, dan fibrinolisis terhadap infeksi8
kondisi vital pasien, terdapat kriteria inflamasi,
Tabel 2. Kriteria Sepsis5 kriteria hemodinamik, dan kriteria gangguan
fungsi organ.5
Kriteria SIRS Suhu : <36°C atau >38°C
Nadi : 90 kali/menit
Laju napas : >20/menit atau PaCO2 <32 mmHg Tabel 4. Skor quick SOFA6,13
Leukosit <4000/mm3 atau > 12000/mm3
Kriteria qSOFA
Kriteria Hemodinamik Tekanan darah sistolik <90 mmHg, Tekanan arteri rerata <70 mmHg atau tekanan darah
Laju pernapasan >22x/menit
sistolik turun >40 mmHg
Saturasi darah vena <70% Perubahan status mental/kesadaran
Indeks kardiak >3,5L/menit/m Tekanan darah sistolik <100 mmHg
Kriteria Inflamasi Jumlah leukosit > 12000/mm3 atau < 4000/mm3 atau ditemukan sel leukosit muda >10%
Kadar protein C reaktif meningkat >2 kali nilai normal
Kadar procalcitonin meningkat >2 kali nilai normal Keterbatasan dan kelebihan dua kriteria
Kriteria Gangguan Fungsi PaO2/FIO2 < 300 mmHg tersebut dirangkum dalam tabel 5.
Organ Produksi urin <0,5 mg/kgBB
Gangguan pembekuan darah
Ileus MANAJEMEN SEPSIS
Trombositopenia
Terdapat perubahan bermakna surviving
Ikterus
Kriteria Perfusi Jaringan Kadar laktat >3 mmol/L
sepsis campaign 2018 dari rangkaian 3 jam, 6
Pengisian kapiler melambat jam, menjadi rangkaian 1 jam awal.4 Tujuan

682 CDK-280/ vol. 46 no. 11 th. 2019

 ANALISIS

perubahan ini adalah diharapkan terdapat
perubahan manajemen resusitasi awal,
terutama mencakup penanganan hipotensi
pada syok sepsis.4
Pengukuran Kadar Laktat (Rekomendasi
lemah, bukti penelitian lemah)4
Peningkatan kadar laktat dapat menunjukkan
beberapa kondisi di antaranya hipoksia
jaringan, peningkatan glikolisis aerobik
yang disebabkan peningkatan stimulasi
beta adrenergik atau pada beberapa kasus
lain. Peningkatan kadar laktat >2mmol/L
harus diukur pada kondisi 2-4 jam awal dan
dilakukan tindakan resusitasi segera.4
Kultur Darah (Pengalaman terbaik peneliti)4
Pengambilan kultur darah dilakukan segera,
hal tersebut berguna untuk meningkatkan
optimalisasi pemberian antibiotik dan
identifikasi patogen. Kultur darah sebaiknya
dalam 2 preparat terutama untuk kuman
aerobik dan anaerobik. Pengujian kultur
juga dapat menyingkirkan penyebab sepsis,
apabila infeksi patogen tidak ditemukan maka
pemberian antibiotik dapat dihentikan.4
Antibiotik Spektrum Luas (Rekomendasi
kuat, bukti penelitian Sedang)4
Pemberian antibiotik spektrum luas sangat
direkomendasikan pada manajemen awal.
Pemilihan antibitiotik disesuaikan dengan
bakteri empirik yang ditemukan.4
Cairan Intravena (Rekomendasi kuat, bukti
penelitian Lemah)4
Pemberian cairan merupakan terapi awal
resusitasi pasien sepsis, atau sepsis dengan
hipotensi dan peningkatan serum laktat.
Cairan resusitasi adalah 30 mg/kgBB cairan
kristaloid; tidak ada perbedaan manfaat antara
koloid dan kristaloid.4 Pada kondisi tertentu
seperti penyakit ginjal kronis, dekompensasi
kordis, harus diberikan lebih hati –hati.14
Beberapa teknik untuk menilai respons cairan:

Tabel 3. Kriteria sepsis 1992-20165,11,12

Kriteria Sepsis 1 ( 1992) Sepsis 2 ( 2011) Sepsis 3 ( 2016 )

Sepsis Kriteria SIRS bila ditemukan 2 gejala atau lebih tanda Kriteria SIRS ditambah dengan fokal infeksi Skor SOFA ≥ 2
sebagai berikut : Disertai dengan kriteria hemodinamik, inflamasi, qSOFA ≥2
Suhu >38°C atau <36°C dan kriteria gangguan fungsi organ
Detak jantung >90 kali/menit
Frekuensi pernapasan >20 kali/menit atau
PaCO2<32 mmHg
Jumlah leukosit >12000 atau <4000/mm3 atau
ditemukan sel leukosit muda >10%
Disertai dengan fokal infeksi
Sepsis berat Kriteria sama Kriteria sama Definisi sepsis berat dihilangkan
Syok sepsis Kriteria sama Kriteria sama Sepsis dengan hipotensi
Kadar serum laktat ≥2 mmol/L yang menetap
walaupun telah diberikan terapi cairan sehingga
dibutuhkan pemberian vasopressor untuk
mempertahankan MAP > 65 mmHg

Tabel 3. Sequential organ failure assessment (SOFA)6,13

Sofa Score
No Sistem Organ
0 1 2 3 4
1 Respiratory PO/FiO2 mmHg ≥400 <400 <300 <200 dengan bantuan respirasi <100 dengan bantuan respirasi
(Kpa)
2 Koagulasi Platelet,x 105/ ≥150 <150 <100 <50 <20
mm5
3 Hepar, bilirubin mg/dL <1,2 <1,2-1,9 2,0-5,9 6,0-11,9 >12,0
(mol/L)
4 Kardiovaskuler MAP ≥70 mmHg MAP < 70 mmHg Dopamin <5 ug/kg/menit atau Dopamin 5,1-15 ug/kg/menit Dopamin >15 atau epinefrin >0,1
Dobutamin (dosis berapapun ) atau epinefrin ≤ 0,1 ug/kg/menit ug/kg/menit
atau norepinefrin ≤ 0,1 ug/kg/
menit
5 Sistem saraf pusat, Glasgow 15 13-14 10-12 6-9 <6
Coma Scale (GCS)
6. Renal, kreatinin, mg/dL <1,2 1,2-19 2,0-3,4 3,5-4,9 >5.0
umol/L), urine output mL/ <500 <200
hari

Ket : Dosis dobutamin dalam ug/kg/menit, FiO2 ; Fraksi Oksigen inspirasi, PO2; tekanan parsial oksigen, MAP; mean arterial pressure

Tabel 5. Keterbatasan dan kelebihan kriteria SIRS dan SOFA

Sepsis SIRS SOFA

Keterbatasan Kriteria SIRS tidak spesifik
(ditemukan kasus SIRS namun tidak ada proses
infeksi melalui hasil kultur)6,9
Keunggulan
Assessment untuk identifikasi kegagalan organ tidak untuk mendefinisikan sepsis14
„„ Lebih dari 75% pasien diduga infeksi dengan qSOFA score >2 dan skor SOFA positif mengindikasikan
disfungsi organ dan suspek sepsis4
„„ Kriteria qSOFA mudah digunakan dan membantu klinisi memberikan tatalaksana awal tanpa
menunggu hasil laboratorium10,14

CDK-280/ vol. 46 no. 11 th. 2019 683

 ANALISIS

1. Passive leg raising test.
Penilaian ini untuk menilai pasien sepsis
kategori responder atau non-responder, dengan
sensitivitas 97% dan spesifisitas 94%.15 Bila
pulse pressure bertambah > 10% dari baseline,
dianggap responder. Penilaian ini bertujuan
untuk menilai peningkatan cardiac output
dengan penambahan volume.15
Diagram. Rekomendasi pemberian vasopresor dan steroid pada manajemen syok sepsis.17
Dosis Norepinefrin dimulai hingga 35-90 ug/min
untuk mencapai MAP 65 mmHg
Target MAP tercapai Target tidak tercapai dan tidak
respin dengan pemberian NE

2. Fluid challenge test.

Ne dilanjutkan atau Vasopressin ditingkatkan
Mengukur kemaknaan perubahan isi sekuncup penambahan vasopresor menjadi 0.03 unit per menit*
jantung (stroke volume) atau tekanan sistolik 0.03 unit tiap menit untuk
mengantisipasi pengurangan
arterial, atau tekanan nadi (pulse pressure). dosis NEP
Pemberian cairan dapat mengembalikan Target MAP tercapai Target MAP tidak tercapai
distribusi oksigen dalam darah dan perfusi
ke organ vital untuk mencegah ganguan
Dosis NEP ditingkatkan 20-50ug per menit
kerusakan organ.15 untuk mencapai target MAP

3. Stroke Volume Variation (SVV).

Penilaian variasi isi sekuncup jantung akibat *Pemberian steroid dipertimbangkan Target MAP Tambahkan
tercapai fenilefrin 300-
perubahan tekanan intra-toraks saat pasien **Berikan pemberian IV Steroid 300 ug per menit
menggunakan ventilasi mekanik. Syarat untuk meningkatkan
***Pedoman SSC diam terhadap pemberian fenilefrin MAP
penilaian responsivitas cairan dengan metode
ini adalah:15
„„ Pasien dalam kontrol ventilasi mekanis Catatan :
penuh Pertimbangkan dopamin vasopressor alternatif jika terdapat sinus bradikardia
„„ Volume tidal 8-10 mL/kgBB (predicted Pertimbangkan pemberian fenilefrin apabila timbul takiaritmia berbahaya akibat pemberian norepinefrin atau
body weight), epinefrin
„„ Tidak ada aritmia. Pasien masuk kategori Berdasarkan penilitian seusai dengan EBM tidak ditemukan batasan pemberian norepinefrin , epinefrin dan
responder bila SVV ≥12%. fenilefrin. Rentang dosis yang dicantumkan pada alogritma ini berdasarkan pengalaman peneliti. Dosis
maksimal dievaluasi berdasarkan respons fisiologis.

Selain SVV, Pulse Pressure Variation (PPV)
juga dapat dipergunakan untuk menilai
responsivitas cairan.15
Pemberian Vasopressor (Rekomendasi kuat,
bukti penelitian cukup)
Manajemen resusitasi awal bertujuan untuk
mengembalikan perfusi jaringan, terutama
perfusi organ vital. Jika tekanan darah
tidak meningkat setelah resusitasi cairan,
pemberian vasopressor tidak boleh ditunda.4
Vasopressor harus diberikan dalam 1 jam
pertama untuk mempertahankan MAP >65
mmHg.4 Dalam review beberapa literatur
ditemukan pemberian vasopressor/inotropik
sebagai penanganan awal dari sepsis.4
Pemilihan Vasopressor
Norepinefrin direkomendasi sebagai
vasopresor lini pertama. Penambahan
vasopressin (sampai 0,03 U/menit) atau
epinefrin untuk mencapai target MAP dapat
dilakukan.15,17
Dopamin sebagai vasopresor alternatif
norepinefrin hanya direkomendasikan untuk
pasien tertentu, misalnya pada pasien berisiko
rendah takiaritmia dan bradikardi relatif.12,15
Penggunaan dopamin dosis rendah untuk
proteksi ginjal sudah tidak direkomendasikan
lagi.15 Dobutamin disarankan diberikan pada
hipoperfusi menetap meskipun sudah diberi
cairan adekuat dan vasopresor.15 Steroid dapat
digunakan apabila dengan norepinefrin target
MAP masih belum tercapai.12
INDIKATOR KEBERHASILAN RESUSITASI
AWAL
Evaluasi Mean Arterial Pressure (MAP)
MAP merupakan driving pressure untuk perfusi
jaringan atau organ terutama otak dan ginjal.
Batas rekomendasinya adalah 65 mmHg.15
Penetapan target MAP yang lebih tinggi
(85 mmHg dibandingkan 65 mmHg) justru
meningkatkan risiko aritmia.15 Target MAP
lebih tinggi mungkin perlu dipertimbangkan
pada riwayat hipertensi kronis.12,15,18
Laktat
Laktat sebagai penanda perfusi jaringan
dianggap lebih objektif dibandingkan
pemeriksaan fisik atau produksi urin.15
Keberhasilan resusitasi pasien sepsis dapat
dinilai dengan memantau penurunan kadar
laktat, terutama jika awalnya mengalami
peningkatan kadar laktat.15
Tekanan Vena Sentral (CVP) dan Saturasi
Vena Sentral (SvO2)
Tekanan CVP normal adalah 8-12 mmHg.
CVP sebagai parameter panduan tunggal
resusitasi cairan tidak direkomendasikan lagi.15
Jika CVP dalam kisaran normal (8-12 mmHg),
kemampuan CVP untuk menilai responsivitas
cairan (setelah pemberian cairan atau fluid
challenge) terbukti tidak akurat.15 Penggunaan
target CVP secara absolut seharusnya
dihindari, karena cenderung mengakibatkan
resusitasi cairan berlebihan.15
CO2 gap (Perbedaan kadar karbondioksida
arteri dan vena (Pv-a CO2))
Peningkatan produksi CO2 merupakan salah

684 CDK-280/ vol. 46 no. 11 th. 2019


OUTLINE
Etiology of Burn Injury
Pathophysiology of Burn Injury
Basic Treatment of Burn Injury
Specific Treatment of Burns
Attenuation of the Hypermetabolic Response
Special Considerations: Electrical and Chemical Burns
Outcomes
Burn Units
Summary
More than 500,000 burn injuries occur annually in the United
States.1 Although most of these burn injuries are minor, approxi-
mately 40,000 to 60,000 burn patients require admission to a
hospital or major burn center for appropriate treatment. The
devastating consequences of burns have been recognized by the
medical community and significant amounts of resources and
research have been dedicated, successfully improving these dismal
statistics.2 Specialized burn centers (Box 19-1) and advances in
therapy strategies, based on improved understanding of resuscita-
tion, enhanced wound coverage, more appropriate infection
control, improved treatment of inhalation injury, and better
support of the hypermetabolic response to injury, have further
improved the clinical outcome of this unique population of
patients during the past years.3,4 However, severe burns remain a
devastating injury affecting nearly every organ system and leading
to significant morbidity and mortality.5,6
ETIOLOGY OF BURN INJURY
There is no greater trauma than major burn injury, which can be
classified according to different burn causes and different depths
(Box 19-2). Of all cases, nearly 4000 people die of complications
related to thermal injury.7 As in all trauma-related deaths, burn
deaths generally occur either immediately after the injury or weeks
later as a result of multisystem organ failure. Sixty-six percent of
all burns occur at home, and fatalities are predominant in the
extremes of age—the very young and the elderly. The most
common causes of burn are flame and scald burns.8 Scald burns
are most common in children up to 5 years of age.8 There is a
significant percentage of burns in children that are due to child
abuse. A number of risk factors have been linked to burn injury,
specifically age, location, demographics, and low economic status.9
These risk factors underscore the fact that most burn injuries
and fatalities are preventable and mandate intervention and
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For personal use only. No other uses without permission. Copyright ©2020. Elsevier Inc. All rights reserved.
CHAPTER 19
Burns
Marc G. Jeschke, David N. Herndon
prevention strategies. Overall, no single group is immune to the
public health debt caused by burns.
Location plays a major role in the risk for and treatment of a
burn. The available resources in a given community greatly influ-
ence morbidity and mortality. A lack of adequate resources affects
the education, rehabilitation, and survival rates for burn victims.
An individual with a severe burn in a resource-rich environment
can receive care within minutes, whereas a burned person in an
austere environment may suffer for an extended time waiting for
care. Ideal treatment of burns requires the collaboration of sur-
geons, anesthesiologists, occupational therapists and physiothera-
pists, nurses, nutritionists, rehabilitation therapists, and social
workers just to accommodate the very basic needs of a major burn
survivor.10 Any delay in reaching these resources compounds a
delay in resuscitation and thus adds to the mortality risk.11 For
those who have access to adequate burn care, survival from a
major burn is the rule, no longer the exception. In fact, the sur-
vival rate for all burns is 94.6%, but for at-risk populations, in
communities lacking medical, legal, and public health resources,
survival can be nearly impossible.8
PATHOPHYSIOLOGY OF BURN INJURY
Local Changes
Locally, thermal injury causes coagulative necrosis of the epider-
mis and underlying tissues; the depth of injury depends on the
temperature to which the skin is exposed, the specific heat of the
causative agent, and the duration of exposure. Burns are classified
into five different causal categories and depths of injury. The
causes include injury from flame (fire), hot liquids (scald), contact
with hot or cold objects, chemical exposure, and conduction of
electricity (Box 19-2). The first three induce cellular damage
by the transfer of energy, which induces coagulation necrosis.
Chemical burns and electrical burns cause direct injury to cellular
505
512 SECTION III Trauma and Critical Care

Burn wound

↑↑ Oxygen consumption ↑↑ 20-fold

Catecholamines Intestine

Heart Serum Alanine Ammonia

↑↑ Glucagon
↑↑ Cardiac output ↑↑ Heart rate ↑↑ Cortisol ↑↑ Insulin Glutamine

Glutamine
Nitrogen
↑↑ Kidney
Wasting
Ammonia

Bone
↓↓ Calcium Liver
Alanine Glutamine
↓↓ Magnesium Urea Ammonia
Muscle
Glucose Glycogen
Fat stores Glucose
Glucose
Glycolysis Lactate
↑ Fractures Glycolysis Lactate
↓ Bone mineral content
↓ Bone mineral density Pyruvate
Pyruvate
Lipid complexes
↑↑ Fatty acids
↑↑ Glycerol ↑↑ Lactate
FIGURE 19-7 Effects of metabolic dysfunction after burn injury. (From Williams FN, Jeschke MG, Chinkes
DL, et al: Modulation of the hypermetabolic response to trauma: Temperature, nutrition, and drugs. J Am
Coll Surg 208:489–502, 2009.)

conditions are based on depressed cellular function in all parts of
the immune system, including activation and activity of neutro-
phils, macrophages, T lymphocytes, and B lymphocytes. With
burns of more than 20% TBSA, impairment of these immune
functions is proportional to burn size.
Macrophage production after burn injury is diminished, which
is related to the spontaneous elaboration of negative regulators of
myeloid growth. This effect is enhanced by the presence of endo-
toxin and can be partially reversed with granulocyte colony-
stimulating factor (G-CSF) treatment or inhibition of prostaglandin
E2. Investigators have shown that G-CSF levels actually increase
after severe burn. However, bone marrow G-CSF receptor expres-
sion is decreased, which may in part account for the immunode-
ficiency seen in burns. Total neutrophil counts are initially
increased after burn injury, a phenomenon that is related to a
decrease in cell death by apoptosis. However, neutrophils that are
present are dysfunctional in terms of diapedesis, chemotaxis, and
phagocytosis. These effects are explained, in part, by a deficiency
in CD11b/CD18 expression after inflammatory stimuli, decreased
respiratory burst activity associated with a deficiency in p47phox
activity, and impaired actin mechanics related to neutrophil
motile responses. After 48 to 72 hours, neutrophil counts decrease
somewhat, like macrophages, with similar causes.
T-helper cell function is depressed after a severe burn that is
associated with polarization from the interleukin-2 and interferon-γ
cytokine-based T-helper 1 (Th1) response toward the Th2 response.
The Th2 response is characterized by the production of interleukin-4
and interleukin-10. The Th1 response is important in cell-mediated
immune defense, whereas the Th2 response is important in
antibody responses to infection. As this polarization increases, so
does the mortality rate. Administration of interleukin-10 antibod-
ies and growth hormone has partially reversed this response and
improved mortality rate after burn injury in animals. Burn also
impairs cytotoxic T-lymphocyte activity as a function of burn size,
thus increasing the risk of infection, particularly from fungi and
viruses. Early burn wound excision improves cytotoxic T-cell
activity.
BASIC TREATMENT OF BURN INJURY
Prehospital Management
Before undergoing any specific treatment, burned patients must
be removed from the source of injury and the burning process
stopped. Inhalation injury should always be suspected, and 100%
oxygen should be given by face mask. While the patient is being
removed from the source of injury, care must be taken so that the
rescuer does not become another victim. All caregivers should be
aware that they might be injured by contact with the patient or
the patient’s clothing. Universal precautions, including wearing of
gloves, gowns, mask, and protective eyewear, should be used
whenever there is likely to be contact with blood or body fluids.
Burning clothing should be extinguished and removed as soon as
possible to prevent further injury. All rings, watches, jewelry, and
belts should be removed because they retain heat and can produce
a tourniquet-like effect. Room temperature water can be poured
on the wound within 15 minutes of injury to decrease the depth
of the wound, but any subsequent measures to cool the wound
should be avoided to prevent hypothermia during resuscitation.

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Table 92.1 Burn Prophylaxis
PREVENT FIRES
Install and use smoke detectors.
Control the hot water thermostat; in public buildings, maximum
water temperature should be 48.9°C (120°F).
Keep fire, matches, and lighters out of the reach of children.
Avoid cigarette smoking, especially in bed.
Do not leave lit candles unattended.
Use flame retardant–treated clothing.
Use caution when cooking, especially with oil.
Keep cloth items off heaters.
PREVENT INJURY
Roll, but do not run, if clothing catches fire; wrap in a blanket.
Practice escape procedures.
Crawl beneath smoke if a fire occurs indoors.
Use educational materials.*
*National Fire Protection Association pamphlets and videos.
burns of all sizes is 99%. Death is more likely in children with irreversible
anoxic brain injury sustained at the time of the burn. It is well known
that burns occur in predictable patterns. Sources of burns include,
by season:
Winter:
◆ Glass front fireplaces/pellet stoves and radiators increase hand burns.
◆ Treadmill injuries as more people exercise inside—child imitates
adults or young child touches belt.
Summer:
◆ Fireworks, sparkler—temperatures reach 537.8°C (1,000°F).
◆ Burn contact with hot grill; hand/feet burn from hot embers.
◆ Lawnmowers
Spring/Fall:
◆ Burning leaves
◆ Gasoline burns
◆ Tap water scalds are essentially preventable through a combination
of behavioral and environmental changes.
Pediatricians can play a major role in preventing the most common
burns by educating parents and healthcare providers. Simple, effective,
efficient, and cost-effective preventive measures include the use of
appropriate clothing and smoke detectors and the planning of routes
for emergency exit from the home. The National Fire Protection Associa-
tion (NFPA) recommends replacing smoke detector batteries annually
and the smoke detector alarm every 10 yr (or earlier, if indicated on
the device). Child neglect and abuse must be seriously considered when
the history of the injury and the distribution of the burn do not match.
ACUTE CARE, RESUSCITATION, AND ASSESSMENT
Indications for Admission
Burns covering >10% of total body surface area (BSA), burns associated
with smoke inhalation, burns resulting from high-tension (voltage)
electrical injuries, and burns associated with suspected child abuse or
neglect should be treated as emergencies and the child hospitalized
(Table 92.2). Small 1st- and 2nd-degree burns of the hands, feet, face,
perineum, and joint surfaces also require admission if close follow-up
care is difficult to provide. Children who have been in enclosed-space
fires and those who have face and neck burns should be hospitalized
for at least 24 hr for observation for signs of central nervous system
(CNS) effects of anoxia from carbon monoxide (CO) poisoning and
pulmonary effects from smoke inhalation.
First Aid Measures
Acute care should include the following measures:
1. Extinguish flames by rolling the child on the ground; cover the child
with a blanket, coat, or carpet.
2. After determining that the airway is patent, remove smoldering
clothing or clothing saturated with hot liquid. Jewelry, particularly
rings and bracelets, should be removed or cut away to prevent
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Chapter 92 ◆ Burn Injuries 615
Table 92.2 Indications for Hospitalization for Burns
Burns affecting >10% of BSA
Burns >10–20% of BSA in adolescent/adult
3rd-degree burns
Electrical burns caused by high-tension wires or lightning
Chemical burns
Inhalation injury, regardless of the amount of BSA burned
Inadequate home or social environment
Suspected child abuse or neglect
Burns to the face, hands, feet, perineum, genitals, or major joints
Burns in patients with preexisting medical conditions that may
complicate the acute recovery phase
Associated injuries (fractures)
Pregnancy
BSA, Body surface area.
Table 92.3 Acute Treatment of Burns
First aid, including washing of wounds and removal of devitalized
tissue
Fluid resuscitation
Provision of energy requirements
Control of pain
Prevention of infection—early excision and grafting
Prevention of excessive metabolic expenditures
Control of bacterial wound flora
Use of biologic and synthetic dressings to close the wound
constriction and vascular compromise during the edema phase in
the first 24-72 hr after burn injury.
3. In cases of chemical injury, brush off any remaining chemical, if
powdered or solid; then use copious irrigation or wash the affected
area with water. Call the local poison control center for the neutralizing
agent to treat a chemical ingestion.
4. Cover the burned area with clean, dry sheeting and apply cold (not
iced) wet compresses to small injuries. Significant large-burn injury
(>15% of BSA) decreases body temperature control and contraindicates
the use of cold compresses.
5. If the burn is caused by hot tar, use mineral oil to remove the tar.
6. Administer analgesic medications.
Emergency Care
Supportive measures are as follows (Table 92.3 and Table 92.4)
1. Rapidly review the cardiovascular and pulmonary status and document
preexisting or physiologic lesions (asthma, congenital heart disease,
renal or hepatic disease).
2. Ensure and maintain an adequate airway, and provide humidified
oxygen by mask or endotracheal intubation (Fig. 92.1). The latter
may be needed in children who have facial burns or a burn sustained
in an enclosed space, before facial or laryngeal edema becomes evident.
If hypoxia or CO poisoning is suspected, 100% oxygen should be
used (see Chapters 81 and 89).
3. Children with burns >15% of BSA require intravenous (IV) fluid
resuscitation to maintain adequate perfusion. In an emergency situation
if IV access is unattainable, an intraosseous line should be placed.
When inserting central lines to provide high-volume fluid, special
attention should be paid to use a very-small-caliber catheter in small
children to avoid injury to the vascular lining, which may predispose
to formation of clots. All inhalation injuries, regardless of the extent
of BSA burn, require venous access to control fluid intake. All high-
tension and electrical injuries require venous access to ensure forced
alkaline diuresis in case of muscle injury to avoid myoglobinuric
renal damage. Lactated Ringer solution, 10-20 mL/kg/hr (normal
saline may be used if lactated Ringer solution is not available), is
initially infused until proper fluid replacement can be calculated.
Consultation with a specialized burn unit should be made to coordinate
 Chapter 92 ◆ Burn Injuries 617

Table 92.5 Categories of Burn Depth

2ND-DEGREE, OR PARTIAL-THICKNESS, 3RD-DEGREE, OR FULL-THICKNESS,
1ST-DEGREE BURN BURN BURN
Surface appearance Dry, no blisters Moist blebs, blisters Dry, leathery eschar
Minimal or no edema Underlying tissue is mottled pink and Mixed white, waxy, khaki, mahogany,
Erythematous white, with fair capillary refill soot-stained
Blanches, bleeds Bleeds No blanching or bleeding
Pain Very painful Very painful Insensate
Histologic depth Epidermal layers only Epidermis, papillary, and reticular layers of Down to and may include fat,
dermis subcutaneous tissue, fascia, muscle,
May include domes of subcutaneous layers and bone
Healing time 2-5 days with no scarring Superficial: 5-21 days with no grafting Large areas require grafting, but small
Deep partial: 21-35 days with no infection; areas may heal from the edges after
if infected, converts to full-thickness burn weeks

Superficial Deep Full- viable. Fluid losses and metabolic effects of deep dermal (2nd-degree)
Superficial dermal dermal thickness burns are essentially the same as those of 3rd-degree burns.
Full-thickness, or 3rd-degree, burns involve destruction of the entire
Epidermis epidermis and dermis, leaving no residual epidermal cells to repopulate
the damaged area. The wound cannot epithelialize and can heal only by
wound contraction or skin grafting. The absence of painful sensation and
capillary filling demonstrates the loss of nerve and capillary elements.
Technologies are being used to help accurately determine the depth
Dermis of burns. Laser Doppler imaging can be used from 48 hr to 5 days after
the burn. It produces a color map of the affected tissue; yellow indicates
second-degree burns, reflecting the presence of capillaries, arterioles,
and venules, and blue reflects very low or absence of blood flow, which
indicates third-degree burns. Its accuracy is up to 95%, and with accurate
Sub- assessment, the proper treatment can be applied without delay. Doppler
cutaneous imaging can be used in both outpatients and inpatients.
Another technology called reflectance confocal microscopy (RCM),
Fig. 92.2 Diagram of different burn depths. (From Hettiaratchy S, can be combined with optical coherence tomography (OCT) to visualize
Papini R: Initial management of a major burn. II. Assessment and tissue morphology at the subcellular level. It determines if the cells are
resuscitation, BMJ 329:101–103, 2004.) damaged and enables detection of skin morphologic changes up to
1 mm in depth. It provides accurate determination of the depth of the
burn, allowing for the appropriate treatment.

7. All wounds should be wrapped with sterile dressings until it is decided
whether to treat the patient on an outpatient basis or refer to an
appropriate facility.
8. A CO measurement (carboxyhemoglobin [HbCO]) should be obtained
for fire victims and 100% oxygen administered until the result is
known.
9. Review child immunization. Burns <10% BSA do not require tetanus
prevention, whereas burns >10% need tetanus immunization. Use
diphtheria, tetanus toxoids, and acellular pertussis (DTaP) for tetanus
prophylaxis for children <11 yr old, and use tetanus, diphtheria, and
pertussis (TdaP) for children >11 yr old (see Chapter 238).
Classification of Burns
Proper triage and treatment of burn injury require assessment of the
extent and depth of the injury (Table 92.5 and Fig. 92.2). 1st-degree
burns involve only the epidermis and are characterized by swelling,
erythema, and pain (similar to mild sunburn). Tissue damage is usually
minimal, and there is no blistering. Pain resolves in 48-72 hr; in a small
percentage of patients, the damaged epithelium peels off, leaving no
residual scars.
A 2nd-degree burn involves injury to the entire epidermis and a
variable portion of the dermal layer (vesicle and blister formation are
characteristic). A superficial 2nd-degree burn is extremely painful because
many remaining viable nerve endings are exposed. Superficial 2nd-degree
burns heal in 7-14 days as the epithelium regenerates in the absence of
infection. Mid-level to deep 2nd-degree burns also heal spontaneously
if wounds are kept clean and infection free. Pain is less with these burns
than in more superficial burns because fewer nerve endings remain
Estimation of Body Surface Area for a Burn
Appropriate burn charts for different childhood age-groups should be
used to accurately estimate the extent of BSA burned. The volume of
fluid needed in resuscitation is calculated from the estimation of the
extent and depth of burn surface. Mortality and morbidity also depend
on the extent and depth of the burn. The variable growth rate of the
head and extremities throughout childhood makes it necessary to use
BSA charts, such as that modified by Lund and Brower or the chart
used at the Shriners Hospital for Children in Boston (Fig. 92.3). The
rule of nines used in adults may be used only in children >14 yr old
or as a rough estimate to institute therapy before transfer to a burn
center. In small burns, <10% of BSA, the rule of palm may be used,
especially in outpatient settings; the area from the wrist crease to the
finger crease (the palm) in the child equals 1% of the child’s BSA.
TREATMENT
Outpatient Management of Minor Burns
A patient with 1st- and 2nd-degree burns of <10% BSA may be treated
on an outpatient basis unless family support is judged inadequate or
there are issues of child neglect or abuse. These outpatients do not
require a tetanus booster (unless not fully immunized) or prophylactic
penicillin therapy. Blisters should be left intact and dressed with bacitracin
or silver sulfadiazine cream (Silvadene). Dressings should be changed
once daily, after the wound is washed with lukewarm water to remove
any cream left from the previous application. Very small wounds,
especially those on the face, may be treated with bacitracin ointment
and left open. Debridement of the devitalized skin is indicated when
the blisters rupture. A variety of wound dressings and wound membranes

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