Step 7

1. Bagaimana anatomi dan fisiologi kulit?

 Struktur kulit
Kulit terdiri atas 2 lapisan utama yaitu epidermis dan dermis. Epidermis merupakan
jaringan epitel yang berasal dari ektoderm, sedangkan dermis berupa jaringan ikat
agak padat yang berasal dari mesoderm. Di bawah dermis terdapat selapis jaringan
ikat longgar yaitu hipodermis, yang pada beberapa tempat terutama terdiri dari
jaringan lemak.

Epidermis
Epidermis terdiri atas 5 lapisan yaitu, dari dalam ke luar, stratum basal, stratum spinosum,
stratum granulosum, stratum lusidum, dan stratum korneum

Stratum basal (lapis basal, lapis benih)

Lapisan ini terletak paling dalam dan terdiri atas satu lapis sel yang tersusun berderet-deret di atas
membran basal dan melekat pada dermis di bawahnya. Selselnya kuboid atau silindris. Intinya besar,
jika dibanding ukuran selnya, dan sitoplasmanya basofilik. Pada lapisan ini biasanya terlihat
gambaran mitotik sel, proliferasi selnya berfungsi untuk regenerasi epitel. Sel-sel pada lapisan ini
bermigrasi ke arah permukaan untuk memasok sel-sel pada lapisan yang lebih superfisial.
Pergerakan ini dipercepat oleh adalah luka, dan regenerasinya dalam keadaan normal cepat.

Stratum spinosum (lapis taju)

Lapisan ini terdiri atas beberapa lapis sel yang besar-besar berbentuk poligonal dengan inti lonjong.
Sitoplasmanya kebiruan. Bila dilakukan pengamatan dengan pembesaran obyektif 45x, maka pada
dinding sel yang berbatasan dengan sel di sebelahnya akan terlihat taju-taju yang seolah-olah
menghubungkan sel yang satu dengan yang lainnya. Pada taju inilah terletak desmosom yang
melekatkan sel-sel satu sama lain pada lapisan ini. Semakin ke atas bentuk sel semakin gepeng.

Stratum granulosum (lapis berbutir)

Lapisan ini terdiri atas 2-4 lapis sel gepeng yang mengandung banyak granula basofilik yang disebut
granula keratohialin, yang dengan mikroskop elektron ternyata merupakan partikel amorf tanpa
membran tetapi dikelilingi ribosom. Mikrofilamen melekat pada permukaan granula.

Stratum lusidum (lapis bening)

Lapisan ini dibentuk oleh 2-3 lapisan sel gepeng yang tembus cahaya, dan agak eosinofilik. Tak ada
inti maupun organel pada sel-sel lapisan ini. Walaupun ada sedikit desmosom, tetapi pada lapisan ini
adhesi kurang sehingga pada sajian seringkali tampak garis celah yang memisahkan stratum
korneum dari lapisan lain di bawahnya.

Stratum korneum (lapis tanduk)

Lapisan ini terdiri atas banyak lapisan sel-sel mati, pipih dan tidak berinti serta sitoplasmanya
digantikan oleh keratin. Selsel yang paling permukaan merupa-kan sisik zat tanduk yang terdehidrasi
yang selalu terkelupas.

Lapisan Dermis (korium, kutis vera, true skin) => terdiri dari lapisan elastik dan fibrosa pada
dengan elemen-elemen selular dan folikel rambut.

o Pars Papilare => bagian yang menonjol ke epidermis, berisi ujung serabut
saraf dan pembuluh darah.
o Pars Retikulare => bagian bawah yang menonjol ke subkutan. Terdiri dari
serabut penunjang seperti kolagen, elastin, dan retikulin. Dasar (matriks)
lapisan ini terdiri dari cairan kental asam hialuronat dan kondroitin sulfat,
dibagian ini terdapat pula fibroblas. Serabut kolagen dibentuk oleh fibroblas,
selanjutnya membentuk ikatan (bundel) yang mengandung hidroksiprolin dan
hidroksisilin. Kolagen muda bersifat elastin, seiring bertambahnya usia,
menjadi kurang larut dan makin stabil. Retikulin mirip kolagen muda. Serabut
elastin biasanya bergelombang, berbentuk amorf, dan mudah mengembang
serta lebih elastis.

Lapisan Subkutis (hipodermis) => lapisan paling dalam, terdiri dari jaringan ikat longgar
berisi sel lemak yang bulat, besar, dengan inti mendesak ke pinggir sitoplasma lemak yang
bertambah. Sel ini berkelompok dan dipisahkan oleh trabekula yang fibrosa. Lapisan sel
lemak disebut dengan panikulus adiposa, berfungsi sebagai cadangan makanan. Di lapisan ini
terdapat saraf tepi, pembuluh darah, dan getah bening. Lapisan lemak berfungsi juga sebagai
bantalan, ketebalannya berbeda pada beberapa kulit. Di kelopak mata dan penis lebih tipis, di
perut lebih tebal (sampai 3 cm).

FUNGSI KULIT

1. Fungsi Proteksi
Kulit punya bantalan lemak, ketebalan, serabut jaringan penunjang yang dapat
melindungi tubuh dari gangguan :
o fisis/ mekanis : tekanan, gesekan, tarikan.
o kimiawi : iritan seperti lisol, karbil, asam, alkali kuat
o panas : radiasi, sengatan sinar UV
o infeksi luar : bakteri, jamur

Beberapa macam perlindungan :

o Melanosit => lindungi kulit dari pajanan sinar matahari dengan mengadakan
tanning (penggelapan kulit)
o Stratum korneum impermeable terhadap berbagai zat kimia dan air.
o Keasaman kulit kerna ekskresi keringat dan sebum => perlindungan kimiawo
terhadap infeksi bakteri maupun jamur
 o Proses keratinisasi => sebagai sawar (barrier) mekanis karena sel mati
melepaskan diri secara teratur.
2. Fungsi Absorpsi => permeabilitas kulit terhadap O2, CO2, dan uap air
memungkinkan kulit ikut mengambil fungsi respirasi. Kemampuan absorbsinya
bergantung pada ketebalan kulit, hidrasi, kelembaban, metabolisme, dan jenis
vehikulum. PEnyerapan dapat melalui celah antar sel, menembus sel epidermis,
melalui muara saluran kelenjar.
3. Fungsi Ekskresi => mengeluarkan zat yang tidak berguna bagi tubuh seperti NaCl,
urea, asam urat, dan amonia. Pada fetus, kelenjar lemak dengan bantuan hormon
androgen dari ibunya memproduksi sebum untuk melindungi kulitnya dari cairan
amnion, pada waktu lahir ditemui sebagai Vernix Caseosa.
4. Fungsi Persepsi => kulit mengandung ujung saraf sensori di dermis dan subkutis.
Saraf sensori lebih banyak jumlahnya pada daerah yang erotik.
o Badan Ruffini di dermis dan subkutis => peka rangsangan panas
o Badan Krause di dermis => peka rangsangan dingin
o Badan Taktik Meissner di papila dermis => peka rangsangan rabaan
o Badan Merkel Ranvier di epidermis => peka rangsangan rabaan
o Badan Paccini di epidemis => peka rangsangan tekanan
5. Fungsi Pengaturan Suhu Tubuh (termoregulasi) => dengan cara mengeluarkan
keringat dan mengerutkan (otot berkontraksi) pembuluh darah kulit. Kulit kaya
pembuluh darah sehingga mendapat nutrisi yang baik. Tonus vaskuler dipengaruhi
oleh saraf simpatis (asetilkolin). Pada bayi, dinding pembuluh darah belum sempurna
sehingga terjadi ekstravasasi cairan dan membuat kulit bayi terlihat lebih edematosa
(banyak mengandung air dan Na)
6. Fungsi Pembentukan Pigmen => karena terdapat melanosit (sel pembentuk pigmen)
yang terdiri dari butiran pigmen (melanosomes)
7. Fungsi Keratinisasi => Keratinosit dimulai dari sel basal yang mengadakan
pembelahan, sel basal yang lain akan berpindah ke atas dan berubah bentuknya
menjadi sel spinosum, makin ke atas sel makin menjadi gepeng dan bergranula
menjadi sel granulosum. Makin lama inti makin menghilang dan keratinosit menjadi
sel tanduk yang amorf. Proses ini berlangsung 14-21 hari dan memberi perlindungan
kulit terhadap infeksi secara mekanis fisiologik.
8. Fungsi Pembentukan Vitamin D => kulit mengubah 7 dihidroksi kolesterol dengan
pertolongan sinar matahari. Tapi kebutuhan vit D tubuh tidak hanya cukup dari hal
tersebut. Pemberian vit D sistemik masih tetap diperlukan.

2. Mengapa luka bakar dapat menyebabkan bula?

3. Apa saja klasifikasi derajat luka bakar?

- First-degree (superficial thickness, affecting the epidermis only) burns are

typically benign, very painful, heal without scarring and do not require surgery.

- Burns extending into the underlying skin layer (dermis) are classed as partial
thickness or second-degree; these burns frequently form painful blisters. These
burns range from superficial partial thickness, which are homogeneous, moist,
 hyperaemic and blanch, to deep partial thickness, which are less sensate, drier,
may have a reticular pattern to the erythema and do not blanch.

- Third-degree (full thickness) and fourth-degree burns require surgery and,

paradoxically, usually present with almost no pain.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224101/

4. Bagaimana interpretasi pf Vital Sign: RR: 28 x/menit, TD: 100/70 mmHg, N: 100
x/menit?
If the burn area exceeds 30% of the total body surface area, cytokines released from
the burn area and other inflammatory mediators reach levels that will produce a
systemic response [13]. An inflammatory reaction also occurs as a result of a minor
thermal injury lasting for 20–60 seconds and at a temperature of 51–60°C. Burn shock
period can be examined in three periods:
Early period (exudative period):
It covers the first 36–72 hours after trauma. Vasodilatation is the first response to
trauma in the burn area. Systemic inflammatory mediators (histamine, TNF-α, IL-1,
IL-6, GM-CSF, interferon-ɤ, and prostaglandins) are excessively released from both
 the burn site and from other tissues. Capillary permeability increases, due to
inadequate tissue perfusion, intracellular sodium increases, and edema develops in the
cells [27]. Burn shock developed after burns is hypovolemic shock and is directly
proportional to the extent and severity of burns. In adults 20%, in children younger
than 12 years of age 10%, of burn area leads to a higher risk for hypovolemic shock
development [4, 24]. Hypovolemia resulting from circulatory fluid loss due to edema,
occurs within the first 2 days utmost. Hemodynamic insufficiency develops due to
decreased blood volume. As circulation in the brain, kidneys, liver, muscles, and
gastrointestinal system deteriorates, oxygenation is reduced. Ischemia develops in the
tissues as a result of hypovolemia and slowing down of blood flow. Damage to cells that
develops in hypoxia leads to dysfunction in organs [13, 24]. Clinical signs of hypovolemic
shock are observed as follows:
- Pale, moist, cool skin.
- Hyperthermia have coldness at extremities.
- Tachycardia and hypotension.
- Fast and shallow breathing.
- Decrease in urine volume.
Intermediate period (intoxication period):

Includes 2–4 weeks after burn. During this period, the formation of edema stops and polyuria
develops. While edema is regressing, the denatured proteins released from the cells pass through
the circulation to form the intoxication case. At the end of the first week after burn, the
hemodynamic situation is completely reversed and there is an abnormally high cardiac output
accompanied by vasodilatation in the burn patient. On the 10th day after the burn, the cardiac
output is increased by 2.5 times of normal [28].

Late (infectious) period:

Acute and chronic infections may occur during this period. The cellular and humoral immune
response is suppressed in direct proportion to the size of the burn. Lymphopenia develops
chemotaxis, phagocytosis, and migration of neutrophils are reduced. IL-2 level decreases in burns
that hold large surface area. IL-1, IL-6, and IL-8 levels decrease in the first week after burn [23].
Increased catabolism and capillary leakage result in reduced circulating IgG, IgA, and IgM. The
decrease in IgG, especially after burn injuries, is closely related to septic complications [13, 29]. With
respect to the grade of the burn, T cell activation is impaired, creating a predisposing condition for
viral and fungal infections

5. Mengapa didapatkan urin hanya 5cc dan berwarna kuning kemerahan setelah 30
menit?
RENAL

Defining acute renal failure in the burn population has been problematic, with various
studies reporting ranges from 0.5 to 30%.22,33 In the past, the International Acute
Dialysis Quality Initiative group standardized the definition of acute renal
insufficiency by developing the RIFLE criteria.22,33 The RIFLE criteria define three
different grades of acute renal injury (risk, injury, and failure) based on glomerular
filtration rate, urine output, and two clinical outcome parameters (loss and end-stage
kidney disease).22,33 In 2007, the Acute Kidney Injury Network (AKIN) developed a
 modified standard for diagnosis and classifying acute kidney injury (AKI). Chung et
al.34 compared a cohort of patients using the RIFLE criteria and AKIN criteria. The
determined in-hospital mortality was significantly higher using the AKIN criteria at
0.877 (95% confidence interval: 0.848–0.906) when compared with the RIFLE
criteria at 0.838 (95% confidence interval: 0.801–0.874; P = .0007).34 The results of
this study suggested that the AKIN criteria may be more precise and more predictive
of death than the RIFLE criteria.34

AKI related to thermal injury is most likely to occur at two distinct time points: early
during resuscitation or late secondary to sepsis.22 Early AKI has been shown to be
associated with early multiple organ dysfunction and higher mortality risk.35
Increasing size and depth of burns are key factors determining AKI.33 Prevention of
AKI requires early and aggressive fluid resuscitation and preservation of normal renal
perfusion.22 Global parameters of perfusion (lactate, base deficit, and central venous
saturation) are more appropriate than urine output alone in reflecting the degree and
recovery from a hypoperfused state, or a state of shock.22

The pathophysiology of late AKI is altered from that of early AKI, and remains a
serious problem within the burn intensive care unit.22 Sepsis or septic shock accounts
for up to 87% of the cases of acute renal failure within the burn intensive care unit.22
Late AKI is multifactorial, but primarily relates to the systemic inflammatory
response that accompanies a septic event such as generalized vasodilation and a
hypercoagulabe state.22 These result in AKI via a decrease in renal perfusion:
globally via vasodilation resulting in decreased systemic blood pressure and locally
by formation of microthrombi in the glomeruli.22 Ultimately, renal replacement
therapy has been shown to be only marginally affective in reducing mortality rates,
and prevention still serves as the most effective treatment

6. Mengapa pasien mengalami suara serak dan dahak berwarna hitam ketika batuk?
Pada kebakaran dalam ruang tertutup atau bila luka terjadi di wajah, dapat terjadi kerusakan
mukosa jalan napas karena gas, asap, atau uap panas yang terhisap. Oedem laring yang
ditimbulkannya dapat menyebabkan hambatan jalan napas dengan gejala sesak napas,
takipnea, stridor, suara serak dan dahak bewarna gelap akibat jelaga.

7. Mengapa didapatkan nyeri dan kesemutan pada tangan kiri pasien?

8. Mengapa dokter memberikan diberikan oksigenasi dengan masker 10 L/menit serta

infus RL 30 tetes permenit?

- Cairan kristaloid adalah ion (garam) dengan berat molekul rendah disertai atau
tanpa glukosa
- cairan kristaloid cepat seimbang dan terdistribusi ke seluruh rongga cairan
ekstraseluler
- Kristaloid didominasi oleh cairan air steril dengan elektrolit sehingga mirip dengan
kandungan mineral dari plasma darah manusia.
 - Kristaloid tersedia dalam berbagai formulasi, dari yang hipotonik daripada  plasma
hingga yang isotonik atau hipertonik. Salah satu formulasi yang paling sering, normal
saline 0,9%, dirancang untuk meniru konsentrasi mineral dan elektrolit plasma
manusia, namun masih ada perbedaan substansial.
- Alternatif selain normal salin yang sering digunakan adalah Ringer laktat yang lebih
ketat meniru konsentrasi elektrolit plasma manusia serta mengandung sejumlah
kecil laktat.[3]

http://herdiantrisufriyana.com/jenis-jenis-cairan-intravena/

http://kedokteran.unsoed.ac.id/Files/Kuliah/modul%20/Genap
%20I%20-%20Pemasangan%20Infus.pdf

9. Apa saja etiologi dari luka bakar dan perbedaannya?

10. Bagaimana cara menentukan luas luka bakar?
Lund and Browder diagrams for estimating burn size in terms of TBSA.
In adults, the ‘Rule of Nines’ (that is, using multiples of 9) is used to assess the proportion of the total
body surface area (TBSA) affected and to help guide immediate treatment decisions, such as amount
of fluid resuscitation, that are based on the size of the burn injury. However, owing to different head
to body size ratios, the proportion of the TBSA affected in children is estimated differently; the Rule
of Nines is inaccurate. Another challenge is the body habitus. For example, the Rule of Nines and the
estimate that each hand comprises 1% of the TBSA are inaccurate in patients who have obesity or
cachexia265. The body areas are separated by colour and the numbers are percentages of the TBSA and
include front and back coverage; for example, ‘32’ in the diagram of the trunk relates to the chest,
abdomen and back that make up 32% of the TBSA. The hand, including the palm, fingers and back of
the hand, represents 2% of the TBSA and can be a useful tool for quick calculation of the size of a
burn — especially irregularly shaped scald burns
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224101/

11. Bagaimana menentukan trauma inhalasi pada pasien?

12. Bagaimana penanganan pertama luka bakar?

Untuk luka yang severe

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224101/

13. Apa perbedaan penanganan luka bakar terbuka dan tertutup?

14. Bagaimana monitoring cairan pada pasien?

15. Bagaimana tatalaksana pasien dengan escar pada tangan kirinya?

EARLY EXICISION AND GRAFTING (E&G)
 Dengan metode ini eschar di angkat secara operatif dan kemudian luka ditutup dengan
cangkok kulit (autograft atau allograft ), setelah terjadi penyembuhan, graft akan
terkelupas dengan sendirinya. E&G dilakukan 3-7 hari setelah terjadi luka, pada
umumnya tiap harinya dilakukan eksisi 20% dari luka bakar kemudian dilanjutkan
pada hari berikutnya. Tapi ada juga ahli bedah yang sekaligus melakukan eksisi pada
seluruh luka bakar, tapi cara ini memiliki resiko yang lebih besar yaitu : dapat terjadi
hipotermi, atau terjadi perdarahan masive akibat eksisi. Metode ini mempunyai
beberapa keuntungan dengan penutupan luka dini, mencegah terjadinya infeksi pada
luka bila dibiarkan terlalu lama, mempersingkat durasi sakit dan lama perawatan di
rumah sakit, memperingan biaya perawatan di rumah sakit, mencegah komplikasi
seperti sepsis dan mengurangi angka mortalitas. Beberapa penelitian membandingkan
teknik E&G dengan teknik konvensional, hasilnya tidak ada perbedaan dalam hal
kosmetik atau fungsi organ, bahkan lebih baik hasilnya bila dilakukan pada luka bakar
yang terdapat pada muka, tangan dan kaki. Pada luka bakar yang luas (>80% TBSA),
akan timbul kesulitan mendapatkan donor kulit. Untuk itu telah dikembangkan
metode baru yaitu dengan kultur keratinocyte. Keratinocyte didapat dengan cara
biopsi kulit dari kulit pasien sendiri. Tapi kerugian dari metode ini adalah
membuthkan waktu yang cukup lama (2-3 minggu) sampai kulit (autograft) yang baru
tumbuh dan sering timbul luka parut. Metode ini juga sangat mahal 6

ESCHAROTOMY
Luka bakar grade III yang melingkar pada ekstremitas dapat menyebabkan iskemik
distal yang progresif, terutama apabila terjadi edema saat resusitasi cairan, dan saat
adanya pengerutan keropeng. Iskemi dapat menyebabkan gangguan vaskuler pada
jarijari tangan dan kaki. Tanda dini iskemi adalah nyeri, kemudian kehilangan daya
rasa sampai baal pada ujung-ujung distal. Juga luka bakar menyeluruh pada bagian
thorax atau abdomen dapat menyebabkan gangguan respirasi, dan hal ini dapat
dihilangkan dengan escharotomy. Dilakukan insisi memanjang yang membuka
keropeng sampai penjepitan bebas

16. Apa saja indikasi perawatan dan pemberian cairan resusitasi pada pasien luka bakar?
17. Bagaimana pencegahan kontraktur luka bakar?
It is far better principle to prevent contractures rather than treat them. Major burn cases
have declined due to improvements in health and safety at work and domestically (12). First
aid is vital to prevent burn extending deep into the dermis. First aid should include removal
of clothes at the site of burn, placing the injured site under a tepid tap of water for a
minimum of 20 minutes and wrapping the site in cling film. Upon admission, burns should be
assessed to gauge the size, the depth of burn and the mechanism of injury. This is a priority
but unfortunately burns are not always assessed sufficiently. One study showed 30% of
patients performed appropriate first aid and furthermore74% of burns upon admission were
not assessed adequately (2). Laser Doppler Imaging (LDI) is used to determine the blood flow
at the burn injury site. This provides an accurate description at the depth of the burn. It is a
useful aid to deciding when a burn will likely heal. LDI is used between 2-5 days following a
burn injury

A clinician should determine from their assessment if the burn is likely to heal before or after
21 days. Cubison et al. concluded that there is a low risk of hypertrophic scarring if the burn
 healed conservatively before 21 days. Only intermediate burns that are expected to heal
after 21 days were likely to develop a hypertrophic scar should receive primary excision and
skin graft. Burns expected to heal before 21 days may be dressed with Biobrane, skin
allografts or with simple dressings. Biobrane is a biosynthetic silicon dressing which contains
an embedded sheet of nylon. This is left on the wound and provides the wound with a 3D
structure to heal to. The nylon sheet causes blood and sera to clot forming a firm dressing
(13). Cadaveric allografts provide temporary closure of the wound. Such allografts behave
like normal skin but are rejected may require replacement. Application of such dressings
help to prevent early desiccation, prevent infection, reduce loss of water or proteins and
electrolytes.

There is general agreement that major burns should be treated with aggressive excision and
skin grafting. Split skin grafts (SSGs) should only be reserved for burns likely to heal after 21
days (5). Large burns require multiple operations and areas should be prioritised. Potentially,
early excision and skin grafts will be delayed at certain sites, leading to prolonged healing
time and scarring. Also, the total amount of skin available for a graft should be determined.
A shortage of skin will require the use of a mesh graft as opposed to a sheet split skin graft. A
mesh graft however will contract greater than a sheet SSG.

Schneider et al. concluded the importance of therapeutic positioning and intensive therapy
intervention. The study of 985 patients concluded that 38.7% of patients developed a
contracture at hospital discharge. The shoulder was the most common joint to undergo
contracture (38%), followed by the elbow (34%) and the knee (22%) (14).

Following a burn injury over the surface of a joint, splintage should be used to place a joint in
a position which will later allow a patient to maintain essential function e.g. eating, drinking,
going to the toilet. There are a wide range of splints which stretch the skin and maintain
positions of function (12, 15, 17). Burns to the flexor surface of the skin increase the risk of
contracture as the flexor muscles are stronger than the extensors. Full co-operation is
essential for reducing long term pain, providing a greater range of movement and reducing
the requirement for further surgery.

Physiotherapy is important to prevent scar formation and limit contractures. Celis et al.
showed that patients receiving additional, supportive physiotherapy required less surgery
for burn contractures than a group receiving basic support (16). Adequate analgesia
alongside patient education is a priority as patients must move their affected joints despite
perceived pain (14, 17).
file:///C:/Users/Asus/Downloads/burnschaptercopy.pdf

18. Bagaimana komplikasi luka bakar?

The complications of the injury vary up to a great extent depending on the affected location,
tissue and the degree of severity. Scar formation and deformity due to burns cause
psychological discomfort in patients (Perera et al., 2015)
Systemic and local both type of complications is caused by burn. Fluid loss and breakdown of
skin integrity is major contributor of systemic complications. Contractures, scarring and
eschars are the local complications of burn injury (Rowan et al., 2015).
 Systemic
The risk of developing systemic complications is directly proportional to the total body
surface area (TBSA) involved in burn injury. Following are the risk factors of severe systemic
complications and mortality.
- Burns of more than 40% of TBSA
- Age of greater than 60 year or less than 2 year
- Presence of concurrent smoke inhalation or major trauma Hypovolemia and infection
are the most common systemic complications (Singh et al., 2007).

Local
Eschar “rigidness and death of tissue caused by deep burns”. Respiration can be compromise
by an eschar around the thorax and viability of limbs and digits is endangered by ischemia
(Rowan et al., 2015).
Scarring and contractures due to healing of deep burns; contracture deformities can appear
at the joints depending on the extent of the scar.

Infection in burns
Bacterial growth on damaged skin along with immunosuppression causes wound infection,
invasive sepsis and may lead to death. The mortality rate caused by hypovolemia and
hyperosmolar shock is reduced with the increase of resuscitation procedures in burn
patients (Lee et al., 2014).
https://scihub.wikicn.top/10.3329/icpj.v5i12.30411

19. Bagaimana prognosis luka bakar?

Future perspectives

Extended burn injuries cause systemic modification of the patient’s clinical conditions that usually
worsen the prognosis. Hypovolaemia, respiratory insufficiency and shock are only a few of such
changes. The pathophysiologic mechanisms that underlie them are complex and involve almost all
organs and body systems. Apoptotic processes following burn injury have been described
increasingly. Future potential therapeutic targets which need to be addressed are the clinical
significance of this systemic phenomenon and the development of promising antiapoptotic drugs
with the intriguing possibility to block the ‘systemic apoptotic response’ and its pathophysiologic
effects. For instance, specific therapies could derive from the experimental application of selective
antiapoptotic drugs i.e. selective inhibitors of death receptors, caspases or the proteasome complex.
Another potential pathway of new therapeutic options after thermal injuries is gene expression
profiling, which has inspired new hope for finding genes involved in complications resulting from
burn injury. Therefore, genetic dissection of burn injury should be carried out in a global context. A
similar investigative approach is the understanding of Pseudomonas aeruginosa burn wound
infections by profiling gene expression. Pseudomonas represents a key opportunistic pathogen
causing severe acute and chronic nosocomial infections. It is prevalent in burn wounds and generally
multi-drug resistant. Understanding the genetic programs underlying infection is essential to develop
highly needed new strategies for prevention and therapy. Future efforts should focus on the
identification of direct virulent factors and elucidation of their mode of action. These new data sets
obtained from global transcriptional profiling could be essential for the development of new targets
and options for the prevention and intervention of burn wound infections.