Referat

Trauma and Triad

(Relationship Between Hipothermi and Acidosis Metabolic)

Oleh
Latipah Binti Latip, S.Ked 04011381320082

Pembimbing

BAGIAN DEPARTEMEN ANESTASI DAN TERAPI INTENSIF

FAKULTAS KEDOKTERAN UNIVERSITAS SRIWIJAYA
RSUP Dr. MOHAMMAD HOESIN PALEMBANG
2017
 KATA PENGANTAR

Alhamdulillah, puji syukur kepada Tuhan karena atas berkat dan rahmat-Nya
sehingga penulis dapat menyelesaikan referat yang berjudul Supraventrikular
Takikardi dengan baik.
Di kesempatan ini penulis juga mengucapkan terima kasih yang sebesar-
besarnya kepada dr, Hj Endang Melati Maas, Sp. An. KIC. KAP selaku pembimbing
yang telah membantu penyelesaian referat ini.
Penulis menyadari bahwa dalam penulisan referat ini masih banyak terdapat
kesalahan dan kekurangan. Oleh karena itu, segala saran dan kritik yang bersifat
membangun sangat kami harapkan. Demikianlah penulisan referat ini, semoga
bermanfaat

Palembang, Mei 2017

Penulis

i
 HALAMAN PENGESAHAN

REFERAT

Judul

Trauma and Triad

(Relationship Between Hipothermi and Acidosis Metabolic)

Oleh:

Latipah Binti Latip, S. Ked 040113281320082

Telah diterima dan disetujui sebagai salah satu syarat mengikuti Kepaniteraan Klinik
Senior di Bagian Ilmu Penyakit Dalam Fakultas Kedokteran Univesitas Sriwijaya
stase di RSUP DR. Moh. Hoesin Palembang 3 Maret 15 Mei 2017.
Palembang, Mei 2017

ii
 DAFTAR ISI
Halaman
KATA PENGHANTAR.................................................................................................
i
HALAMAN PENGESAHAN.......................................................................................
ii
DAFTAR ISI .................................................................................................................
iii
BAB I PENDAHULUAN..............................................................................................
1
BAB II TINJAUAN PUSTAKA...................................................................................
3
2.1 Trauma triage..........................................................................................................
8
2.1.1 Guidelines for field trige of injured patients- United States, 2011...................
8
2.1.2. 2011 Field Triage Guideline Recommendations .............................................
9
2.2.2.1. Changes in 2011 Guidelines for Field Triage of Injured Patients
Guidelines
........................................................................................................................
9
2.2. Hypothermia......................................................................................................
10
2.3. Acidosis .............................................................................................................
10
2.4. Coagulopathy ....................................................................................................
11
2.5. EMS Management of the Lethal Triad ..............................................................
12

iii
BAB III KESIMPULAN...............................................................................................
23
DAFTAR PUSTAKA....................................................................................................
28

iv
 BAB I
PENDAHULUAN

Meskipun ada kemajuan besar dalam perawatan trauma selama 30 tahun

terakhir, trauma masih merupakan salah satu penyebab utama kematian pada semua
kelompok usia.1 Di Amerika Serikat, cedera yang tidak disengaja adalah penyebab
utama kematian bagi orang berusia 1- 44 tahun (7). Pada tahun 2008, cedera
menyumbang sekitar 181.226 kematian di Amerika Serikat (8). Pada tahun 2008,
sekitar 30 juta orang yakni cedera parah untuk mengunjungi gawat darurat rumah
sakit (ED); 5,4 juta (18%) dari pasien yang cedera ini diangkut oleh personil EMS
(9). Dari pelbagai jenis kematian, pendarahan menyumbang hingga 40% dan tetap
merupakan penyebab utama kematian terkait trauma..2,3
Memastikan bahwa pasien trauma yang cedera parah dirawat di pusat trauma
memiliki dampak yang besar terhadap kelangsungan hidup mereka (10). Idealnya,
semua orang dengan luka parah yang mengancam jiwa akan dibawa ke pusat trauma
Tingkat I atau Tingkat II, dan semua orang dengan luka yang kurang serius akan
dibawa ke pusat trauma tingkat rendah atau komunitas ED. Namun, perbedaan
pasien, luka gaib, dan kompleksitas penilaian pasien di lapangan dapat
mempengaruhi keputusan triase..
Pada tahun 2011, Panel berkumpul kembali untuk meninjau Pedoman 2006 dalam
konteks literatur yang baru diterbitkan serta pengalaman negara bagian dan
masyarakat lokal yang bekerja untuk menerapkan Panduan dan membuat
rekomendasi mengenai perubahan atau modifikasi Panduan.
Tiga serangkai hipotermia, asidosis dan koagulopati telah diakui sebagai penyebab
kematian yang signifikan pada pasien dengan luka traumatis. Pada tahun 1982,
sebuah penelitian menggambarkan sebuah "siklus setan berdarah" di mana
perdarahan dan cedera jaringan menyebabkan triad yang dapat diprediksi ini sebagai
faktor yang menyulitkan.4 Pada akhirnya, triad ini mengakibatkan perdarahan dan
kematian yang memburuk. Penulis penelitian menyarankan pengobatan hipotermia,
asidosis dan koagulopati pada trauma memerlukan perhatian sebanyak yang
ditekankan secara tradisional pada penanganan luka operasi.4
Hari ini, kami menyadari bahwa untuk berhasil menyadarkan pasien trauma kritis,
semua penyedia layanan darurat harus memiliki pemahaman yang kuat tentang triad
mematikan. Pemahaman ini seharusnya menjadi batu penjuru untuk semua intervensi
yang diberikan kepada pasien trauma pendarahan. Waktu tidak diobati, hipotermia,
asidosis dan koagulopati menghasilkan dan menyebarluaskan satu sama lain, yang
akhirnya menghasilkan kemajuan yang dapat diprediksi namun tidak dapat
dipulihkan menuju kematian.
 BAB II
PEMBAHASAN

2.1. Trauma triage

2.1.1. Guidelines for field triage of injured patients United States, 2011
In April 2011, the Panel met to discuss the articles, recommendations of the
working group, and the experiential base from states and communities implementing
the Guidelines, and to reaffirm or revise the Guidelines. In the sources reviewed,
Injury Severity Score (ISS) >15, where available, was used as the threshold for
identifying severe injury; however, other factors (e.g., need for prompt operative care
and intensive care unit [ICU] admission) also were considered. A threshold of 20%
positive predictive value (PPV) to predict severe injury was used to place criteria into
discussion for inclusion as mechanism-of-injury criteria. A review of NHTSAs
National Automotive Sampling System-Crashworthiness Data System (NASS-CDS)
(23) and Crash Injury and Research Engineering Network (CIREN) (24) information
also was undertaken to inform the Panel on the high-risk automobile-crash criterion.
The final recommendations of the Panel were based on the best available
evidence. When definitive research evidence was lacking, the Panel based its
revisions and recommendations on the expert opinion of its members. Consensus
among the Panel members on specific recommendations and modifications was not
required.
FIGURE 2. Guidelines for field triage of injured patients United States, 2011

Abbreviation: EMS = emergency medical services.

* The upper limit of respiratory rate in infants is >29 breaths per minute to maintain a higher level of overtriage for infants.

Trauma centers are designated Level I-IV. A Level I center has the greatest amount of resources and personnel for care of the
injured patient and provides regional leadership in education, research, and prevention programs. A Level II facility offers
similar resources to a Level I facility, possibly differing only in continuous availability of certain subspecialties or sufficient
prevention, education, and research activities for Level I designation; Level II facilities are not required to be resident or
fellow education centers. A Level III center is capable of assessment, resuscitation, and emergency surgery, with severely
injured patients being transferred to a Level I or II facility. A Level IV trauma center is capable of providing 24-hour
physician coverage, resuscitation, and stabilization to injured patients before transfer to a facility that provides a higher level
of trauma care.
Any injury noted in Step Two or mechanism identified in Step Three triggers a yes response. Age <15 years.
4 Intrusion refers to interior compartment intrusion, as opposed to deformation which refers to exterior damage.
5 Includes pedestrians or bicyclists thrown or run over by a motor vehicle or those with estimated impact >20 mph
with a motor vehicle.
8 Local or regional protocols should be used to determine the most appropriate level of trauma center within the
defined trauma system; need not be the highest-level trauma center.

Age >55 years.

9 Patients with both burns and concomitant trauma for whom the burn injury poses the greatest risk for morbidity and
mortality should be transferred to a burn center. If the nonburn trauma presents a greater immediate risk, the patient may be
stabilized in a trauma center and then transferred to a burn center.
10 Patients who do not meet any of the triage criteria in Steps One through Four should be transported to the most
appropriate medical facility as outlined in local
6

2.1.2. 2011 Field Triage Guideline Recommendations

2.1.2.1. Changes in 2011 Guidelines for Field Triage of Injured Patients
guidelines

Step One: Physiologic Criteria

Change GCS <14 to GCS13
Add or need for ventilatoy support to respiratory criteria

Step Two: Anatomic Criteria

Change all penetrating injuries to head, neck, torso and extremities
proximal to elbow and knee to all penetrating injuries to head, neck, torso and
extremities proximal to elbow or knee
Change flail chest to chest wall instability or deformaity (e.g. flail chest)
Change crushed, degloved, or mangled extremity to crushed,
degloved, mangled, or pulseless extremity
Change amputation proximal to wrist and ankle to amputation
proximal to wrist or ankle

Step Three: Mechanism-of-Injury Criteria

Add including roof to intrusion criterion

Step Four: Special Considerations

Add the following to older adult criteria
SBP <110 might represent shock after age 65 years
Low-impact mechanisms (e.g., ground-level falls) might result in severe injury
Add patients with head injury are at high risk for rapid deterioration to
anticoagulation and bleeding disorders criterion
 Remove end-stage renal disease requiring dialysisand time-sensitive
extremity injury

Transition Boxes
Change layout of the figure
Modify specific language of the transition boxes

2.2 Hypothermia
Normal human body temperature is 35.637.8 degrees C with hypothermia
being defined as a core temperature < 35 degrees C. 5 In one study, it was found that
almost half of EMS-transported trauma patients had a temperature < 36 degrees C on
arrival to the ED.6 Important to note is that there was no association between season
of the year and frequency of hypothermia. At highest risk were those patients older
than 65 and those who had been entrapped. 6 In addition, hypothermia in trauma has
been associated with a significantly increased mortality compared to patients with the
same body temperature from environmental exposure alone. In a study of 71 trauma
victims, a core temperature < 32 degrees C was associated with 100% mortality
independent of the presence of shock, injury severity or volume of fluid
resuscitation.7 Because hypothermia in a trauma patient predicts such a poor
outcome, the traditional classification system of hypothermia has been revised for
use in this vulnerable patient population. (See Table 1--below.)
Even mild hypothermia in a trauma patient can result in devastating
physiologic consequences. (See Table 2.) Of particular concern is the effect of
hypothermia on the coagulation system.8 The coagulation system is a temperature-
and pH-dependent series of complex enzymatic reactions that result in the formation
of blood clots to stop both internal and external hemorrhage.
Coagulopathy is the term used to describe a broad group of disease states in
which there is an impaired ability of this coagulation system to synthesize blood
clots.5 Its been repeatedly demonstrated that as a patients core temperature
decreases, so does the bodys ability to stop bleeding. This is a result of impaired
platelet function, inhibition of the clotting factors, and inappropriate activation of
clot breakdown.8
 Hypothermia in trauma patients is caused by a multitude of factors.
Hemorrhagic shock, traumatic brain injuries, and alcohol intoxication impair the
bodys ability to regulate its core temperature.8 In addition, patients at the extremes of
age and those with certain medical conditions such as diabetes or thyroid disease are
at higher risk to develop hypothermia after trauma. 8 Furthermore, those patients with
prolonged exposure to the environment as during an extrication and those with
severe burns are at risk for rapid heat loss causing profound hypothermia.
Lastly, an important care consideration for a trauma patient is the temperature
of the fluids and blood products we infuse as well-intentioned therapy. Room
temperature normal saline (2025 degrees C) is very hypothermic relative to the
desired normal body temperature. Thus, large volume resuscitations with even room
temperature IV fluids can significantly contribute to this arm of the lethal triad.

2.3. Acidosis
 A pH level is a measure of the bloods acidity on a scale of 014; water has a
neutral pH of 7.0. A healthy individual maintains a physiologically normal pH of
7.357.45 through a complex balance of hydrogen ions (acids) and buffers
predominately controlled by the pulmonary and renal systems.\
Acidosis is defined as an arterial pH < 7.35 and can result from a variety of
disease states. However, in trauma patients the major contributor is poor perfusion to
the tissues. Anemia from acute blood loss, peripheral vasoconstriction in response to
hypothermia and blood loss, and overall decreased cardiac output severely impair
oxygen delivery to the tissues. This results in tissue oxygen demand far exceeding
oxygen delivery. Thus, to make functional energy, the bodys cells are forced to
utilize anaerobic metabolism instead of the normal aerobic metabolism, resulting in
the production of lactic acid as a byproduct.9
As a trauma patients perfusion worsens, lactic acid rapidly accumulates in
the tissues. This causes the bodys pH to drop, resulting in a severe metabolic
acidosis. Its important to note that this process frequently occurs in the presence of
normal or only slightly abnormal vital signs.
An additional cause of acidosis in the trauma patient is excessive
resuscitation using unbalanced crystalloid solutions such as normal saline. 10 With a
pH around 5.5, normal saline is far more acidic than the desired normal blood pH. In
large-volume resuscitations, normal saline predictably causes its own metabolic
acidosis as a result of the high chloride content.11 This hyperchloremic metabolic
acidosis only serves to compound the existing lactic acidosis of trauma. Furthermore,
theres evidence that excessive use of normal saline with its high chloride content
may increase systemic tissue inflammation and thereby contribute to the
coagulopathy of trauma.11 Lactated Ringers (LRs) is an imperfect substitution:
Although its pH is 6.5, LR contains lactate and is incompatible with many
medications and blood products.
Lastly, a trauma patient may also have respiratory acidosis. This is a result of
hypoventilation due to respiratory depression or obstruction resulting in hypercapnia
(increased CO2 levels). Common causes of a respiratory acidosis in trauma include
narcotic or alcohol use, traumatic brain injuries, flail chest or preexisting medical
conditions such as chronic obstructive pulmonary disease.
 With severe acidemia (pH < 7.20), disastrous consequences can occur. 12 (See
Table 3.) For the trauma patient, one of the most harmful effects is that their
coagulation system can become severely impaired. In one study, the function of part
of the coagulation system was reduced by 5570% when the pH dropped from 7.4 to
7.0.13
Figure 1: The lethal triad

Figure 2: How the lethal triad relates to other aspects of trauma

2.4. Coagulopathy
 Coagulopathy can occur for a number of reasons; however, regardless of the
specific cause, coagulopathy results in the potential for continued hemorrhage in the
bleeding trauma patient.
Coagulopathy in trauma is a common occurrence, present in nearly one in
four severely injured patients arriving at the ED. Furthermore, its presence is
associated with a four-fold increase in mortality. 1416 The coagulopathy of trauma
occurs not only because of hypothermia and acidosis as previously discussed, but
also as a result of losing clotting factors through hemorrhage and hemodilution, and
the bodys use and subsequent depletion of both platelets and clotting factors.9
Dilutional coagulopathy occurs when we resuscitate a bleeding trauma patient with
fluid or blood products that dont contain the same clotting factors lost in the acutely
hemorrhaged whole blood.10 Crystalloids such as normal saline and packed red blood
cells dilute the remaining clotting factors circulating in the trauma victims blood.
Furthermore, in the critically injured, through a complex series of enzymatic
reactions, the clotting cascade can become abnormally activated, causing excessive
clot formation and subsequent breakdown (fibrinolysis) out of proportion to the
injury.9 This abnormal and excessive activation of the coagulation system rapidly
consumes the bodys remaining clotting factors, resulting in a further deficiency of
the essential factors needed to achieve hemorrhage control.
Lastly, EMS providers should be aware of those trauma patients who have a
baseline coagulopathy because of preexisting medical conditions. Examples include
those patients on anticoagulant therapy such as warfarin (Coumadin) or a novel oral
anticoagulant such as dabigatran for stroke prevention in the setting of atrial
fibrillation. These patients and those with chronic liver or renal failure have an
increased risk of developing a truly life-threatening coagulopathy and hemorrhage
after trauma.17
2.5. Emergency Medical Services (EMS) Management of the Lethal

Triad
There are several simple steps providers can and should follow to battle the lethal
triad.
1. The triad begins and ends with bleeding, so find the bleeding and stop it. Hold
pressure, use combat gauze, apply a tourniquet, bind the pelvis, etc. (See the
article Training & speed are crucial: Options, issues & training to prevent death
from massive blood loss, by Joe Holley, MD, FACEP, in the JEMS December
2013 supplement, Putting the clamp on hemorrhage: How a simple, effective
point-of-injury tool will transform the way bleeding is controlled in the field.)
2. Do not stop your search for bleeding with the first source you find, as others may
exist.
3. Always assume your patients temperature is dropping right before your eyes,
because it is, and much faster than youd expect.
4. Strip em and flip em, but not with reckless abandon. Make every effort to
expose only those body parts youre examining in the moment and keep the
remainder of the patient covered.
5. Patients can and will become hypothermic in conditions you consider warm.
Prioritize limiting a patients exposure to the environment, especially during
prolonged extrications.
6. Place a warm blanket between the newly extricated patient and your cold, hard
backboard.
7. Turn up the heat in your ambulance. If you arent sweating, its certainly not
warm enough. (Ideally, 27 degrees C.)
8. Promptly remove wet or bloody clothes and replace with a warm blanket.
Shivering wastes valuable cellular energy and oxygen in an attempt to stay warm
while producing more lactate, contributing to acidosis.
9. We dont bleed normal saline, so limit crystalloid infusion as much as possible. It
contributes to the patients acidosis and dilutes the remaining clotting factors in
your patients blood. IV fluids may improve a number, but may actually hurt your
patient in the long run.
10. Except in those patients with a traumatic brain injury, utilize a permissive
hypotension resuscitation strategy. Our goal should be to maintain tissue
perfusion typically defined as the presence of a radial pulse or normal mental
status. We should avoid overly aggressive fluid administration to normalize blood
pressure, which can pop the clot and worsen hemorrhage. (See Vital
pathways: Detect & treat symptoms related to hemorrhagic shock, by Peter
Taillac, MD, FACEP and Chad Brocato, DHSC, CFO, JD, from the JEMS
October 2012 issue and Add a little salt: Permissive hypotension in trauma
resuscitation, by Jeff Beeson, DO, FACEP, EMT-P and Trenton Starnes,
NREMT-P in the JEMS April 2013 issue.)
11. Whenever possible, administer only warmed fluids. (Ideally 40 degrees C.)
12. Measure prehospital lactate levels when available to more accurately detect
cryptic shock in trauma patients with normal vital signs. End-tidal carbon dioxide
may also be a useful marker.
13. Monitor and maximize oxygenation.
14. Treat causes of hypoventilation to prevent a respiratory acidosis.
15. Identify high-risk patients with a baseline coagulopathy due to medications or
preexisting medical conditions.
16. Administer tranexamic acid (TXA)an antifibrinolytic that prevents clot
breakdown and thus decreases blood lossif your system permits its use. TXA
has been shown to decrease mortality in two large trauma studies. (See TXA: A
difference-maker for trauma patients? Role of tranexamic acid in EMS &
preoperative trauma management, by Jeffrey M. Goodloe, MD, NREMT-P,
FACEP; David S. Howerton, NREMT-P; Duffy McAnallen, NREMT-P and
Howard Reed, NREMT-P, in the JEMS April 2013 issue.)
 BAB III
KESIMPULAN

When faced with the unique challenge of resuscitating a criticaly ill trauma
patient in dynamic and austere prehospital environment, knowledge of and respect
for the lethal triad is mission critical. Simply stated, haemorrhage in trauma causes
acidosis, hypothermia and coagulopathy. Result in continued hemoorahage,
beginning a truly self sustaining and deadly cyvcle.
With the exception of hypothermia, EMS is not routinely capable of knowing
exactly which arms of the lethal triad are present in real time for given trauma
patient-the degree of acidosis or severity of coagulopathy is usually determined by
lab testing. Despite this, EMS is uniquely positioned to combat this silent cycle of
death before its spirals out of control.
At the end of the day, recognition and prevention of this lethal triad can be
more effective tan treatmenet. A variety of seemingly imple but truly significant
actions and inactions by EMS at both the scene snd durng transport can directly
prevent or slow the progression of the lethal triad. As time pssses, the three arns of
the triad become so tightly interwoven that it becomes nearly impossivel to stop and
reverse the cyvle. Thus, EMS personnel on the front lines of our nations trauma
stsmtem have the very rela opportunity to improve the outcomes for the millions of
people injured annually.

23
 DAFTAR PUSTAKA

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Statistics (WISQARS). Retrieved Feb. 11, 2014, from
www.cdc.gov/injury/wisqars/.
2. Sauaia A, Moore Fa, Moore EE, et al. Epidemiology of trauma deaths: A
reassessment. J Trauma. 2007;62(2):307310.
3. Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome:
An overview of epidemiology, clinical presentations, and therapeutic
considerations. J Trauma. 2006;60(Suppl. 6):S3S11.
4. Kashuk JL, Moore EE, Millikan JS, et al. Major abdominal vascular trauma
A unified approach. J Trauma. 1982;22(8):672679.
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6. Helm M, Lampl L, Hauke J, et al. Accidental hypothermia in trauma patients.
Is it relevant to preclinical emergency treatment? Anaesthesist.
1995;44(2):101107.
7. Tsuei BJ, Kearney PA. Hypothermia in the trauma patient. Injury.
2004;35(1):715.
8. Soreide E, Smith CE. (2005.) Hypothermia in trauma victimsfriend or foe?
Trauma Care International. Retrieved Feb. 10, 2014, from
www.itaccs.com/traumacare/archive/05_01_Winter_2005/friendorfoe.pdf .
9. Weingart S, Meyers CM. (March 1, 2008.) Thoughts on the resuscitation of
the critically ill trauma patient. EMCrit Blog. Retrieved Feb. 10, 2014, from
www.emcrit.org/podcasts/trauma-resus-part-i/.
10. Ho AM, Karmakar MK, Contardi LH, et al. Excessive use of normal saline in
managing traumatized patients in shock: A preventable contributor to
acidosis. J Trauma. 2001;51(1):173177.
11. De Backer D, Cortes DO. Characteristics of fluids used for intravascular
volume replacement. Best Pract Res Clin Anaesthesiol. 2012;26(4):441451.
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first of two parts. N Engl J Med. 1998;338(1):2634.

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13. Meng ZH, Wolberg AS, Monroe DM, et al. The effect of temperature and pH
on the activity of factor VIIa: Implications for the efficacy of high-dose factor
VIIa in hypothermic and acidotic patients. J Trauma. 2003;55(5):886891.
14. Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma.
2003;54(6):11271130.
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mortality in trauma. J Trauma. 2003;55(1):3944.
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17. Lewis AM. Trauma triad of death emergency. Nursing. 2000;30(3):6264.

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