2. DEFINISI CEDERA OTAK
•Kelainan otak disebabkan oleh trauma
mekanik eksternal
•menyebabkan gangguan fisik, kognitif
dan psikososial
•sementara atau menetap
•berhubungan dengan berbagai tingkat
kesadaran. (Traumatic Brain Injury)
Indonesia, Perhimpunan Dokter Spesialis Saraf. "Panduan praktik klinis neurologi." Jakarta: Perhimpunan Dokter Spesialis Saraf
Indonesia (2016).
3. KLASIFIKASI
Kelainan Patologis
• Fokal
• Difus
Waktu Kejadian
• Primer
• Sekunder
Mekanisme
• Tembus Peluru
• Adanya Fraktur
• dll
Derajat Penurunan
Kesadaran
Indonesia, Perhimpunan Dokter Spesialis Saraf. "Panduan praktik klinis neurologi." Jakarta: Perhimpunan Dokter Spesialis Saraf
Indonesia (2016).
4. KATEGORI GCS GAMBARAN KLINIS CT Scan
Minimal
(Simple Head Injury)
15 Pingsan (-),
Defisit neurologis (-)
Normal
Ringan
(Mild Head Injury)
13–15 Pingsan < 10 menit,
Defisit neurologis (-)
Normal
Sedang
(Moderate Head Injury)
9 – 12 Pingsan > 10 menit - 6 jam
Defisit neurologis (+)
Abnormal
Berat
(Severe Head Injury)
3 – 8 Pingsan > 6 jam,
Defisit neurologis fokal (+)
Abnormal
(Frank, 2005; Wijoto, 2008
KLASIFIKASI berdasarkan
PENURUNAN KESADARAN
5. MEKANISME CEDERA KEPALA
menurut Gennarelli dan Thibault
Mekanisme
Kontak
Mekanisme
Akselerasi
• Akselerasi
translasi
• Akselerasi rotasi
• Akselerasi
angulasi
: otak bergerak sesuai
garis lurus
: kombinasi
translasi dan rotasi
Kleiven, S. (2020). Biomechanics and
Prevention. In Management of Severe
Traumatic Brain Injury (pp. 25-32).
Springer, Cham.
8. ICP Directed Therapy
• Continuous monitoring of ICP has become the cornerstone in
neuromonitoring as it reflects the mass effect that predisposes to
cerebral injury and herniation.
• They support an ICP of 20 mmHg as the upper threshold beyond
which treatment should generally be initiated.
• Treatment of ICP has adverse effects. The risk of infection increases
significantly after 3 days of monitoring. In the case of continuous
cerebrospinal fluid (CSF) drainage, continuous intraventricular
measurement of ICP may become unreliable.
Narotam, P. K., Morrison, J. F., & Nathoo, N. (2009). Brain tissue oxygen monitoring in traumatic brain injury and major trauma: outcome analysis of a brain tissue oxygen–directed therapy. Journal of
neurosurgery, 111(4), 672-682.
Zeiler, F. A., Ercole, A., Cabeleira, M., Beqiri, E., Zoerle, T., Carbonara, M., ... & Czosnyka, M. (2021). Patient-specific ICP epidemiologic thresholds in adult traumatic brain injury: a CENTER-TBI validation
study. Journal of neurosurgical anesthesiology, 33(1), 28-38.
MILES, Darryl K., et al. Predictors of intracranial hypertension in children undergoing ICP monitoring after severe traumatic brain injury. Child's Nervous System, 2020, 36.7: 1453-1460.
9. ICP Management
• External ventricular drains (EVD), can also be used for continuous or
intermittent drainage of CSF as a means to decrease ICP.
• Open or continuous EVD have been associated with better ICP
lowering than intermittent or closed EVD, although EVD monitors
have not been shown to be superior to intraparenchymal ICP
monitors.
• Intraparenchymal monitors are placed directly into brain tissue but
may not accurately measure pressure in the CSF due to pressure
gradients that occur after TBI.
• If ICP remains elevated, continuous CSF drainage is employed. If the
CPP remains low, MAP is increased using a combination of volume
expansion and pressors.
10. The Brain Trauma Foundation (BTF)
recommendation (Level IIB)
• ICP monitoring in patients with severe TBI (GCS <9) and abnormal CT
scan to reduce 2 week and in-hospital mortality.
• CSF drainage be considered to reduce ICP in patients with a GCS <6
within the first 12 hours of injury.
• General goals maintain an ICP <20 and CPP between 50–70,
depending on autoregulatory status.
DASH, Hari Hara; CHAVALI, Siddharth. Management of traumatic brain injury patients. Korean journal of anesthesiology, 2018, 71.1: 12-21.
Zeiler, F. A., Ercole, A., Cabeleira, M., Beqiri, E., Zoerle, T., Carbonara, M., ... & Czosnyka, M. (2021). Patient-specific ICP epidemiologic
thresholds in adult traumatic brain injury: a CENTER-TBI validation study. Journal of neurosurgical anesthesiology, 33(1), 28-38.
11. Previous Research
1. In a study evaluating compliance with the 3rd edition of the BTF ICP
monitoring guidelines
o Patients who underwent ICP monitoring had less in-hospital mortality and less
herniation-related mortality
o But longer ICU and hospital length of stay compared to patients who did not
undergo ICP monitoring.
2. Large observation studies and retrospective analysis with severe TBI have shown
that patients with monitored and controlled ICP had better outcome than those
whose ICP was not controlled. But some studies have indicated that despite
extremely high ICP, intense, aggressive management of CPP can lead to good
neurological outcomes
3. In contrast, the Benchmark Evidence from South American Trials: Treatment of
Intracranial Pressure (BEST:TRIP) multicenter randomized clinical trial from 6
hospitals and 324 ICU patients with severe TBI ICP monitoring was not superior
to care based on imaging and physical exam.
Vella MA, Crandall ML, Patel MB. Acute Management of Traumatic Brain Injury. Surg Clin North Am. 2017 Oct;97(5):1015-
1030. doi: 10.1016/j.suc.2017.06.003. PMID: 28958355; PMCID: PMC5747306.
12. CPP directed therapy
• The clinical use of CPP is based on theoretical suggestions that
maintaining optimal cerebral blood flow (CBF) is necessary to meet
the metabolic needs of the injured brain.
• The goal preserve the ischemic penumbra and avoid exacerbation
of secondary insults, such as excitotoxicity, free radical production,
and inflammation.
• Higher CPP may contribute to various complications and low CPP has
concerns of their own.
• The issue now is to balance CPP and the question of optimal CPP
needs to be addressed.
Prabhakar H, Sandhu K, Bhagat H, Durga P, Chawla R. Current concepts of optimal cerebral perfusion pressure in traumatic brain injury. J
Anaesthesiol Clin Pharmacol. 2014 Jul;30(3):318-27. doi: 10.4103/0970-9185.137260. PMID: 25190937; PMCID: PMC4152669.
13. CPP Management
• Transcranial Doppler ultrasonography is a non-invasive technique
that measures CBF velocity, where differences in CBF velocity are
used to estimate differences in CBF.
• Jugular bulb monitoring of arteriovenous oxygen content difference
(AVDO2) utilizes a central line placed in the jugular bulb and a
peripheral arterial line.
• The difference in oxygen content between blood entering and leaving
the brain can be calculated to provide a global picture of supply and
demand.
Prabhakar H, Sandhu K, Bhagat H, Durga P, Chawla R. Current concepts of optimal cerebral perfusion pressure in traumatic brain injury. J
Anaesthesiol Clin Pharmacol. 2014 Jul;30(3):318-27. doi: 10.4103/0970-9185.137260. PMID: 25190937; PMCID: PMC4152669.
14. CPP Management
• Cerebral microdialysis is a technique whereby a catheter is placed in
the penumbra, or area adjacent to the traumatized brain, and used to
evaluate the local biochemical environment.
• Brain tissue oxygen tension can be measured with a parenchymal
probe but is highly dependent on placement, provides a very focal
measurement of oxygenation, and may not be an appropriate
surrogate for global perfusion.
• In its most recent guidelines, the BTF provides level III
recommendations for measurement of AVDO2, the optimization of
which has been associated with favorable outcomes 6 months after
injury. It is recommended to avoid AVDO2 <50%.
Prabhakar H, Sandhu K, Bhagat H, Durga P, Chawla R. Current concepts of optimal cerebral perfusion pressure in traumatic brain injury. J
Anaesthesiol Clin Pharmacol. 2014 Jul;30(3):318-27. doi: 10.4103/0970-9185.137260. PMID: 25190937; PMCID: PMC4152669.
15. Optimal threshold for CPP following TBI
• The individual parameters of CPP (blood pressure and ICP) have been
shown to be critically related to outcome from TBI.
• Systemic hypotension is highly associated with poor outcome
• As well, elevated ICP predicts increased mortality and less recovery.
• However, the critical CPP threshold is still debatable.
• Role of neuromonitoring to determine optimum CPP
• The response of brain to injury is heterogenous. Considerable
uncertainty exists about the optimal level of CPP required to restore
the cerebral oxygenation. The role of neuromonitoring in
determining the optimal CPP for patients with TBI is investigated.
Kinoshita K, Sakurai A, Utagawa A, Ebihara T, Furukawa M, Moriya T, Okuno K, Yoshitake A, Noda E, Tanjoh K. Importance of cerebral perfusion
pressure management using cerebrospinal drainage in severe traumatic brain injury. Acta Neurochir Suppl. 2006;96:37-9. doi: 10.1007/3-211-
30714-1_9. PMID: 16671420.
16. Role of neuromonitoring to determine
optimum CPP
• The response of brain to injury is heterogenous.
• Considerable uncertainty exists about the optimal level of CPP
required to restore the cerebral oxygenation.
• The role of neuromonitoring in determining the optimal CPP for
patients with TBI is investigated.
Kinoshita K, Sakurai A, Utagawa A, Ebihara T, Furukawa M, Moriya T, Okuno K, Yoshitake A, Noda E, Tanjoh K. Importance of cerebral perfusion
pressure management using cerebrospinal drainage in severe traumatic brain injury. Acta Neurochir Suppl. 2006;96:37-9. doi: 10.1007/3-211-
30714-1_9. PMID: 16671420.
18. • 80% kematian Cedera Kepala
disebabkan oleh proses berkelanjutan
dari iskemi otak.
• Target pengelolaan adalah mencegah
proses iskemik dan kerusakan
sekunder otak yang disebabkan oleh
proses ekstraserebral.
Penyebab Kematian
pada Cedera Kepala
McIntyre, A., Mehta, S., Aubut, J., Dijkers, M., & Teasell, R. W. (2013). Mortality among older adults after a traumatic brain injury: a meta-
analysis. Brain injury, 27(1), 31-40.
19. Kematian cedera otak sekunder (9 H)
1. Hipoksemia (Hipoksia, anemia, CO)
2. Hipotensi (Hipovolemi, ggn jantung, pneumothorax)
3. Hiperkapnia (Distress pernafasan)
4. Hipokapnia (Hiperventilasi)
5. Hipertermi (Hipermetabolisme / reaksi stres)
6. Hiperglikemi (Hipotermia / dekstrose)
7. Hipoglikemia (cairan hipotonik)
8. Hipoproteinemia (malnutrisi)
9. Hiponatremia (SIADH)
McIntyre, A., Mehta, S., Aubut, J., Dijkers, M., & Teasell, R. W. (2013). Mortality among older adults after a traumatic brain injury: a meta-
analysis. Brain injury, 27(1), 31-40.
20. Daugherty, J., Waltzman, D., Sarmiento, K., & Xu, L. (2019). Traumatic brain injury–related deaths by race/ethnicity, sex, intent, and
mechanism of injury—United States, 2000–2017. Morbidity and Mortality Weekly Report, 68(46), 1050.
21. McIntyre, Amanda, et al. "Mortality among older adults after a traumatic brain injury: a meta-analysis." Brain injury 27.1 (2013): 31-40.
22. Bouzat, P., Sala, N., Payen, J. F., & Oddo, M. (2013). Beyond intracranial pressure: optimization of cerebral blood flow, oxygen,
and substrate delivery after traumatic brain injury. Annals of intensive care, 3(1), 1-9.
23. CBF :
50 mg/100 mg/menit
MAP: 60-160 mmHg
AUTOREGULASI CEREBRAL
PERTAHANKAN!
Rangel-Castilla, Leonardo, et al. "Cerebral pressure autoregulation in traumatic brain injury." Neurosurgical focus 25.4 (2008): E7.
Calviello, Leanne, et al. "Cerebral autoregulation monitoring in acute traumatic brain injury: what’s the evidence?." (2017).
31. HIPERVENTILASI PADA TBI
Gouvea Bogossian, Elisa, et al. "Hyperventilation in adult TBI patients: how to approach it?." Frontiers in
Neurology 11 (2021): 580859.
33. LUND THERAPHY
• Lund concept 1990 to 1991 at the University Hospital of Lund,
Sweden.
• initiated because of the high mortality rate of these patients at that
time, and because of the weak physiological and clinical support of
the standard therapies used.
• Lund therapy is a theoretical approach mainly based on physiological
and pathophysiological hemodynamic principles of brain volume and
brain perfusion regulation, and is characterized by the treatment of
intracranial pressure (ICP) and maintenance of cerebral perfusion
(the ICP and perfusion-guided approach).
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
Grände PO. The Lund concept for the treatment of patients with severe traumatic brain injury. J Neurosurg Anesthesiol. 2011 Oct;23(4):358-62. doi:
10.1097/01.ana.0000405612.20356.84. PMID: 21908989.
Grände PO. Critical Evaluation of the Lund Concept for Treatment of Severe Traumatic Head Injury, 25 Years after Its Introduction. Front Neurol. 2017 Jul
4;8:315. doi: 10.3389/fneur.2017.00315. PMID: 28725211; PMCID: PMC5495987.
34. TREATMENT OF ICP
• Post Trauma CPP ↑
• Vasopressors CPP ↑
• CPP ↑ ↑ hydrostatic capillary pressure transcapillary filtration
and aggravate the vasogenic brain oedema
• Lund therapy accepting a lower CPP than the initially
recommended 70 mm Hg and by avoiding vasopressors.
• The Lund concept even advocates the use of antihypertensive
treatment in terms of b-1 blockade, a-2 agonists, and angiotensin II
antagonists to counteract the development of edema.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
Gra¨nde PO. The Lund concept for the treatment of severe head trauma–physiological principles and clinical application. Intensive Care Med. 2006;32:1475–1484.
35. BLOOD VOLUME EXPANDERS
• Lund concept hypovolemia-induced activation of the baroreceptor
reflex release of catecholamines into the plasma and adverse
vasoconstriction in the penumbra zone with aggravation of the
hypoxia.
• Lund concept, albumin is recommended as the main plasma volume
expander—preferably a 20% solution due to its more effective
absorbing effect, an effect that is beneficial to reduce interstitial
volume not only for the injured brain but also for the rest of the
body.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
36. BLOOD VOLUME EXPANDERS
• Lund concept, blood transfusions (only leukocyte-depleted blood) up
to a hemoglobin concentration above 12 g/dL are recommended, as
the red blood cells are not only essential for oxygenation of the brain
but also for maintenance of normal blood volume.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
37. TREATMENT TO IMPROVE PERFUSION
• CPP remains in the range of 60 to 70 mm Hg in most adult patients
treated with Lund therapy.
• If nessesary to control ICP, a minimum CPP of 50 mmHg has been
accepted in adults and 40 mmHg in small children after an individual
evaluation, but only if the patient is treated towards normovolemia
with the fluid therapy advocated in the LC.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
Gra¨nde PO. The Lund concept for the treatment of severe head trauma–physiological principles and clinical application. Intensive Care Med. 2006;32:1475–1484.
38. OSMOTHERAPY
• Osmotherapy is not used in Lund therapy due to the lack of scientific
and physiological support and due to documented side effects.
• Osmotherapy ICP-reducing effect is transient and, at least for
mannitol and urea, is followed by a rebound increase in ICP some
hours after the infusion, aggravating the brain edema.
• Mannitol may also be associated with renal insufficiency and severe
electrolyte disturbances.
Grände PO. The Lund concept for the treatment of patients with severe traumatic brain injury. J Neurosurg Anesthesiol. 2011 Oct;23(4):358-62. doi:
10.1097/01.ana.0000405612.20356.84. PMID: 21908989.
Holbeck S, Bentzer P, Gra¨nde PO. Effects of hypertonic saline, mannitol, and urea with regard to absorption and rebound filtration in cat skeletal muscle. Crit Care Med.
2002;30:212–217.
39. LUNG FUNCTION
• Lund theraphy strongly advocating positive endexpiratory pressure
(PEEP).
• PEEP is an important measure to reduce atelectasis
• Hyperventilation is not used in Lund therapy, as it may aggravate the
hypoxia in the penumbra zone.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
40. ANTISTRESS THERAPY
• Wake-up tests are accepted in many neurointensive care units to
evaluate the status of the patient, which also implies the use of
mainly short-acting sedatives such as propofol.
• Wake-up tests are not a component of Lund therapy due to stress
effects, increase in ICP and the release of catecholamines in
plasma reduced perfusion of the brain.
• Sedatives are not discontinued until ICP has been stabilized at a
normal level and until weaning from the ventilator will be successful.
Koskinen, L-O. D., Olivecrona, M., & Grände, P-O. (2014). Severe Traumatic Brain Injury Management and Clinical Outcome Using the Lund Concept. Neuroscience, 283(Jun
25), 245-255. https://doi.org/10.1016/j.neuroscience.2014.06.039
Gra¨nde PO. The Lund concept for the treatment of severe head trauma–physiological principles and clinical application. Intensive Care Med. 2006;32:1475–1484.
41. TEMPERATURE
• Active cooling has never been a component of the Lund concept
• potential side effects inherent in the significant stress and
catecholamine release initiated by the difference between body
temperature and the temperature value set by the thermostat, with
the risk of reducing cerebral circulation of the penumbra zone.
• Lund therapy involves the treatment of high fever pharmacologically
instead.
Gra¨nde PO, Reinstrup P, Romner B. Active cooling in traumatic brain-injured patients: a questionable therapy? Acta Anaesthesiol Scand. 2009;53:1233–1238.
Grände PO. The Lund concept for the treatment of patients with severe traumatic brain injury. J Neurosurg Anesthesiol. 2011 Oct;23(4):358-62. doi:
10.1097/01.ana.0000405612.20356.84. PMID: 21908989.
42. DRAINAGE OF CSF AND DECOMPRESSIVE
SURGERY
• CSF drainage is accepted in the Lund concept to control an elevated
ICP (only through ventricular drainage), especially if there are signs of
hydrocephalus.
• Decompressive craniotomy is the last therapeutic measure to prevent
brain stem herniation in Lund therapy.
Gra¨nde PO. The Lund concept for the treatment of severe head trauma–physiological principles and clinical application. Intensive Care Med. 2006;32:1475–1484.
43. Grände PO. Critical Evaluation of the Lund Concept for Treatment of Severe Traumatic Head Injury, 25 Years after Its Introduction. Front Neurol. 2017 Jul
4;8:315. doi: 10.3389/fneur.2017.00315. PMID: 28725211; PMCID: PMC5495987.
Editor's Notes
Metabolisme otak : aerob
Oksigenasi otak bergantung pada suplai oksigen dan konsumsi
Berhubungan dengan CBF dan selisih oxygen content pada arteri (CaO2) and vena (CvO2) oxygen contents
CBF × (CaO2 – CvO2)}
CaO2 merupakan penentu signifikan delivery oksigen, dan bergantung pada Hb, saturasi (SaO2), and, tekanan parsial oksigen dalam arteri (PaO2).
Gagal napas pada hipoksemia sistemik menyebabkan hipoksia serebral, terutama bila terjadi gangguan serebral (contoh : perubahan tonus vaskuler untuk mempertahankan CBF)
Optimalisasi Hb dapat memperbaiki oksigenasi otak pada kasus tertentu
Oxygen delivery terutama dipengaruhi CBF,
Yang ditentukan oleh CPP, MAP, ICP, cerebral vasoreactivity, dan autoregulasi serebralRestriksi delivery oxygen karena mikrosirkulasi, yang akan menurunkan difusi oksigen pada sel otak
Meningkatnya konsumsi oksigen dapat diamati pada pasien agitasi, hipertermi, dan kejang
CBF is significantly influenced by PaCO2 levels. When PaCO2 drops below 20mmHg, vasoconstriction of brain blood vessel occurs, leading to a decrease in ICP as the final outcome. Many conditions are responsible for maintain oxygenation balance in brain, divided into extracranial and intracranial causes. Hypoxia, hypotension, hypo/hyper PaCO2, and anemia are extracranial causes while intracranial causes is increased in ICP. When there is a rise in PaCO2 may induce a brain blood vessel dilatation causing ICP increase and contribute to an increase in cerebral blood volume leading to brain edema, likely resulting in a poor outcome for patients. On the other hand, when PaCO2 drops, vasoconstriction of brain blood vessel occurs, leading to a decrease in ICP and cerebral blood volume.9
Patients that experience TBI often develop hypercapnia, a condition where CO2 level in circulation is rising. When hypercapnia develops after a TBI that can be caused by airway obstruction or respiratory insult, hyperventilation therapy is mandatory for decreasing the ICP
Cerebral blood flow is one of the most important determinants of brain oxygen delivery. As discussed previously, arterial blood pressure and CPP are the major modifiable variables of brain oxygenation. This implicates that manipulating blood pressure and CPP may be the first and often the most effective intervention to optimize CBF and oxygen supply to injured brain tissue. Second-tier interventions to improve PbtO2 despite CPP modifications include optimization of systemic oxygenation (lung protective ventilation and maintenance of strict normoxia) [43] and red blood cell transfusion if hemoglobin is below 9 g/dl [44] (Figure 4). However, other mechanisms may reduce brain tissue oxygenation. Among these, diffusion-limited oxygen delivery plays a key role and might explain why PbtO2 can be reduced despite oxygen delivery (PvO2) and CBF are normal [17]. In clinical practice, this may explain why in some circumstances brain tissue hypoxia can occur despite ICP/CPP being within normal ranges [22]. Without anemia or hypoxia, low PbtO2 despite adequate CBF probably reflects microcirculatory dysfunction and pericapillary edema [17]. This has important implications for the management of PbtO2 and the response of PbtO2 to therapeutic interventions.
FIGURE 1. A practical approach on how to manage controlled hyperventilation and hypocapnia in traumatic brain injury (TBI) patients. Acute intracranial hypertension (ICHT) = life-threatening elevation in ICP, in particular when signs of herniation (i.e., anisocoria, apnea, hypertension, bradycardia) are present. ICHT, intracranial pressure close to the critical threshold for therapy without signs of herniation; HV, controlled hyperventilation and hypocapnia. Green and red circles refers to the potential use (green) or contraindication (red) to the use of HV. NM, neuromonitoring. *In case of diffuse brain injury but with high potential risk of tissue hypoxia. **Adjusted on neuromonitoring.