EMERGENCY MANAGEMENT OF

TRAUMATIC BRAIN INJURY AND STROKE

IN EMERGENCY ROOM AND INTENSIVE CARE UNIT

ASWIN WIKANTAMA
in Seminar Kesehatan
Holistic and Comprehensive Approach to Neurological Case: Head Trauma and Stroke
30TH of June 2024
 dr. Aswin Wikantama, Sp.An,
FISQua
Pendidikan:
S1 Profesi : Pendidikan Dokter UNS tahun 2001-2008
PPDS : Anestesiologi dan Terapi Intensif UGM tahun 2016-2020
Fellowship : International Society for Quality in Health care tahun 2023
Pekerjaan : ITS PKU Muhammadiyah Surakarta
• Dosen Progdi keperawatan dan kebidanan ( th 2020-2023)
Lembaga Akreditasi Rumah Sakit Indonesia (LARSI)
• Surveyor Akreditasi (th 2022-sekarang)
RS PKU Muhammadiyah Karanganyar
• Dokter Spesialis Anestesi Fulltimer (th 2020 – sekarang)
• Ketua Subkomite Keselamatan Pasien Komite Mutu (th 2020 – 2023)
• Ketua KSM Anestesi dan Terapi Intensif (th 2023 – sekarang)
• Direktur Utama RS (th 2023 – sekarang)
Keorganisasian:
• Anggota Perdatin (Perhimpunan Dokter Spesialis Anestesiologi dan Terapi Intensif) Cabang Solo Raya
• Surveior LARSI (Lembaga Akreditasi Rumah Sakit Indonesia) (2021-skrng)
• Koordinator MCCC (Muhammadiyah Covid-19 Command Center) PDM Surakarta(2020-2023)
• Wakil Ketua MDMC/LRB (Lembaga Resiliensi Bencana) PDM Surakarta (2014-skrng)
TRAUMATIC BRAIN INJURY
 FACTORS AFFECTING TBI MORTALITY

Traumatic Brain Injury Disorders

Head trauma contributes to more than 50% of
deaths from all accident cases.
01
The characteristics of this head trauma cause
neurological abnormalities which include: (1) Systemic
02 factors that cause hypoxia, hypercapnia, or hypotension
(2) the shape and extent of subdural, epidural, or
intracranial hematoma (3) increased intracranial
Fifty percent of patients with severe traumatic brain
injury suffer from hypotension and hypoxia.
03 pressure
 GCS
OUTCOME
SURVIVAL GCS score less than 11 within 24 hours has a
GCS score has a strong influence on the poor outcome. There is an association between
chances of survival and recovery in lower score of GCS and worse outcomes
traumatic brain injury patients (Okasha, (Lingsma et al. , 2014; Maas et al. 2011).
et al, 2014).

GCS as a clinical parameter

Early GCS Other complication

A low initial GCS at the
assessment the condition of patients with traumatic brain
start of the injury will injury with skull fractures is explained to have ten
have a poor outcome times of the potential to experience neurological
(Okasha, et al, 2014). deficits and the outcome will be worse, as assessed
using GCS (Joseph et al, 2015).
 MANAGEMENT

Early management objectives:

1. Providing adequate oxygen

2. Maintaining sufficient blood pressure to maintain brain perfusion
3. Avoiding secondary brain injury
4. Identifying mass lesions requiring surgery
 HOW TO MANAGE TBI PATIENTS IN THE EMERGENCY ROOM
Handling with primary survey and secondary survey
Primary survey
A : There is possibility of airway obstruction at GCS < 9. Clear the airway, suction, use
oropharyngeal airway.
B : Use nasal canule to NRM, SpO2 target of > 90 % (or if possible more than 95%).
C: Control blood pressure, MAP target of < 110.
D : Decreased consciousness  evaluate GCS after oxygenation and fluid resuscitation,
make sure there are no sedative or relaxant drugs because valid GCS can be evaluated
after these three procedures have been done.
E : Look for other signs of trauma. Use a cervical collar because there is possibility of
cervical problem on head injury patients.
After the handling of primary survey, the secondary survey continues.
Anamnesis: AMPLE.
Secondary survey: re-evaluate ABCDE after primary survey, check laboratory markers, blood
gas analysis, and X-ray.
Patients with indication for intubation  GCS score < 9, signs of cerebral herniation,
progressive loss of consciousness.
Plan Rapid Sequence Intubation. Ensure there is no increase in intracranial pressure.
Administer lidocaine at a dose of 1.5 – 2 mg/kg and fentanyl at a dose of 2-5 mcg/kgBB.
Consult to neurosurgery department. If the head CT scan result shows bleeding, a
craniotomy is recommended.
Perform all supportive examinations. Complete laboratory examination, blood gas analysis,
head CT scan, cervical X-ray, chest X-ray.
 TARGET FOR OXYGENATION AND BLOOD PRESSURE ACCORDING TO
TRAUMATIC BRAIN FOUNDATION

• According to TBF 2016, the target for systolic blood pressure is ≥ 100 at the
age of 50-69 years, ≥ 110 at the age of 15-49 years or over 70 years.

• SpO2 oxygenation target of > 90% according to TBF 2016, cerebral perfusion
pressure target of 60-70mmHg and intracranial pressure therapy need to be
performed if it results in more than 22.
 Procedures to Reduce ICP
Perform 15-300 head up position. Make sure there are no upper vein dams.
Monitor ICP.
First tier: ventricular drainage, administer mannitol of 0.25 – 1 gram/kg in 10-15 minutes,
hyperventilate with PCO2 target of 30-35.
Second tier: hyperventilation, PCO2 target of 25-30. Barbiturate coma. Hypothermia.
Decompressive craniectomy.
Pharmacology: drugs that can be administered: lidocaine of 1.5 – 2 mg/kg, fentanyl of 2-5 mcg/kg.
Prevent other factors that can increase intracranial pressure such as coughing, vomiting, straining,
hypertension, and hypercarbia.
 Management and Treatment
Recommendations
1. Intracranial Complications:
a. CT head scan without contrast or MRI when the neurological findings are unexplained by
computed tomography
b. Maintain hemodynamic stability with goal of systolic BP > 90-mmHg using isotonic fluid
resuscitation.
c. Continuous pulse oximetry monitoring to maintain O2 saturation > 90% or PaO2 > 60 mm Hg using
supplemental oxygen
d. Hypoxemia not corrected with supplemental O2, GCS < 9 or inability to maintain the airway
warrants bag mask ventilation or rapid sequence endotracheal intubation
e. Brief periods of hyperventilation therapy of 20 breaths per minute (PaCO2 < 35 mmHg) should be
used as a temporizing measure when clinical signs of cerebral herniation.
f. Patients with signs of progressive neurological deterioration referable to the intracranial lesion,
medically refractory intracranial hypertension, or signs of mass effect on CT scan should be
evaluated by a Neurosurgeon.
 Management and Treatment
Recommendations

2. Pharmacological complications
a. Management and treatment include discontinuation of the offending medication and
supportive treatment of symptoms.
b. Benzodiazepines are not recommended as sleep aids in patients with TBI due to
adverse side effects, may be used for control of muscle rigidity, agitation and tremor.
 Management and Treatment
Recommendations

3. Infectious complications
a. Diagnosis is made in light of presenting clinical features, positive culture, and
or radiological evidence of infection.
b. Antimicrobial Therapy
1. Initial empiric anti-infective therapy is indicated in patients with sepsis to
include one or more drugs
2. Antimicrobial regimen should be reassessed daily for potential de-escalation to
the most appropriate single therapy
3. Use of procalcitonin levels or similar biomarkers
4. Duration of therapy is typically 7–10 days
5. Antimicrobial agents should not be used in patients with severe inflammatory
states determined to be of noninfectious cause.
6. Source Control
4. Endocrine and metabolic complications
a. Central diabetes insipidus
1. Acute phase CDI warrants immediate hormone replacement therapy with
desmopressin and hypotonic fluids guided by the urine output and the plasma
sodium.
2. Chronic phase CDI is maintained with oral desmopressin.
b. SIADH/CSW
3. Acute symptomatic hyponatremia (<48jam): correction with hypertonic saline
3%
4. Chronic hyponatremia (>48jam): Correction should be no faster than 0.5
mmol/h to avoid the risk of osmotic demyelination syndrome
1. In the secondary survey during anamneses what is meant by AMPLE is

A. Alergy, meal, post stroke, last medication, event

B. Anamneses, medication, past illness, last meal, event
C. Alergy, medication, past illness, last meal, event
D. Anamneses, meal, post stroke, last medication, event

C. Alergy, medication, past illness, last meal, event

STROKE
 Stroke Subtypes
Ischemic stroke most common.
Stroke
A common cause of persistent
disability in US adults
Commonalities for SAH, ICH,
Ischemic Severe Ischemic Stroke:
ICH
• Predominant risk factor is
SAH
hypertension
• Dysphagia is common, and
may lead to pneumonia.
Swallowing evaluations should
be performed prior to oral
© 2021 Society of Critical Care Medicine
feedings
 Severe Stroke

Occlusion of the middle cerebral artery or internal carotid (middle and anterior
cerebral artery) is the prototypical severe stroke

Presentation:
•Gaze preference toward the side of stroke (frontal eye fields allow eyes to look to
the other side), e.g., eyes look left for a large left-sided stroke
•Weakness on the other side of the body, e.g., right sided weakness for a left sided
stroke
•If left sided stroke, inability to speak or follow commands, even if alert
•If right sided stroke, trouble with visuo-spatial orientation (“whose hand is this?”).
More often mis-diagnosed, and not scored as intensely on the NIH Stroke Scale, so
seems less severe.
© 2021 Society of Critical Care Medicine
 Acute Stroke Therapeutics

• Tissue plasminogen activator: t-PA, for use within 4.5 hours of

symptom onset (extended from 3 hours, with some exclusion
criteria).
• Works for all stroke subtypes.
• Endovascular: Large vessel occlusion discovered on imaging, or
mismatch in amount of brain tissue that is under perfused, but
not dead.
• Endovascular indications are changing quickly.
© 2021 Society of Critical Care Medicine
 Hemicraniectomy

• For use in middle cerebral artery infarction where perfusion cannot be

restored.
• Cerebral edema often leads to brain herniation, typically in 2-5 days.
• Hemicraniectomy is removal of the skull on the affected side,
typically within 48 hours of stroke.
• Brain can swell out of the side of the hemicraniectomy, minimizing
brainstem compression.
• Improves survival, typically with moderately severe disability (e.g., needs
assistance with daily living, mRS 4) at one year.
• Early neurosurgical consultation appropriate.

© 2021 Society of Critical Care Medicine

 Hemicraniectomy Example

Clot in left middle Evolving infarction After

cerebral artery (low density, scant hemicraniectomy, no
(hyperdense MCA midline shift) significant midline
sign, arrow) shift

Follow-up: Had deep venous thrombosis, received warfarin. Discharged after 3 weeks to
rehabilitation. At two years, required help with daily living, wheelchair (mRS 4), sociable.

© 2021 Society of Critical Care Medicine

 Subarachnoid Hemorrhage
Dx
• Presentation: “Worst headache of life” and “first” headache like this.

• Mandates CT. If CT negative, perform lumbar puncture (LP).

• LP is most helpful when the diagnosis is most in question.

• 5-10% of patients with SAH are initially misdiagnosed.

• Most common mistake is not obtaining CT

• Misdiagnosis increases potential for aneurysm rebleeding and poor

outcome © 2021 Society of Critical Care Medicine
 Severity of SAH

• Clinical grading – Hunt and Hess scale, from I (mild

headache, best) to V (coma, worst prognosis).
• Required for Stroke Centers.
• CT grading by Fisher grade (and modified forms),
accounting for “thick” subarachnoid blood on the CT.
• More subarachnoid blood increases the risk of delayed
cerebral ischemia (“vasospasm”)

© 2021 Society of Critical Care Medicine

 Targeting early rebleeding risk

• The initial goal of SAH care is to limit the risk of rebleeding by blood pressure
control, optimization of abnormal coagulation parameters and early aneurysm
repair
• Most centers actively control elevated blood pressure to a goal systolic blood
pressure of 140 mmHg or less before open surgical or endovascular treatment
of the ruptured aneurysme
• Extremes of blood pressure on admission (MAP > 130 or < 70 mmHg) have
also been associated with poor outcome after SAH

© 2022 Society of Critical Care Medicine

 Hyponatremia

• SIADH and cerebral salt wasting are common after SAH.

(Distinction is euvolemia versus hypovolemia.)
• Focus on volume resuscitation may disguise some cerebral
salt wasting as SIADH.
• Without specific treatment, [Na] < 130 mEq/L is common;
resulting cerebral edema may worsen neurologic
examination
• Hypertonic saline use common (more detail in elevated ICP
session)
© 2021 Society of Critical Care Medicine
 Seizure and Seizure
Medications

• Seizures occur in about 10% of patients.

• Prophylactic phenytoin independently linked to more complications
(more fever), worse clinical outcomes, and worse cognitive outcomes
• EEG monitoring for patients with altered mental status.
• Routine 30-60 minute EEG detects only about 50% of patients with
subclinical seizures

© 2021 Society of Critical Care Medicine

 Fever

• Fever is common after SAH, much more common than

infection
• Fever is independently linked to worse clinical outcome
• Interventions beyond acetaminophen (e.g., cardiac arrest type
temperature control) have not been linked to improved
outcomes, but do increase ICU interventions and complications

© 2021 Society of Critical Care Medicine

 SAH Summary

• Thick SAH on CT increases risk for vasospasm

and delayed cerebral ischemia
• Prevent cerebral infarction from vasospasm
with nimodipine
• Search for subclinical seizures with EEG if indicated
(typically altered consciousness), but do not use
prophylactic phenytoin

© 2021 Society of Critical Care Medicine

 Intracerebral Hemorrhage (ICH)

•ICH Score on presentation for

severity
• 1 point for GCS 5-12, 2 points 3-4
• 1 point for infratentorial
• 1 point for volume >=30 mL
• 1 point for age >= 80 years
• 1 point for intraventricular hemorrhage

© 2021 Society of Critical Care Medicine

 Hematoma Expansion
• Larger hematomas lead to worse outcome
• Coagulopathy should be reversed rapidly
Cause Treatment

Novel oral anticoagulant (e.g., Specific antibody (idarucizumab).

dabigatran, rivaroxaban) Potentially andexanet alpha (FXa
inhibitor antidote), prothrombin complex
concentrate (changing rapidly)

Warfarin Prothrombin complex concentrate

Aspirin NOT Platelet transfusion

Desmopressin improves platelet activity,
but no prospective trials

P2Y12 Inhibitors (e.g., clopidogrel, ticagrelor) Unknown

© 2021 Society of Critical Care Medicine

 Blood Pressure Lowering

• Current guidelines are BP should be lowered from 150-220 mm Hg

to 140 mm Hg.
• More BP reduction increases risk of renal failure.

© 2021 Society of Critical Care Medicine

 Seizures and Seizure Medications

• Similar to SAH
• Prophylactic phenytoin independently associated with more fever and
reduced independence
• Prophylactic levetiracetam independently associated with worse
cognitive function, but not with more fever or reduced independence
• EEG monitoring should be considered, especially for altered
consciousness.
• Routine EEG not sensitive
• Seizures should be treated

© 2021 Society of Critical Care Medicine

 Cerebellar ICH

• Cerebellar ICH has a high risk of brainstem

compression.
• Neurosurgical consultation should be obtained early for
evaluation for cerebellar decompression

© 2021 Society of Critical Care Medicine

 Deep Venous Thrombosis

• DVT is common after ICH

• Increased risk with paretic limbs, withholding of
anticoagulants (e.g., anticoagulant prescribed for DVT, leading to
ICH, with reversal of anticoagulant)
• Minidose heparin for DVT prophylaxis is likely safe after 3 – 5
days from ICH if hematoma is stable on CT

© 2021 Society of Critical Care Medicine

 ICU management

• Patient positioning
• Fluids
• Prevention of seizures
• Management of hyperglycemia
• Management of elevated ICP
• Intraventricular trombolytic theraphy
• Surgical intervention for ICH
• Deep venous thrombosis prophylaxis
© 2022 Society of Critical Care Medicine
2. which is not management in the emergency department
in stroke patients with intracerebral hemorrhage….

A. Blood pressure control

B. Initial emergency ICP management
C. Fever and glycemic control
D. Always care in ICU

D. Always care in ICU

 DAFTAR PUSTAKA

• Bisri, T., 2012. Terapi Intensif Cedera kepala. In: Penanganan Neuroanestesia dan Critical Care: Cedera Otak Traumatik.
Bandung: Fakultas Kedokteran Universitas Padjadjaran-Bandung, p. 143.
• Bisri, T., Wargahadibrata, H. & Surahman, E., 1997. In: Neuroanestesi. Bandung: Saga Olahcitra.
• Lingsma, H., Rozzenbeek, B., Steyerberg, E., Murray, G., & Maas, A., 2014. Early prognosis in traumatic brain injury: from
prophecies to predictions. Lancet Neurol, 9, 543
• Maas, Engel, & Lingsma, 2011. Prognostic After Trauma Brain Injury. Humans Neurological Surgery, sixth edition, chapter
340, 3497
• Roberts, Pamela R. & Todd, S.Rob, 2022. Comprehensive critical care: adult. Third edition. Society of critical care
medicine. USA
• Traumatic Brain Foundation 2016
• Traumatic Brain Foundation 2023
THANK YOU