Raised ICP: What are our option? - Pathophysiology intracranial hypertension. - Use Brain Trauma Foundation Guideline (first-tier and second-tier therapy). - On going research is the effect of TH to decrease ICP.

1. Raised ICP: What are our option?
Tatang Bisri
Universitas Padjadjaran Bandung
Sebagian slide diambil dari NACC course versi 2014

2. PATHOPHYSIOLOGY

3. Normal ICP in
healthy adult
5-15 mmHg.
ICP >20 mmHg
accepted as
Intracranial
Hypertension
Figure: Idealized intracranial pressure volume relationships. From: Shapiro,
H.M. Intracranial hypertension: Therapeutic and anaesthetic considerations.
Anesthesiology 43: 445-471, 1975
Intracranial
contents:
Brain tissue,
intravascular
blood, CSF.

4. Causes of Intracranial Hypertension
• Traumatic brain injury
• Brain tumor
• Subarachnoid
hemorrhage
• Brain swelling from
cerebral infarction
• Intracerebral hematoma
• Extracerebral
hematoma
• Acute hydrocephalus
• Cerebral venous
thrombosis
• Anoxic-ischemic
encephalopathy
• Brain infarction after
acute occlusion MCA
• Abscess
• Meningitis
• Hypertensive
encephalopathy
Roper AH. Pract Neurol 2014;14:152-8, Stocchetti N, Maas AIR. N Eng J Med 2014;170:2121-30

5. Pathophysiology: Main causing increased ICP
Condition Mass
effect
Edema Vasodila-tation
Disturbed
circulation
of CSF
TBI + + +
SAH
+
+
Spontaneous ICH
+
+
++
Cerebral venous
thrombosis
+ ++
Abscess + +
Brain Tumor + +
Stocchetti N, Maas AIR. N Eng J Med 2014;170:2121-30

6. Primary and Secondary Brain Injury
Primary Brain Injury
• Result from the biomechanical effect of forces applied to
the skull and brain at the time of insult and are manifested
within miliseconds.
• Curently, there is no treatment for the primary brain injury.
Secondary Brain Injury
• Occurs in the minutes, hours, or days after the impact.
• Represent complicating processes initiated by primary
brain injury such as ischemia, brain swelling and edema,
intracranial hemorrhage, intracranial hypertension, and
herniation.
• Secondary injury can be treatment and avoid.

7. Secondary insult that can contribute to hypoxic
and/or Ischemic Brain Damage
Systemic/Extracranial
• Hypoxemia
• Hypotension
• Anemia
• Hypocarbia
• Hypercarbia
• Pyrexia
• Hyponatremia
• Hypoglicemia
• Hyperglicemia
Intracranial
• Hematoma
• Raised ICP
• Seizure
• Infection
• Vasospasm
Cottrell and Young’s Neuroanesthesia
2010

8. Systemic Cause of Increased ICP
Vasodilatation of
cerebral vessel
Fever, Seizure, Hypercarbia,
Hypoxemia, Hypotension
Increased venous
pressure
Neck torsion or compression
Pneumothorax, Ventilator
asynchrony, increased abdominal
pressure
Increased arterial
pressure
Pain, bladder distension
Cellular edema Hyponatremia

9. Increases ICP
• Both intracranial and systemic event contribute to
increased ICP after TBI.
• In the 1st hour: expansion of hematoma is the main
threat.
• In the following days: water accumulation (edema),
disrupted autoregulation, ischemia, contusion
expansion lead to further increases ICP.
• Mechanical effect of increases ICP: distortion of brain
tissue, mid line shift, herniation.
• Vascular effect of increases ICP: impaired CPP
(CPP=MAP-ICP).

10. TREATMENT

11. Still remember ABCDE Neuroanesthesia??
 A = Clear airway
 B = Control ventilation, normocapnia at TBI and
slight hypocapnia at brain tumor.
 C = Avoid high increase or decrease of BP, avoid
increase of cerebral venous pressure,
normovolemia, iso-osmoler.
 D = Avoid drugs & anesthesia technique will
increase ICP, give drugs with brain protection
effect.
 E = environment (temperature control) target
35 degree C in OR

12. Treatment of
Intracranial
Hypertension
First-tier
Therapy
BTF Guideline
2007
Hypot
herm,
DC
Treatment
if ICP>20
mmHg

13. Insert ICP monitoring
• Severe TBI, abnormal CT-scan (hematoma, contusion,
swelling, herniation, compress basal cysterna).
• Severe TBI with normal CT-scan if 2 or more features are
note at admission: age over 40 year, unilateral or
bilateral motor posturing, or systolic BP < 90 mmHg.
• Treatment should be initiated if ICP threshold above 20
mmHg.
BTF Guidelines 2007
• Placement of intracerebral catheter is relative
contraindicated in patient with coagulopathy (i.e increase
Prothrombin time, partial thromboplastin time, or
platelet count <100.000 per microliter).
Stocchetti N, Maas IAR. N Engl J Med 2014

14. Maintain CPP
• CPP 50-70 mmHg.
• Aggresive attempt CPP > 70 mmHg should be
avoided because of the risk of ARDS.
• CPP < 50 mmHg should be avoided, because
the injured brain show sign of ischemia.
BTF guideline 2007. Bendo AA. In: Cottrell and Young’s
Neuroanesthesia 2010

15. First-tier Therapy: Ventricular Drainage
• Requires insertion catheter and the effect only
temporary.
• Part of insert ICP monitor with ventricular
catheter.

16. First-tier Therapy: Hyperventilation
• Risks of inducing cerebral ischemia
– Moderate hypocapnia (PaCO2 <34 mmHg)
found to ↑vol of severely hypoperfused
tissues despite improvements in CPP and ICP
• Effects are transient – prolonged HV (>4 hrs) will
lead to rebound ↑ ICP when discontinued
Coles JP et al. Crit Care Med 2002; 30:1950-59

17. CO2‐ CBF Reactivity
•↓PaCO2 causes
cerebral
vasoconstriction
•↓ 3% CBF per
mmHg
↓ PaCO2
•Highly effective in
rapidly lowering ICP
Stocchetti N et al. J Neurotrauma 1993; 10:187
Stocchetti N et al. Chest 2005; 127:1812-27
Robertson C CCJM 2004; 71:S14-15

18. First-tier Therapy: Mannitol
• Reduce ICP within few minutes: Immediate plasma
expanding effect, reduce Ht, increase deformability
erythrocytes, reduce blood viscosity, increase CBF,
increase cerebral oxygen delivery.
• Osmotic effect delayed for 15-30 minute, and persist
90 minute-6h.
• Osmolarity must be monitored and should no exceed
320 mOsm/l.
• Rebound effects to be relevant only with a defective
BBB or treatment > 4 days.

19. Second-tier therapy:
• If increase ICP refracter to first-tier therapy.
• Refractory elevation in ICP as a spontaneous
increase ICP >15 minutes within a 1 hour period,
despite optimized first-tier intervention.
• Hiperventilation to achieved PaCO2 < 30 mmHg
(SJO2, AVDO2, and/or CBF monitoring is
recommended), high dose barbiturate therapy,
consider hypothermia, consider hipertensive
therapy, consider decompresive craniectomy.

20. Second-tier Therapy: hypothermia
ICP Lowering effect
–lower CMRO2 → ↓CBF and ↓ CBV → ↓ ICP
Neuroprotective effects
 Retard the ischaemic (inhibits release of
excitotoxic mediators)
 Prevents disruption of the
blood‐brain‐barrier cascade

21. Jiang JY, et al. Journal of Cerebral
Blood Flow & Metabolism 2006
• Long-term mild hypothermia (33-35 0C)
significantly improve outcome of severe TBI
patient with cerebral contusion and
intracranial hypertension without significant
complication.
• 5 days long-term cooling is more efficacious
than 2 days of short-term cooling.

22. Sadaka F, Veremakis C. Brain injury
2012;26(7-8):899-908
• A systematic review: 18 studies
• 13 RCT, 5 observational studies.
• Therapeutic hypothermia 32-34 degree C, was
effective in controlling ICH.
• Conclusions: Pending result from large multi
center studies evaluating the effect of TH on
ICH and outcome, TH should be included as a
therapeutic option to control ICP in patient
with severe TBI

23. The Eurotherm3235Trial
• European society of intensive care medicine study of
HT (32-35°C) for ICP reduction after TBI (the
Eurotherm3235Trial)
• This is a pragmatic, multi-centre RCT examining the
effects of hypothermia 32-35°C, titrated to reduce
ICP <20 mmHg, on morbidity and mortality 6 months
after TBI.
• Enrollment 1800 pts over 41 months, started in April
2010.

24. Second-tier Therapy: decompresive
craniectomy
• DECRA trial: Randomly assigned 155 adult with
severe diffuse TBI and intracranial hypertension.
• For patient severe TBI and increased ICP that was
refractory to 1st tier therapy.
• Result: Decrease mean ICP and duration of
ventilatory support and ICU stay but associated
with significant worst outcome at 6 months, as
measured by GOSE score.
Cooper DJ, et al. N Engl J Med 2011;1493-502

25. Second-tier Therapy:
High dose barbiturate therapy
• Eisenberg Pentobarbital Protocol: Loading dose
pentobarbital 10 mg in 10 minutes or 5 mg/kg/h for
3 hours, and maintenance dose 1 mg/kg/h.
• Thiopental: loading dose 10-20 mg/kg bolus during
30 minutes followed 3-5 mg/kg/h.
• Thiopental: loading dose 5-11 mg/kg followed 4-6
mg/kg/h.
• Propofol: loading dose 1-2 mg/kg followed 2-10
mg/kg/h.
BTF Guideline 2007;Torbey MT. Neurocritical Care 2010

26. Cause of and Possible Therapy for Increased ICP
in TBI: Extracranial Cause
Variable Possible Therapeutic
Airway Obstruction Airway clearance, possible tracheal intubation
Hypoxemia Oxygenation and ventilation
Hypercarbia Ventilation
Hypertension associated
Analgesia and sedation
with pain
Coughing or straining Sedation, paralysis
Jugular venous obstruction Correction of neck position, draining
pneumothorax
Abdominal distention Nasogastric tube
Fever Antipyretic drugs
Hypoosmolaity Hyperosmolar fluids
Stocchetti N, Maas AIR. N Eng J Med 2014

27. Cause of and Possible Therapy for Increased ICP
in TBI: Intracranial Cause
Variable Possible Therapeutic
Hematoma (EDH, Acute SDH,
ICH)
Surgical evacuation,
decompressive craniectomy
Contusion Surgical evacuation,
decompressive craniectomy
Disturbance in CSF Drainage CSF
Edema Hyperosmolar fluids,
decompressive craniectomy
Vasodilatation Mild hyperventilation,
barbiturate
Seizure Antiepileptic medication
Stocchetti N, Maas AIR. N Eng J Med 2014

28. Risk of Treatment
Treatment Risk
Intubation, normocarbic
ventilation
Coughing, ventilator asynchrony, VAP
Increased Sedation Hypotension
Ventricular CSF drainage Infection
Hyperoosmolar therapy Negative fluid balance, hypernatremia,
kidney failure
Induced hypocapnia Excessive vasoconstriction and ischemia
Hypothermia Fluid and electrolyte disturbances and
infection
Barbiturates Hypotension and increased number of
infection
Decompressive
craniectomy
Infection or delayed hematoma, subdural
effusion, hydrocephalus
Stocchetti N, Maas IAR. N Engl J Med 2014

29. Conclusion
• Pathophysiology intracranial hypertension.
• Use Brain Trauma Foundation Guideline (first-tier
and second-tier therapy).
• On going research is the effect of TH to
decrease ICP.

30. TERIMAKASIH