Download - pengelolaan hipertensi intrakranial
Raised ICP: What are our option?
Tatang Bisri
Universitas Padjadjaran Bandung
Sebagian slide diambil dari NACC course versi 2014
PATHOPHYSIOLOGY
Figure: Idealized intracranial pressure volume relationships. From: Shapiro,
H.M. Intracranial hypertension: Therapeutic and anaesthetic considerations.
Anesthesiology 43: 445-471, 1975
Normal ICP in healthy adult 5-15 mmHg.
ICP >20 mmHg accepted as Intracranial Hypertension
Intracranial contents: Brain tissue, intravascular blood, CSF.
Causes of Intracranial Hypertension
• Traumatic brain injury
• Brain tumor
• Subarachnoid hemorrhage
• Brain swelling from cerebral infarction
• Intracerebral hematoma
• Extracerebralhematoma
• 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
Condition Mass effect
Edema Vasodila-tation
Disturbed circulation of CSF
TBI + + +
SAHSpontaneous ICH
++
++
++
Cerebral venous thrombosis
+ ++
Abscess + +
Brain Tumor + +
Pathophysiology: Main causing increased ICP
Stocchetti N, Maas AIR. N Eng J Med 2014;170:2121-30
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.
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
Vasodilatation of cerebral vessel
Fever, Seizure, Hypercarbia, Hypoxemia, Hypotension
Increased venous pressure
Neck torsion or compressionPneumothorax, Ventilator asynchrony, increased abdominal pressure
Increased arterial pressure
Pain, bladder distension
Cellular edema Hyponatremia
Systemic Cause of Increased ICP
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).
TREATMENT
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
Treatment of Intracranial Hypertension
First-tier Therapy
BTF Guideline 2007
Hypotherm, DC
Treatment if ICP>20 mmHg
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
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
First-tier Therapy: Ventricular Drainage
• Requires insertion catheter and the effect only temporary.
• Part of insert ICP monitor with ventricular catheter.
First-tier Therapy: Hyperventilation
• Risks of inducing cerebral ischemia
– Moderate hypocapnia (PaCO2 <34 mmHg) found to ↑vol of severely hypoperfusedtissues 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
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; 10:187Stocchetti N et al. Chest 2005; 127:1812-27Robertson C CCJM 2004; 71:S14-15
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.
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.
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
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.
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
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.
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
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
Variable Possible Therapeutic
Airway Obstruction Airway clearance, possible tracheal intubation
Hypoxemia Oxygenation and ventilation
Hypercarbia Ventilation
Hypertension associated with pain
Analgesia and sedation
Coughing or straining Sedation, paralysis
Jugular venous obstruction Correction of neck position, draining pneumothorax
Abdominal distention Nasogastric tube
Fever Antipyretic drugs
Hypoosmolaity Hyperosmolar fluids
Cause of and Possible Therapy for Increased ICP in TBI: Extracranial Cause
Stocchetti N, Maas AIR. N Eng J Med 2014
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
Cause of and Possible Therapy for Increased ICP in TBI: Intracranial Cause
Stocchetti N, Maas AIR. N Eng J Med 2014
Treatment Risk
Intubation, normocarbicventilation
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
Decompressivecraniectomy
Infection or delayed hematoma, subdural effusion, hydrocephalus
Risk of Treatment
Stocchetti N, Maas IAR. N Engl J Med 2014
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.
TERIMAKASIH