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pengelolaan hipertensi intrakranial


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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.

Published in: Health & Medicine
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pengelolaan hipertensi intrakranial

  1. 1. Raised ICP: What are our option? Tatang Bisri Universitas Padjadjaran Bandung Sebagian slide diambil dari NACC course versi 2014
  3. 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. 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. 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. 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. 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. 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. 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. 10. TREATMENT
  11. 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. 12. Treatment of Intracranial Hypertension First-tier Therapy BTF Guideline 2007 Hypot herm, DC Treatment if ICP>20 mmHg
  13. 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. 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. 15. First-tier Therapy: Ventricular Drainage • Requires insertion catheter and the effect only temporary. • Part of insert ICP monitor with ventricular catheter.
  16. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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.