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