ICP management - Dr. Gliozzo

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June 03, 2020

ICP management - Dr. Gliozzo

ICP management - Dr. Gliozzo



June 03, 2020


  1. Intraoperative Management of Intracranial Hematomata Department of Anesthesiology and Perioperative

    Medicine Presenter: Dr. Thomas Gliozzo, MD CA-1 Moderator: Dr. Sagar Mungekar, MD
  2. Objectives 1. To identify the neurophysiologic changes associated with space-occupying

    lesions 2. To articulate the anesthetic management of patients with neurological hematomata 3. To assess the measures of controlling intracranial pressure intraoperatively
  3. Cushing’s Triad • Increasing ICP decreased cerebral blood flow to

    Ventral Medullary Center  regulation of respiration is compromised – Bradypnea/Agonal Breathing and Increased PCO2 • Increased PCO2  Sympathetic outflow – systemic hypertension • commonly widened pulse pressure • Carotid Sinus stimulation  increased vagal tone – bradycardia
  4. Cerebral Blood Flow • 15% of CO; 25% of O2

    consumption • CBF = CPP/CVR – Avg. CBF = 50mL/100g brain tissue/min – Cortical grey matter – 75-80mL/100g tissue/min – Subcoritcal white matter – 20mL/100g tissue/min – Cerebral impairment – 20-25mL/100g tissue/min – Isoelectric EEG – 15-20mL/100g tissue/min – Irreversible brain damage - <10mL/100g tissue/min • Influenced by CMRO2, CPP, PaCO2, PaO2, autoregulation, temperature and anesthesia – CBF changes 1-2mL/100g tissue/min for every 1mmHG of PaCO2 change between 20-80
  5. Cerebral Blood Flow - CBF, respiratory rate, CO2 relationship: -

    Hyperventilation – very effective measure for acutely decreasing CBF in patients w/ elevated ICP - If MAPs < 50, PaCO2 has minimal influence on CBF - Hyperventilation effect wanes with time HCO3 - takes 2-5 hours to equilibrate - In operative neurosurgery, target PaCO2 = 30mmHg is sufficient for permissive hyperventilation
  6. Autoregulation • Ability of an organ to adjust vascular resistance

    to maintain normal blood flow despite changing perfusion pressure
  7. Cerebral Metabolic Rate of O2 • Average is 3-3.5mL O2

    /100g tissue/min • What Increases CMRO2 ? 1. Elevated regional brain activity 2. Seizures 3. Hyperthermia 4. IV anesthetics such as ketamine • What Decreases CMRO2 ? 1. Hypothermia 2. Inhalational anesthetics 3. Deep sleep 4. Comatose states for every 1°C decrease in temperature, CMR decreases, ultimately decreasing CBF by 7%
  8. Question • Which of the following has the fastest impact

    on decreasing ICP? a) Increasing respiratory rate from 10 bpm to 14 bpm b) Decreasing PEEP from 8 - 3 c) Administering 20% Mannitol IV d) Elevating head of the bed e) Opening External Ventricular Drain
  9. Patient Positioning for NSGY cases • Prone +/- pinning •

    180º supine/prone • 180º head bump (incline) • Sitting – EAM is 20cm above heart – For every 10cm above heart, pressure decreases by 7.5mmHg
  10. None
  11. Glasgow Coma Scale • Gross predictor of TBI severity, does

    not predict outcomes • Does not incorporate brain stem reflexes • Limitations: – Affected by other factors altering level of consciousness and impairments – impaired hearing, language barriers – not useful for intoxicated patients • GCS 3 just for showing up • GCS 8 or less – severe TBI, many sources recommend intubation for airway protection – Must use overall picture of patient and not just the number • Motor score of 2,3,4 is useful to determine severity of TBI and area of brain affected – Decerebrate – lesion is below red nucleus – Decorticate – lesion above red nucleus – Flexion withdrawal – higher cortex
  12. FOUR Score (Full Outline of UnResponsiveness) • When is it

    useful? – Intubated in field – When brainstem impairment is suspected • Score: 0-16 • Studies have shown it is more exact and practical • Better predictor of early outcomes from TBI – Eye exam includes tracking – Eliminates verbal response and replaces with brainstem reflexes
  13. None
  14. Patient Positioning • Sitting – offers surgeon great exposure to

    posterior cranial fossa and posterior cervical spine – Advantages for Anesthesia: • access to airway • decreased facial swelling • improved ventilation – Advantages for surgeon: • increased field visualization • possibly decreased blood loss – Disadvantages: • Increased risk of venous air embolism (>25% incidence) and paradoxical air embolism • gravitational traction on UE w/ risk of neurovascular injury • hypotension from pooling of blood in lower body • Excessive cervical flexion – impedes both arterial flow causing hypoperfusion – venous drainage causing congestion – Compression of ETT – macroglossia, increased peak pressure – Decreased respiratory excursion
  15. Venous Air Embolism • Risk Factors: – operative site is

    above the heart – veins in the cut-edge of bone and dural veins may not collapse when transected • Air enters pulmonary circulation – Microbubbles - bronchoconstriction with release of inflammatory/endothelial mediators and pulmonary edema • Endothelial damage: accumulation of platelets, fibrin, lipid droplets • Activation of complement and free radicals  capillary damage and non-cardiogenic pulmonary edema • V/Q mismatch – increased alveolar dead space w/ hypoxemia and hypercapnia – Larger bubbles - trapped in right ventricle leading to RV failure • Decreased pulmonary VR  decreased CO  tachyarrhythmia/bradyarrhythmia  arrest • Death is usually from cardiovascular collapse and arterial hypoxemia – Morbidity: 5mL of air – Mortality: as little as 20mL of air
  16. Venous Air Embolism • Detecting air embolism: 1) TEE –

    sensitivity = 76% o Capability: 0.02mL/kg of air 2) Precordial doppler ultrasound w/ EtCO2 – sensitivity = 40% o Left/right parasternal between 2nd and 3rd ribs o Capability: 0.05mL/kg of air 3) CVC: diagnostic and therapeutic – if correctly positioned at junction of SVC and RA o Possibility of aspirating air 4) Pulmonary Artery Catheter – increased pulmonary artery pressure o Normal: 20-30/8-15 mmHg o Systolic > 40 mmHg 5) Standard ASA monitors: o Blood pressure – hypotension o EKG – RV strain & ST depressions (low sensitivity) o Stethoscope – “mill-wheel” murmur (constant machine-like murmur)
  17. Venous Air Embolism Paradoxical Air Embolism Mid-Esophageal (90º) view RA

    SVC LA
  18. RA SVC LA RA App

  19. None
  20. Venous Air Embolism • Treatment: 1) Notify surgeon if suspected

    2) Irrigation of operative site, apply occlusive dressings to all bone edges 3) Compression of Internal Jugular Veins 4) Place patient in head-down position, Durant Maneuver 5) 100% O2, IVF, pressor support * PEEP – can reverse pressure gradient between left and right atria and predispose air passage across PFO