Critical Care Management of Adults with Brain Injury - PowerPoint Presentation

1. Critical Care Management of Adults with Brain InjuryStephan Salvia, RN, MSN, FNP-BC, RNFA

2. ObjectivesState common causes and pathophysiology of intracranial hypertensionIdentify signs & symptoms of intracranial hypertensionDiscuss different Intracranial Pressure (ICP) monitoring devices Describe strategies used to treat patients with intracranial hypertension

3. Brain Injury PRIMARY: Initial injury. (Trauma) Can be fatal Or Can lead to…SECONDARY: Subsequent neuronal destruction (occurs within minutes, days, weeks)

4. Secondary Brain InjuryIntracranial causesNeurotoxic cascades, Calcium-Channel Disturbance, Oxygen Free Radicals Extracranial causesRespiratory failure, Hypovolemia (Hypotension), Hypercapnea, Acidosis, Infection, Seizure.

5. Monro-Kellie DoctrineFixed Volume (V.) inside the skullV. Brain parenchyma (85%)V. Cerebral Spinal Fluid (10%)V. Blood (5%)Brain + CSF + Blood = Intracranial Pressure (ICP)* An increased volume in one component must lead to a decreased volume in other components to maintain normal ICP or else ICP will rise*

6. Diffuse Axonal Injury (DAI)

7. Tumor

8. Hydrocephalus

9. Intraparenchymal Hemorrhage

10. Subarachnoid Hemorrhage (SAH)

11. Subdural Hematoma (SDH)

12. Epidural Hematoma (EDH)

13. ICP Components1- Brain2- Blood 3- CSF And…

14. ICP extra-components

15. ICP extra-components

16. Intracranial HypertensionICP > 20mm Hg > 5 minutesIntracranial Hypertension may lead to direct injury to brain parenchyma or indirectly by compressing vasculature.Resulting in herniation syndromes, seizures, stroke, and/or brain death.

17. Herniation Syndromes

18. Intracranial Hypertension SymptomsNon-Focal and Focal neurological deficitsChange in level of consciousness, confusion, headache, nausea/vomiting, vision changes, dizziness, weakness, language deficitsCushing’s Triad (Late Signs!) 1) Irregular breathing pattern 2) Bradycardia 3) Systolic Hypertension

19. Signs & Symptoms

20. Signs & Symptoms

21. Signs & Symptoms

22. Neurological ExaminationMental StatusGlasgow Coma ScaleShould not be used alone in evaluating coma and predicting prognosisNot intended to be converted to a single scoreComponent Score (E4,V5,M6) more important than totalLevel of Consciousness (LOC)Must follow commands for thorough examinationCranial NervesOrientationLanguage Deficits

23. Neurological ExaminationEyesPupils Size, Shape, Reaction to Light, AccommodationMedications side effectsExtra Ocular Movements 9 cardinal positionsCranial Nerve (3,4,6) palsyVisual FieldsEyelid positionPtosis

24. Neurological ExaminationMotor & SensoryMotorFollows commandsLook for asymmetry: Hemiparesis/HemiplegiaPronator DriftSensoryLight Touch/Sharp TouchGrimaces to noxious stimuli

25. Neurological ExaminationReflexesDeep Tendon Reflexes: Can help distinguish Upper Motor Neuron lesion Vs. Lower Motor Neuron lesionHyporeflexia: 0-1+Normal: 2+Hyper-reflexia: 3-5+MyelopathyHoffman’s SignBabinski Test

26. Neurological ExaminationUnconscious/UncooperativeExam limited in patients unable to follow commands Sedated/comatose/delirium/toxicPupilsSize and ReactivityFixed/Dilated pupils (Ominous Sign)Motor ResponsesLocalized/Withdraws to noxious stimuliPosturing (Ominous Sign)ReflexesCorneal ReflexGag ReflexOculocephalic (Contraindicated in cervical injuries)Oculovestibular (Contraindicated in ruptured TM)

27. Neurological ExaminationPosturingCan occur unilaterally or bilaterallyDecorticateArms flexed towards “Core”Indicates damage to corticospinal tractDecerebrateArms Extend toward (More “E’s” in decerebrate)Indicates injury to brainstemDo not confuse with purposeful movement

28. ICP monitoringIndications No universally accepted guidelinesTypically used in patients with Traumatic Brain Injury (TBI) and Glasgow Coma Scale < 8.Abnormal CT head with decreased LOCICP monitoring not always used & is based on neurosurgeon’s intuition…may provide little benefit in care of patient.

29. ICP monitoringGoal: To be used as a therapeutic goal to help prevent and improve secondary brain injuryNon-invasive monitoringSigns and symptoms based on examinationoptic nerve sheath ultrasound, CT/MRI, transcranial doppler, fundoscopy, tympanic membrane displacementInvasiveVentriculostomy/External Ventriculostomy Drain (EVD)Microtransducers

30. ICP Monitoring RisksHemorrhageInfection (low rate)CSF leakDrift (loss of accuracy)Fiberoptics: up to 2 mm Hg/dayVentriculostomy: up to 11 mg Hg/8 hoursMigrationBe careful not to rip out!!!

31. ICP monitoringVentriculostomyVentriculostomy is GOLD standardExternal Ventricular Drain (EVD) more reflective of global ICPAdvantage: Therapeutic CSF drainage, accuracy.Disadvantage: Increased risk for infection, more difficult to place, maintain fixed reference

32. Ventriculostomy

33. Ventriculostomy

34. VentriculostomySet UpSecure to poleTransducer leveled at tragus (use string-level or laser-level)Set to cm H2O(caution not to confuse with mm Hg)Zero Q shift, position changes, and reconnecting to monitorStopcock off to patient . Open to atmosphere.Continuous Drainage Transduce ICP hourlyStopcock open to patient. Off to drainStopcock off to burette to accurately measure CSF hourly. Open to drainage bag to reset.

35. VentriculostomyClampingClamp for transducing accurate ICP (Off to drain/Open to patient)Clamp and re-level after each position changeClamp during suctioning/vomitingClamp for transport unless unstable ICPAs per facility protocolClamp during weaning

36. VentriculostomyCSF drainage/samplingCSF sampling: as per facility policyCell count, cytology, culture, protein/glucoseNever “bullet” CSF sample. Always hand deliver.Document color/clarityClear/sanguineous/purulentChange in colorNotify Neurosurgeon anything outside of parameter>20 mL/hour or < 0mL/hourSignificant change in amount of drainage

37. VentriculostomyNot-Leveled correctlyTransducer above Foramen of Monro (tragus)False Low ICP (Intracranial hypertension undetected)Under Drainage  Increased ICPTransducer below Foramen of Monro (tragus)False High ICPExcessive Drainage  stretching of Bridging Veins  Subdural Hematoma (SDH)

38. VentriculostomyUnder-DrainageCorrect level?Occlusion? Stopcocks clamped/tubing kinked/catheter pulled out?Check patency (Quickly)Lower burette/Drop EVD. Observe for drainageRaise burette. Observe CSF meniscus for pulsation. No pulsation = not patent. (CSF flows in a pulsatile manner, matching the pressure waves in vessels caused by beating heart)Manual ICP: assess where meniscus is on mmHgNotify NeurosurgeryReposition CatheterIrrigate tubing

39. MicrotransducersFiberoptic, strain gauge, and pneumatic sensorsPlaced in different locations including: subdural, epidural, intraparenchymal spacesAdvantage: Less invasive. No need for leveling. Ease of use.Disadvantage: no therapeutic drainage (newer models have combined ventricular catheters).

40. Microtransducers

41. Fiberoptic a.k.a “Bolt”Keep battery plugged in (low battery life)Unplug only for transportMost are not MRI conditional (safe)Connect ICP monitor to bedside monitorSynchronize/Recalibrate often (every shift)+/- 1mm Hg drift is normal. Always use ICP monitor… Not bedside monitor if there’s a differenceOptimize scale for waveform analysisRed Depth Indicator Monitor for migration

42. ICP Waveform

43. Cerebral Perfusion Pressure (CPP)CPP = MAP – ICPCPP maintained > 60 mm Hg to ensure adequate Cerebral Blood Flow (CBF)Autoregulation is the ability of the brain to maintain constant Cerebral Blood Flow (750mL/minute)Autoregulation is only effective when CPP is between 50-150mmHg.Impaired autoregulation results in fluctuating CBF with changes in Systemic Blood Pressure (SBP)

44. Cerebral Blood Flow (CBF)Maintaining sufficient CBF to meet Cerebral Metabolic Rate (CMR) is important in preventing secondary brain injuryCBF = CPP / Cerebral Vascular Resistance (CVR)CVR = pressure across cerebrovascular bed from arteries to veinsCVR similar to Systemic Vascular ResistanceCVR= Controlled by AutoregulationVasoconstriction =  CVRVasodilation =  CVRAverage CBF = 50mL/100gram(brain)/minute

45. Cerebral Blood Flow (CBF)Extrinsic Factors:SBP, Cardiac Output, Blood Viscosity, Vascular toneIntrinsic Factors:PaCO2, PaO2, ICPVasodilation= hypercarbia, hypoxia, acidosisVasoconstriction= hypocarbia, increased PaO2, alkalosisOther Factors:Medications, Temperature, Pain, Seizures, etc.

46. Brain Code Tier 0Maintain quiet environment (less stimulation)HOB elevated 30 degrees with head neutral/cervical collar not too tight (facilitates venous return)General MonitoringVitals: Normal Temp, Pulse Ox, Blood Pressure…Labs: Normal PCO2, PO2, Serum Sodium…Analgesics/Sedation; maximize comfort/minimize over-sedationStool Softeners/GI regimen  prevent valsava maneuver Seizure prophylaxis

47. Brain CodeTier 1Osmotic Therapy: Hypertonic Saline (HTS) Mannitol: (hemodynamically unstable)Strict I&O, monitor serum sodium & osmolaritySodium Bicarb: Slow IVP (1 amp over 5 minutes…works similar to HTS)CSF drainage If not already in progress

48. Brain CodeTier 2Propofol Paralytics: Train of 4 (peripheral nerve stimulator)  Obtain baseline Facial: eyebrow twitchingUlnar: thumb twitchPosterior tibial: plantar flexion of great toeCPP optimization (Increase MAP  Increase CPP)Vasopressors PRN

49. Brain CodeTier 3Barbituate ComaHyperventilation : PCO2 down to 25-30 mm HgTachyphylaxis: Results diminish quickly > 6 hours carries risk for cerebral ischemiaInduced Hypothermia (ROSC after cardiac arrest)Decompressive SurgeryMay have undergone surgically intervention initially in some circumstances.

50. OutcomesGood RecoveryModerately DisabledSeverely DisabledVegetative StateBrain Death (Legally Dead)

51. Thank You!Questions???

52. ReferencesMurthy, T., Bhatia, P., Sandhu, K., Prabhakar, T., Gogna, R. (2005). Secondary brain injury: prevention and intensive care management. Indian Journal of Neurotrauma, volume 2. 7-12.Raboel, P., Bartek, J., Andresen, M., Bellander, M., Romner, B. (2012). Intracranial pressure monitoring: invasive versus non-invasive methods- a review. Critical Care Research and Practice, 2012. 1-14.White, J., Sheth, K. Neurocritical Care for the Advanced Practice Clinician. Cham, Switzerland: Springer International Publishing.