Downloaded 77 times
Uploaded byKode Sashanka
Icp monitoring &brainherniation
ICP waveforms provide information about intracranial dynamics and compliance. The normal ICP waveform has three peaks - P1, P2, and P3. An elevated P2 compared to P1 indicates increased intracranial pressure. Lundberg waves reflect fluctuations in ICP and cerebral blood flow. Invasive ICP monitoring is usually done via an external ventricular drain, while noninvasive methods include optic nerve sheath diameter. Brain herniation, such as subfalcine or descending transtentorial herniation, can occur due to increased intracranial mass or pressure.
More Related Content
Similar to Icp monitoring &brainherniation
![Apporach to lung biopsy [Auto-saved].pptx latest](https://cdn.slidesharecdn.com/ss_thumbnails/apporachtolungbiopsyauto-saved-251211225655-93258539-thumbnail.jpg?width=640&height=640&fit=bounds)
Icp monitoring &brainherniation
- 1. ICP waveforms &monitoring Dr Sashanka
- 2.
- 3.
- 5.
- 8. “compliance reflects theability of the intracranial system to compensate for increases in volume without subsequent increases in ICP. When compliance is decreased, even small increases in intracranial volume result in large increases in ICP.”
- 9. Normal ICP It isdifficult to establish a universal “normal value” for ICP as it depends on age, body posture and clinical conditions. The upper limit of normal ICP – 15 mm Hg (5 – 10 mm Hg) Physiologic increase – Coughing, sneezing – 30-50 mm Hg
- 10.
- 11. ICP monitoring waveforms Flowof 3 upstrokes in one wave. P1 = (Percussion wave) represents arterial pulsation P2 = (Tidal wave) represents intracranial compliance P3 = (Dicrotic wave) represents venous pulsation In normal ICP waveform P1 should have highest upstroke, P2 in between and P3 should show lowest upstroke. On eyeballing the monitor, if P2 is higher than P1 - it indicates intracranial hypertension.
- 13. Related to Cardiac cycle: within individual waves Respiratory cycle : between consecutive waves
- 15. ICP waveform –pulsatile Baseline is referred to as ICP Magnitude of baseline, amplitude & periodicity of pulsatile components Earliest sign of ↑ ICP – Changes in pulsatile components
- 16. Flat EVD clogged /kinked Patient expired
- 17. ↑⁄↓ amplitude Increasing CSFvolume (or decreased) If a large volume of CSF is drained off, the waveform will decrease in amplitude. Missing bone flap
- 18. Prominent P1 wave Thesystolic BP is too high
- 19. Diminished P1 wave Ifthe systolic BP is too low, P1 decreases and eventually disappears, leaving only P2. P2 and P3 are not changed by this.
- 20. Prominent P2 wave Themass lesion is increasing in volume The intracranial compliance has decreased An inspiratory breath hold (as ICP will also rise)
- 21. Diminished P2 andP3 waves Hyperventilation
- 22. Rounded ICP waveform ICPcritically high
- 23.
- 25.
- 26. Lundberg A waves Increasesof ICP sustained for several minutes and then return spontaneously to baseline, which is slightly higher than the preceding one. Results from ↑ cerebrovascular volume due to vasodilatation (Lundberg) Results from normal compensatory response to decreases in CPP. Hence give vasopressors. (Rosner) – But may enhance lesion size & edema
- 27. 4 phases: 1.Drift phase: ↓ CPP → vasodilatation 2.Plateau phase : Vasodilatation → ↑ ICP 3.Ischemic response phase : ↓ CPP → Cerebral ischemia → Brainstem vasomotor centres → Cushing response 4.Resolution phase : Cushing response → Restores CPP
- 29.
- 30. Lundberg B waves Shortelevations of modest nature (10 – 20 mm Hg) 0.5 – 2 Hz Relate to vasodilatation secondary to respiratory fluctuations in PaCO2 Seen in ventilated patients (?) Secondary to intracranial vasomotor waves, causing variations in CBF Reflects ↑ ICP in a qualitative manner
- 31.
- 32.
- 33. Lundberg C waves Morerapid sinusoidal fluctuation (0.1 Hz) Corresponds to Traube-Hering-Meyer fluctuations in arterial pressure brought about by oscillations in baroreceptor and chemoreceptor reflex control systems Sometimes seen in normal ICP waveform High amplitude – pre-terminal, seen on top of A waves
- 34.
- 35. Why look atICP waveform analysis? “…provides information about intracranial dynamics that can help identify individuals who have decreased adaptive capacity and are at risk for increases in ICP and decreases in CPP, which may contribute to secondary brain injury and have a negative impact on neurologic outcome.” C.J Kirkness et. al; J Neurosci Nurs. 2000 Oct; 32(5):271-7.
- 36. The main indicationsfor ICP monitoring are: Glasgow Coma Scale (GCS ) < 8 Posturing (extension, flexion) Bilateral or unilateral pupil dilation (except with Epidural Hematomas) CT Scan results showing edema and/or mid-line shift Physical assessment /neurological assessment findings which indicate a need for monitoring
- 37.
- 38. Methods of ICP measurement Technology externalstrain gauge catheter tip (internal) strain gauge fibre-optic Location Ventricular (EVD/IVC) Intraparenchymal Subarachnoid Subdural/Extradural External Fontanelle
- 39. External Ventricular Drain EVDconnected to external strain gauge is the gold standard for measuring ICP Tip in foramen of Monro Extensive history, low cost, reliability, therapeutic Success rate of cannulation – 82%
- 41. Malposition: 4 –20% Did not have significant clinical sequelae Occlusion : By brain matter / blood clots Flush EVD Hemorrhage : 0 – 15% (1.1%) Most asymptomatic Intervention in 0.5%
- 42. Infection : 0– 22% (8.8%) Risk factors : IVH, SAH, craniotomy, CSF leakage, systemic infection, depressed skull # Duration of catheterization & irrigation of catheter Venue of insertion – No difference Extended tunneling Sandalcioglu - <5 vs >5 cm – 83% vs 17% Leung – No difference Prophylactic catheter exchange : No difference
- 43. Prophylactic antibiotics: Periprocedural vsnone – No difference Periprocedural vs entire duration – No difference Guidelines for the Management of Severe Traumatic Brain Injury – No antibiotic prophylaxis Antibiotic impregnated catheter: Rifampin + Minocycline (Zabramski) – 9.4 to 1.3% Cost
- 44. When to pullthe EVD out? CT evidence of resolution of cerebral oedema, and Improvement of ICP (consistently under 20-25) Or if the EVD is infected.
- 45. Fibreoptic ICP monitor Cathetertip measures the amount of light reflected off a pressure sensitive diaphragm Intraparenchymal Camino ICP monitor Ease of insertion – Right frontal Also in the region with pathology Can be inserted in severely compressed ventricles or those with midline shift Low risk of hemorrhage and infection Zero drift: Recalibration cannot be performed 2 mm Hg (first 24 hrs); 1 mm Hg (first 5 days) – Manufacturer 0.5 – 3.2 mm Hg drift - Actual
- 47. Miniature Strain Gauge CodmanMicroSensor ICP Transducer Microchip pressure sensor at the tip of a flexible nylon cable that produces different electricity based on pressure Intraventricular (Correlation coefficient 0.97 with EVD, Drift 0.2 mm Hg) Intraparenchymal (Less accurate) Subdural space (Not enough studies)
- 48. Spiegelberg Parenchymal Transducer Airpouch at the tip that is maintained at constant volume Pressure transducer located in ICP monitor Recalibration can be made easily Good correlation with ICP measured by ventriculostomy
- 50. Compliance Monitor Experimental stage Changein volume per unit change in pressure Spielberg compliance monitor injects small amount of air into the air balloon pouch and measures the pressure response to this change in volume Inverse relationship between compliance and ICP
- 51. Noninvasive ICP monitoring CT,clinical examination, monitoring pressure in epidural space Optic Nerve Sheath Diameter (ONSD) Measured by ultrasound Critical value is different in different studies Venous Opening Pressure (VOP) Measured by venous ophthalmodynamometry Requires dilatation of pupil Performed intermittently – Only screening purpose Cochlear fluid pressure, Flow velocity in intracranial arteries, Delay in VEPs
- 52. Pediatric ICP monitoring ICPmonitoring only as an option for treating patients with severe traumatic brain injury (GCS < 8) Similar complication rates as in adults
- 53.
- 56. BRAIN HERNIATION • mostcommon types – Subfalcine herniation – descending transtentorial herniation • Others – Posterior fossa herniations • ascending transtentorial herniation • tonsillar herniation – Transalar herniation • Rare but important types – transdural/transcranial herniations – brain displacements across the sphenoid wing
- 57.
- 58. Subfalcine herniation • mostcommon • supratentorial mass in one hemicranium • affected hemisphere pushes across the midline under the inferior "free" margin of the falx, extending into the contralateral hemicranium
- 60. Subfalcine herniation: imaging Axialand coronal images show that •cingulate gyrus •anterior cerebral artery (ACA) •internal cerebral vein (ICV) are pushed from one side to the other under the falx cerebri. The ipsilateral ventricle appears compressed and displaced across the midline
- 62. Complications • unilateral obstructivehydrocephalus – foramen of Monro occlusion • Periventricular hypodensity with "blurred" margins of the lateral ventricle – Fluid accumulates in the periventricular white matter
- 63. Complications • When severe,the herniating ACA can be pinned against the inferior "free" margin of the falx cerebri 🡪 secondary infarction of the cingulate gyrus
- 65.
- 66.
- 67. Descending transtentorial herniations• thesecond most common • a hemispheric mass • initially produces subfalcine herniation • As the mass effect increases, the uncus of the temporal lobe is pushed medially begins to encroach on the suprasellar cistern hippocampus follows hippocampus effaces the ipsilateral quadrigeminal cistern both the uncus and hippocampus herniate inferiorly through the tentorial incisura
- 68. "Dysautonomia, Multisystem Atrophyand Parkinson's." Dysautonomia, Multisystem Atrophy and Parkinson's. N.p., n.d. Web. 18 Nov. 2014
- 70. Descending transtentorial herniation • Unilateral •Bilateral ;"central“ – Severe
- 71. unilateral DTH: imaging early uncusis displaced medially Ipsilateral aspect of the suprasellar cistern effaced Ipsilateral prepontine + cerebellopontine angle cistern enlarged
- 73. Descending transtentorial herniation As DTHincreases hippocampus also herniates medially quadrigeminal cistern compression midbrain pushed toward the opposite side of the incisura
- 74. Descending transtentorial herniation severe cases entiresuprasellar and quadrigeminal cisterns are effaced. The temporal horn can even be displaced almost into the midline
- 76. bilateral DTH both hemispheresbecome swollen the whole central brain is flattened against the skull base All the basal cisterns are obliterated hypothalamus and optic chiasm are crushed against the sella turcica
- 79. Complete bilateral DTH bothtemporal lobes herniate medially into the tentorial hiatus midbrain and pons displaced inferiorly through the tentorial incisura The angle between the midbrain and pons is progressively reduced from 90° to almost 0°
- 81. Complications • CN III(oculomotor) nerve compression – CN III palsy • PCA occlusion as it passes back up over the medial edge of the tentorium – secondary PCA (occipital) infarct
- 84. Kernohan notch • Asthe herniating temporal lobe pushes the midbrain toward the opposite side of the incisura – contralateral cerebral peduncle is forced against the hard edge of the tentorium • Pressure ischemia 🡪 ipsilateral hemiplegia – the "false localizing" sign
- 88. Duret hemorrhage "Top-down" masseffect displaces the midbrain inferiorly closes the midbrain-pontine angle Perforating arteries from basilar artery are compressed and buckled
- 89. hypothalamic and basal gangliainfarcts complete bilateral DTH perforating arteries from the circle of Willis compression against the central skull base hypothalamic and basal ganglia infarcts
- 93.
- 95. Tonsillar herniation • Thecerebellar tonsils are displaced inferiorly and become impacted into the foramen magnum. • congenital (e.g., Chiari 1 malformation) – mismatch between size and content of the posterior fossa • Acquired – an expanding posterior fossa mass pushing the tonsils downward—more common – intracranial hypotension: abnormally low intraspinal CSF pressure • tonsils are pulled downward
- 96. Tonsillar herniation: imaging •Diagnosing tonsillar herniation on NECT scans may be problematic. Cisterna magna obliteration
- 98. Tonsillar herniation: imaging •MR: much more easily diagnosed • In the sagittal plane – the tonsillar folia become vertically oriented – the inferior aspect of the tonsils becomes pointed – Tonsils > 5 mm (or 7 mm in children) below the foramen magnum are generally abnormal • especially if they are peg-like or pointed (rather than rounded)
- 99. Tonsillar herniation: imaging •In the axial plane, T2 scans show that the tonsils are impacted into the foramen magnum – obliterating CSF in the cisterna magna – displacing the medulla anteriorly
- 101.
- 102.
- 104. Ascending transtentorial herniation •causedby any expanding posterior fossa mass –Neoplasms > trauma
- 106. Complications •Acute intraventricular obstructive hydrocephalus –causedby compression of the cerebral aqueduct
- 109. OTHER LESS COMMONHERNIATION: TRANSALAR TRANSDURAL TRANSCRANIAL HERNIATIONS
- 110. Transalar Herniation •brain herniatesacross the greater sphenoid wing (GSW) or "ala" •ascending > descending
- 111. Ascending transalar herniation •causedby a large middle cranial fossa mass •An intratemporal or large extraaxial mass Temporal lobe + sylvian fissure + MCA up and over the greater sphenoid wing
- 117. References •Osborn, Anne G."Secondary Effects and Sequellae of CNS Trauma."Osborn's Brain: Imaging, Pathology, and Anatomy. Salt Lake City, UT: Amirsys Pub., 2013. N. pag. Print. •Osborn, Anne G. "Cerebral Vasculature: Normal Anatomy and Pathology."Diagnostic Neuroradiology. St. Louis: Mosby, 1994. N. pag. Print.