Raised Intracranial Pressure

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  • 1. Raised Intracranial pressure By Wafaa Laimon Resident in Pediatrics MUCH
  • 2. 2
  • 3. OUTLINES:  Definition of intracranial pressure(ICP).  Physiology of cerebral circulation.  Causes of raised ICP.  Clinical presentation of raised ICP.  Measurement of ICP.  Management of raised ICP.
  • 4. INTRACRANIAL PRESSURE (ICP) is the pressure exerted by cranial contents on the dural envelope.  It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF).  ICP= P cerebrum +P blood +P csf  Intracranial volume=brain volume+cerebral blood volume+csf volume (Monro –Kellie hypothesis)  Normal intracranial pressure is below 10 mmHg.
  • 5. Compliance: is the ability to tolerate an increase in volume without a corresponding increase in Pressure. Relationship of intracranial volume to intracranial pressure (ICP). At normal brain compliance ICP increases only slightly as intracranial volume increases . A further increase in volume results in a steep rise in ICP.
  • 6. Cerebral autoregulation: (A) In the normal situation, cerebral blood flow remains constant over a wide range of cerebral perfusion pressure. (B) in acute head injury, the autoregulatory curve is shifted to the Right. (C) in some cases of acute head injury, autoregulation is lost and cerebral blood flow becomes pressure dependent.
  • 7. Regulation of cerebral blood flow: Pressure Autoregulation Metabolic Autoregulation
  • 8. Pressure autoregulation CPP=MAP-ICP  CPP= effective pressure that results in blood flow to the brain.  MAP=Mean Arterial Blood Pressure. •CBF remains constant with variations in MAP in the range(50-150 mmHg). • Beyond these limits or with acute brain insult this autoregulation is disturbed.
  • 9. CPP=MAP-ICP  Arterial hypotension-- -- reduced CBF--  Increased ICP-- reduced CPP cerebral ischemia. reduced CPP -- reduced CBF-- cerebral ischemia.
  • 10. Metabolic autoregulation  CBF is sensitive to changes in PaCO2 and PaO2. Metabolic autoregulation is resistant to acute brain injury.  Hypoventilation-- increase PaCO2-increase CBF-- increase ICP.  Hyperventilation-- reduce PaCO2-- reduce CBF -- decrease ICP.  Arterial hypoxemia--- increase in CBF and ICP.  Increase in PaO2-- cerebral vasoconstriction.
  • 11. PATHOLOGY  When to say intracranial hypertension?? If ICP more than 20 mmHg more than 5 minutes. Degrees  Mild:20-29 mmHg.  Moderate:30-40 mmHg.  Severe:more than 4o mmHg.
  • 12. Causes of raised ICP according to mechanism:  Brain edema: • Cytotoxic • Vasogenic • Interstitial  Increased cerebral blood flow: • • • • • Hypoxemia Hypercarbia Hyperpyrexia Convulsion Hypertension  Increased CSF volume(obstruction-excess production).  Pathological volume(mass-hemorrage).
  • 13. Clinical manifestations of increased ICP  What is the outcome of raised ICP??
  • 14. Clinical manifestations of increased ICP Non specific manifestations Neurological manifestations Complications
  • 15. Clinical presentation of raised ICP 1 2 Non specific manifestations Neurological manifestations •Headache and vomiting. •Cushing response. •Disturbed conscious level. •Sluggish pupillary reaction to light and may be dilatation. •Increased Muscle tone and exaggerated deep tendon reflexes. •Hyperventilation with deep inspiration and expiration. 3 Complications •Ischemia. •Tonic convulsions. •Herniation syndromes.
  • 16. What are herniation syndromes?
  • 17. Central herniation  Increased pressure in both cerebral hemispheres→downward displacement of the diencephalon through the tentorium → brainstem compression.  Stages: Diencephalic stage:     withdraws to noxious stimuli, increased rigidity or decorticate posturing. small, reactive pupils. preserved oculocephalic and oculovestibular reflexes. yawns, sighs, or Cheyne-Stokes breathing. Midbrain-upper pons stage: • • • • decerebrate posturing or no movement. mid-position pupils that may become irregular and unreactive. abnormal or absent oculocephalic and oculovestibular reflexes. hyperventilation.
  • 18. Lower pons-medullary stage: • no spontaneous motor activity. • lower extremities may withdraw to plantar stimulation. • mid-position fixed pupils. • absent oculocephalic and oculovestibular reflexes. • ataxic respirations. Medullary stage: • generalized flaccidity. • absent pupillary reflexes and ocular movements. • slow irregular respirations. • death.
  • 19. Uncal herniation  Uncus of the temporal lobe is displaced medially over the free edge of the tentorium.  Ipsilateral third-nerve palsy (ptosis, pupil fixed and dilated, eye deviated down and out).  Ipsilateral hemiparesis from compression of the contralateral cerebral peduncle (Kernohan notch).  posterior cerebral artery compression.
  • 20. Subfalcine (Cingulate) herniation  Increased pressure in one cerebral hemisphere leads to herniation of cingulated gyrus underneath falx cerebri.  Compression of anterior cerebral artery leads to paraparesis.
  • 21. Tonsillar herniation  Increased pressure in the posterior fossa leads to brainstem compression.  Loss of consciousness (RAS).  Focal lower cranial nerve dysfunction.  Respiratory and cardiovascular dysfunction with relative preservation of upper brainstem function, such as pupillary light reflexes and vertical eye movements.
  • 22. a) Subfalcial (cingulate) herniation ; b) uncal herniation c) downward (central, transtentorial) herniation d) external herniation e) tonsillar herniation.
  • 23. Tonsillar heniation
  • 24. IMAGING CT BRAIN sensitive in detecting extrabrain pathology. Exclude secondary cause e.g tumor-mass. Brain edema. HOWEVER Inferior resolution compared with MRI. Missed pathology such as small bleeds.
  • 25.  Diffuse Injury Type I  no CT visible intracranial pathology  Diffuse Injury Type II  cisterns present with midline shift 0-5 mm  no high- or mixed-density lesion > 25 cc  Diffuse Injury Type III(swelling)  cisterns compressed or absent with midline shift 0-5 mm  no high- or mixed-density lesion > 25 cc  Diffuse Injury Type IV (shift)  midline shift > 5 mm  no high- or mixed-density lesion > 25 cc  Evacuated Mass Lesion  any lesion surgically evacuated  Non-Evacuated Mass Lesion  high- or mixed-density lesion > 25 cc
  • 26.       Which patient will present with raised ICP? Patient(a) OR Patient(b) ?
  • 27. MRI More sensitive in detecting nonhemorrhagic and brain stem lesions. Detection of diffuse axonal injury. Distinguishing subdural blood from subdural hygromas and pathologic collections of CSF. PET -SPECT NIRS TRANSCRANIAL DOPPLER
  • 28. ICP MONITORING Sites of ICP measurement: Extradural. Subdural. Intraparenchymal. Intraventricular. Lumbar subarachnoid.
  • 29. Intraparenchymal ICT monitoring
  • 30. External ventricular drainage
  • 31. LUMBAR PUNCTURE???
  • 32. Management of raised ICP Decompressive craniectomy Forced hyperventilation Barbiturate coma Tris buffer Hypothermia Positioning Hyperventilation Hyperosmolar therapy Induced hypertension arterial
  • 33. First tire Positioning:  Moderate head elevation at an angle 15-30.  This enhances cerebral venous return decreases ICP.  Higher angle will decrease cerebral blood flow.  Neutral position as turning head to one side will reduce cerebral venous return.
  • 34. Adequate ventilatory support:  Evidence based medicine has not identified perfect ventilation but adapted to your patient.  Avoid fighting of the patient with ventilator.  Effect of PEEP on MAP should be taken in consideration.  Hyperventilation.
  • 35. Hyperventilation:  It is a rescue maneuver in impending or frank herniation.  Keep PaCo2 between 30-35 mmHg.  Lowering paCO2 by 1 mmHg reduces CBF by 4%.
  • 36. CPP=MAP-ICP CPP Concept:  In case of intra-Cranial hypertension,autoregulation is triggered by pharmacologically increasing MAP.  Drugs of choice are norepinephrine(0.1 mic/kg/min)or dopamine(4–10 mic/kg/min).  Goal in TBI is MAP level of >70mmHg.
  • 37. CPP CONCEPT ↑ICP Text CPP=MAP-ICP ↑CBV ↓CVR Text ↓CPP
  • 38. Drugs: Lidocaine(1.5 mg/kg IV bolus) before intubation and to reduce ICP. Thiopental(1-2 mg/kg) IV bolus. Midazolam. Fentanyl. WHY??
  • 39. Hyperosmolar treatment  Mannitol  Hypertonic saline Effective in few minutes How does it act??? Dosage??
  • 40. MANNITOL Mechanism: 1)Osmotic diuresis(Intact BBB). 2)Decrease blood viscosity----cerebral vasoconstriction. 3)Free radicle scavenger. Precautions: 1)Serum osmolalrity. 2)CVP. 3)Renal functions. 4)Hyperglycemia. 5)Rebound brain edema.
  • 41. Hypertonic saline It can be given till serum osmolarity 36o mosmol. It acts also as volume expander. It maintains MAP.
  • 42. Second-tier treatment  Forced hyperventilation:  Hyperventilation down to a paCO2 of 25-30mmHg  Carries the risk of cerebral ischemia.  Barbiturate coma:  Suppress the cerebral metabolic rate for oxygen(CMRO2).  Terminate convulsions.  Scavenge free oxygen radicals.  Decrease a cerebral hyperthermic response to ischemia.
  • 43.  Hypothermia  Tris buffer:  Acidosis removes the Mg lock from the NMDA receptor— facilitating excitotoxicity.  High pH protects energy-dependent glutamate porter sytems and thus delays onset of excitotoxicity.  Tris buffer corrects intracellular acidosis and increases the buffering capacity of CSF.  Tham(trishydroxymethylaminomethane) (1 mg/kg intravenously)
  • 44.  Steroids: • in vasogenic brain edema around brain tumors,hematoma or postoperative. • Dexamethasone .25 mg/kg every 6 h IV. • Methyl predinsolone 1-2 mg/kg every 6 h
  • 45.  Indomethacin: The non-selective cyclooxygenase inhibitor--Reduce ICP following TBI or intracranial surgery.
  • 46. Hyperoncotic treatment  The concept assumes importance of vasogenic edema and colloid-osmotic pressure  Aim is to reduce capillary pressure----precapilary arterioles are constricted with dihydroergotamine(DHE)  (DHE) also constrict cerebral veins---reducingCBF  Dose:4 mic/kg intravenously.
  • 47. Hepatic Encephalopathy  Hyperammoniemia is the key via  Glutamine accumulation .  free radicle release.  Osmolar therapy:Mannitol-HS  Hyperventilation  Maitainance of MAP.  Ornithine-L-Aspartate.  Hypothermia.
  • 48. Diabetic Ketoacidosis Brain Edema Cytogenic or vasogenic???
  • 49. Hypoxic–Ischemic Brain Injury  Hypothermia is strongly tried especially in neonates.  Cytogenic brain edema.  Reperfusion injury----Vasogenic brain edema.
  • 50. Infectious Causes  Types of brain edema.  What is the role of fluid restriction??  Lumbar puncture.To do OR not to do??  What is the role of steroids??
  • 51. Mass Lesions: Tumors and Hydrocephalus
  • 52. Thanks…. But it’s not the end !!!
  • 53. Always remember:  Patient with raised ICP is critically ill patient. So Don not forget A,B,C,D.  Papilledema is a late sign, And Pupilary dilatation deprive you from precious sign
  • 54. Always remember:  Whatever the cause of raised ICP the initial management will be the same.  Don not rush to lumbar puncture or even CT brain until you stabilize your patient.  CT brain is important to diagnose some secondary causes of raised ICP.  Monitoring of ICP is valuable esp. in cases of TBI.
  • 55. Thank You for Being Patient Till the End