1 / 60

Treating Elevated ICP in the TBI Patient

Treating Elevated ICP in the TBI Patient. Andrew Asimos, MD Director of Emergency Stroke Care Neuroscience and Spine Institute Carolinas Medical Center, Charlotte, NC Adjunct Associate Professor, Department of Emergency Medicine University of North Carolina School of Medicine at Chapel Hill.

omer
Télécharger la présentation

Treating Elevated ICP in the TBI Patient

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Treating Elevated ICP in the TBI Patient

  2. Andrew Asimos, MDDirector of Emergency Stroke CareNeuroscience and Spine InstituteCarolinas Medical Center, Charlotte, NCAdjunct Associate Professor, Department of Emergency MedicineUniversity of North Carolina School of Medicine at Chapel Hill

  3. Attending PhysicianEmergency MedicineCarolinas Medical CenterDepartment of Emergency MedicineCharlotte, NC

  4. Session Objectives • Present a relevant patient case • State key clinical questions • Outline the procedure for treating elevated ICP

  5. A Clinical Case

  6. Clinical History • 18 year old male non-helmeted skateboarder, struck his head on driveway • Closest L1TC one hour by helicopter • Being taken to non-trauma center ED • Prehospital care: IV, O2 via NRB mask, monitor • Intermittently combative • Attempting immobilization

  7. Physical Exam • 98.8 100/60 110 12 pulse ox 95% • Gen: Intermittently agitated • Head: Scalp abraisions, soft tissue selling over R temporal-parietal region, hemotympanum • Face: Several abrasions • Eyes: 4 mm, equal, reactive

  8. Physical Exam • Chest: BSBE, no crepitus • Cardiac: Tachycardia without murmur • Abd: Soft, FAST negative • Pelvis: Stable to compression • Ext: No long bone deformity, abrasions

  9. Neurologic Exam • Motor: Withdraws to painful stimuli, no posturing, no pathological reflexes • Eyes: Open to painful stimuli, PERL • Verbal: Perseverating speech • Sensory: No sensory level

  10. Provisional Diagnosis • Moderate to Severe TBI • GCS Score ≈ 9-10

  11. Key Clinical Questions • In the setting of acute TBI, what are the clinical signs and symptoms of increased ICP? • What imaging findings suggest impending herniation syndrome in the TBI patient? • How should patients with suspected increased ICP in the setting of TBI be managed? • What are the roles for the following therapies in the setting of suspected increased ICP: mannitol, hyperventilation, steroids, seizure prophylaxis, and skull trephination?

  12. Initial CT

  13. Treating Elevated ICP inthe TBI Patient : Key Clinical Concepts

  14. ICP Detection Pearls • VS don’t change until late in the clinical course of increased ICP and herniation • Signs and symptoms of increased ICP in TBI • GCS score of 8 or less • Decreased level of consciousness • Cranial nerve findings • Eye exam is key • CT scans showing ventricle or cistern abnormalities, or midline shift

  15. Eye Examination in Suspected Increased ICP

  16. Brain Herniation • Cranial contents compartmentalized by a layering of dura mater • Folding dura forms distinct brain compartments • Falx cerebri – separates 2 hemispheres • Tentorium cerebelli – separates infratentorial structures from supratentorial structures • Expansion of IC contents limited by skull and these compartments

  17. Transtentorial Herniation • Brain traverses tentorium at the level of the incisura • Divided into • Descending • Largest category • Mass effect in the cerebrum pushes supratentorial brain through incisura to the posterior fossa • Ascending • Mass effect in posterior fossa leads to brain extending through the incisura in an upward

  18. Central Transtentorial Herniation • Causes • Diffuse and severe TBI swelling • Centrally located, supratentorial masses • Thalamic hemorrhage • Lesions of the frontal, parietal, & occipital lobes • Downward movement of the diencephalon and rostral midbrain through the tentorial notch

  19. Diagnosing Central Transtentorial Herniation • Progressive rostrocaudal deterioration of brainstem function • Compression of diencephalic structures causes lethargy, apathy, or confusion • Loss of upward gaze due to compression of the diencepahlic pretectal area against the posterior tentorial incisura • Extensor plantar responses, paratonia, ipsilateral decortication, contralateral decerebration • Pupils dilate to midposition because of sympathetic and parasympathetic dysfuction • Hyperventilation • Decerebrate rigidity • Autonomic dysregulation • VS do not change until late

  20. Uncal Herniation • Associated with supratentorial masses and masses in the temporal fossa • Subdural or epidural hematoma, large MCA stroke, temporal lobe tumor • Medial portion of the temporal lobe (uncus) displaces over the tentorial notch • Causing compression of • Ipsilateral oculomotor nerve and brainstem compression • Occasionally the ipsilateral PCA

  21. Diagnosing Uncal Herniation • Classically, a stepwise progression • Early clinical sign is dilatation of the ipsilateral pupil • Compression of the parasympathetic fibers traveling on the periphery of the third nerve • Loss of the light reflex, ipsilateral ptosis, “down and out” eye • Patient may be surprisingly alert • Contralateral hemiparesis • Compression of the ipsilateral cerebral peducle against the free edge of the tentorium • Rarely ipsilateral hemiparesis (Kernohan’s phenomenon) • Consciousness deteriorates • Midbrain compession, sometimes associated hemorrhage, with compromise of the ascending portion of the RAS • Bilateral pupillary dilation • Changes in VS may not occur until just prior to fatal herniation • Respiratory changes and bradycardia

  22. Descending Transtentorial Herniation

  23. Imaging Findings of Descending Transtentorial Herniations

  24. Imaging Findings of Uncal Herniation Usual six pointed star appearance of the suprasellar cistern Truncated suprasellar cistern on the ipsilateral side of the herniation

  25. Right Uncal Herniation

  26. Descending Transtentorial Shift to the Left

  27. Durette Hemorrhage:A Complication of Descending Transtentorial Herniation

  28. Featured Procedures or Protocols • Treatment protocol for the management of elevated intracranial pressure (ICP) • Skull trephination for the management of suspected uncal herniation due to an expanding epidural hematoma

  29. Elevated ICP Therapy:The Procedure

  30. BTF Guidelines for the Management of Severe Traumatic Brain Injury Management and Prognosis of Severe Traumatic Brain Injury Brain Trauma Foundation, Inc, American Association of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  31. BTF TBI Treatment Guidelines • Head Injury Guidelines Task Force (AANS) • Initial draft 2000, revision due 2006 • Key Concept • Evidence based TBI treatment guidelines exist and are widely available Brain Trauma Foundation, Inc, American Association of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  32. Elevated ICP Rx Procedure • Evaluate globally all resuscitation needs

  33. Initial Management • No Standards or Guidelines • Options • Complete and rapid physiologic resuscitation • No specific treatment for intracranial hypertension in the absence of signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial explanations Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  34. Hypoxia and Hypotension in TBI Chesnut RM et al. J Trauma 34(2):216-22, 1993 Feb.

  35. Elevated ICP Rx Procedure • Evaluate globally all resuscitation needs • Do not provide prophylactic osmotherapy • Only with clinical deterioration • Do not use prophylactic hyperventilation

  36. Mannitol • Standards • There are insufficient data to support a treatment standard for the use of mannitol • Guidelines • Mannitol is effective for control of raised ICP after severe head injury • Effective doses range from 0.25 g/kg body weight to 1 gm/kg body weight Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  37. Mannitol • Options • The indications for the use of mannitol prior to ICP monitoring are signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial explanations • Avoid hypovolemia by fluid replacement • Intermittent boluses may be more effective than continuous infusion Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  38. Mannitol • Appropriate dosing range in the ED is 0.25-1.4 g/kg administered “wide open” • The Cochrane Review concludes high-dose mannitol (1.4 g/kg) appears to be preferable to conventional-dose mannitol in the pre-operative management of patients with acute intracranial hematomas Roberts I et al. Mannitol for acute traumatic brain injury. Cochrane Injuries Group Cochrane Database of Systematic Reviews 2005.

  39. Elevated ICP Rx Procedure • Evaluate globally all resuscitation needs • Do not provide prophylactic osmotherapy • Only with clinical deterioration • Do not use prophylactic hyperventilation • Only with clinical deterioration

  40. Hyperventilation • Standards • In the absence of increased ICP, chronic prolonged hyperventilation therapy (PaCO2 <25 mm Hg) should be avoided after severe traumatic brain injury • Guidelines • The use of prophylactic hyperventilation (PaCO2 <35 mm Hg) therapy during the first 24 hours after severe traumatic brain injury should be avoided because it can compromise CPP during a time when CBF is reduced Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  41. Hyperventilation • Options • Hyperventilation therapy may be necessary for brief periods • When there is acute neurologic deterioration • For longer periods if there is intracranial hypertension refractory to sedation, paralysis, cerebrospinal fluid drainage, and osmotic diuretics Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  42. Elevated ICP Rx Procedure • Evaluate globally all resuscitation needs • Do not provide prophylactic osmotherapy • Only with clinical deterioration • Do not use prophylactic hyperventilation • Only with clinical deterioration • Consider seizure prophylaxis

  43. Seizure Prophylaxis • Standards • Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate is not recommended for preventing late post-traumatic seizures • Guidelines • None Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  44. Seizure Prophylaxis • Options • It is recommended as a treatment option that anticonvulsants may be used to prevent early post-traumatic seizures in patients at high risk for seizures following head injury • Phenytoin and carbamazepine have been demonstrated to be effective in preventing early post-traumatic seizures • Available evidence does not indicate that prevention of early post-traumatic seizures improves outcome following head injury Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  45. Elevated ICP Rx Procedure • Evaluate globally all resuscitation needs • Do not provide prophylactic osmotherapy • Only with clinical deterioration • Do not use prophylactic hyperventilation • Only with clinical deterioration • Consider seizure prophylaxis • Do not use steroids

  46. Steroids • Standards • The use of steroids is not recommended for improving outcome or reducing ICP in patients with severe TBI • Guidelines • None • Options • None Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

  47. Steroids • Conclusions • In the absence of a meta-analysis, we feel most weight should be placed on the result of the largest trial • The increase in mortality with steroids in this trial suggest that steroids should no longer be routinely used in people with traumatic head injury Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. Cochrane Injuries Group Cochrane Database of Systematic Reviews 2005.

  48. Indications for Emergent Cranial Decompression • To evacuate extradural hematomas • To reverse clinical signs of tentorial herniation • Rapid, progressive neurologic deterioration • Timely inavailability of a neurosurgeon

  49. Gather Up What You will Need

More Related