Online Module:

1. Online Module: Traumatic Brain Injury and increased ICP Intracranial Hematomas Spontaneous Subarachnoid Hemorrhage Herniation Syndromes

2. Traumatic Brain Injury and Increased ICP

3. Practically speaking, the brain is protected by a rigid case, within which there is no “extra” space.

4. The Cranial Vault • Skull (holds three things) • Brain • Blood • Cerebro-Spinal Fluid (CSF) • An increase in any one of these three “compartments” displaces the other two. • The principle buffer in the system is CSF. • Only small volume increases can be tolerated before intracranial pressure (ICP) begins to rise.

5. The Monroe-Kellie Doctrine • Increase in one constituent necessitates a compensatory decrease in the volume of another constituent.

6. Compliance • Because the three constituents that take up residence within the cranial vault are housed within a relatively rigid container, small increases in volume can drastically increase the intracranial pressure • This is the concept of compliance. • Compliance = change in volume/change in pressure

7. Normal Cerebral Metabolism • Brain tissue relies on aerobic metabolism – gets starved for oxygen very quickly because it has no real backup energy reserve. • Normal cerebral metabolism requires a blood flow of approximately 50 mL/100g/min. • Serious neurological deficits begin to occur at 20 mL/100g/min. • Prolonged Cerebral Blood Flow > 12 mL/100g/min. results in cerebral infarction.

8. MAP and ICP • MAP = “Mean Arterial Pressure” • Defined as: [(2 x DBP) + (SBP)]/3 • This is literally the average arterial blood pressure over a single cardiac cycle. • ICP = “Intra-Cranial Pressure” • 15 mmHg is getting into the upper limits of normal in you and me. • MAP – ICP = CPP

9. Cerebral Perfusion Pressure • Cerebral Perfusion Pressure is key to brain tissue survival. • CPP = MAP – ICP • This takes measurable physiologic parameters into account to determine if the individual is able to adequately oxygenate brain tissue. It is the net pressure of blood delivery to the brain. • In a normal adult, CPP is generally regulated between 70 and 90 mmHg (can be more or less).

10. Cerebral Metabolism • In the uninjured brain, the arterioles regulate CBF to the brain over MAPs ranging from 50-150 mmHg. • Outside of this range, the arterioles lose the ability to autoregulate, and blood flow becomes dependent upon blood pressure (this is called pressure-passive flow). • MAPs less than 50 run risk of ischemia due to decreased blood flow, while MAPs greater than 150 causes excess CBF that can contribute to increased intracranial pressure. • Autoregulation is impaired in the injured brain.

11. Cerebral Autoregulation

12. Summing that up - • Normal anatomy implies a fixed space in skull where small increase in volume causes large increase in pressure. • Perfusion of brain tissue is impaired by anything that’s taking up space or decreasing blood delivery to the tissue. • Normal autoregulation processes that help the brain maintain homeostasis are impaired after injury.

13. The TRAUMATIC neuro exam • When dealing with “Emergency” neurological evaluation, you MUST MUST MUST MUST MUST KNOW the concept of the Glascow Coma Scale!!!!!!!

14. Clinical Assessment: GCS

15. Diagnostic Imaging • This is a great way to get past the handicap of having a relatively inflexible surface to evaluate. • Often provides you the information you need to ANTICIPATE a problem or PREVENT its occurrence before it becomes clinically apparent. • Newer diagnostic imaging modalities have REVOLUTIONIZED management of intracranial pathology (the benefit to traumatic brain injury is immeasurable)!

16. “Reading head films 101” • #1 – Identify the modality • #2 – Orient yourself • #3 – Describe what you see; don’t just try to find what’s abnormal • #4 – Pay attention to symmetry! • #5 – Pay attention to proportion

17. The CT Scan • The CT scan single-handedly revolutionized the landscape for head-trauma. • Allows quick evaluation of intracranial space (and skull). • Good for acute eval. • “Fancy X-ray”

18. Traumatic Brain Injury • Two general types of injury: • Primary – represents the direct result of the initial trauma. • Fracture • Cerebral contusion • Vascular disruption • Secondary – results from the evolution of the initial injury or complications. (This is what we aim to minimize) • Hypoxia and ischemia • Cerebral edema • Intracranial hypertension (ICH)

19. Cerebral Ischemia • This is the mechanism that underlies “secondary” injury to the brain. • It all comes back around to Cerebral Perfusion Pressure. • Remember that you’ve got two opposing forces – the mean arterial pressure “pushing” oxygenated blood into brain tissue, and intracranial pressure pushing back. • CPP = MAP - ICP

20. Bottom Line • You need adequate CPP to maintain viable brain tissue. • Once past the primary injury, secondary injury sets in as the volume of any one (or more) of the three constituents starts to increase and cerebral ischemia occurs. • ICP begins to rise relatively quickly once the extra volume increases (especially beyond ~100 cc’s.) • Generally, 60 – 70 mmHG is the target CPP for patients with TBI. • It is thought that ICP should be treated once it hits a threshhold of 20 mmHg.

21. Symptoms and Signs of Elevated ICP • Triad • Headache, nausea, vomiting • Cranial nerve palsies • Papilledema • Usually from a more chronic process • Vital sign changes • Cushing’s • Arterial hypertension and bradycardia • Respiratory changes

22. Papilledema Swelling of the optic nerve head with engorgement of the retinal veins Presence almost always indicates raised intracranial pressure.

23. Management of Elevated ICP: Airway/ventilator support Maintain adequate CPP Osmotic diuresis Hypertonic saline Sedation/analgesia Hypothermia Neuromuscular blockade Barbiturate coma Glycemic control CSF drainage Craniectomy

24. Therapeutic Modalities for Reduction of ICP

25. Intracranial Hematomas

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27. Epidural Hematoma • Typically younger patients • Patients may present with alterations in consciousness, headache, nausea/vomiting, etc. • Evidence of trauma: Contusion, laceration, or bony step-off may be observed on the head (should have high clinical suspicion).

28. Epidural Hematoma • “Classic presentation”: Impact on side of head with “lucid interval,” then CT scan demonstrating biconvex (lenticular – “lens shaped”) hematoma causing brain compression and midline shift. • Deterioration can be rapid. • Prognosis is generally excellent if managed aggressively!!! • Mortality estimated as high as 20%!

29. Epidural Hematoma • Epidural Hematomas – 90% seen in head trauma with a skull fracture that crosses a portion of the middle meningeal artery/vein. • Middle meningeal artery is torn approximately 2/3rds of the time. • Blood which collects in the epidural space is limited by the intracranial sutures, where the dural membrane is closely adherent to the inside of the calvarium.

30. Epidural Hematoma

31. Skull Fracture

32. Epidural Hematoma (underneath skull fracture)

33. Epidural Hematoma • Generally, treatment is surgical. • Can sometimes manage small EDHs conservatively if they are asymptomatic (but you still MUST get these patients to a Neurosurgeon so that if the EDH evolves or clinical picture worsens they can receive immediate treatment. • What really hurts these patients is delay in diagnosis, delay in transfer, i.e. anything that delays treatment!!!

34. Epidural Hematoma

35. Epidural Hematoma

36. Subdural Hematoma • Come in three different “flavors”: • Acute • Subacute • Chronic • Don’t be fooled!!! Acute to Chronic SDHs are different clinical entities!

37. Acute Subdural Hematoma • About twice as common (or more) as EDHs. • Major difference compared to EDH – magnitude of primary injury is usually much higher in acute SDH (mortality is HIGHER!). • Two most common causes of Acute SDH: • Accumulation of blood around parenchymal laceration • Tearing of surface/bridging vessels from acceleration-deceleration during violent head motion • Mechanism of injury: “brain rattles inside head.” • Much higher risk in patients on anticoagulation!

38. Acute SDHs • Typically an older patient who suffers some type of head injury (or suspected injury) and gets a CT scan in the ER. • Radiographically, what you typically see is a HYPER-dense CRESCENT-shaped fluid collection that CROSSES SUTURE LINES!!! • Associated parenchymal bleeding, even subarachnoid blood is not an uncommon finding.

39. Acute SDH • 30-day mortality is between 50 and 80%! • Dramatic difference between mortality of EDH and Acute SDH is secondary to the magnitude of primary brain injury, which is typically much greater in the setting of Acute SDH than EDH. • Also they are usually older patients.

40. Acute Subdural Hematoma

41. Acute Subdural Hematoma

42. Acute Subdural Hematoma

43. Acute Subdural Hematoma

44. Acute Subdural Hematoma

45. Compare: EDH vs acute SDH

46. Chronic SDHs • Generally occur in elderly (avg age of presentation is 63 yrs) • Other risk factors: alcohol abuse, coagulopathies, fall risk, seizures, etc. • Anything that impairs blood clotting, coagulation, etc. • Patients can present any of a multitude of different ways: TIA-type symptoms, headache, confusion, lethargy, speech trouble, weakness, etc. • Often, no known history of trauma or event.

47. Chronic SDHs • Prevailing thought is that Chronic SDHs evolve from small / asymptomatic acute SDHs. • Blood within the subdural space causes inflammatory response; fibroblasts invade, neomembranes form, neovascularization occurs. • Chronic SDHs can be very complex, multi-lobed structures. • Tend to gradually get larger over time.

48. Chronic SDHs • On CT scans, these are CRESCENT-shaped HYPO-dense lesions that cross suture lines. • Not uncommon to see lobules within the fluid collection. • Not uncommon to see subacute or even acute blood within a chronic SDH. • Treatment is surgical when symptomatic or (generally speaking) once thickness exceeds 1cm.

49. Chronic SDHs • Bilateral occurrence as often as 25% of the time

50. Acute vs. Chronic SDHs