Swelling, Itching Brain: - PowerPoint Presentation

Slide1

Swelling, Itching Brain:Management of Cerebral Edema and Increased Intracranial Pressure

Deepak S Nair, MD

Stroke Neurology &

Neurocritical

Care

OSF Healthcare – Illinois Neurological InstituteSlide2

DisclosuresNo financial (or other) conflicts of interest to discloseSlide3

Objectives

Describe the pathologic mechanism of malignant cerebral edema.

Review the current treatment modalities for cerebral edema/intracranial pressure.

Propose an algorithmic approach to ICP crisis in cerebral edema.

NOTE: this discussion is intentionally limited to ischemic strokeSlide4

Stages of Cerebral EdemaSlide5

Pathophysiology of Cerebral Edema – part 1

Cytotoxic edema

Occurs within minutes of tissue injury (ischemic cascade)

Water moves from extracellular space to intracellular space

NO increase in total brain volume – no significant “swelling”

Ischemic cascade

Reduced oxygen & glucose

 reduced ATP

Failure of Na/K pump  influx of Na into cell (depolarization)

Water follows Na  cellular swelling

Membrane failure  influx of Ca into cell  cell death/ruptureSlide6

Can we stop this?Slide7

Can we stop this?NOPESlide8

Can we stop this?

Well…

Hyperacute

intervention to stop the ischemic cascade

Ischemic Stroke

 thrombolysis, endovascular

thrombectomy

Hemorrhagic Stroke  prevent

rebleeding

, surgical resection??

Status  abort the seizures (

benzo’s

, AEDs, sedatives)

Infection  antibiotics, steroids??

This is most effective in the setting of ischemic stroke…

But, cytotoxic edema is inevitable, because it happens too fast…Slide9

Pathophysiology of Cerebral Edema – part 2

Vasogenic

edema, stage 1 (a.k.a., Ionic edema)

Cytotoxic edema

 Na/water gradient across intact BBB

Edema of endothelial cells 

transcapillary

flux of Na

Water follows Na  increased extracellular water content

Vasogenic

edema, stage 2

Endothelial damage

 breakdown of BBB

Leakage of plasma & proteins/ions into extracellular space

Water follows proteins/ions  increased water content of brainSlide10

Can we stop this??Slide11

Can we stop this??

NOPESlide12

Can we stop this??

Well…

BBB disruption

Osmotic agents only effective if they are blocked by an intact BBB

Leakage of osmotic agents into tissue can worsen edema

Occluded capillary flow

Arterial flow may be already blocked by thrombus (ischemic stroke)

Tissue edema eventually compresses the capillaries

Limited movement of water from edematous tissue

In ischemic stroke, this tends to be ineffective, because of all the aboveSlide13

What the heck??Is this the end of the talk??Slide14

What the heck??Edema sucks, and we can’t do anything about it??Slide15

What the heck??Maybe we should start over…Slide16

Swelling, Itching Brain:Management of Increased Intracranial Pressure

Deepak S Nair, MD

Stroke Neurology &

Neurocritical

Care

OSF Healthcare – Illinois Neurological InstituteSlide17

DisclosuresNo financial (or other) conflicts of interest to discloseSlide18

ObjectivesDescribe the pathologic mechanism of ICP crisis.

Review the current treatment modalities for ICP crisis.

Propose an algorithmic approach to managing ICP crisis. Slide19

Increased Intracranial PressureSlide20

Treatment Options for ICP Crisis

Standard measures

Surgery

 if/when indicated

Medical management

ICP monitoring

Ventilator optimization

Osmotherapy

Barbiturate coma

Therapeutic hypothermia

InvestigationalSlide21

Standard Measures

ABC’s

Head/neck position

Mild sedation

Avoid hyponatremia

Avoid hypotonic fluids

Avoid hyperglycemic fluids

Avoid/prevent fever

Avoid/prevent seizuresSlide22

Decompressive HemicraniectomySlide23

Hyper-osmolar Therapy

Mannitol

Non-metabolized sugar alcohol, used for diuresis

Creates an osmotic gradient across an intact BBB

Diffusion of water into intravascular space, decreases brain water content

Lowers ICP, typically when

sOsm

is ~320

mOsm

Can induce renal failure, so must monitor

osmolar

gap

Hypertonic saline

Multiple formulations (3%

 23.4%)

Creates osmotic gradient, decreases brain water content

Lowers ICP, when serum Na is 145 – 155, or higher in selected patients

Increases intravascular volume  beneficial effects on CPP/CBF/oxygenation

Rapid reversal can lead to rebound edema, so titrate off slowlySlide24
Slide25

Putting it all together

Anticipate cerebral edema, based on stroke severity

Initiate “Standard Measures” for all severe strokes

Monitor for edema/ICP crisis

Serial neuro exams

Serial imaging

ICP monitoring, if/when appropriate

Team-based approach

Stroke/Neurology

Neurosurgery

Critical Care

Do not delay treatmentSlide26
Slide27

Questions…Slide28

References

Treadwell, S. D., and B.

Thanvi

. "Malignant Middle Cerebral Artery (MCA) Infarction: Pathophysiology, Diagnosis and Management." Postgraduate Medical Journal (2010): n.

pag

. Print.

Ryu

, Justine H., Brian P. Walcott, Kristopher T.

Kahle

, Sameer A.

Sheth

, Randall T. Peterson, Brian V.

Nahed

, Jean-Valery C. E.

Coumans

, and J. Marc

Simard

. "Induced and Sustained Hypernatremia for the Prevention and Treatment of Cerebral Edema Following Brain Injury."

Neurocritical

Care 19.2 (2013): 222-31. Print.

Kahle

, K. T., J. M.

Simard

, K. J. Staley, B. V.

Nahed

, P. S. Jones, and D. Sun. "Molecular Mechanisms of Ischemic Cerebral Edema: Role of

Electroneutral

Ion Transport." Physiology 24.4 (2009): 257-65. Web.

Torre-Healy, Andrew, Nicholas F. Marko, and Robert J. Weil. "Hyperosmolar Therapy for Intracranial Hypertension." 

Neurocritical

Care

 17.1 (2011): 117-30. Print.

Lukitsch

, Ivo. "Hypernatremia." 

Background, Pathophysiology, Epidemiology

.

EMedicine

/Medscape, 08 Sept. 2016. Web. 05 Apr. 2017.