Cerebral Edema and Fluids

Question 1

What are the type of cerebral edema?

Answer 1

1. Vasogenic (most common) caused by disruption of the BBB from mechanical trauma, inflammatory lesions, hypertension, tumors, infarction.
2. Osmotic - from relative interstitial hyperosmolality (compared to plasma) in the presence of an intact BBB.
3. Compressive - from obstruction of interstitial fluid bulk flow pathways
4. Hydrocephalic - from obstruction of CSF bulk flow

Question 2

What is “vascular” brain swelling?

Answer 2

Brain swelling that is not cerebral edema per se but is caused by arterial dilation or venous obstruction.

Question 3

What is “cellular” brain swelling?

Answer 3

Not cerebral edema, per se, but is caused by cytotoxic injuries such as hypoxemia, ischemia or metabolic disease.

Question 4

Why are “vascular” and “cellular” brain swellings not just called cerebral edema?

Answer 4

Because total brain water is not necessarily increased which is what cerebral edema is, by definition.

Question 5

What is the definition of cerebral edema?

Answer 5

Cerebral edema is an increase in brain water.

Question 6

How would you treat cerebral edema?

Answer 6

ABCs then address underlying cause which may include antihypertensive therapy.
Elevation of head to 30 degrees
Hyperventilation
Diuretics (mannitol, furosemide)
Steroids (for vasogenic edema surrounding brain tumors, abscesses, infection, subdural hematoma, postop swelling and pseudotumor cerebri. Don’t seem to be effective for head trauma).

Question 7

Are steroids of any use for the treatment of cerebral edema?

Answer 7

Perhaps for for vasogenic edema surrounding brain tumors, abscesses, CNS infections, subdural hematoma, postop swelling and pseudotumor cerebri. Don’t seem to be effective for head trauma.

Question 8

How does mannitol work as a diuretic in patients with cerebral edema and what are some implications of its use?

Answer 8

• Mannitol is an osmotic diuretic that begins to work in 5 minutes and reaches peak effect in 30 - 45 minutes.
• Theoretically disruption of the BBB not only limits its effectiveness, the extravasation of mannitol into the parenchyma could worsen the cerebral edema. It also could initially increases intravascular volume and causes cerebral vasodilation increasing ICP with initiation of its use.
• Conversely, it decreases CSF production and acts as a free radical scavenger.

Question 9

What is the difference between oncotic pressure and osmotic pressure?

Answer 9

With regards to plasma, oncotic pressure is a component of the osmotic pressure of plasma. Specifically, oncotic pressure refers to the osmotic pressure due to proteins > 30 Kdaltons in molecular weight like albumin.

Question 10

What is the difference between the peripheral endothelial barrier and the blood brain barrier?

Answer 10

The peripheral endothelial barrer has wide junctions that are permeable to water, sodium but not proteins. Hence, oncotic pressure is the primary determinant of water flux across peripheral capillaries. The BBB has very small junctions that are impermeable not just to proteins but also to sodium. As a result both oncotic and osmotic pressures determine water flux across the BBB.

Question 11

Which is superior crystalloids or colloids in a patient with cerebral edema?

Answer 11

Colloids may allow more sustained increases in intravascular volume and improve cerebral blood flow but no improvement in survival has been demonstrated. In fact, the starches have shown to have deleterious renal and coagulation side effects, albumin may worsen outcome. Hypertonic saline must be used with caution. Dextrose may worsen neurologic outcome.

Question 12

What should the fluid status goal be for a patient with cerebral edema?

Answer 12

Maintaining euvolemia is now favored over the once popular approach of running patients dry.

Question 13

Via what mechanism may relative hyperglycemia worsen neurologic outcome under conditions of cerebral ischemia?

Answer 13

The purported mechanism is the increased production of lactate using glucose as a substrate with subsequent intracellular acidosis.

Question 14

What are the hemodynamic effects of mannitol?

Answer 14

Transiently decreases PVR and can cause hypotension if given quickly (under 10 minutes) this is why it is given over 30 minutes.
Delayed effects of fluid overload include pulmonary edema/CHF exacerbation
Diuresis may result in hypovolemia

Question 15

By what mechanism do steroids potentially help in cerebral edema?

Answer 15

1. stabilization of endothelial membranes
2. increased cerebral capillary lysosomal activity
3. inhibition of neurotoxic release
4. electrolyte shifts favoring capillary efflux
5. increased glucose utilization

Question 16

What is the difference between osmolarity and osmolality?

Answer 16

Osmolarity is the number of osmoles of solute per liter of solution. Osmolality is number of osmoles of solute per kg of solvent.

Question 17

If brain interstitial osmolarity were 285 mosm/L and that in the blood were acute raised to 295 after mannitol administration, what would the resultant gradient be in terms of mm Hg?

Answer 17

Ever 1 mOsm of concentration difference across the BB produces a pressure of 19.3 mm Hg, so a difference of 10 mOsm/L would create a 193 mm Hg gradient driving fluid out of the brain and into the intravascular space.

Question 18

Which has a higher osmolarity: LR or NS?

Answer 18

NS has an osmolarity of 308 mOsm/L whereas LR has a lower one of 273 mOsm/L

Question 19

What is normal serum osmolarity?

Answer 19

285 mOsm/L

Question 20

Does the decrease in oncotic pressure from use of large volume of crystalloids cause cerebral edema?

Answer 20

It may make a small contribution towards cerebral edema but the osmotic effect of oncotic forces is generally very small on the order of 23 - 27 mm Hg.