Brain Edema & It’s Management

Introduction
Intracranial dynamics describes the interactions of the
contents—brain parenchyma, blood and CSF—within the
cranium.
CSF Blood
10% 10%

Brain
80%
 Introduction

CPP = MAP – ICP

Intracranial Blood Ischemic

Pressure perfusion necrosis
pressure
Cerebral blood CBF
is generally independent of mean arterial pressure but it is closely
regulated by arterial PaCO₂ systemically and locally by regional
factors such as release of endothelin and NO flow
.
Brain edema
is a life-threatening condition

Brain edema
is defined as an abnormal accumulation of fluid within the brain
parenchyma, producing a volumetric enlargement of the tissue.
 Mechanism of brain edema
Induced by factors that influence the permeability of BBB like
• changes in the BBB
• Changes blood osmolality
• Dysregulated blood flow
• ↑ capillary Pressure
It can be consequence of
1.cerebral trauma 2.massive cerebral infarction,
3.Hemorrhage 4.abscess
5.Tumor 6.allergy
7.Sepsis 8.hypoxia
9.other toxic or metabolic disorders
1. Cytotoxic
Permeability of the BBB is normal and edema results from a
disturbance in ionic homeostasis.
2- Vasogenic
due to a breakdown of the tight endothelial junctions → disturb BBB
→↑vascular permeability → accumulation of edema fluid in the
extracellular spaces

This type of edema is seen in response to

• Trauma
• Tumors
• Focal inflammation
• Late stages of cerebral ischemia
3- Interstitial cerebral edema
• Result from acute obstructive hydrocephalus.
• CSF pushed into extracellular space in
extracellular spaces of the periventricular
white matter in hydrocephalous
4- Osmotic cerebral edema
• Result from dilution of blood (↓ osmolarity)

• Normally CSF and brain’s extracellular fluid osmolarity is slightly

lower than plasma.

• If ↓ plasma osmolarity, the brain osmolality will exceed the serum

osmolality creating an abnormal pressure gradient result in water
influx into the brain causing edema.
Causes of Osmotic cerebral edema include
1. Hyponatremia
2. SIADH
3. Hemodialysis
4. Rapid reduction of blood glucose in DKA
5. Rapid correction of hypernatremia
6. Infusion of hypotonic solusion.
5-Hydrostatic
• This form of cerebral edema is seen in acute, malignant
hypertension.

• It is thought to result from disturbance of the autoregulation of

cerebral blood circulation with direct transmission of pressure to
cerebral capillary with transudation of fluid into the ECF.
 Clinical presentation
Manifestation of ↑ICP
• Headache
• Vomiting
• Diplopia , visual loss
Cushing triad: Hypertension, Bradycardia, Irregular respiration
Siezure
Disturbed conscious level
Herniation syndromes
Clinical signs of brain edema start to appear when ICP exceed 30mmHg
 Cerebral edema

Pathological increase in the water content of the brain

Increased intracranial pressure

Neurological deterioration

Herniation

Death
 Management

1. Optimizing Head and Neck Positions

30 ̊elevation of the head in patients is essential for decreasing CSF hydrostatic
pressure.

Maintain CPP between 50 – 65 mmhg

2.Ventilation and Oxygenation
• Hypoxia and hypercapnia are potent cerebral vasodilator
• Maintain PaCO2 (25 - 30 mmHg) to support adequate CBF or CPP
to brain
• maintain PaO2 at approximately 100 mmHg
• Pt should be intubated in:
1. GCS scores less than or equal to 8
2. Patients with poor upper airway reflexes be intubated for airway protection.
3. Pulmonary disorder eg ARDS, aspiration pnemonia
3. Seizure Prophylaxis
• Phenobarb. and phenytoin specially in brain trauma

4. Osmotherapy
Mannitol 0.25 – 1 g/kg I.V over 20 min
3% Saline 0.1 – 1 ml/kg/hr

5. Diuretics
Furosemide 1 – 2 mg/kg
6. Corticosteroid
dexamethasone, are the preferred steroidal agents, due to their low
mineralocorticoid activity
 Other Lines
1. Controlled hypothermia→ (32 -34 C) ↓ the rate of metabolism in the
brain.

2. Lumbar CSF drainage

3. Craniectomy
 Supportive

• Avoid hypoglycemia or hyperglycemia

• Foley catheter should be inserted
• High caloric intake