How to identify cerebral edema (vascular origin, cytotoxicity, interstitial) in clinical notes?

Cerebral edema is divided into vasogenic cerebral edema, cellular cerebral edema and interstitial cerebral edema
.

Vasogenic brain edema

Vasogenic brain edema

Due to the damage and destruction of the blood-brain barrier, the permeability of the capillaries increases, and the water exudation increases, which is caused by the accumulation of the surrounding blood vessels and the intercellular substance
.

At this time, some protein substances permeate into the extracellular fluid through the blood vessel wall along with the water, which increases the osmotic pressure of the extracellular fluid, and the water seeps out from the blood vessel wall, resulting in the continued development of cerebral edema.

The following figure (Figure 1~Figure 3) shows glioblastoma.
The tumor compresses the surrounding brain tissue or obstructs cerebral venous return, increases the venous pressure, the absorption of the cerebrospinal fluid circulation machine, and the tumor's biological toxicity, etc.
The brain tissue of the patient is affected, the blood-brain barrier is damaged or destroyed, the permeability of the blood vessel wall is increased, and localized angiogenic brain edema is produced
.

Figure 1 FLAIR sequence tumor is slightly hyperintensive, irregular hyperintensity edema is seen in the white matter around the tumor, which outlines the local white matter morphology

Figure 1 FLAIR sequence tumor is slightly hyperintensive, irregular hyperintensity edema in the white matter surrounding the tumor, outlines the local white matter morphology Figure 1 FLAIR sequence tumor is slightly hyperintensive, irregular hyperintensity edema in the white matter surrounding the tumor, Outline the local white matter morphology

Figure 2 T1 enhanced scan shows that the tumor solid has a rosette enhancement, while the surrounding edema has no enhancement

Figure 2 T1 enhanced scan shows that the tumor solid has a rosette enhancement, but the surrounding edema has no enhancement .
Figure 2 T1 enhanced scan shows that the tumor solid has a rosette enhancement, but the surrounding edema has no enhancement.

Figure 3 The spectrum shows that the Cho peak is significantly higher, and the NAA peak is reduced

Figure 3 The spectrum shows that the Cho peak is significantly increased and the NAA peak is reduced .
Figure 3 The spectrum shows that the Cho peak is significantly increased and the NAA peak is reduced.

Cellular brain edema

Cellular brain edema

Cellular brain edema is different pathogenic factors that change the internal and external environment of cells.
Hypoxia in brain tissue affects nerve cell metabolism, cell membrane system dysfunction, reduced mitochondrial adenosine triphosphate production, and decreased activities of nerve cell membranes such as sodium-potassium pump and calcium-magnesium pump , So that the sodium, potassium and calcium plasma exchange barrier inside and outside nerve cells
.

These factors can cause intracellular edema

Fig.
4 In patients with acute cerebral infarction, DWI showed that the left frontal lobe has obvious flaky high signal, and the responsible blood vessel is the frontal branch of the left middle cerebral artery

Fig.
4 In patients with acute cerebral infarction, DWI shows obvious flaky hyperintensity in the left frontal lobe, and the responsible vessel is the frontal branch of the left middle cerebral artery .
Fig.
4 In patients with acute cerebral infarction, DWI shows obvious signs in the left frontal lobe.
Sheet-like high signal, the responsible blood vessel is the frontal branch of the left middle cerebral artery

Interstitial brain edema

Interstitial brain edema

Also known as hydrocephalus hydrocephalus, it is common in obstructive hydrocephalus
.

Different etiologies cause obstructive hydrocephalus, which enlarges the ventricular system, especially the lateral ventricle, causing the intraventricular pressure to be significantly higher than the pressure in the brain tissue

Figure 5 A patient with obstructive hydrocephalus, bilateral lateral ventricles were significantly dilated, and crescent-shaped long T2 edema bands were visible near the anterior horns of the lateral ventricles

Figure 5 A patient with obstructive hydrocephalus, bilateral lateral ventricles were significantly dilated, and a crescent-shaped long T2 signal edema zone can be seen near the anterior horn of the lateral ventricle .

Figure 6 In the DWI sequence, the medulloblastoma tissue cells are tightly arranged, showing a typical high signal

Figure 6 In DWI sequence, medulloblastoma tissue cells are densely arranged, showing typical high signal .

Figure 7 T1 enhanced sagittal four ventricle lesions showed mild uneven enhancement

Figure 7 T1 enhanced sagittal fourth ventricle lesions showed mild uneven enhancement Figure 7 T1 enhanced sagittal fourth ventricle lesions showed mild uneven enhancement

Figure 8 Differential diagnosis of various types of cerebral edema

Figure 8 Differential diagnosis of various types of cerebral edema Figure 8 Differential diagnosis of various types of cerebral edema Leave a message here