Brain edema
| Classification according to ICD-10 | |
|---|---|
| G93.6 | Brain edema |
| P11.0 | Brain edema from birth injury |
| S06.1 | Traumatic brain edema |
| ICD-10 online (WHO version 2019) | |
When cerebral edema , according to Reichardt (1904) a form of brain swelling (cerebral increase in volume), it is caused by damage to the blood-brain barrier or the blood-cerebrospinal fluid barrier to edema , so to fluid retention in the brain .
causes
The cerebral edema is a complication of pathological processes (e.g. tumors , inflammation , poisoning , vascular processes) or disruption of the water-electrolyte balance of the brain that occurs after injuries , operations and after successfully treated cardiac arrest . The fluid accumulation occurs predominantly intracellularly in the astrocytes continue.
Cerebral edema can also result from the influence of high altitude and the associated reduced oxygen partial pressure in the breath, especially when climbing at high altitude . See also high altitude brain edema (HACE).
Diagnosis
In quantitative disturbances of consciousness and general signs of increased intracranial pressure lends itself to the history survey and neurological examination, a ophthalmoscopy at which a positive result in papilledema would show. The imaging examination of the inside of the skull using computed tomography or magnetic resonance imaging provides security .
to form
Cerebral edema can occur perifocally , i.e. surrounding localized brain damage, or also generalized. A distinction is made between vasogenic , cytotoxic and interstitial brain edema:
The vasogenic form is based on a permeability disorder of the blood-brain barrier or an increased permeability of the capillary vessels , which leads to the influx of fluid into the interstitium. The underlying diseases here are head trauma , infections, abscesses and brain tumors .
In cytotoxic brain edema, the intracellular space of the brain increases as a result of a partial local breakdown of the sodium-potassium pump , as sodium passes into the cells and draws chlorine ions and water with it. Causes are global or local oxygen deficiency , liver failure and hypotonic hyperhydration as well as the late phase of a traumatic brain injury.
An interstitial edema is by an obstruction of cerebrospinal fluid , or a rapid decrease of the glucose -, sodium or - urea conditionally levels in the blood.
consequences
Since the brain has little opportunity to expand due to the bony skull surrounding it, cerebral edema is usually a serious disease, especially since the swelling brain can also compress the sinuses , which ensure the blood flow from the brain. The intracranial pressure increases, which leads to a decrease in the cerebral perfusion pressure and thus the cerebral blood flow. A ischemia with a result of infarction and brain damage is a continuing through to brain death may result.
Treatment options
The treatment options are geared towards lowering the increased intracranial pressure and mostly relate to a ventilated intensive care patient .
- The standard is an upper body elevation of 15–30 °
- Pressure relief by draining CSF through an external ventricular drainage
- Trepanation / craniectomy to give the brain additional space
- u. U. osmotically effective diuretic , e.g. E.g .: mannitol , glycerin , to create an osmotic gradient between plasma and tissue and thereby drain the brain.
- short-term hyperventilation in the event of an acute critical increase in intracranial pressure
- Use of TRIS (buffering intracellular acidosis ) or barbiturates (lowering the cerebral metabolism)
- Mild therapeutic hypothermia
Web links
Individual evidence
- ↑ Friedrich Unterharnscheidt: Pathology of the nervous system VI.C: Traumatology of the brain and spinal cord Traumatic damage to the brain (forensic pathology) . Springer Verlag, Berlin, Heidelberg 1994, ISBN 978-3-642-78265-7 , pp. 148 ( limited preview in Google Book search).
- ↑ a b Pschyrembel, Clinical Dictionary, 261st edition, keyword “brain edema”.
- ↑ Verena Kollmann - Fakler: Prognosis criteria and outcome of hypoxic brain damage after cardiovascular arrest , Munich 2011.
- ↑ H. Bechtelsheimer u. a .: Textbook of general pathology and pathological anatomy . 32nd edition. Springer, Berlin, Heidelberg 1986, ISBN 978-3-662-00683-2 , pp. 495 ( limited preview in Google Book search).
- ↑ Hackett, Roach: High Altitude Cerebral Edema in: HIGH ALTITUDE MEDICINE & BIOLOGY, Volume 5, Number 2, 2004.
- ↑ a b Stefan Silbernagl, Florian Lang: Pocket Atlas of Pathophysiology . 4th edition. Thieme Verlag, Stuttgart 2013, ISBN 978-3-13-102194-6 , p. 384 ( limited preview in Google Book Search).
- ^ A b Hans Walter Striebel: Operative Intensive Care Medicine: Safety in Clinical Practice; with 229 tables . Schattauer, Stuttgart 2008, ISBN 978-3-7945-2480-8 , p. 508 f . ( limited preview in Google Book search).
- ↑ a b c d e f Lothar Ulrich (ed.): Thiemes intensive care and anesthesia . Thieme, Stuttgart 2005, ISBN 978-3-13-130910-5 , p. 387 f . ( limited preview in Google Book search).
- ↑ a b German Society for Neurology: Guideline on intracranial pressure ( memento of the original from September 23, 2015 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. 2012, p. 10.
- ↑ German Society for Neurology: Guideline on intracranial pressure ( Memento of the original from September 23, 2015 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. 2012, p. 7.
