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[The internal environment and intracranial hypertension]
C Ichai1, J F Ciais, D Grimaud
1Département d'anesthésie-réanimation, hôpital Saint-Roch, Nice, France.
Annales Francaises D'Anesthesie Et De Reanimation
|January 1, 1997
Summary
Intracranial pressure management involves understanding fluid dynamics. Hypotonic solutions can worsen cerebral edema and intracranial hypertension, while osmotic therapy with mannitol is a key treatment.
Area of Science:
- Neurology
- Neurosurgery
- Critical Care Medicine
Background:
- Intracranial pressure (ICP) is determined by cerebral tissue volume, cerebrospinal fluid volume (CSFV), and cerebral blood volume (CBV), governed by the Monro-Kelly equation.
- The integrity of the blood-brain barrier (BBB) dictates how osmotic and hydrostatic pressure gradients influence water movement and cerebral tissue volume.
- Cerebral blood flow (CBF) regulation, primarily through cerebral vascular resistances, significantly impacts CBV and consequently ICP.
Purpose of the Study:
- To elucidate the effects of various physiological factors and therapeutic interventions on intracranial pressure (ICP).
- To evaluate the impact of osmotic and hydrostatic gradients, as well as specific solutes, on cerebral edema and ICP.
- To review established and potential therapeutic strategies for managing acute intracranial hypertension (ICHT).
Main Methods:
- Review of physiological principles governing intracranial pressure.
- Analysis of experimental data regarding the effects of osmotic pressure, hypoosmolarity, and solute types on cerebral edema.
- Examination of the role of CO2, temperature, and glucose in modulating CBF and ICP.
- Assessment of therapeutic interventions including osmotic therapy, hyperventilation, hypothermia, and glucose control.
Main Results:
- Plasma hypoosmolarity increases cerebral water content and ICP when the BBB is intact; hypooncotic solutes do not affect ICP.
- Hypotonic solutes are contraindicated in ICHT due to potential aggravation of cerebral edema.
- Hyperventilation effectively reduces ICP by inducing cerebral vasoconstriction, but requires careful monitoring to avoid ischemia; hyperthermia worsens ICHT, while moderate hypothermia is beneficial.
- Hyperglycemia can exacerbate ICHT through lactic acidosis and cytotoxic edema, necessitating glucose control.
Conclusions:
- Osmotic therapy, particularly with mannitol, is a cornerstone in managing acute ICHT.
- Careful selection of intravenous fluids is crucial, avoiding hypotonic solutions in patients with ICHT.
- Management strategies for ICHT should consider factors like CO2 levels, temperature, and glucose control to optimize outcomes.