Medication Summary
Acetazolamide (ACZ) and furosemide (FUR) treat posthemorrhagic hydrocephalus in neonates. Both are diuretics that also appear to decrease secretion of CSF at the level of the choroid plexus. ACZ can be used alone or in conjunction with FUR. The combination enhances efficacy of ACZ in decreasing CSF secretion by the choroid plexus. If ACZ is used alone, it appears to lower risk of nephrocalcinosis significantly.
Medication as treatment for hydrocephalus is controversial. It should be used only as a temporary measure for posthemorrhagic hydrocephalus in neonates, or when shunting is not possible.
Carbonic anhydrase inhibitors
Class Summary
These agents inhibit an enzyme found in many tissues of the body that catalyzes a reversible reaction in which carbon dioxide becomes hydrated and carbonic acid dehydrated. These changes may result in a decrease in CSF production by the choroid plexus.
Acetazolamide (Diamox)
Noncompetitive reversible inhibitor of enzyme carbonic anhydrase, which catalyzes the reaction between water and carbon dioxide, resulting in protons and carbonate. This contributes to decreasing CSF secretion by choroid plexus.
Loop diuretics
Class Summary
These agents increase excretion of water by interfering with the chloride-binding cotransport system, which results from inhibition of reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule.
Furosemide (Lasix)
Mechanisms proposed for lowering ICP include lowering cerebral sodium uptake, affecting water transport into astroglial cells by inhibiting cellular membrane cation-chloride pump, and decreasing CSF production by inhibiting carbonic anhydrase. Used as adjunctive therapy with ACZ in temporary treatment of posthemorrhagic hydrocephalus in neonates.
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Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.
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Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.
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Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.
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Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recovery (FLAIR) sequences. Note that apical cuts (lower row) do not show enlargement of the sulci, as is expected in generalized atrophy. Pathological evaluation of this brain demonstrated hydrocephalus with no microvascular pathology corresponding with the signal abnormality (which likely reflects transependymal exudate) and normal brain weight (indicating that the sulci enlargement was due to increased subarachnoid cerebrospinal fluid [CSF] conveying a pseudoatrophic brain pattern).
