Osmotherapy in neurocritical care

Bhardwaj, Anish

doi:10.1007/s11910-007-0079-2

Cited by 38 publications

(34 citation statements)

References 57 publications

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“…D-mannitol, a sugar alcohol used in treating elevated ICP (Bhardwaj 2007), shrank the tissue by 14 per cent. The effect of D-mannitol on tissue volume could be explained by its brain tissue partition coefficient that describes the ratio of osmolyte concentration in the bathing media to inside the tissue.…”

Section: Discussionmentioning

confidence: 99%

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Elkin

Shaik

Morrison

2010

Phil. Trans. R. Soc. A.

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Cerebral oedema or brain tissue swelling is a significant complication following traumatic brain injury or stroke that can increase the intracranial pressure (ICP) and impair blood flow. Here, we have identified a potential driver of oedema: the negatively charged molecules fixed within cells. This fixed charge density (FCD), once exposed, could increase ICP through the Donnan effect. We have shown that metabolic processes and membrane integrity are required for concealing this FCD as slices of rat cortex swelled immediately (within 30 min) following dissection if treated with 2 deoxyglucose + cyanide (2DG+CN) or Triton X-100. Slices given ample oxygen and glucose, however, did not swell significantly. We also found that dead brain tissue swells and shrinks in response to changes in ionic strength of the bathing medium, which suggests that the Donnan effect is capable of pressurizing and swelling brain tissue. As predicted, a non-ionic osmolyte, 1,2 propanediol, elicited no volume change at 2000 × 10 −3 osmoles l −1 (Osm). Swelling data were well described by triphasic mixture theory with the calculated reference state FCD similar to that measured with a 1,9 dimethylmethylene blue assay. Taken together, these data suggest that intracellular fixed charges may contribute to the driving forces responsible for brain swelling.

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Section: Discussionmentioning

confidence: 99%

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Elkin

Shaik

Morrison

2010

Phil. Trans. R. Soc. A.

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“…7,56 In fact, their discovery was fortuitous since the original aim was to study CSF flow dynamics and electrolyte composition, as urged by Harvey Cushing. 10 Cushing recognized the importance of a neurosurgeon's ability to understand and manage hydrocephalus.…”

Section: History Of Hyperosmolar Agents and The Discovery Of Ureamentioning

confidence: 99%

“…45 In addition, it was contraindicated in patients who were already dehydrated. 7,32 Finally, due to the potential for platelet dysfunction, urea was contraindicated in patients with an intracranial hemorrhage prior to evacuation of the hematoma. 7,32 Urea was also found to be associated with several relevant side effects.…”

Section: Limitations and Complications Associated With Ureamentioning

confidence: 99%

“…7,32 Finally, due to the potential for platelet dysfunction, urea was contraindicated in patients with an intracranial hemorrhage prior to evacuation of the hematoma. 7,32 Urea was also found to be associated with several relevant side effects. Infusion of large quantities of urea led to nausea, vomiting, and diarrhea in awake patients.…”

Section: Limitations and Complications Associated With Ureamentioning

confidence: 99%

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The history of urea as a hyperosmolar agent to decrease brain swelling

Otvos

Kshettry

Benzel

2014

FOC

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In 1919, it was observed that intravascular osmolar shifts could collapse the thecal sac and diminish the ability to withdraw CSF from the lumbar cistern. This led to the notion that hyperosmolar compounds could ameliorate brain swelling. Since then, various therapeutic interventions have been used for the reduction of intracranial pressure and brain volume. Urea was first used as an osmotic agent for the reduction of brain volume in 1950. It was associated with greater efficacy and consistency than alternatives such as hyperosmolar glucose. Its use became the standard of clinical practice by 1957, in both the intensive care unit and operating room, to reduce intracranial pressure and brain bulk and was the first hyperosmolar compound to have widespread use. However, the prime of urea was rather short lived. Reports of side effects and complications associated with urea emerged. These included coagulopathy, hemoglobinuria, electrocardiography changes, tissue necrosis with extravasation, and a significant potential for rebound intracranial hypertension. Mannitol was introduced in 1961 as a comparable and potentially superior alternative to urea. However, mannitol was initially purported to be less effective at rapidly reducing intracranial pressure. The debate over the two compounds continued for a decade until mannitol eventually replaced urea by the late 1960s and early 1970s as the hyperosmolar agent of choice due to the ease of preparation, chemical stability, and decreased side effect profile. Although urea is not currently the standard of care today, its rise and eventual replacement by mannitol played a seminal role in both our understanding of cerebral edema and the establishment of strategies for its management.

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“…If an external ventricular drain is present, diversion of cerebrospinal fluid can be helpful as well. Use of hyperosmolar substances is the mainstay of therapy for cerebral edema, with or without associated intracranial hypertension (Bhardwaj 2007). Infusion of a hyperosmolar substance serves to generate an osmotic gradient across the blood-brain-barrier, which reduces cerebral edema by drawing water out of the brain tissue.…”

Section: Cerebral Edema Intracranial Hypertension and Cerebral Perfumentioning

confidence: 99%