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==Medical Therapy==
==Medical Therapy==


* To decrease ICP, medications can be administered by increasing the absorption of Cerebrospinal fluid (CSF) or decreasing its production. Such medicines include diuretics like [[acetazolamide]] and lasix.
The best treatment of elevated ICP is to address its underlying cause
* steroids can reduce inflammation (if this is a contributing factor to increased ICP), and may help to prevent vision loss. However, steroids have also been known to cause increased ICP, especially with a change in dosage. However, if a severe inflammatory condition exist, such as [[multiple sclerosis]], steroids with anti-inflammatory effects such as Methylprednisolone and prednisone can help.
 
* The removal of potentially causative medicines including tetracyclines and vitamin A analogues may help decrease ICP, however this is only necessary if the medication is truly felt to contribute to ICP increase.
* [[Mannitol]] — Osmotic diuretics reduce brain volume by drawing free water out of the tissue and into the circulation, where it is excreted by the kidneys, thus dehydrating brain parenchyma<ref>{{cite journal |author=Paczynski RP |title=Osmotherapy. Basic concepts and controversies |journal=Crit Care Clin |volume=13 |issue=1 |pages=105–29 |year=1997 |month=January |pmid=9012578 |doi= |url=}}</ref>,<ref>{{cite journal |author=Nath F, Galbraith S |title=The effect of mannitol on cerebral white matter water content |journal=J. Neurosurg. |volume=65 |issue=1 |pages=41–3 |year=1986 |month=July |pmid=3086519 |doi=10.3171/jns.1986.65.1.0041 |url=}}</ref>,<ref>{{cite journal |author=Bell BA, Smith MA, Kean DM, ''et al.'' |title=Brain water measured by magnetic resonance imaging. Correlation with direct estimation and changes after mannitol and dexamethasone |journal=Lancet |volume=1 |issue=8524 |pages=66–9 |year=1987 |month=January |pmid=2879175 |doi= |url=}}</ref>. The most commonly used agent is mannitol. It is prepared as a 20 percent solution, and given as a bolus of 1 g/kg. Repeat dosing can be given at 0.25 to 0.5 g/kg as needed, generally every six to eight hours. Use of any osmotic agent should be carefully evaluated in patients with renal insufficiency.
 
* [[Furosemide]]- 0.5 to 1.0 mg/kg intravenously, may be given with mannitol to potentiate its effect<ref>{{cite journal |author=Wilkinson HA, Rosenfeld SR |title=Furosemide and mannitol in the treatment of acute experimental intracranial hypertension |journal=Neurosurgery |volume=12 |issue=4 |pages=405–10 |year=1983 |month=April |pmid=6406929 |doi= |url=}}</ref>,<ref>{{cite journal |author=Pollay M, Fullenwider C, Roberts PA, Stevens FA |title=Effect of mannitol and furosemide on blood-brain osmotic gradient and intracranial pressure |journal=J. Neurosurg. |volume=59 |issue=6 |pages=945–50 |year=1983 |month=December |pmid=6415245 |doi=10.3171/jns.1983.59.6.0945 |url=}}</ref>. However, this effect can also exacerbate dehydration and hypokalemia
 
* [[Glycerol]] and [[urea]]- were used historically to control ICP via osmoregulation; however, use of these agents has decreased because equilibration between brain and plasma levels occurs more quickly than with mannitol.
 
* [[Hypertonic saline bolus]] — Hypertonic saline in bolus doses may acutely lower intracranial pressure; however, the effect of this early intervention on long-term clinical outcomes remains unclear<ref>{{cite journal |author=Bhardwaj A, Ulatowski JA |title=Hypertonic saline solutions in brain injury |journal=Curr Opin Crit Care |volume=10 |issue=2 |pages=126–31 |year=2004 |month=April |pmid=15075723 |doi= |url=}}</ref>.
 
* [[Glucocorticoids]] — Glucocorticoids were associated with a worse outcome in a large randomized clinical trial of their use in moderate to severe [[head injury]]<ref>{{cite journal |author=Roberhttp://wikidoc.org/index.php?title=Papilledema_medical_therapy&action=submitts I, Yates D, Sandercock P, ''et al.'' |title=Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial |journal=Lancet |volume=364 |issue=9442 |pages=1321–8 |year=2004 |pmid=15474134 |doi=10.1016/S0140-6736(04)17188-2 |url=}}</ref>. They should not be used in this setting.In addition, glucocorticoids are not considered to be useful in the management of [[cerebral infarction]] or [[intracranial hemorrhage]].In contrast, glucocorticoids may have a role in the setting of intracranial hypertension caused by brain tumors and CNS infections.  
 
* [[Hyperventilation]] — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of intracranial blood; a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF. Hyperventilation also results in respiratory alkalosis, which may buffer post-injury acidosis. The effect of hyperventilation on ICP is short-lived (1 to 24 hours)<ref>{{cite journal |author=Laffey JG, Kavanagh BP |title=Hypocapnia |journal=N. Engl. J. Med. |volume=347 |issue=1 |pages=43–53 |year=2002 |month=July |pmid=12097540 |doi=10.1056/NEJMra012457 |url=}}</ref>. Following therapeutic hyperventilation, the patient's respiratory rate should be tapered back to normal over several hours to avoid a rebound effect Therapeutic hyperventilation should be considered as an urgent intervention when elevated ICP complicates cerebral edema, intracranial hemorrhage, and tumor. Hyperventilation should not be used on a chronic basis, regardless of the cause of increased ICP be tapered back to normal over several hours to avoid a rebound effect.


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Revision as of 05:11, 18 July 2012


Medical Therapy

The best treatment of elevated ICP is to address its underlying cause

  • Mannitol — Osmotic diuretics reduce brain volume by drawing free water out of the tissue and into the circulation, where it is excreted by the kidneys, thus dehydrating brain parenchyma[1],[2],[3]. The most commonly used agent is mannitol. It is prepared as a 20 percent solution, and given as a bolus of 1 g/kg. Repeat dosing can be given at 0.25 to 0.5 g/kg as needed, generally every six to eight hours. Use of any osmotic agent should be carefully evaluated in patients with renal insufficiency.
  • Furosemide- 0.5 to 1.0 mg/kg intravenously, may be given with mannitol to potentiate its effect[4],[5]. However, this effect can also exacerbate dehydration and hypokalemia
  • Glycerol and urea- were used historically to control ICP via osmoregulation; however, use of these agents has decreased because equilibration between brain and plasma levels occurs more quickly than with mannitol.
  • Hypertonic saline bolus — Hypertonic saline in bolus doses may acutely lower intracranial pressure; however, the effect of this early intervention on long-term clinical outcomes remains unclear[6].
  • Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large randomized clinical trial of their use in moderate to severe head injury[7]. They should not be used in this setting.In addition, glucocorticoids are not considered to be useful in the management of cerebral infarction or intracranial hemorrhage.In contrast, glucocorticoids may have a role in the setting of intracranial hypertension caused by brain tumors and CNS infections.
  • Hyperventilation — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of intracranial blood; a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF. Hyperventilation also results in respiratory alkalosis, which may buffer post-injury acidosis. The effect of hyperventilation on ICP is short-lived (1 to 24 hours)[8]. Following therapeutic hyperventilation, the patient's respiratory rate should be tapered back to normal over several hours to avoid a rebound effect Therapeutic hyperventilation should be considered as an urgent intervention when elevated ICP complicates cerebral edema, intracranial hemorrhage, and tumor. Hyperventilation should not be used on a chronic basis, regardless of the cause of increased ICP be tapered back to normal over several hours to avoid a rebound effect.

References

  1. ↑ Paczynski RP (1997). "Osmotherapy. Basic concepts and controversies". Crit Care Clin. 13 (1): 105–29. PMID 9012578. Unknown parameter |month= ignored (help)
  2. ↑ Nath F, Galbraith S (1986). "The effect of mannitol on cerebral white matter water content". J. Neurosurg. 65 (1): 41–3. doi:10.3171/jns.1986.65.1.0041. PMID 3086519. Unknown parameter |month= ignored (help)
  3. ↑ Bell BA, Smith MA, Kean DM; et al. (1987). "Brain water measured by magnetic resonance imaging. Correlation with direct estimation and changes after mannitol and dexamethasone". Lancet. 1 (8524): 66–9. PMID 2879175. Unknown parameter |month= ignored (help)
  4. ↑ Wilkinson HA, Rosenfeld SR (1983). "Furosemide and mannitol in the treatment of acute experimental intracranial hypertension". Neurosurgery. 12 (4): 405–10. PMID 6406929. Unknown parameter |month= ignored (help)
  5. ↑ Pollay M, Fullenwider C, Roberts PA, Stevens FA (1983). "Effect of mannitol and furosemide on blood-brain osmotic gradient and intracranial pressure". J. Neurosurg. 59 (6): 945–50. doi:10.3171/jns.1983.59.6.0945. PMID 6415245. Unknown parameter |month= ignored (help)
  6. ↑ Bhardwaj A, Ulatowski JA (2004). "Hypertonic saline solutions in brain injury". Curr Opin Crit Care. 10 (2): 126–31. PMID 15075723. Unknown parameter |month= ignored (help)
  7. ↑ Roberhttp://wikidoc.org/index.php?title=Papilledema_medical_therapy&action=submitts I, Yates D, Sandercock P; et al. (2004). "Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial". Lancet. 364 (9442): 1321–8. doi:10.1016/S0140-6736(04)17188-2. PMID 15474134.
  8. ↑ Laffey JG, Kavanagh BP (2002). "Hypocapnia". N. Engl. J. Med. 347 (1): 43–53. doi:10.1056/NEJMra012457. PMID 12097540. Unknown parameter |month= ignored (help)
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