Papilledema medical therapy: Difference between revisions

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* [[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.
* [[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.


 
* '''[[Weight]] Reduction-'''  Medically and surgically induced weight reduction (eg, gastric banding or gastric bypass procedures) may be necessary in morbidly obese patients. Case series of [[idiopathic intracranial pressure]] patients undergoing gastric surgery report improvement of symptoms and signs including papilledema, headache, tinnitus, and cerebrospinal fluid pressure.<ref>{{cite journal |author=Sugerman HJ, Felton WL, Sismanis A, Kellum JM, DeMaria EJ, Sugerman EL |title=Gastric surgery for pseudotumor cerebri associated with severe obesity |journal=Ann. Surg. |volume=229 |issue=5 |pages=634–40; discussion 640–2 |year=1999 |month=May |pmid=10235521 |pmc=1420807 |doi= |url=}}</ref> <ref>{{cite journal |author=Nadkarni T, Rekate HL, Wallace D |title=Resolution of pseudotumor cerebri after bariatric surgery for related obesity. Case report |journal=J. Neurosurg. |volume=101 |issue=5 |pages=878–80 |year=2004 |month=November |pmid=15540933 |doi=10.3171/jns.2004.101.5.0878 |url=}}</ref>
* '''[[Weight]] Reduction-'''  Medically and surgically induced weight reduction (eg, gastric banding or gastric bypass procedures) may be necessary in morbidly obese patients. Case series of [[idiopathic intracranial pressure]] patients undergoing gastric surgery report improvement of symptoms and signs including papilledema, headache, tinnitus, and cerebrospinal fluid pressure.<ref>
 
 


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

Revision as of 16:38, 18 July 2012

Overview

The best treatment of papilledema is to address its underlying cause. However the root cause of papilledema is increase intracranial pressure.Drugs are use to decrease intracranial pressure. These drugs acts mainly by either decreasing cerebrospinal fluid production or by increasing its outflow.

Medical Therapy

  • Acetazolamide — Carbonic anhydrase inhibitors are believed to reduce the rate of cerebrospinal fluid production. Acetazolamide is the usual first line treatment for idiopathic intracranial hypertension. Acetazolamide is successful in managing symptoms and stabilizing vision in 47 to 67 percent of patients [34-36].[1][2]Although a sulfa allergy is reported to be a relative contraindication to acetazolamide use, there is little clinical or pharmacologic basis for this recommendation.
  • 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[3] [4] [5]. The most commonly used agent is mannitol. 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[6] [7]. 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[8].
  • Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large randomized clinical trial of their use in moderate to severe head injury[9]. 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)[10]. 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.
  • Weight Reduction- Medically and surgically induced weight reduction (eg, gastric banding or gastric bypass procedures) may be necessary in morbidly obese patients. Case series of idiopathic intracranial pressure patients undergoing gastric surgery report improvement of symptoms and signs including papilledema, headache, tinnitus, and cerebrospinal fluid pressure.[11] [12]

References

  1. ↑ Matthews YY (2008). "Drugs used in childhood idiopathic or benign intracranial hypertension". Arch Dis Child Educ Pract Ed. 93 (1): 19–25. doi:10.1136/adc.2006.107326. PMID 18208981. Unknown parameter |month= ignored (help)
  2. ↑ Youroukos S, Psychou F, Fryssiras S, Paikos P, Nicolaidou P (2000). "Idiopathic intracranial hypertension in children". J. Child Neurol. 15 (7): 453–7. PMID 10921516. Unknown parameter |month= ignored (help)
  3. ↑ Paczynski RP (1997). "Osmotherapy. Basic concepts and controversies". Crit Care Clin. 13 (1): 105–29. PMID 9012578. Unknown parameter |month= ignored (help)
  4. ↑ 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)
  5. ↑ 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)
  6. ↑ 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)
  7. ↑ 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)
  8. ↑ 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)
  9. ↑ 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.
  10. ↑ 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)
  11. ↑ Sugerman HJ, Felton WL, Sismanis A, Kellum JM, DeMaria EJ, Sugerman EL (1999). "Gastric surgery for pseudotumor cerebri associated with severe obesity". Ann. Surg. 229 (5): 634–40, discussion 640–2. PMC 1420807. PMID 10235521. Unknown parameter |month= ignored (help)
  12. ↑ Nadkarni T, Rekate HL, Wallace D (2004). "Resolution of pseudotumor cerebri after bariatric surgery for related obesity. Case report". J. Neurosurg. 101 (5): 878–80. doi:10.3171/jns.2004.101.5.0878. PMID 15540933. Unknown parameter |month= ignored (help)
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