X-Message-Number: 33220
Date: Wed, 12 Jan 2011 18:16:03 -0800 (PST)
From: 
Subject: hypertonic saline for brain edema


A number of CI's clinical reports make mention of tissue edema. FYI: In 
mainstream medicine, injections of hypertonic saline have replaced mannitol, due
to its greater efficacy in treating edema. Although saline may not be the 
optimal stabilization solution, it is already available to funeral directors.

BMC Neurosci. 2010 Dec 10;11:153.

A comparative study on the efficacy of 10% hypertonic saline and equal volume of
20% mannitol in the treatment of experimentally induced cerebral edema in adult
rats.

Zeng HK, Wang QS, Deng YY, Jiang WQ, Fang M, Chen CB, Jiang X. Department of 
Emergency & Critical Care Medicine, Guangdong General Hospital, Guangdong 
Academy of Medical Sciences, Guangzhou 510080, PR China.
Abstract

BACKGROUND: Hypertonic saline and mannitol are commonly used in the treatment of
cerebral edema and elevated intracranial pressure (ICP) at present. In this 
connection, 10% hypertonic saline (HS) alleviates cerebral edema more 
effectively than the equal volume of 20% mannitol. However, the exact underlying
mechanism for this remains obscure. This study aimed to explore the possible 
mechanism whereby 10% hypertonic saline can ameliorate cerebral edema more 
effectively than mannitol.

RESULTS: Adult male Sprague-Dawley (SD) rats were subjected to permanent 
right-sided middle cerebral artery occlusion (MCAO) and treated with a 
continuous intravenous infusion of 10% HS, 20% mannitol or D-[1-3H(N)]-mannitol.
Brain water content (BWC) as analyzed by wet-to-dry ratios in the ischemic 
hemisphere of SD rats decreased more significantly after 10% HS treatment 
compared with 20% mannitol. Concentration of serum Na+ and plasma crystal 
osmotic pressure of the 10% HS group at 2, 6, 12 and 18 h following permanent 
MCAO increased significantly when compared with 20% mannitol treated group. 
Moreover, there was negative correlation between the BWC of the ipsilateral 
ischemic hemisphere and concentration of serum Na+, plasma crystal osmotic 
pressure and difference value of concentration of serum Na+ and concentration of
brain Na+ in ipsilateral ischemic hemisphere in the 10% HS group at the various
time points after MCAO. A remarkable finding was the progressive accumulation 
of mannitol in the ischemic brain tissue.

CONCLUSIONS: We conclude that 10% HS is more effective in alleviating cerebral 
edema than the equal volume of 20% mannitol. This is because 10% HS contributes 
to establish a higher osmotic gradient across BBB and, furthermore, the 
progressive accumulation of mannitol in the ischemic brain tissue counteracts 
its therapeutic efficacy on cerebral edema.
PMID: 21143951
Free text>
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004923/pdf/1471-2202-11-153.pdf


J Neurosci Nurs. 2008 Dec;40(6):362-8.

Challenging the gold standard: should mannitol remain our first-line defense 
against intracranial hypertension?
Infanti JL. Hospital of the University of Pennsylvania, Philadelphia, USA.
Abstract

  Mannitol has long been the "gold standard" for treatment of cerebral edema and
  refractory intracranial hypertension in traumatic brain injury, subarachnoid 
  hemorrhage, and stroke. Studies performed in animals have shown that 
  hypertonic saline (HS), in doses ranging from 3% to 10%, may be more effective
  than mannitol in treating these populations. Recently, randomized clinical 
  trials have evaluated the efficacy and safety of HS versus mannitol in the 
  treatment of elevated intracranial pressure (ICP). This research has been 
  prompted by mounting concern about the side effects of mannitol, the limited 
  ability to give multiple doses of the drug, and an increased understanding of 
  cerebral physiology. Four studies have compared the use of HS and mannitol in 
  brain-injured populations. These studies have shown that not only is HS a safe
  drug (no patients experienced adverse effects), it is also more efficient in 
  reducing ICP. Efficiency is defined as the drug's ability to decrease ICP to 
  acceptable levels and to maintain lower ICPs for a longer duration of time. It
  is important for nurses who administer osmotic diuretics to evaluate and 
  understand the current research to provide educated and appropriate care.
PMID: 19170304

Neurosurgery. 2005 Oct;57(4):727-36; discussion 727-36.

Effects of 23.4% sodium chloride solution in reducing intracranial pressure in 
patients with traumatic brain injury: a preliminary study.

Ware ML, Nemani VM, Meeker M, Lee C, Morabito DJ, Manley GT. Department of 
Neurological Surgery, University of California, San Francisco, California 94110,
USA.
Abstract

  OBJECTIVE: Mannitol is the standard of care for patients with increased 
  intracranial pressure (ICP), but multiple administrations of mannitol risk 
  renal toxicity and fluid accumulation in the brain parenchyma with consequent 
  worsening of cerebral edema. This preliminary study assessed the safety and 
  efficacy of small-volume injections of 23.4% sodium chloride solution for the 
  treatment of intracranial hypertension in patients with traumatic brain injury
  who became tolerant to mannitol.

METHODS: We retrospectively reviewed the charts of 13 adult patients with 
traumatic brain injury who received mannitol and 23.4% sodium chloride 
independently for the treatment of intracranial hypertension at San Francisco 
General Hospital between January and October 2003. Charts were reviewed to 
determine ICP, cerebral perfusion pressure, mean arterial pressure, serum sodium
values, and serum osmolarity before and after treatment with 23.4% sodium 
chloride and mannitol. Complications were noted.

RESULTS: The mean reductions in ICP after treatment were significant for both 
mannitol (P < 0.001) and hypertonic saline (P < 0.001); there were no 
significant differences between reductions in ICP when comparing the two agents 
(P = 0.174). The ICP reduction observed for hypertonic saline was durable, and 
its mean duration of effect (96 min) was significantly longer than that of 
mannitol treatment (59 min) (P = 0.016). No complications were associated with 
treatment with hypertonic saline.

CONCLUSION: This study suggests that 23.4% hypertonic saline is a safe and 
effective treatment for elevated ICP in patients after traumatic brain injury. 
These results warrant a rigorous evaluation of its efficacy as compared to 
mannitol in a prospective randomized controlled trial.
PMID: 16239885



Here rank order of effectiveness was  beta-hydroxybutyrate > glycerine > saline.

Jpn J Pharmacol. 2001 Oct;87(2):143-50.

Effect of beta-hydroxybutyrate, a cerebral function improving agent, on cerebral
hypoxia, anoxia and ischemia in mice and rats.

Suzuki M, Suzuki M, Sato K, Dohi S, Sato T, Matsuura A, Hiraide A. Shimizu 
Research Center, Research and Development Division, Shimizu Pharmaceutical Co., 
Ltd., Shizuoka, Japan.
Abstract

  Although improving energy metabolism in ischemic brain has been accepted for 
  the treatment of cerebrovascular diseases, administration of glucose, as an 
  energy substrate, would aggravate ischemic brain damage via activating 
  anaerobic glycolysis, which leads to lactate accumulation. 
  Beta-hydroxybutyrate (BHB) is one of the ketone bodies that can be utilized as
  an energy source during starvation. The purpose of our study was to define 
  the protective effects of BHB on brain damage induced by hypoxia, anoxia and 
  ischemia. The isotonic solution of BHB administered 30 min before the 
  induction of ischemia at doses over 50 mg x kg(-1) x h(-1) showed remarkable 
  protective effects against hypoxia and anoxia. BHB administered immediately 
  after a bilateral carotid artery ligation at a dose of 30 mg x kg(-1) x h(-1) 
  significantly suppressed the elevation of cerebral water and sodium contents 
  as well as maintaining high ATP and low lactate levels. In contrast, glycerin,
  a hypertonic agent, substantially reduced the water content but did not show 
  any significant effect on other parameters. We demonstrated that BHB, unlike 
  glycerin, when used as an energy substrate in ischemic brain, has protective 
  effects on cerebral hypoxia, anoxia and ischemia-induced metabolic change.
PMID: 11700013
Free text>
http://www.jstage.jst.go.jp/article/jjp/87/2/143/_pdf

Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=33220