Experimental Cerebral Effects of Intravenous Fluid Therapy

  • M. H. Zornow
Conference paper


Intracranial hypertension resulting from cerebral edema is a major cause of morbidity and mortality in patients with traumatic brain injury. In the noninjured brain, water movement between the vasculature and the brain parenchyma is determined primarily by osmolar gradients. Administration of hypertonic solutions such as mannitol or concentrated saline solutions produces a brain-to-plasma osmotic gradient favoring the movement of water out of the brain parenchyma and into the vessels. This osmotic gradient can be maintained due to the high reflection coefficients for sodium ions, chloride ions, and mannitol, which effectively prevent them from crossing the blood-brain barrier.

Cryogenic lesions have long been used to model the pathophysiology of traumatic brain injury. These lesions are highly reproducible and it is a simple matter to vary their intensity depending on the goals of the studies. Many of the histologic features of traumatic brain contusions are found in cryogenic lesions, including cytolysis of neurons, petechial hemorrhages, an inflammatory response as evidenced by the accumulation of monocytes and leukocytes, and the appearance of edematous tissue at the periphery of the lesion. Using cryogenic lesions, various investigators have examined the ability of hypertonic solutions to decrease brain edema and control intracranial hypertension. Although most studies have concluded that hypertonic saline is superior to isotonic solutions, there is little or no evidence that it is superior to more conventional therapy with an equiosmolar dose of mannitol.

One of the most promising new techniques for study of cerebral edema is the use of magnetic resonance imaging (MRI). This technology should allow the serial noninvasive measurement of regional brain water content. Additional studies are required to correlate MRI findings with more direct measures of brain water content.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Baxt WG, Moody P (1987) The differential survival of trauma patients. J Trauma 27:602–606PubMedCrossRefGoogle Scholar
  2. Cascino T, Baglivo J, Szewczykowski J, Posner JB, Rottenberg DA (1983) Quantitative CT assessment of furosemide- and mannitol- induced changes in brain water content. Neurology (Cleve) 33:898–903PubMedCrossRefGoogle Scholar
  3. Clasen RA, Brown DVL, Leavitt S, Hass GM (1953) The production by liquid nitrogen of acute closed cerebral lesions. Surg Gynecol Obstet 96:605–616PubMedGoogle Scholar
  4. Clasen RA, Prouty RR, Bingham WG, Martin FA, Hass GM (1957) Treatment of experimental cerebral edema with intravenous hypertonic glucose, albumin, and dextran. Surg Gynecol Obstet 104:591–606PubMedGoogle Scholar
  5. Fenstermacher JD (1984) Volume regulation of the central nervous system. In: Staub NC, Taylor AE (eds) Edema. Raven, New YorkGoogle Scholar
  6. Gazendam J, Go KG, van Zanten AK (1979) Composition of isolated edema fluid in cold-induced brain edema. J Neurosurg 51:70–77PubMedCrossRefGoogle Scholar
  7. Kaieda R, Todd MM, Warner DS (1989) Prolonged reduction in colloid oncotic pressure does not increase brain edema following cryogenic injury in rabbits. Anesthesiology 71:554–560PubMedCrossRefGoogle Scholar
  8. Klatzo I, Piraux A, Laskowski EJ (1955) The relationship between edema, blood-brain barrier and tissue elements in a local brain injury. J Neuropathol Exp Neurol 17:548–564CrossRefGoogle Scholar
  9. Kurtzke JF (1982) The current neurologic burden of illness and injury in the United States. Neurology (NY) 32:1207–1214PubMedCrossRefGoogle Scholar
  10. Marshall LF, Bowers SA (1985) Medical management of head injury. Clin Neurosurg 29:312–325Google Scholar
  11. Mintorovitch J, Yang GY, Shimizu H, Kucharczyk J, Chan PH, Weinstein PR (1994) Diffusion-weighted magnetic resonance imaging of acute focal cerebral ischemia: comparison of signal intensity with changes in brain water and Na+, K+-ATPase activity. J Cereb Blood Flow Metab 14:332–336PubMedCrossRefGoogle Scholar
  12. Orita T, Nishizaki T, Kamiryo T, Harada K, Aoki H (1988) Cerebral microvascular architecture following experimental cold injury. J Neurosurg 68:608–612PubMedCrossRefGoogle Scholar
  13. Peters RM, Hargens AR (1981) Protein vs electrolytes and all of the Starling forces. Arch Surg 116:1293–1298PubMedCrossRefGoogle Scholar
  14. Peters RM, Shackford SR, Hogan JS, Cologne JB (1986) Comparison of isotonic and hypertonic fluids in resuscitation from hypovolemic shock. Surg Gynecol Obstet 163:219–224PubMedGoogle Scholar
  15. Prough DS, Johnson JC, Poole GV, Stullken EH, Johnston WE, Royster R (1985) Effects on intracranial pressure of resuscitation from hemorrhagic shock with hypertonic saline versus lactated Ringer’s solution. Crit Care Med 13:407–411PubMedCrossRefGoogle Scholar
  16. Reulen HJ (1976) Vasogenic brain oedema. Br J Anaesth 48:741–751PubMedCrossRefGoogle Scholar
  17. Serieller MS, Zornow MH, Oh YS (1991) A comparison of the cerebral and hemodynamic effects of mannitol and hypertonic saline in a rabbit model of acute cryogenic brain injury. J Neurosurg Anesth 3:291–296CrossRefGoogle Scholar
  18. Schmoker J, Zhuang J, Shackford S (1991) Hypertonic fluid resuscitation improves cerebral oxygen delivery and reduces intracranial pressure after hemorrhagic shock. J Trauma 31:1607–1613PubMedCrossRefGoogle Scholar
  19. Starling EH (1896) On the absorption of fluids from the connective tissue spaces. J Physiol (Lond) 19:312–326PubMedGoogle Scholar
  20. Walsh JC, Zhuang J, Shackford SR (1991) A comparison of hypertonic to isotonic fluid in the resuscitation of brain injury and hemorrhagic shock. J Surg Res 50:284–292PubMedCrossRefGoogle Scholar
  21. Weed LH, McKibben PS (1919) Experimental alteration of brain bulk. Am J Physiol 48:531–555Google Scholar
  22. Zornow MH, Todd M, Moore S (1987) The acute cerebral effects of changes in plasma osmolality and oncotic pressure. Anesthesiology 67:936–941PubMedCrossRefGoogle Scholar
  23. Zornow MH, Scheller MS, Shackford SR (1989) Effect of a hypertonic lactated Ringer’s solution on intracranial pressure and cerebral water content in a model of traumatic brain injury. J Trauma 29:484–488PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • M. H. Zornow

There are no affiliations available

Personalised recommendations