DOCSLIB.ORG

Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach Review Article Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach Jerry Yee ,1 Naushaba Mohiuddin,2 Tudor Gradinariu,1 Junior Uduman,1 and Stanley Frinak1 Abstract Cerebral edema, in a variety of circumstances, may be accompanied by states of hyponatremia. The threat of brain injury from hypotonic stress-induced astrocyte demyelination is more common when vulnerable patients with hyponatremia who have end stage liver disease, traumatic brain injury, heart failure, or other conditions undergo overly rapid correction of hyponatremia. These scenarios, in the context of declining urinary output from CKD and/or AKI, may require controlled elevations of plasma tonicity vis-a`-vis increases of the plasma sodium concentration. We offer a strategic solution to this problem via sodium-based osmotherapy applied through a conventional continuous RRT modality: predilution continuous venovenous hemofiltration. KIDNEY360 1: 281–291, 2020. doi: https://doi.org/10.34067/KID.0000382019 Introduction continuous venovenous hemofiltration (CVVH) (11,12), Generally, sodium-based osmotherapy (SBO) is tonicity continuous venovenous hemodialysis (13), or con- therapy with the aim of reducing cerebral edema during tinuous venovenous hemodiafiltration (14). states of hypotonic hyponatremia. Depending on the circumstance, plasma tonicity may be increased or decreased. Because the sodium concentration ([Na]) General Principles of SBO in the plasma at any time (t), PNa(t), and accompa- SBO can be implemented as a stepwise approach nying anions constitute the bulk of plasma tonicity, based on established biophysical principles govern- SBOispredicatedongradualalterationofPNa,in ing sodium transit via predilution CVVH. The follow- contrast to the relatively rapid PNa increases imposed ing urea- and sodium-based kinetic methodology by steep dialysate-to-plasma [Na] gradients associ- involves six steps: (1) establishing a time-dependent ∇ ated with conventional hemodialysis. Generally, [Na] gradient [ Na(t)] between the plasma and a fl osmotherapy is carried out when there is severe hypo- replacement uid (RF) based on a sodium concentra- natremia, oligo-anuria, and inability to excrete sufficient tion adjustment ratio (NaAR) (Figure 1), (2)estima- electrolyte-free water to maintain isotonicity (1–3). Thus, tion of total body water (TBW), (3) determination of SBO has played a role in patients with end stage liver sodium ion dialysance (DNa)thatapproximatesthe fi disease and advanced heart failure. urea hemo lter transfer rate, (4) on-treatment predic- Osmotic demyelination syndrome may transpire in tion of PNa(t), (5) determination of sodium balance, and patients who are hyponatremic with end stage liver (6)troubleshooting. disease after abrupt PNa elevations during orthotopic liver transplantation (4,5). Correspondingly, presurgical Predilution CVVH fi elevation of PNa among individuals prone to osmotic RF is infused postblood pump and prehemo lter at a fi fl demyelination may be prophylactic. Less commonly, speci ed rate (QRF)intotheplasma ow (QP)toraise supranormal PNa elevations have been imposed during (or lower) PNa from its pretreatment level, NaPre or traumatic brain injury or intracerebral hemorrhage to PNa(0), to its post-treatment level, NaPost or PNa(t) reduce brain swelling (6,7). (Figure 1). Employing a fixed-volume model where To rectify severe plasma hypotonicity, a relatively TBW volume is constant and analogizing to estab- hypertonic/hypernatric solution is administered in a lished urea kinetic principles, the rate change of PNa controlled fashion during continuous renal replacement can be computed over a specified time interval therapy (CRRT), and PNa is increased at rates consis- (15,16). Thus, sodium advected from the RF gradually tent with consensus guidelines (8). Controlled PNa increases NaPre to NaPost, with their difference equal- elevations can be achieved by hemodialysis, but spe- ing DNa (Equation 1). cial device- and protocol-specificmodifications are To produce an [Na] gradient, a stock RF (RF1) of required to avoid dialysis disequilibrium syndrome nominal [Na] NaRF1 is adjusted to NaRF2, thereby (9). Sustained low-efficiency dialysis or slow contin- establishing ∇Na(0), the maximal [Na] gradient at time uous ultrafiltration with simultaneous infusion of a (0) (Equation 2). DNa is also the product of ∇Na(0) and D ∇ solution relatively hypernatric to PNa is also feasible NaAR, and NaAR is the ratio of Na to Na(0) (Equa- (10). In terms of CRRT, SBO has been conducted with tion 3). 1Division of Nephrology and Hypertension, Henry Ford Hospital, Detroit, Michigan; and 2St. Clair Specialty Physicians, Roseville, Michigan Correspondence: Dr. Jerry Yee, Division of Nephrology and Hypertension, Henry Ford Hospital, 2799 West Grand Boulevard, CFP-514, Detroit, MI 48202. Email: [email protected] www.kidney360.org Vol 1 April, 2020 Copyright © 2020 by the American Society of Nephrology 281 282 KIDNEY360 Replacement RF2 Fluid ∇Na(t) NaRF2 Q QP RF2 PNa(t) Hemofilter Blood Pump DNa·t DNa – NaAR=1–e V QP – QUF QRF2 + QUF Figure 1. | Plasma sodium concentration is exponentially changed by the replacement fluid sodium concentration and flow rates of plasma, replacement fluid, and ultrafiltration. The extracorporeal circuit is comprised of a hemofilter and replacement fluid. The plasma inflow rate (QP) ∇ is advected by a sodium concentration [Na]-adjusted replacement fluid (NaRF2). The sodium concentration [Na] gradient, Na(t), equals the [Na] difference between NaRF2 and plasma sodium concentration at any time (t), PNa(t). The sodium concentration adjustment ratio (NaAR) is defined by sodium ion dialysance (DNa), time, and total body water volume (Watson volume, V). Hemofilter effluent equals the sum of RF2 flow rate ∇ (QRF2) and net ultrafiltration flow rate (QUF). Na(t), [Na] gradient at time (t) or PNa(t)-to-NaRF2 difference; RF2, [Na]-adjusted replacement fluid 2. DNa 5 NaPost 2 NaPre (Equation 1) Step 1: Establishing the Sodium Concentration Gradient ∇ ð0Þ 5 2 Na NaRF2 NaPre (Equation 2) Replacement Fluids ∇ To generate Na(0), the sodium-adjusted RF [Na], NaRF2, NaAR5 DNa=∇Nað0Þ 5 ðNaPost 2 NaPreÞ=ðNaRF2 2 NaPreÞ is often simply assigned an [Na] that is 6–10 mM greater than (Equation 3) NaPre.However,NaRF2 can be more rationally determined from intrinsic parameters of predilution CVVH (Tables 1 and D fi 2). First, by predetermining a target NaPost, Na is de ned. Sodium Kinetic Principles Second, estimation of NaAR from URR (Equations 3 and 4) The NaAR is a function of treatment time (t), TBW (V, and rearrangement of Equation 3 yields NaRF2 as Equation 5. Watson volume), and D . The NaAR is similar to the urea Na 5 1 ðD = Þ reduction ratio (URR, Equation 4), with equivalence of NaRF2 NaPre Na NaAR (Equation 5) DNa to the urea clearance constant, KUrea (Equation 4, A and B). In summary, urea kinetics function to approximate NaAR. These principles are illustrated by the following example. Case 1. A 42-year-old man, 178 cm and 90 kg, is anuric URR 5 ðBUNð0Þ 2 BUNðtÞÞ=ðBUNð0Þ 2 BUN Þ Dialysate with stage 3 AKI. He has no peripheral edema. Laboratory 2 z = 5 5 2 KUrea t V ð Þ URR 1 e Equation 4A data: NaPre, 116 mM; BUN(0), 80 mg/dl; hematocrit, 0.25. The target BUN and PNa after 24 hours of CVVH are 48 mg/dl and 124 mM, respectively. First, NaAR approximating URR 2 z = 5 2 DNa t V “ ” NaAR 1 e (Equation 4B) is calculated, with BUNDialysate as zero. KIDNEY360 1: 281–291, April, 2020 Sodium-Based Osmotherapy, Yee et al. 283 Table 1. Sodium-based osmotherapy parameters Row Parameter Definition Units 1 DNa Post-treatment [Na] minus mmol/l, mM pretreatment [Na] 2 ∇Na(0) [Na] gradient at time (t)50 mmol/l, mM 3 [Na] Sodium concentration mmol/l, mM 4 SNa Sodium balance mmol 5DNa Dialysance of sodium ion ml/min fl 6 Eff-NaRF Effective replacement uid [Na] from mmol/l, mM combined infusions of NaRF1 and NaH 7 NaAR Sodium concentration adjustment Dimensionless ratio fi 8NaH [Na] of a de ned hypo-, iso-, mmol/l, mM hypertonic solution H 9NaPre Pretreatment PNa, i.e., PNa(0) mmol/l, mM 10 NaPost End treatment PNa mmol/l, mM 11 NaRF1 RF1 [Na], unadjusted replacement mmol/l, mM fluid 12 NaRF2 RF2 [Na], sodium-adjusted mmol/l, mM replacement fluid 13 PNa(t) Plasma [Na] at time (t) mmol/l, mM fl 14 QH Solution H ow rate ml/min fl 15 QB,QP Respective blood and plasma uid ml/min flow rates fl fl 16 QRF Replacement uid ow rate ml/min fi fl 17 QUF Net ultra ltration ow rate ml/min fl 18. QEff Combined ow rate of QRF1 and QH ml/min 19 RF1 Replacement fluid 1 — 20 RF2 Replacement fluid 2 — 21 t Time min 22 URR Urea reduction ratio Dimensionless 23 V Total body water, i.e., Watson volume ml, L 24 V4M Volume of added hypertonic saline ml, L (23.4%, 4 M) 25 VRF1 Volume of RF1 ml, L 26 VRF2 Volume of RF2 ml, L 27 VW Volume of added sterile water ml, L Variables and abbreviations used in text and equations. NaAR URR 5 ðBUNð0Þ 2 BUNð1440ÞÞ=BUNð0Þ Replacement Fluid Manipulation 5 ð80 2 48Þmg=dl=80mg=dl 5 0:4 In predilution CVVH SBO, the NaRF1 is frequently low- ered from a nominal level of 130 or 140 mM. For Case 1, D ∇ Na can be adjusted to an Na of 136 mM by several Second, after NaAR is determined, Na, Na(0), and NaRF2 RF1 RF2 are calculated. methods (Figure 3) (11,12): method 1, diluting RF1 (NaRF1 140 mM) with 147 ml sterile water; method 2, exchanging 143 ml of RF1 (Na 140 mM) for sterile water; and method D 5 2 5 2 5 RF1 Na NaPost NaPre 124 mM 116 mM 8 mM 3, addition of 7.8 ml of 4 M saline (23.4%) to 5 L of RF1 ∇Nað0Þ 5 DNa=NaAR 5 8 mM=0:4 5 20 mM solution (NaRF1 130 mM).
Load more

Recommended publications
  • Driving Cerebral Perfusion Pressure with Pressors: How, Which, When?
    Driving Cerebral Perfusion Pressure with Pressors: How, Which, When? J. A. MYBURGH Department of Intensive Care Medicine, The St George Hospital, Sydney, NEW SOUTH WALES ABSTRACT In traumatic brain injury, cerebral hypoperfusion is associated with adverse outcome, particularly in the early phases of management. This has resulted in the increased use of drugs such as adrenaline, noradrenaline, dopamine and phenylephrine to augment or maintain systemic blood pressures at near normal levels. This is now part of standard practice and is endorsed by the Brain Trauma Foundation guidelines. It probably matters little which agent is used, provided appropriate monitoring is in place and those reversible causes of hypotension are promptly excluded and treated. However, blindly applying management guidelines to all patients may negate these early benefits. The time has come move away from artificially separated concepts of “intracranial pressure” versus “cerebral perfusion pressure” based strategies. These should be considered in parallel and applied to an individual patient, rather than making the patient fit into an all-encompassing treatment algorithm. A paradigm shift from a “set and forget” philosophy to one of “titration against time” to achieve appropriate therapeutic targets is now required. In this context the rational use of vasoactive agents to optimise cerebral perfusion pressure may be employed. On the basis of limited animal and human evidence, noradrenaline appears to be the most appropriate catecholamine for traumatic brain injury, although definitive, targeted trials are required. (Critical Care and Resuscitation 2005; 7: 200-205) Key words: Cerebral perfusion, inotropic agents, resuscitation, head injury, review The recognition of the importance of defending simplistic.
    [Show full text]
  • Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood- Brain Barrier Disruption After Experimental Stroke in Mice
    RESEARCH ARTICLE Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood- Brain Barrier Disruption after Experimental Stroke in Mice Emil Zeynalov1*, Susan M. Jones1, Jeong-Woo Seo1, Lawrence D. Snell2, J. Paul Elliott3 1 Swedish Medical Center, Neurotrauma Research, Englewood, Colorado, United States of America, 2 Colorado Neurological Institute, Englewood, Colorado, United States of America, 3 Colorado Brain and Spine Institute, Englewood, Colorado, United States of America a11111 * [email protected] Abstract OPEN ACCESS Background Citation: Zeynalov E, Jones SM, Seo J-W, Snell LD, Stroke is a major cause of morbidity and mortality. Stroke is complicated by brain edema Elliott JP (2015) Arginine-Vasopressin Receptor and blood-brain barrier (BBB) disruption, and is often accompanied by increased release of Blocker Conivaptan Reduces Brain Edema and arginine-vasopressin (AVP). AVP acts through V1a and V2 receptors to trigger hyponatre- Blood-Brain Barrier Disruption after Experimental Stroke in Mice. PLoS ONE 10(8): e0136121. mia, vasospasm, and platelet aggregation which can exacerbate brain edema. The AVP doi:10.1371/journal.pone.0136121 receptor blockers conivaptan (V1a and V2) and tolvaptan (V2) are used to correct hypona- Editor: Muzamil Ahmad, Indian Institute of Integrative tremia, but their effect on post-ischemic brain edema and BBB disruption remains to be elu- Medicine, INDIA cidated. Therefore, we conducted this study to investigate if these drugs can prevent brain Received: May 25, 2015 edema and BBB disruption in mice after stroke. Accepted: July 29, 2015 Methods Published: August 14, 2015 Experimental mice underwent the filament model of middle cerebral artery occlusion Copyright: © 2015 Zeynalov et al.
    [Show full text]
  • Critical Care and Resuscitation • Volume 11 Number 2 • June 2009 151 POINTS of VIEW
    POINTS OF VIEW Mannitol or hypertonic saline for intracranial hypertension? A point of view Luis B Castillo, Guillermo A Bugedo and Jorge L Paranhos Osmotically active solutions have been used for more than ABSTRACT 30 years in the treatment of intracranial hypertension. The traditional agent of choice has been mannitol, but hyper- Osmotically active solutions, particularly mannitol, have tonicCrit saline Care has Resusc recently ISSN: emerged 1441-2772 as an1 Junealternative. Here, been used for more than 30 years in the treatment of we discuss2009 11 the2 151-154 systemic and cerebral effects of these two intracranial hypertension. Recently hypertonic saline has ©Crit Care Resusc 2009 substances,www.jficm.anzca.edu.au/aaccm/journal/publi- as well as their side effects and complications, emerged as an alternative to mannitol. Both solutions are and cations.htmmake recommendations about their clinical use. used worldwide, and their indications and long-term side Points of View effects are well known. More recently, knowledge about their effects has increased, both limiting and expanding Mannitol their clinical use. Here, we compare the systemic and Mannitol has been the agent of choice in osmotherapy for cerebral effects of mannitol and hypertonic saline, as well as cerebral injury since the 1960s. It is a mannose-derived their side effects and complications. Finally, we make simple alcohol, which is easy to prepare and use, stable in recommendations about their clinical use. solution, inert, not metabolised, freely filtered by the kidneys without being reabsorbed, and low in toxicity. Its Crit Care Resusc 2009; 11: 151–154 distribution volume corresponds to the extracellular com- partment.1-7 The effects of mannitol on the central nervous For editorial comment, see page 94 system have been well described, but the mechanisms are still not completely understood.
    [Show full text]
  • Critical Care Management and Monitoring of Intracranial Pressure
    REVIEW J Neurocrit Care 2016;9(2):105-112 https://doi.org/10.18700/jnc.160101 eISSN 2508-1349 Critical Care Management and Monitoring of Intracranial대한신경집중치료학 Pressure회 Jeremy Ragland, MD and Kiwon Lee, MD, FACP, FAHA, FCCM Division of Critical Care, Department of Neurological Surgery, The University of Texas Health Science Center at Houston, Neuroscience and Neurotrauma Intensive Care Unit, Memorial Hermann Texas Medical Center, The Mischer Neuroscience Institute, Houston, Texas, USA Patients with brain injury of any etiology are at risk for developing increased intracranial Received December 15, 2016 pressure. Acute intracranial hypertension is a medical emergency requiring immediate Revised December 16, 2016 intervention to prevent permanent damage to the brain. Intracranial pressure as an absolute Accepted December 16, 2016 value is not as valuable as when one investigates other important associated variables such Corresponding Author: as cerebral perfusion pressure and contributing factors for an adequate cerebral blood flow. Kiwon Lee, MD, FACP, FAHA, FCCM This manuscript reviews a number of various interventions that can be used to treat acute Division of Critical Care, Neuroscience intracranial hypertension and optimize cerebral perfusion pressure. Management options and Neurotrauma Intensive Care Unit, are presented in an algorithm-format focusing on current treatment strategies and treatment The University of Texas Health Science goals. In addition to the efficacy, clinicians must consider significant adverse events that are Center at Houston, Memorial Hermann associated with each therapy prior to initiating treatment. The initial step includes elevation Texas Medical Center, The Mischer of head of the bed and adequate sedation followed by osmotic agents such as mannitol and Neuroscience Institute, 6431 Fannin St.
    [Show full text]
  • Fluids and the Neurosurgical Patient
    Anesthesiology Clin N Am 20 (2002) 329–346 Fluids and the neurosurgical patient Concezione Tommasino, MD* Institute of Anesthesiology and Intensive Care, University of Milano, Department of Anesthesia and Intensive Care, San Raffaele Hospital, Via Olgettina, 60 20132, Milano, Italy The fluid management of neurosurgical patients presents special challenges for anesthesiologists and intensivists [1]. Neurosurgical patients often receive diu- retics (eg, mannitol, furosemide) to treat cerebral edema and/or to reduce intracranial hypertension. Conversely, they may also require large amounts of intravenous fluids to correct preoperative dehydration and/or to maintain intra- operative and postoperative hemodynamic stability as part of therapy for vaso- spasm, for blood replacement, or for resuscitation. For a long time restrictive fluid management has been the treatment of choice in patients with brain pathology, growing from fear that fluid administration could enhance cerebral edema [2]. It is well known that fluid restriction, if pursued to excess (hypovolemia), may result in episodes of hypotension, which can increase intracranial pressure (ICP) and reduce cerebral perfusion pressure, and the consequences can be devastating [3]. It is unfortunate that little substantial human data exist concerning the impact of fluids on the brain, or which can guide rational fluid management in neurosurgical patients. However, it is possible to examine those factors that influence water movement into the brain, and to make some reasonable recommendations. This review will address some of the physical determinants of water move- ment between the intravascular space and the central nervous system (CNS). Subsequent sections will address specific clinical situations with suggestions for the types and volume of fluids to be administered.
    [Show full text]
  • Reduction of Cerebral Edema After Traumatic Brain Injury Using an Osmotic Transport Device
    JOURNAL OF NEUROTRAUMA XX:1–7 (Month XX, 2014) ª Mary Ann Liebert, Inc. DOI: 10.1089/neu.2014.3439 Reduction of Cerebral Edema after Traumatic Brain Injury Using an Osmotic Transport Device Devin W. McBride,1 Jenny I. Szu,2 Chris Hale,1 Mike S. Hsu,2 Victor G.J. Rodgers,1 and Devin K. Binder 2 Abstract Traumatic brain injury (TBI) is significant, from a public health standpoint, because it is a major cause of the morbidity and mortality of young people. Cerebral edema after a TBI, if untreated, can lead to devastating damage of the remaining tissue. The current therapies of severe TBI (sTBI), as outlined by the Brain Trauma Foundation, are often ineffective, thus a new method for the treatment of sTBI is necessary. Herein, the reduction of cerebral edema, after TBI, using an osmotic transport device (OTD) was evaluated. Controlled cortical impact (CCI) was performed on adult female CD-1 mice, and cerebral edema was allowed to form for 3 h, followed by 2 h of treatment. The treatment groups were craniectomy only, craniectomy with a hydrogel, OTD without bovine serum albumin (BSA), and OTD. After CCI, brain water content was significantly higher for animals treated with a craniectomy only, craniectomy with a hydrogel, and OTD without BSA, compared to that of control animals. However, when TBI animals were treated with an OTD, brain water content was not significantly higher than that of controls. Further, brain water content of TBI animals treated with an OTD was signifi- cantly reduced, compared to that of untreated TBI animals, TBI animals treated with a craniectomy and a hydrogel, and TBI animals treated with an OTD without BSA.
    [Show full text]
  • Serum Sodium Values and Their Association with Adverse Outcomes in Moderate-Severe Traumatic Brain Injury (TBI)
    University of Massachusetts Medical School eScholarship@UMMS UMass Center for Clinical and Translational 2012 UMass Center for Clinical and Science Research Retreat Translational Science Research Retreat May 22nd, 4:30 PM - 6:00 PM Serum sodium values and their association with adverse outcomes in moderate-severe traumatic brain injury (TBI) Lucia Rivera Lara University of Massachusetts Medical School Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/cts_retreat Part of the Anesthesiology Commons, Clinical Epidemiology Commons, Health Services Research Commons, Neurology Commons, Surgery Commons, and the Trauma Commons Repository Citation Rivera Lara L, Muehlschlegel S, Carandang RA, Ouillette C, Hall WR, Anderson FA, Goldberg RJ. (2012). Serum sodium values and their association with adverse outcomes in moderate-severe traumatic brain injury (TBI). UMass Center for Clinical and Translational Science Research Retreat. https://doi.org/ 10.13028/40gv-kp57. Retrieved from https://escholarship.umassmed.edu/cts_retreat/2012/posters/55 Creative Commons License This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License. This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in UMass Center for Clinical and Translational Science Research Retreat by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. SERUM SODIUM VALUES AND THEIR ASSOCIATION WITH ADVERSE OUTCOMES IN MODERATE-SEVERE TRAUMATIC BRAIN INJURY (TBI) Lucia Rivera-Lara1; Susanne Muehlschlegel, MD, MPH1,2,3; Raphael Carandang, MD1,3; Cynthia Ouillette, RN1; Wiley Hall, MD1,3; Fred Anderson, PhD 3,4; Robert Goldberg, PhD5 Departments of 1Neurology (Div.
    [Show full text]
  • Medical Management of Cerebral Edema
    Neurosurg Focus 22 (5):E12, 2007 Medical management of cerebral edema AHMED RASLAN, M.D.,1 AND ANISH BHARDWAJ, M.D.1, 2, 3 Departments of 1Neurological Surgery, 2Neurology, and 3Anesthesiology and Peri-Operative Medicine, Oregon Health and Science University, Portland, Oregon PCerebral edema is frequently encountered in clinical practice in critically ill patients with acute brain injury from diverse origins and is a major cause of increased morbidity and death in this subset of patients. The consequences of cerebral edema can be lethal and include cerebral ischemia from compro- mised regional or global cerebral blood flow (CBF) and intracranial compartmental shifts due to intracra- nial pressure gradients that result in compression of vital brain structures. The overall goal of medical management of cerebral edema is to maintain regional and global CBF to meet the metabolic require- ments of the brain and prevent secondary neuronal injury from cerebral ischemia. Medical management of cerebral edema involves using a systematic and algorithmic approach, from general measures (optimal head and neck positioning for facilitating intracranial venous outflow, avoidance of dehydration and sys- temic hypotension, and maintenance of normothermia) to specific therapeutic interventions (controlled hyperventilation, administration of corticosteroids and diuretics, osmotherapy, and pharmacological cere- bral metabolic suppression). This article reviews and highlights the medical management of cerebral edema based on pathophysiological principles in acute brain injury. KEY WORDS • cerebral blood flow • cerebral edema • controlled hyperventilation • intracranial pressure • osmotherapy EREBRAL edema, simply defined as an increase in tion of these fundamental subtypes of edema, although brain water content (above the normal brain water one can predominate depending on the type and duration C content of approximately 80%) and invariably a re- of injury.
    [Show full text]
  • Therapy for Cerebral Edema Possible New Mechanism Underlying
    Possible new mechanism underlying hypertonic saline therapy for cerebral edema Adam Chodobski Journal of Applied Physiology 100:1437-1438, 2006. doi:10.1152/japplphysiol.01560.2005 You might find this additional information useful... This article cites 10 articles, 1 of which you can access free at: http://jap.physiology.org/cgi/content/full/100/5/1437#BIBL Medline items on this article's topics can be found at http://highwire.stanford.edu/lists/artbytopic.dtl on the following topics: Chemistry .. Osmosis Physiology .. Rats Neuroscience .. Brain Edema Medicine .. Brain Injuries Medicine .. Edema Medicine .. Epidemiology Updated information and services including high-resolution figures, can be found at: http://jap.physiology.org/cgi/content/full/100/5/1437 Downloaded from Additional material and information about Journal of Applied Physiology can be found at: http://www.the-aps.org/publications/jappl This information is current as of April 14, 2006 . jap.physiology.org on April 14, 2006 Journal of Applied Physiology publishes original papers that deal with diverse areas of research in applied physiology, especially those papers emphasizing adaptive and integrative mechanisms. It is published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2005 by the American Physiological Society. ISSN: 8750-7587, ESSN: 1522-1601. Visit our website at http://www.the-aps.org/. J Appl Physiol 100: 1437–1438, 2006; doi:10.1152/japplphysiol.01560.2005. Invited Editorial Possible new mechanism underlying hypertonic saline therapy for cerebral edema ϩ ϩ Ϫ CEREBRAL EDEMA IS A SIGNIFICANT cause of mortality in patients activity of the Na -K -2Cl cotransporter, an important cell with traumatic brain injury and ischemic or hemorrhagic volume regulator, and its ability to affect the function of the stroke.
    [Show full text]
  • The Management of Brain Edema in Brain Tumors Evert C.A
    The management of brain edema in brain tumors Evert C.A. Kaal and Charles J. Vecht This review focuses on pathophysiology, clinical signs, and Introduction imaging of brain edema associated with intracranial tumors Brain edema is a prominent feature of brain cancer and and its treatment. Brain edema in brain tumors is the result of often contributes to neurologic dysfunction and impaired leakage of plasma into the parenchyma through dysfunctional quality of life. This review focuses on treatment of brain cerebral capillaries. The latter type of edema (ie, vasogenic edema in brain tumors. Clinical features of patients with edema) and the role of other types in brain tumors is brain tumors are discussed, followed by pathologic and discussed. Vascular endothelial growth factor-induced pathophysiologic aspects of brain edema, and methods dysfunction of tight junction proteins probably plays an for diagnosing its presence. The practice of corticoste- important role in the formation of edema. Corticosteroids are roid administration, corticosteroid dependency, and the mainstay of treatment of brain edema. When possible, withdrawal effects are discussed, together with a number corticosteroids should be used in a low dose (eg, 4mg of new agents that can influence the development of dexamethasone daily) to avoid serious side effects such as brain edema. myopathy or diabetes. Higher doses of dexamethasone (16 mg/day or more), sometimes together with osmotherapy Clinical presentation (mannitol, glycerol) or surgery, may be used in emergency Papilledema, occipital headache worsening in the morn- situations. On tapering, one should be aware of the possible ing, nausea and vomiting, abnormal eye movements, and development of corticosteroid dependency or withdrawal impaired consciousness are the classic signs of raised in- effects.
    [Show full text]
  • Manucher Javid, Urea, and the Rise of Osmotic Therapy for Intracranial Pressure
    LEGACY—INSTITUTIONS AND PEOPLE TOPIC LEGACY—INSTITUTIONS AND PEOPLE Manucher Javid, Urea, and the Rise of Osmotic Therapy for Intracranial Pressure Therapy with hypertonic solutions is one of the mainstays of neurosurgical treatment Brandon G. Rocque, MD, MS for all types of neurological injury. Although the initial research with hypertonic agents in the early decades of the 20th century showed great promise for these agents to Department of Neurological Surgery, Uni- versity of Wisconsin, Madison, Wisconsin lower intracranial pressure, this research also showed a considerable rate of adverse effects and complications. By the 1940s and 1950s, hypertonic therapy had been dis- Correspondence: counted as unsafe and was rarely used in neurosurgery. In the late 1950s, Manucher J. Brandon G. Rocque, MD, 600 Highland Ave, K4/822, Javid and Paul Settlage at the University of Wisconsin began experimenting with Madison, WI 53711. infusions of urea as an agent to control intracranial pressure. Their experiments were E-mail: [email protected] wildly successful, and urea became a drug of major importance to neurosurgeons worldwide in only a few years. This article chronicles the work of Javid and Settlage, Received, January 21, 2011. Accepted, October 19, 2011. including a discussion of the early research on hypertonic agents, the initial difficulty Published Online, November 8, 2011. the Wisconsin researchers had in disseminating their results, the widespread acceptance that followed, and the impact that these discoveries had on the neurosurgical com- ª Copyright 2011 by the munity. The prominent place that hypertonic agents now hold in the armamentarium of Congress of Neurological Surgeons neurosurgeons is owed to the work of Dr Javid, as illustrated in this historical analysis.
    [Show full text]
  • Effects of Conivaptan Versus Mannitol on Post-Ischemic Brain Injury and Edema
    Eurasian J Med 2019; 51(1): 42-8 Original Article Effects of Conivaptan versus Mannitol on Post-Ischemic Brain Injury and Edema Betul Can1 , Semih Oz2 , Varol Sahinturk3 , Ahmet Musmul4 , İbrahim Ozkan Alatas1 ABSTRACT Objective: The aim of this study was to compare the effects of conivaptan, an arginine vasopressin antago- nist, and mannitol, a sugar alcohol, on cerebral ischemia-induced brain injury and edema in rats. Materials and Methods: Fifty-eight 8-week-old male Sprague Dawley rats were randomly divided into five groups: control, ischemia–reperfusion (I/R)+saline, I/R+mannitol, I/R+10 mg/ml conivaptan, and I/R+20 mg/ ml conivaptan. Cerebral ischemia was induced by common carotid artery occlusion for 30 minutes. Saline, mannitol, or conivaptan were administered intravenously at the onset of reperfusion. Blood and brain tissue samples were taken at the 6th hour of reperfusion. The electrolytes (Na+–K+–Cl−), osmolality, arginine va- sopressin, albumin, progranulin (PGRN), neuron-specific enolase (NSE), and myeloperoxidase activity were measured in rat serum samples. Brain frontal/hippocampal sections were stained with hematoxylin–eosin and TUNEL techniques to evaluate histopathological changes. Results: Statistical analyses revealed that conivaptan caused significant changes in the electrolyte, NSE, and PGRN levels and osmolality when compared with mannitol. Conivaptan treatment showed positive effects on serum biochemistry and tissue histology. Cite this article as: Can B, Oz S, Sahinturk V, Musmul A, Alatas IO. Effects of Conivaptan versus Conclusion: Our findings revealed that conivaptan shows more diuretic activity than mannitol and triggers Mannitol on Post-Ischemic Brain Injury and Edema. neither any damages nor edema in the brain tissue.
    [Show full text]