dialysis brain injury davenport.pdf

Review Article Practical guidance for dialyzing a hemodialysis patient following acute brain injury Andrew DAVENPORT UCL Center for Nephrology, Royal Free & University College Medical School, London, UK Abstract The incidence of acute brain injury in chronic hemodialysis patients is increasing, as the dialysis population is becoming increasingly older, often hypertensive, at risk of ischemic and/or hemor- rhagic stroke, and subdural hemorrhage.
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  Review Article Practical guidance for dialyzing ahemodialysis patient following acutebrain injury Andrew DAVENPORT UCL Center for Nephrology, Royal Free & University College Medical School, London, UK  Abstract The incidence of acute brain injury in chronic hemodialysis patients is increasing, as the dialysispopulation is becoming increasingly older, often hypertensive, at risk of ischemic and/or hemor-rhagic stroke, and subdural hemorrhage. Standard intermittent hemodialysis treatments typicallylead to an increase in cerebral swelling, which can exacerbate underlying cerebral damage. In crit-ically ill patients, continuous modes of renal replacement therapy may be required, but dependingupon the clinical condition, simple modifications to standard intermittent therapies may suffice, andalloweffectivedeliveryofrenalreplacementtherapy,butensurethatpatientoutcomes bothin termsof mortality and residual functional brain damage is no different between those with normal renalfunction and those on the chronic dialysis program. Key words:  Hemodialysis, stroke, subdural, intracranial hemorrhage, anticoagulation INTRODUCTION Over the last decade, the age of the average hemodialysispatient has increased, and these elderly patients are at risk of both ischemic and hemorrhagic stroke due to their increasedburden of atherosclerotic disease and hypertension. 1,2 In addition, the number of patients developing sub-dural hemorrhages has also increased over the lastdecade, 3 whether this is due to the increasing use of cou-marin anticoagulants for atrial fibrillation and othercardiac conditions, and also catheter access problemshas yet to be determined.Standard intermittent hemodialysis has been repeat-edly shown to increase cerebral water content in chronicdialysis patients attending for outpatient treatment. 4 Theretention of waste products of metabolism and acidosisthat develops in end-stage kidney failure leads to in-creased plasma, extracellular, and intracellular osmolality.In the brain, the astrocytes play a key role in maintainingextracellular homeostasis. These cells respond to changesin extracellular fluid tonicity by regulating Na/K ex-change, and by accumulating intracellular osmoles, notonly urea but also other retained osmolytes, by producingglycine, glycerol, myoinositol, and sorbitols, 5 which en-able these cells to regulate cerebral extracellular volume.However, during hemodialysis there is a rapid reductionin plasma urea and osmolality. This sets up a diffusiongradient between the plasma, which has a lower ureaconcentration, and the cerebral extracellular space andthe neurons and glial cells. As water moves transcellularly some 20 times faster than urea, 6 water moves along thisosmotic gradient, back across the blood brain barrier intothe cerebral extracellular tissues, where it is initially takenup by the astrocytes and other glial cells, causing cellswelling.During hemodialysis, there is a rapid correction of theplasma acidosis, due to the diffusion of bicarbonate fromthe dialysate, and at the same time carbon dioxide is lost Correspondence to: A. Davenport, UCL Center forNephrology, Royal Free & University College MedicalSchool, Hampstead Campus, Rowland Hill Street, LondonNW3 2PF, UK.E-mail: Hemodialysis International  2008;  12 :307–312 r 2008 The Authors. Journal compilation r 2008 International Society for Hemodialysis  307  to the dialysate. As bicarbonate is charged, it cannotreadily traverse cell membranes, whereas carbon dioxideis freely diffusible. 7 The relative concentration of bicar-bonate to carbon dioxide, affects pH, 8 pH ¼ pK 0 þ log ½ HCO  3  = ½ H 2 CO 3  and thus it is possible that the rapid passage of bicarbon-ate into the plasma, with some losses of CO 2  into the di-alysate, can lead to an imbalance, with the developmentof a paradoxical intracellular acidosis, 7 due to the trans-port of CO 2  across the blood-brain barrier, 9 which thenexacerbates cerebral astrocyte idiogenic osmole genera-tion and increases water uptake by the cells. CEREBRAL BLOOD FLOW INHEMODIALYSIS PATIENTS Cerebral blood flow, as assessed by transcranial Dopplermeasurements of the middle cerebral artery, decreaseswith age. 10 Similar studies in healthy nonanemic hemo-dialysis patients have shown that cerebral blood flow iseither normal or decreased, 11 with reduced regional cor-tical oxygen supply. Although cerebral blood flow hasbeen shown to respond appropriately to changes in arte-rial carbon dioxide tensions, 12 intradialytic hypotensionshould be avoided, as patients with or at risk of cerebraledema are at increased risk of surges in intracranial pres-sure and reduction in cerebral perfusion pressure, asso-ciated with intradialytic hypotension (Figure 1).During hemodialysis, middle cerebral blood flow fallswith increasing ultrafiltration. 10 Oxygen saturation ini-tially falls during dialysis, and patients may also hypo-ventilate, 13 so patients should be monitored and providedwith supplemental oxygen where appropriate to maintaincerebral oxygen delivery. RENAL REPLACEMENT SUPPORT  Although changes occur to cerebral blood flow and ox-ygen delivery during dialysis therapies, with carefulthought and adjusting treatment the patient survivaland outcome should be similar to that of the nondialy-sis patient. 14 INTERMITTENT HEMOFILTRATION AND/OR DIALYSIS  All standard intermittent therapies, hemofiltration, hemo-dialysis, and hemodiafiltration, will lead to increased ce-rebral swelling, and if the patient has suffered a severeinjury and is unconscious, then most centers would deemcontinuous renal replacement or hybrid therapies as thepreferred treatment. 15 However, if the patient is con-scious, and the brain computed tomography scan only shows limited cerebral damage with no evidence of edema (Figure 2), then many centers would consider in-termittent therapies. 5090110706 8 10 12Time (hrs)0204060    M   A   P  m  m   H  g M e anI   C P mmH g intermittent hemodialysis Figure1  Fall in mean arterial blood pressure (MAP) at thestart of renal replacement therapy, associated with anincrease in intracranial pressure (ICP) and fall in cerebralperfusion pressure (CPP) in a hemodialysis patient postneurosurgical evacuation of subdural hemorrhage. Figure2  Unenhanced computed tomography scan of brainshowing cerebral edema with flattening and narrowing of thelateral ventricles (arrowed). This patient was treated with 1short hemodialysis session, but fitted and was then success-fully treated by continuous renal replacement therapy. Davenport Hemodialysis International  2008;  12 :307–312 308  Treatment should be designed to both slow down therate of change of serum urea and osmolality, and to main-tain cardiovascular stability. Experimental data, particu-larly in dog models of acute renal failure, showed thatslowing down the rate of change in plasma urea, whetherit was by slowing down blood pump speeds or even add-ing urea to the dialysate bath, reduced the amount of ce-rebral edema. 16 Thus, a treatment bundle is required touse a combination of reduced blood and dialysateflows, in combination with a small surface area dialyzer,shortened treatment session time, 17 and avoiding supra-physiological bicarbonate dialysates. 18 Hemofiltrationtechniques, particularly predilutional, will further reducethe rate of urea clearance. Cardiovascular stability can beimproved by choosing a biocompatible dialyzer, andpriming with isotonic bicarbonate to minimize brady-kinin generation, 19 preventing hypotension when pa-tients are first connected to the extracorporeal circuit. 20 Other measures include cooling the dialysate to 35 1 C orusing isothermic dialysis, as moderate cooling has beenshown to be effective in reducing intracranial pressure inpatients with cerebral edema secondary to acute liver fail-ure. 21 High sodium dialysates, reduce the risk of intradi-alytic hypotension, and a recent multicenter trial reportedthat by using a high sodium dialysate, of up to 10mEq/L(10mmol/L) above the serum sodium, the incidence of intradialytic hypotension was no different to that duringcontinuous renal replacement therapies (CRRT). 22 Morerecent work has shown that a hypertonic sodium infusionduring renal replacement therapy can help to reduce in-tracranial pressure. 23 Predilutional hemofiltration tech-niques often increase cooling and may provide greatercardiovascular stability. 24 High ultrafiltration rates shouldbe avoided to prevent intradialytic hypotension, and if available, dialysis machines with relative blood volumemonitoring and/or fuzzy logic may help reduce intradia-lytic hypotension. 25 One study showed that intradialytichypotension could be reduced by connecting the patientdirectly to the extracorporeal circuit, and starting theblood pump at 50mL/min and then increasing up to aflow of around 250mL/min. 26 Glucose containing dialy-sates should be used to prevent hypoglycemia, and ahigher dialysate potassium and calcium concentrationshould be considered to help minimize cardiovascularinstability and arrhythmias.It has been suggested that treatments should preferably be daily, so that pretreatment serum urea values fall, re-ducing time average deviation, aiming for a predialysisblood urea nitrogen of 34mg/dL (12mmol/L). 15 Follow-ing an acute ischemic stroke, there is a zone of potentially reversible injury surrounding the site of irreversibledamage. Typically this takes 12 to 14 days to stabilize,and therefore the alterations in dialysis prescription may have to be continued during this period, dependingupon the clinical course and recovery of the individualpatient. CONTINUOUS THERAPIES Several studies have shown that CRRT provide greatercerebrovascular stability in the patient with overt cerebraledema. 20 Even so, continuous arteriovenous treatments,with slower changes in serum urea and osmolality, lead tofewer changes in intracranial pressure compared withhigh volume exchanges 24 (Figure 3). HYBRID TREATMENTS Hybrid dialysis systems usually utilize standard hemodi-alysis machines, with reduced blood and dialysate flows.However, there is also a batch dialysate system used inEurope, the Genius s system (Fresenius, Bad Homberg,Germany), which uses a different blood pump technol-ogy, so that the blood and dialysate flows are linked. Itmay be because of this technology that circuit clotting isreduced compared with standard hybrid dialysis. 27 TheGenius s can be slowed down to prolong dialysis treat-ment to 12 to 18hours and also has additional cardio-vascular stability due to cooling of the returning venousblood. 28 Thus, hybrid systems can potentially provide analternative therapy for a chronic dialysis patient followinga stroke or subdural hemorrhage by slowing down therate of change of plasma urea concentration and osmol-ality and also reducing cardiovascular instability. 05101520253530Pre 1 2 3 4Time (h)CAVHFHVHF    M  e  a  n   i  n   t  r  a  c  r  a  n   i  a   l  p  r  e  s  s  u  r  e  m  m   H  g Figure3  Changes in mean intracranial pressure (ICP) dur-ing low volume exchange continuous arteriovenous hemo-filtration (CAVHF) and high volume exchange venovenoushemofiltration (HVHF). Hemodialysis for patients with stroke Hemodialysis International  2008;  12 :307–312  309   ANTICOAGULATION Even in cases of acute ischemic brain injury, the blood-brain barrier is disrupted and there is a potential risk of local hemorrhage into the damaged area. Therefore, ex-cessive systemic over-anticoagulation should be avoided.There is an additional risk of hemorrhage around the siteof invasive intracranial pressure monitoring devices, par-ticularly with intraventricular catheters. Anticoagulantfree circuits or regional anticoagulant techniques are tobe preferred, particularly in cases of intracranial hemor-rhage. Anticoagulation free treatments are possible withcareful circuit design, minimizing blood-air interfacesand may be aided by heparin-coated dialyzers. 29 Morerecently, heparin rinsing of dialyzers, which have beensurface modified to adsorb heparin, have been success-fully used to dialyze patients without systemic anticoag-ulation. 30 Otherwise citrate or nafamostat are potentregional anticoagulants. Prostanoids, in particular pros-tacyclin, although a regional anticoagulant may lead tohypotension and reduced cerebral perfusion. 31,32 PERITONEAL DIALYSIS  Although the rate of change of plasma urea and osmol-ality is slower during peritoneal dialysis, there are reportsof raised intracranial pressure during peritoneal dialysis,particularly in patients with acute kidney injury, 33 anddisequilibrium syndrome in children. 34 However, gener-ally the changes in intracranial pressure during peritonealdialysis tend to be much less than those during hemodi-alysis, 33,35 although significant and sustained surges inICP do occur. 33,35 In patients with acute renal failure, theclearances achieved with peritoneal dialysis may not besufficient to control chemistries in catabolic patients, andsimilarly peritoneal dialysis may not adequately controlfluid balance. 35 Nevertheless, many centers including ourown continue to provide peritoneal dialysis followingacute intracranial events and post neurosurgery to thosepatients with end-stage renal failure already establishedon peritoneal dialysis.Recent studies have demonstrated that exchange vol-umes of    2L, particularly when using hypertonic glu-cose concentrations (3.86%), are associated with reducedcardiac output. 36 The change in intra-abdominal pressureassociated with such exchanges leads to a reduction inright atrial filling pressure, and this may cause a fall incardiac output. 37 In patients with compromised cerebralperfusion, particularly those with intracranial hemor-rhage, such reductions in cardiac output and cerebralperfusion may lead to further cerebral ischemia and evendeath 38 (Figure 4).Thus, to prevent such potential reductions in cardiacoutput and cerebral perfusion, the number of hypertoniclarge volume glucose exchanges should be minimized.For chronic kidney disease patients already establishedon peritoneal dialysis, to reduce fluctuations in intra-abdominal pressure, venous return, and cardiac output,a tidal regime may be more appropriate rather thantheir standard continuous ambulatory peritoneal dialysis(CAPD) and/or automated peritoneal dialysis (APD)prescription. ROLE OF OSMOTHERAPY  Mannitol and hypertonic saline have been shown to helpreduce cerebral edema, by removing brain extracellularfluid from those areas of the brain with a functionally in-tact blood-brain barrier. 35 However their main effect inreducing intracranial pressure is probably by expandingthe intravascular volume, and so increasing cerebral per-fusion. Both can be infused during renal replacementtherapy. For mannitol to be effective then, it needs to beinfused over a relatively short period, for example a100mL bolus of 20% mannitol over 10 to 15minutesand then repeated, provided that the serum osmolality remains below 330mOsmol/kg. Similarly, hypertonic sa-line can be infused during intermittent and continuoustherapies to temporarily increase the serum sodium up to150 to 155mmol/L. 15,23  As standard peritoneal dialysissolutions are hyponatremic, hypertonic saline may be required to correct hyponatremia. 0204060800 4 8 12 16Time (h) Cardiac arrest& deathfixed dilatedpupils CAPD 2 l cycles norepinephrine    M   A   P  m  m   H  g Figure4  Changes in mean arterial pressure (MAP) during2.0L peritoneal dialysis exchanges in a peritoneal dialysispatient with intracranial hemorrhage, who died from tento-rial herniation due to cerebral swelling. Davenport Hemodialysis International  2008;  12 :307–312 310
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