Neurocrit Care DOI 10.1007/s12028-014-0063-z

PRACTICAL PEARL

Dialysis-Induced Worsening of Cerebral Edema in Intracranial Hemorrhage: A Case Series and Clinical Perspective Abhay Kumar • Andreia Cage • Rajat Dhar

Ó Springer Science+Business Media New York 2014

Abstract Background Intracranial hemorrhage (ICH) is not an uncommon complication of end-stage renal disease (ESRD), and may be complicated by cerebral edema. Hemodialysis (HD) may induce rapid osmolar and fluid shifts, increasing brain water content with the potential to worsen cerebral edema. The dangers of HD in patients with acute ICH have only been highlighted in isolated reports. Methods Case series and review of relevant literature. Results Two patients with ESRD presented with acute ICH (one with putaminal hematoma, the other with bilateral subdural hematomas) and developed fatal/near-fatal herniation during HD, associated with malignant worsening of cerebral edema. Both had interruptions in dialysis schedule prior to index event. Both were awake initially, but developed cerebral herniation syndrome toward the end of index HD, confirmed on imaging with worsening edema and effaced basal cisterns. In one case, herniation was reversed with hypertonic saline and hyperventilation, but in the other, the patient progressed to brain death despite these measures. We contrast these cases with a young patient with ESRD and large basal ganglia ICH who had

A. Kumar Department of Neurology, Saint Louis University, Saint Louis, MO, USA A. Cage Barnes-Jewish Hospital, Saint Louis, MO, USA R. Dhar (&) Department of Neurology, Washington University School of Medicine, 660 S. Euclid Ave, Campus Box 8111, Saint Louis, MO 63110, USA e-mail: [email protected]

elevated ICPs on admission, but safely underwent continuous veno-venous HD. Conclusions Hemodialysis may worsen cerebral edema in the setting of ICH sufficient to precipitate cerebral herniation. Caution should be exercised when dialysing a patient with an acute mass lesion and reduced intracranial compliance, especially those in whom HD is new or not routine. Delaying HD till risk of edema is attenuated, or ensuring gradual urea removal (such as with continuous hemofiltration) may be advisable. Keywords Hemodialysis  Dialysis disequilibrium syndrome  Herniation  Brain death

Introduction Hemodialysis (HD) is the predominantly used renal replacement therapy in patients with end-stage renal disease (ESRD). The goal of treatment is to restore the body’s fluid/electrolyte environment toward normal, primarily by processes of diffusion wherein urea and other toxic solutes are transported from blood into the dialysate solution and by ultrafiltration, which removes excess body water. These physiologic alterations induce osmolar shifts and may lead to an acute increase in brain water, as demonstrated in animal as well as human studies [1, 2]. Such fluid shifts may lead to the dialysis disequilibrium syndrome (DDS), a constellation of signs and symptoms including nausea, headache, irritability, and agitation. Even a small increase in brain water resulting from HD could precipitate dangerous elevations in intracranial pressure in patients with mass lesions, cerebral edema, and reduced brain compliance; this could lead to worsening encephalopathy,

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Fig. 1 Baseline head CT showing left putaminal hematoma (a) with effaced basal cisterns (b) but open foramen magnum (c). Follow-up imaging at time of herniation demonstrates stable hematoma size (d) but worsening edema (e) and tonsillar herniation (f)

herniation, or even death [3]. This prospect makes management of ESRD patients with brain injuries challenging for the neurointensivist and may necessitate special caution when (re-) initiating HD in such patients. Here, we present two cases where cerebral edema is acutely worsened during HD in patients with acute intracranial hemorrhage (ICH), sufficient to precipitate central and tonsillar herniation, in one case leading to the patient’s death. We present a third case as a counterpoint, in which we successfully employed continuous hemofiltration to avoid HD-induced worsening of edema after ICH. This strategy was based on our review of the literature on brain herniation or cerebral edema with HD, performed using the terms: (dialysis, hemodialysis, renal replacement AND herniation, cerebral edema, and dialysis disequilibrium [or dysequilibrium] syndrome) in PubMed and Google Scholar, restricted to articles in the English language.

Case #1 A 34-year-old woman with ESRD, poorly controlled hypertension, noncompliant with home peritoneal dialysis,

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was found unresponsive. Blood pressure on arrival to the emergency department (ED) was 263/134 mmHg. She was intubated for airway protection with initial arterial blood gas (ABG) 7.26/38/349, serum bicarbonate of 10 mmol/l, and anion gap of 24. Laboratory abnormalities included serum Na 147 mmol/l, BUN 61 mg/dl, and creatinine 10 mg/dl. Head computed tomography (HCT) revealed a 25 ml left putaminal hemorrhage with intraventricular extension and partial effacement of the basal cisterns (Fig. 1a–c). On transfer to the Neuro-ICU (NICU), she was arousable with stimulation, followed simple commands, but had right-sided hemiplegia. She was changed to a pressure support mode of ventilation due to ventilator dyssynchrony. Her neuro exam remained unchanged till a few hours later when she was noted to be intermittently apneic with decreased minute ventilation after being given a dose of fentanyl (for presumed pain). She then became acutely hypertensive, unresponsive and exhibited extensor posturing. Transient hyperventilation was initiated immediately in response to this acute decompensation, felt to be related to acute hypercapnia, with return to her neurological baseline by 60 min after the event. Head CT at the time revealed no change in size of ICH or in edema.

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HD was initiated a few hours after this episode (primarily for metabolic acidosis), using dialysate composition with sodium 140 mEq/l and blood flow rate 400 ml/min. One hour into dialysis, she again became acutely hypertensive and unresponsive; both pupils were fixed and dilated, and she lost corneal and cough reflexes. Clinical evidence of herniation persisted despite cessation of HD, aggressive hyperventilation, and a bolus of 30 ml of 23.4 % hypertonic saline. Head CT showed worsening edema and effacement of the basal cisterns consistent with central and tonsillar herniation, but no increase in hematoma size (Fig. 1d–f). ABG during hyperventilation was 7.54/25/189, bicarbonate 20 mmol/l, while serum Na was 149 mmol/l after hypertonic saline administration, and BUN had fallen to 39 mg/dl after dialysis. Subsequent neurological examinations were consistent with brain death.

Case #2 A 74-year-old woman with ESRD and hypertension was admitted to NICU with drowsiness and left hemiparesis after a fall, with bilateral (right larger than left) acute subdural hematoma (SDH) on HCT (Fig. 2a, b); she was initially managed conservatively including resuming HD without incident. However, her third HD session was terminated prematurely after she developed focal seizures, for which antiepileptic drugs (AED) were initiated. A followup HCT done 3 days later for persistent drowsiness despite seizure control (on continuous EEG monitoring) showed increased left SDH size with crowding of basal cisterns (Fig. 2c, d). Nonetheless, routine HD was reinitiated later that day, with a pre-dialysis BUN of 128. Toward the end of HD, she became acutely unresponsive, and was found to have fixed dilated pupils (right-side larger and irregular). A bedside HCT revealed no change in size of SDH relative to HCT that morning, but complete effacement of basal cisterns with progression of global cerebral edema (Fig. 2e). BUN had fallen to 30 after HD. Patient was rapidly intubated, hyperventilated, and given 350 ml of 5 % saline. With osmotic therapy and hyperventilation, her pupils became equal and sluggishly reactive, and she started to withdraw her right arm. Neurosurgery opted for urgent bedside subdural drainage that evening. By the next morning, she was more awake and localizing with both arms. HCT showed that SDH was partially evacuated, and edema was greatly improved, with open cisterns (Fig. 2f); the next day she began to follow commands again. She did not require further osmotic therapy, ventilatory support could be weaned, and given resolution of edema, and she safely underwent resumption of HD at half-rate with dialysate sodium set at 155 mEq/l.

Counterpoint: Case #3 A 28-year-old man with malignant hypertension and ESRD was evaluated for left-sided weakness followed by unresponsiveness to a GCS of 6, requiring intubation in the ED. HCT showed moderately large right thalamic ICH with intraventricular rupture. He received DDAVP and had a right-sided ventriculostomy placed. His BP was 230/135 in the ED, and it was discovered that he had missed his last HD 2 days earlier. ABG showed metabolic acidosis, and BUN was 68. ICPs remained elevated after EVD insertion. Based on our previous experiences, we deferred HD, and instead initiated CVVHD in consultation with renal service. The HD-catheter placement required 250 ml of 5 % saline to control elevated ICPs (to the 40–60 range when laying flat, prior to osmotic therapy). However, he underwent CVVHD without any elevation in ICP or worsening of edema. In fact, he woke up the next day and was extubated shortly thereafter. After 3 days of continuous UF, he was transitioned back to HD (without systemic heparinization). Unfortunately, on initiation of his third HD session, he became acutely hypertensive and unresponsive, and HCT showed massive rebleeding of ICH; he progressed to brain death shortly thereafter.

Discussion Dialysis disequilibrium syndrome (DDS) consists of a constellation of symptoms which range from nausea, vomiting, and headache, to altered mentation, seizures, coma, and herniation that may occur during or even several hours after HD [1]. These symptoms are thought to result from an acute increase in brain water and are usually seen in patients undergoing hemodialysis for the first time [3, 4], although patients receiving chronic maintenance therapy may also experience DDS [4]. In patients with preexisting cerebral edema from intracranial mass lesions, initiation of HD can result in exacerbation of cerebral edema, leading to severe complications of DDS, as evidenced by the first two cases in our series. Hemodialysis increases brain water content in ESRD as demonstrated on neuroimaging studies [2]. The average increase in brain volume after HD was approximately 3 % of total brain volume. While this may be tolerated or produced only mild symptoms in patients without underlying neurological disease, in patients such as ours with mass lesions, preexisting edema, and decreased compliance, even small increases in volume could precipitate herniation. A combination of factors causes cerebral edema in ESRD patients undergoing hemodialysis. Chronically elevated plasma osmolarity due to uremia leads to generation

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Neurocrit Care Fig. 2 Head CT on admission with bilateral acute subdural hematoma (a) with open basal cisterns (b). Follow-up head CT prior to hemodialysis shows increase in size of SDH (c) with some effacement of basal cisterns (d). Head CT after deterioration shows complete effacement of basal cisterns consistent with herniation (e) while follow-up CT after SDH evacuation shows resolution of edema (f)

of ‘‘idiogenic osmoles’’ within the brain [5]. Additionally, while brain–plasma urea concentrations achieve steady state, rapid hemodialysis could cause ‘‘relative urea abundance’’ in the brain due to poor reflection coefficient of urea [1]. This could be due to deficiency of urea transporters as seen in uremic rodent models [6]. ‘‘Idiogenic

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osmoles’’ and relative urea abundance lead to increased brain–plasma osmolal gradient during HD as plasma osmolality drops acutely. Rapid correction of metabolic acidosis causes paradoxical cerebrospinal fluid (CSF) acidosis, which can further increase the brain–plasma osmolal gradient [7, 8]. The

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resultant increase in brain-plasma osmolal gradients, as plasma urea falls and acidosis resolves, leads to sudden water influx into brain tissue, further facilitated by increased expression of aquaporin channels in the uremic brain [6]. Patients with acute intracranial hemorrhage often have reduced brain compliance, as heralded by the acute sentinel deterioration seen in patient 1 with an episode of hypoventilation/hypercapnia, and the elevations in ICP with positioning patient 3 flat. Radiographic evidence of cerebral edema, especially in the presence of effaced basal cisterns, serves as an additional warning sign that HD (with its resultant further increase in brain water) may not be tolerated. Furthermore, large reductions in BUN (patient 2 had acute reduction by 80, corresponding to an almost 30 mosm/l fall in serum osmolality), high flow rates, or resumption of HD after a period of noncompliance (patient 1) are additional risk factors for accentuated water shifts and worsening of edema. HD has been associated with increased ICP in patients with ICH in previous series [4, 9]. All patients had elevation of ICP within the first hour of HD. Signs of tentorial herniation were seen in a patient with thalamic hemorrhage within 2 h of HD, but it was reversed with CSF drainage through the ventriculostomy catheter. In fact, herniation and global edema have been documented in two patients without intracranial pathology but undergoing HD for sepsis and acute kidney injury [10]. Lower HD rates (50–100 ml/min) or continuous venovenous hemodialysis (CVVHD) do not appear to cause any significant elevations in ICP in previous case series [4, 9, 11]. Daily treatment with reduced hemodialysis rates slows down the plasma urea clearance and fluctuations thereby lowering the plasma–CSF osmotic gradient and minimizing the risk of cerebral edema, as evidenced in Patient 2. Similarly CVVHD provides slower and sustained decrease in plasma osmolytes thus providing improved cerebrovascular stability and less frequent spikes in ICPs as evidenced in Patient 3. These strategies should be considered, especially early after brain injury, and there should be a slow transition to conventional hemodialysis. Higher composition of Na in dialysate (143–146 mEq/l) or preemptive use of mannitol to maintain higher plasma tonicity could also be considered [12]. ICP monitoring in high-risk patients with intracranial pathologies and reduced compliance requiring HD should be considered prior to initiating the treatment. Further studies are needed to better evaluate the optimal strategy for such patients. Above all, goals of hemodialysis and potential risks should be discussed with the

dialysis team when planning resumption/initiation of renal replacement therapy.

Conclusion Patients with ESRD and uremia that develop acute mass lesions such as ICH are at increased risk for developing worsening cerebral edema during HD. Careful consideration of hemodialysis needs should be undertaken in these patients, including potential options of delaying HD or using gradual urea removal with CVVHD. Conflict of interest of interest.

The authors declare that they have no conflict

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Dialysis-induced worsening of cerebral edema in intracranial hemorrhage: a case series and clinical perspective.

Intracranial hemorrhage (ICH) is not an uncommon complication of end-stage renal disease (ESRD), and may be complicated by cerebral edema. Hemodialysi...
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