Dialysis with kayexalate

Kidney failure

2011.06.30 13:21 pwndcake Kidney failure

Got questions about kidney failure or dialysis? Want to share your experience dealing with kidney issues? Feel free to join.
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2021.06.12 17:35 PDUFA_INFO 🦍💎 $ARDX ✋🚀

The selective sodium hydrogen exchanger 3 (NHE3) inhibitor Tenapanor is being developed by Ardelyx Inc for the treatment of constipation-predominant irritable bowel syndrome (IBS-C) and for hyper-phosphataemia in patients with chronic kidney disease (CKD) on dialysis.
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2021.03.30 17:00 sd-SAN The COVID ICU Deck (V6)

Hi all –
For the original thread on The COVID ICU Deck (based on Marino's The ICU Book), please see the link below. The TL;DR – this is an Anki deck for ICU rotation prep based on Marino's text.
https://www.reddit.com/medicalschoolanki/comments/fntw1q/the_covid_icu_deck/
The following link is Version 6 of the deck, with the complete table of contents updated below.
https://drive.google.com/file/d/1ao4NRCeVc-exvaQhaYd_YHjH1PeboH_6/view?usp=sharing
3/28/2024 update: sorry I broke the link for 1+ years... The new link above should work now!

GENERAL UPDATES/COMMENTS –

NEW TO ICU? RECOMMENDED SECTIONS:

COMPLETE TABLE OF CONTENTS (1582 cards):

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2021.02.26 23:00 sd-SAN The COVID ICU Deck V5.2

Hi all –
For the original thread on The COVID ICU Deck (based on Marino's The ICU Book), please see the link below. The TL;DR – this is an Anki deck for ICU rotation prep based on Marino's text.
https://www.reddit.com/medicalschoolanki/comments/fntw1q/the_covid_icu_deck/
The following link is V5.2 of the deck, with the complete table of contents updated below.
https://drive.google.com/file/d/1gsT1vyrrcIaqEzR59V09CD5qVH04UELE/view?usp=sharing

GENERAL UPDATES/COMMENTS –

COMPLETE TABLE OF CONTENTS (1572 cards) –

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2020.11.12 02:50 drag99 Interesting case presentation- 50 something YO man who can't pee

So this is a case not so much about the diagnosis (which is interesting), but the process of getting this patient cared for. For those that want to consider what they would do, I'll break up the post a bit to allow you some space between important decision points.
A little background information about me. I'm a US emergency medicine attending who works in a community/academic setting. This case is at a 14 bed 30,000 annual visit ER in a hospital that is part of a large system of hospitals in the city I live in. We have CT capabilities, an ICU, and most specialties available for consult. I am working an overnight and have 3 nurses and a tech with me.
So its 0450, I am an hour away from ending my uneventful shift when I am told that a 50 something YO gentleman is checking in for generalized weakness and can't pee. They bring him back to a room and I immediately notice that he is LLS (looks like shit) score positive. He is breathing 35x per minute. He is too distressed/tachypneic/weak to talk, so his wife tells me that he has a history of DVTs (on xarelto), peripheral arterial disease, HTN, DMII, and frequent kidney stones and he presented due to feeling poorly and being unable to urinate for the last 2 days, now is too weak to even stand. She states about 5 days ago he urinated out some stones, and 2 days ago he went completely anuric. The wife states that being a stubborn man, she had to beg him to come in this morning.
The rest of his VS are a HR of 81, BP 190/91, temp 37.1 C, O2 96%.
What is the first test you want on this patient? Also, consider what else you are doing and ordering on this patient.
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If you stated an ECG, you are correct.
Now I feel this ECG is fairly obvious, but maybe not so much for medical students, so I'll ask what your interpretation is.
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This ECG demonstrates an irregular, wide complex rhythm with no evidence of sinus activity, with diffuse peaked T-waves consistent with severe hyperkalemia. You will also some right axis deviation, a tall R wave w/ downsloping ST segment in aVR, and a brugada-like pattern in V1 and V2 which is frequently seen in hyperkalemia (along w/ sodium channel blocker toxicity). While peaked t-waves is typically taught to us in med school as what we should look for when concerned for hyperkalemia, isolated peaked t-waves in the setting of hyperkalemia actually does not portend any worse outcome for the patients it is present in. The typical hyperkalemic ECG changes that do portend worse outcomes are absence of p-waves, QRS widening, and bradycardia1 .
As for the rest of the tests I ordered, VBG (as the patient clearly has severe metabolic acidosis from acute renal failure based on his tachypnea), cbc, cmp, CXR, and added on some blood cultures as a just in case.
His VBG came back with a pH of 7.1, pCO2 of 21, and HCO3 of 6. Unfortunately our blood gas analyzers cannot perform istat electrolytes.
I also performed a POCUS of his bladder (because of course every interesting EM case needs some POCUS) while we were obtaining the ECG, which demonstrated an absence of urine which confirmed what I was suspecting.
So how are you going to treat this?
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You should now be focusing on cardiac membrane stabilization and shifting the patients potassium intracellularly. I think of hyperkalemia treatment in 5 separate treatments. You have your membrane stabilizers (calcium gluconate/chloride), your potassium excreters (lasix, kayexalate, ion-exchange resins), your potassium shifters (albuterol, insulin, bicarb), your diluters (fluids), and dialysis.
I avoided lasix because the patient is anuric and avoided kayexalate and ion-exchange resins because they limited utility in the acute setting. I also avoided fluids given the patient was anuric.
If we were to give a hyperkalemic patient fluids, I think there is an interesting conversation to have. Classic teaching would suggest avoiding balanced solutions like lactated ringers due to the presence of potassium in them; however, there is some literature to suggest LR has improved potassium levels compared to NS, at least in renal transplant patients in the OR 2,3,4 . This is likely due to the miniscule amount of potassium in LR (4 mEq) along with with LR's pH (6.5) being closer to physiologic compared to NS (5.5), given that we know acidosis leads to potassium shifting extracellularly.
The first med I gave was 3gm of calcium gluconate (the equivalent of 1gm calcium chloride), then 10u insulin along with an amp of D50, then two amps of bicarb, then a 15mg albuterol neb was started. There has been some discussion in EM circles about reducing insulin dosage to 5u to decrease the incidence of hypoglycemia with similar efficacy in potassium lowering, however, the literature seems to be mixed on this from my own reading5,6 .
The QRS narrowed following calcium administration. While meds were being administered, I made a call to nephrology and our intensivist. The nephrologist stated he would prepare to set up dialysis while myself and the intensivist worked on placing a quinton catheter (I love my consultants, they didn't even bat an eye when I explained that we had no lab values back yet). We then took him quickly to CT to confirm my suspicion that the patient had bilateral ureteral stones with one side having a proximal 1.5cm stone and the other side having a mid ureteral 8mm stone.
I then gave a call to the patient's urologist and we agreed that the more pressing issue was starting dialysis and he could work on placing bilateral percutaneous nephrostomy tubes vs bilateral ureteral stents in a day or two once the patient was off his anticoagulation.
Finally, about an hour and a half after presentation, I got a call from lab stating that the patients creatinine was 20 and his potassium was 8.9.
Of course as I was about to leave my shift about an hour after it ended, and two hours after the patient had arrived. I heard a code blue call in the ICU in the room we transferred him to. So I ran over there. Luckily I did, as when I arrived the patient was in stable-ish V-tach vs a sinusoidal rhythm on the monitor (appeared to be more consistent w/ V-tach), and the intensivist was ready to push amiodarone before I stopped him explaining that giving a medication with sodium channel blocking properties to a severely hyperkalemic patient could potentially kill them. We instead opted for an additional dose of calcium, which did not work, so made the sphincter tightening decision to perform an electrical cardioversion (sphincter tightening because cardioverting a hyperkalemic patient can potentially put the patient into v-fib). Luckily he converted back to his junctional rhythm following cardioversion and was started on dialysis.
The patient was discharged from the hospital 7 days later after bilateral ureteral stents were placed. I went and visited him the last day of his admission and seemed to be doing great, and was thankful that his dialysis line was finally removed.
I think some important conclusions you should have from this case is not to wait for potassium levels before starting therapy on a hyperkalemic patient which highlights the importance of recognizing evidence of hyperkalemia on ECG. Also probably important not to wait 2 days to go to the hospital after becoming anuric.
  1. Durfey, N., Lehnhof, B., Bergeson, A., Durfey, S., Leytin, V., McAteer, K., Schwam, E., & Valiquet, J. (2017). Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events?. The western journal of emergency medicine, 18(5), 963–971. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576635/
  2. O'Malley CM, Frumento RJ, Hardy MA, Benvenisty AI, Brentjens TE, Mercer JS, Bennett-Guerrero E. A randomized, double-blind comparison of lactated Ringer's solution and 0.9% NaCl during renal transplantation. Anesth Analg. 2005 May;100(5):1518-24, table of contents. doi: 10.1213/01.ANE.0000150939.28904.81. PMID: 15845718. https://pubmed.ncbi.nlm.nih.gov/15845718/
  3. Khajavi MR, Etezadi F, Moharari RS, Imani F, Meysamie AP, Khashayar P, Najafi A. Effects of normal saline vs. lactated ringer's during renal transplantation. Ren Fail. 2008;30(5):535-9. doi: 10.1080/08860220802064770. PMID: 18569935. https://pubmed.ncbi.nlm.nih.gov/18569935/
  4. Modi MP, Vora KS, Parikh GP, Shah VR. A comparative study of impact of infusion of Ringer's Lactate solution versus normal saline on acid-base balance and serum electrolytes during live related renal transplantation. Saudi J Kidney Dis Transpl. 2012 Jan;23(1):135-7. PMID: 22237237. https://pubmed.ncbi.nlm.nih.gov/22237237/
  5. LaRue HA, Peksa GD, Shah SC. A Comparison of Insulin Doses for the Treatment of Hyperkalemia in Patients with Renal Insufficiency. Pharmacotherapy. 2017 Dec;37(12):1516-1522. doi: 10.1002/phar.2038. Epub 2017 Nov 27. https://pubmed.ncbi.nlm.nih.gov/28976587/
  6. Moussavi, K., Nguyen, L. T., Hua, H., & Fitter, S. (2020). Comparison of IV Insulin Dosing Strategies for Hyperkalemia in the Emergency Department. Critical care explorations, 2(4), e0092. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7188424/
TLDR: 50 year old anuric, ECG demonstrates severe hyperkalemic changes. Meds given to treat while placing dialysis line. CT obtained demonstrating bilateral ureteral stones. Pt goes into v-tach and is almost given amiodarone. Electrically cardioverted. Started on dialysis. Discharged 7 days later in good health.
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2020.05.14 17:06 sd-SAN The COVID ICU Deck V5.1 (COMPLETE!)

Hi all –
IT'S FINISHED!
For the original thread on The COVID ICU Deck (based on Marino's The ICU Book), please see the link below. The TL;DR – this is an Anki deck for ICU rotation prep based on Marino's text.
https://www.reddit.com/medicalschoolanki/comments/fntw1q/the_covid_icu_deck/
The following link is V5.1 of the deck, with a complete table of contents now described below.
https://drive.google.com/open?id=1e7eJ1La5qXVajr4guaEDB5_3TxUd1Gpa

GENERAL UPDATES/COMMENTS –

COMPLETE TABLE OF CONTENTS (1563 cards) –

For those following along from the beginning...

Thank you for the continued support! I really hope this will help rising subIs & interns feel even slightly more comfortable in the hospital: we're all in this together.
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2020.02.03 12:17 JuniperPublishersICM Hyperkalemia Management in the Oncology Patient: A Case of Sodium Polystyrene Sulfate Induced Bowel Perforation-Juniper Publishers

Abstract
Kayexalate (sodium or calcium polystyrene sulfate) is a cation-exchange resin commonly used to treat hyperkalemia in patients with renal dysfunction. It works by exchanging its bound sodium with potassium in the colon to promote potassium excretion in the stool. This occurs over hours to days, and is known to cause adverse digestive effects including anorexia, nausea, vomiting, and constipation. Bowel necrosis and perforation is an uncommonly recognized, though devastating complication of kayexalate administration. We present a case of a postoperative surgical oncology patient who developed a bowel perforation associated with oral kayexalate administration. We also review the literature to further delineate the relationship between the use of kayexalate and bowel perforation and necrosis, particularly in a surgical oncology patient where this complication has been less frequently documented.
Keywords: Kayexalate; Hyperkalemia; Bowel perforation; Bowel necrosis; Sodium polystyrene sulfate; Calcium polystyrene sulfate

Introduction

Hyperkalemia is a condition commonly encountered in medical and surgical patients and can induce life-threatening cardiac arrhythmias if left untreated. Kayexalate is a cation-exchange resin frequently used to treat this condition. Although rare, there is a known relationship between kayexalate administration and bowel necrosis and it is therefore important to consider this in a patient with abdominal pain who has been treated with oral kayexalate [1,2]. We present a case of a surgical oncology patient who developed spontaneous bowel perforation in the setting of kayexalate administration.

Case Report

The patient is a 60 year old male with past medical history significant for hypertension, hyperlipidemia, diabetes mellitus type II requiring insulin for glucose control and complicated by diabetic nephropathy (baseline creatinine 1.0), congestive heart failure with ejection fraction 30-40%, non-obstructive coronary lesions, moderate pulmonary hypertension and locally advanced left renal cell carcinoma (14cm mass causing renal vein thrombosis and retroperitoneal lymphadenopathy). The patient was not a candidate for neoadjuvant chemotherapy given his multiple medical comorbidities.
He underwent a left radical nephrectomy with regional lymphadenectomy with significant intra-op findings of left colon ischemia requiring left segmental colectomy with primary anastomosis. His postoperative course was significant for severe sepsis requiring initiation of vasopressor support and piperacillin- tazobactam, new onset atrial fibrillation requiring amiodarone, and acute kidney injury resulting in hyperkalemia. He was initially treated in the post-anesthesia care unit for hypotension with crystalloid, albumin and low dose phenylephrine which was weaned off over several hours. The patient was subsequently transferred to the ward. Hyperkalemia was treated with oral kayexalate 15 grams, of which the patient received six doses over the course of postoperative days #3-5 on a six hourly dosing regimen. On postoperative day #7, the patient developed acute abdominal pain and was found to have feculent output from the surgical drains. He was taken back to the operating room for exploratory laparotomy, left colectomy, transverse colostomy and mucous fistula. Postoperatively, he had continued vasopressor requirement with norepinephrine and vasopressin, he remained intubated and required intensive care unit admission. His antibiotic coverage was broadened to vancomycin, meropenem, and micafungin. Pathology of the left colon specimen revealed transmural necro-inflammation, exudative serositis and serosal fibrosis, as well as basophilic crystalloid particles consistent with kayexalate at the site of perforation, which was proximal to the prior viable-appearing anastomosis (Figure 1). Thus, a diagnosis of kayexalate-induced colon ischemia and necrosis was made.
The patient had improvement in his clinical status, was weaned off vasopressor and ventilatory support, demonstrated improvement in his renal function and cardiac function with ejection fraction to 52% and he was discharged from the intensive care unit on post-operative day #6 to the ward, then discharged home with physical and occupational therapy services on post-operative day #19 . The remainder of his course has been unremarkable.

Discussion

Kayexalate is a cation-exchange resin which was first approved by the Food & Drug Administration in 1958 and has since been widely used to treat hyperkalemia [3]. Sorbitol is an osmotic laxative which historically has been added to kayexalate formulations to reduce the incidence of constipation, however there is a well-documented association with kayexalate- sorbitol and bowel necrosis [4,5]. In 2006, the Food and Drug Administration issued a black box warning on kayexalate-sorbitol products, and this formulation has subsequently been removed from the market over the last 10 years [4,5].
Despite the removal of sorbitol from most kayexalate formulations however, there have been numerous case reports of kayexalate administration and bowel necrosis. The incidence is thought to be 0.27% overall, and up to 1.8% during the postoperative period [2,3,6]. There have also been multiple case reports of upper gastrointestinal ulceration due to oral kayexalate administration, although none of these cases have required surgical intervention [7]. The symptoms of intestinal injury have been documented to occur between 3 hours and 11 days following the administration of kayexalate, and mortality from this complication is >30% in cases with gastrointestinal injury [3,5].
Kayexalate can be administered orally or rectally, and works by exchanging its bound sodium with potassium in the colon to promote potassium excretion in stool. Its effect is seen within hours to days, and thus it is not indicated for use as sole therapy in severe hyperkalemia. Although the mechanism of kayexalate induced bowel necrosis is unknown, one suspected mechanism involves the elevated renin levels seen in patients with renal failure who develop hyperkalemia. Renin activates angiotensin II which causes splanchnic vasoconstriction and can predispose the colon to non-occlusive ischemia, especially following dramatic electrolyte and fluid shifts [8]. Norepinephrine, the initial vasopressor indicated in septic shock, is also known to reduce the splanchnic blood flow and this can worsen intestinal vasoconstriction. However, the bowel necrosis and perforation described in cases of kayexalate administration is distinguished from ischemic necrosis by the pathological presence of kayexalate crystals in the bowel wall. Basophilic crystals with a mosaic pattern on Hematoxylin & Eosin stain is pathognomic for the presence of kayexalate.
We present this case to raise clinical suspicion of bowel necrosis and perforation in a patient with abdominal pain, particularly in a surgical oncology patient where this complication has been less frequently documented, after the administration of oral or rectal kayexalate [9,10]. Early diagnosis and prompt surgical intervention is critically important in this rare yet devastating complication of kayexalate administration due to the significant morbidity and mortality associated with this condition. In addition, we recommend the use of alternative treatment strategies for hyperkalemia, including insulin-glucose, diuretics, calcium, bicarbonate, inhaled beta-adrenergic agonists and emergent dialysis in severe, life-threatening hyperkalemia as these are safer and more efficacious therapies when implemented in a timely manner.

Conflict of Interest

We have no financial interest or any conflict of interest.
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2015.01.09 07:30 snapgray07 Nurses of Reddit, lend me your brains

I have an ESRD patient getting dialysis, no bm for 5 days was given a lot of stool softer and laxatives, she hasn't been dialize for 3 days, because her bp was low 2 days ago and the following day her fistula clotted. Her K now is 5.5 and MD order Kayexalate rectal, which I gave with tap water enema..I only gave her 500ml of water I'm scared she might have fluid overload..its been an hour and no output yet..should I give more? Thoughts? Input anyone? .______.
She now stated shes confused and she's seeing things (she's legally blind though -_-) and has and order for UA, shes anuric but dribble sometimes...should I cath her out?
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