University of Washington



Hyperkalemia Case Discussion(Below case is discussed assuming you’ve completed the recommended readings – if you haven’t yet, please do so prior to continuing)Part OneDM is an 81 year old female in the ED accompanied by her daughter. Chief complaint is decreased oral intake, confusion, and lethargy for one day, reports medication compliance and missed dialysis x1.PMHHome MedsAllergies-End Stage Renal DiseaseAllopurinolCodeine-Diabetes Type 2AspirinPCN-cirrhosisCiprofloxacinNarcotic analgesics-hypertensionDarbopoetin-HyponatremiaFurosemide-Hepatic encephalopathyInsulin glargineInsulin lisproRifaximinLabs drawn earlier in the day by hospice nurse include:Hb (i-STAT)?????? ???11.9?g/dL?Na (i-STAT)??????? ???133?mEq/LHCT (i-STAT)?? 35 %?K (i-STAT)???????? ?????? 5.5?mEq/L ?WBC?????????????????????9.91 thousand/microLCl (i-STAT) ?????? ?????? 112?mEq/L ??RBC??????????? ??????????3.64 million/microL ??Total?CO2? (POC)13?mEq/L ?Hb??????????????????????? 12.0?g/dL?AG ?(POC) ??????????????? 15 mmol/L?PLT?????????????????????? 92 thousand/microL ?Glucose(POC)???????????421?mg/dL ??BUN(i-STAT) (POC)????? 104?mg/dLCr (POC)??????????????? ??? 4.0?mg/dL ?Ca (Ionized) (POC)????????1.60 mmol/L ?Questions for Discussion: ?What about this case stands out to you? Given the patient complaint, medical history, and medication list, discuss appropriate pharmaceutical considerations.? What would be appropriate follow up questions and information?Case Discussion Part OneWith DM’s presentation and vague complaints the differential is wide. Initial labs, detailed history and physical assessment will help the team evaluate concern for possibilities such as hepatic encephalopathy, hypoglycemia, UTI, medication interactions or even meningitis. We will want to clarify the extent of her renal disease and her glycemic profile as well as her current electrolytes, fluid status and infectious concerns. Working closely with a multidisciplinary team is vital to narrowing down DM’s differential, but even at this early stage she demonstrates some classic signs of electrolyte disturbance worthy of evaluation.First, DM’s history of renal disease should immediately make us question her potassium balance – the kidney is responsible for clearing 80% of the body’s potassium load(note?), so whenever you think of kidney injury you should think of hyperkalemia and whenever you see hyperkalemia you should wonder about renal function. Her current serum creatinine should allow us to estimate a GFR, although we can also ask if DM is on dialysis, and if so, when her last dialysis session was. Other common causes of hyperkalemia include: (list)…The presence of any of these factors should bring to mind the possibility of hyerpkalemia or any possible contributing role.For DM, we see from her history of diabetes and her home med use that she has access to insulin introducing the possibility of hypoglycemia, and - given the role that insulin plays in potassium balance – hypokalemia. DM’s reported lab values would appear to rule out hypokalemia, although without knowing we can wonder simultaneously about hypoglycemia and hypokalemia.DM’s history of cirrhosis, hyponatremia, and furosemide all put her at risk for hyponatremia, both acute and chronic. Her current status of altered mental status makes this possibility even more of a concern.Part TwoDM continues to demonstrate altered mental status. Heart rate is 60 bpm, SBP?120,?DBP?80,?RR?22 bpm, Temp 36.7. ?DM?is described as “confused but directable”.??? A repeat panel was?run:K 6.7 mEq/L CO2 12 mEq/LNa 130 mEq/LAnion Gap 12 Cl 144 mEq/L Glucose 322 mg/dL BUN 110 mg/dL Cr 4.2 mg/dL ?An?EKG?was run showing the following findings when compared to previous EKGs: concern for?ST?elevations,?QRS?148, Vent rate?59.?Questions for Discussion:? Why was a repeat panel run?? What about these results is concerning — are these labs what you expected??? Why was the?EKG?run?? What is the significance of comparing the?EKG?to previous EKGs and what is the significance of the?EKGfindings? ?What additional information would you like at this point?? Is this a critical situation?? What would you do?next?Case Discusion Part TwoThe labs we see in Part One don’t fully explain the clinical picture - DM’s sodium level may appear marginally low until we notice that her glucose is significantly elevated. Hyperosmolarity resulting from hyperglycemia can falsely lower sodium levels necessitating a correction equation: (1.7 x [(Blood Glucose-100)/100]) to reach a corrected sodium level of 138 which is within normal. It’s also not unusual to encounter significantly low sodium levels in the setting of cirrhosis/hepatic encephalopathy. DM’s potassium is borderline/mildly elevated but not enough to explain what we are seeing, and is lower than we might expect given end stage renal failure and missed dialysis. DM’s anion gap is elevated with a low CO2 suggesting a possible metabolic acidosis, but her glucose level is lower than we might typically expect in frank DKA. In order to truly understand lab values, we need to know when they were drawn and how they were run? Intralab and interlab variation are always consideration, and critical labs requiring action should always be questioned, particularly if they don’t match your clinical picture. If the initial labs for DM were drawn in the morning then these labs may no longer reflect DM’s actual panel. We would want to know if DM’s symptoms have worsened since these labs were drawn. Acute changes in sodium can play a significant role in obtundation, but potassium is also susceptible to dramatic changes in short period of times. This is partially due to the continuous active transport of potassium between intracellular and extracellular. Because potassium is the primary intracellular cation, it is susceptible to falsely elevated lab values, or pseudohyperkalemia. This can happen when red blood cells lyse either as a result of difficulty drawing the sample, difficulty handling the test tube once drawn, or mishandling at any point in the process. Potassium from inside the cell rushes out and produces falsely elevated levels, often in the arena of 6.0 to 8.0. This phenomenon can also be seen in patients with dramatically elevated platelet levels (>1,000,000/cm3) or dramatically elevated white blood cell counts (>70,000/cm3). For this reason elevated potassium should always be confirmed with a redraw, particularly in the absence of any signs and symptoms common to hyperkalemia. For this reason, and given an initial potassium level of 5.5 from the hospice nurse and the subsequent potassium level of 6.7, we should probably draw one more potassium level to confirm the elevated potassium. While we’re waiting for this final potassium redraw, however, we are faced with the question of whether or not to treat her apparent hyperkalemia. If we seek to aggressively lower her potassium and the redraw comes back at 4.0, then we run the risk of inadvertently pushing DM into hypoglycemia. But if we fail to treat, DM may become more symptomatic while we wait. To help us with our decision making, we ask ourselves if DM is demonstrating classic signs and symptoms of hyperkalemia. DM is confused, which is more often associated with sodium abnormalities, but it is certainly possible to see with potassium abnormalities, along with descending paralysis in more severe hyperkalemia. More concerning with hyperkalemia is cardiac toxicity, so at the first suspicion of hyperkalemia an EKG should be run. The extracellular/intracellular potassium gradient is responsible for cardiac repolarization. Because such an overwhelming percentage of the body’s potassium is intracellular (98%), even small changes in extracellular potassium can have dramatic effects on cardiac repolarization leading to some fairly predictable EKG signs:112395022225000 Getting an EKG for DM can help confirm any suspicions of hyperkalemia. It is important to note, however, that the progression and/or severity of EKG changes do not always directly correlate with the serum potassium. In other words, the EKG of a patient with a potassium of 6.5 may look worse than that of a someone else with a K of 7.0. It is important to compare your current EKG to a prior, non-hyperkalemic EKG for appropriate interpretation.As potassium levels rise and repolarization slows, we can begin to see P waves flatten and heart rate slow down, as we see with DM. At potassium levels above 5.5, we may see peaked “tented” T waves, generally in several contiguous leads, and notable peaked compared to previous non-hyperkalemic EKGs. Prolonged PR waves may also be seen. As Potassium levels exceed 6.5 we may see loss of P wave. QRS complexes > 120ms, as we see in DM, are of particular concern, especially if previous EKGs show a normal QRS complex. Potassium levels greater than 8 are often accompanied by dramatic EKG changes and should be considered life-threatening. Levels greater than 8 with normal EKG changes should raise questions about the veracity of the potassium level, but treatment should be initiated while recheck is pending. Part ThreePotassium was redrawn and?DM?received Calcium Gluconate 9mEq while results were being posted.? Redraw confirmed K of 6.7 mEq/L.? Point of care glucose showed blood sugar of 300mg/dL and?DM?was given 5 units of regular insulin iv, 50ml?D50W, 50mEq sodium bicarbonate, 3 amps of albuterol and 30 gm kayexolate.? Nephrology was consulted, DM was admitted to medicine service with diagnosis of hyperkalemia in the setting of chronic kidney disease and plans for dialysis in the morning.Questions for Discussion:Discuss the rationale and appropriateness for DM’s treatments, along with alternatives and controversies in hyperkalemia management. Case Discussion Part ThreeHyperkalemia results from either a high potassium intake, a transcellular potassium shift, or - as we see with DM - decreased potassium excretion. Potassium excretion alterations most often occur due to decreased renal function, as we see in DM, although it can also be caused by medications that interfere with aldosterone like spironolactone and epleronone, calcineurin antagonists like cyclosporine, Bactrim, heparin, and – often overlooked – potassium supplements. Even if DM’s EKG was perfectly normal, potassium levels above 6 are considered risk for “impending” EKG changes, so treatment should be initiated. The safest approach to initial, pre-confirmatory treatment is one that would protect (“stabilize”) cardiac tissue from the toxic effects of potassium without putting DM at risk for hypoglycemia in the event that her potassium was in fact falsely elevated. CalciumThe agent used most commonly to stabilize the myocardium is Calcium, either as the gluconate or the chloride salt. The onset is rapid, with normalization of EKG often seen within minutes of calcium infusion; if 2gm of calcium gluconate is infused without symptom resolution, it is reasonable to repeat a dose. DM received 2 g calcium gluconate (9 mEq) with prompt effects – her QRS quickly normalized, her heart rate increased and her peaked T waves resolved. Calcium’s stabilization lasts for 30-60 minutes, so if symptoms return at this point redosing is required. When giving calcium infusion we must consider calcium gluconate versus calcium chloride. Calcium chloride has the benefit of containing more elemental calcium. One gram of calcium gluconate contains 4.5 mEq of calcium, while 1 gm of calcium chloride contains 13.6 mEq. Calcium chloride is also widely available in code carts in the form of a prefilled syringe. However, calcium chloride is considerably irritating upon administration and can cause significant tissue damage if extravasated. Calcium gluconate is much safer to administer and is generally the preferred agent – 1 to 2gm is often given with good effect. Calcium chloride is best saved for life threatening situations such as systole or impending torsades. Of note, there are case reports of patients on digoxin experiencing digoxin toxicity immediately after receiving iv calcium, but causality is uncertain; iv calcium is generally considered safe even in patients receiving digoxin if the calcium is diluted and given over 15-30 minutes. Consideration should be made in patients actively experiencing digoxin toxicity – some practitioners advocate using magnesium in these patients, although data is limited. Note that Calcium will protect the myocardium from potassium’s toxic effects but will not decrease potassium levels at all. This makes it ineffective as monotherapy, but safe to administer to DM while we are waiting for her conformation draw.ShiftOnce DM’s hyperkalemia is confirmed we begin treatment aimed at reducing potassium levels. The first phase of this treatment is “Shifting”, utilizing agents to shift potassium from the extracellular environment to intracellular. Insulin is often the first agent used for this purpose. ATPase dependent Na-K pumps located in liver and skeletal muscle shift potassium into cells in the presence of insulin and/or adrenergic agonists. 10 units of insulin will usually decrease serum potassium by 0.5-1.0 mEq/L although hypoglycemia becomes a consideration. In renal failure patients clear insulin at a slower rate and run a higher risk of hypoglycemia, so patients with eGFR<30 ml/min often receive 5 units of insulin, as we see in DM. Similar to insulin, adrenergic agonists (albuterol is the preferred agent in hyperkalemia management) will work on the Na-K-ATPase pump and drive potassium back into the cell and can be effective in the acute treatment setting by lowering potassium 0.5-1.0 mEq/L within 30 minutes with a duration of action of at least 2 hours. There is evidence that some patients are resistant to albuterol’s hypokalemic effect, so albuterol is discouraged as monotherapy and is more appropriate as part of a combined treatment approach where it’s been shown to exhibit an additive effect with insulin to reduce serum potassium. In order to achieve an effective dose, 10-20mg of nebulized albuterol should be given – note that this is a much higher dose than often seen but is necessary for effect. DextroseDextrose is often given as part of the hyperkalemia protocol in part to stimulate endogenous production of insulin, but moreover to protect the patient from the hypoglycemic effect of administered insulin. For DM we have two considerations – first of all, dextrose is not always necessary in patients with glucose levels greater than 300 mg/dL so we might argue against giving dextrose in DM. However, patients with decreased renal function are at increased risk of hypoglycemia due to impaired renal clearance of insulin. When CrCl decreases below 30ml/min, insulin clearance can be dramatically prolonged while dextrose metabolism is not impaired at all; patients in renal failure receiving a single amp of dextrose will often clear the dextrose within 20-30 minutes while the hypoglycemic effect of insulin will continue up to 60 minutes after administer. For this reason, many euglycemic patients receiving 10 units insulin and 25gm dextrose will become significantly hypoglycemic within 30-40 minutes of administration. While patients with initial glucose levels above 300mg/dL may not require any dextrose at all, patients with normal glucose levels will require much more than one amp of dextrose ; any appropriate management requires blood glucose monitoring every 20-30 minutes for at least 1 hour following insulin administration. Many protocols address the risk of hypoglycemia by infusing D10W after insulin administration, or by preparing insulin drips in a solution of D10W. Sodium BicarbonateOnce a mainstay of treatment, NaHCO3 was theorized to push potassium into the cell by using a sodium-hydrogen exchange pump. Unfortunately, several studies have failed to show a strong effect for NaHCO3, and bicarb therapy has largely fallen out favor. Some clinicians reserve its use for patients with hyperkalemia and acidemia, where the Na+/H+ exchanger required is more likely to be in an active mode. Limited data suggest a potential additive effect with insulin but overall mixed data suggests that sodium bicarbonate should never be used as monotherapy and is best employed in a combined approach for severely acidotic patients. One might argue that sodium bicarbonate was not clearly indicated in DM, but many clinicians would suggest that if bicarb is to be given, it is better to give in an infusion of 150mEq/L than in a 50 mEq push such as DM received.Sodium Polystyrene SulfonateCation exchange resins like SPS or Kayexalate exchange sodium for potassium, with 30g of SPS potentially removing 120mEq of potassium. SPS should theoretically increase the amount of potassium in stool, and is often mixed with sorbitol to induce osmotic diarrhea. This is not a fast way of decreasing serum potassium, and multiple studies have shown the potassium reducing effects of SPS to be equal to those of other non-resin cathartics. Many clinicians point to the lack of evidence in acute cases as a reason to avoid SPS, along with the risk of GI necrosis. Most studies find them to work slowly over a 24 hour period. However, as in the case of DM, it is often used along with other treatments as a means of eliminating potassium from the body. DM received kayexolate orally although it can also be given rectally – either way SPS should be used cautiously and only when necessary. Loop DiureticsLoop diuretics such as furosemide can be used in patients capable of producing urine, and is an often overlooked mechanism of eliminating potassium. Diuresis may take 15 minutes (IV) or longer (PO) depending on the perfusion of the kidneys. DialysisDialysis is the quickest, most efficient way to remove potassium from the patient’s body. Due to the invasive nature it is reserved for patients already on dialysis with severe hyperkalemia, patients who can often be refractory to traditional hyperkalemia treatments. For these patients dialysis can substantially drop serum potassium levels and (1-1.5meq/L/hr) and is a reasonable first line treatment.For DM’s follow up care, we should further consider continuous cardiac monitoring and serum potassium redraws every 1-4 hours until potassium levels stabilize. Once DM is out of the acute care window we can further pursue ongoing causes of hyperkalemia and means of preventing further hyperkalemia episodes. ................
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