Is the plan to increase torsemide and transition from enoxaparin to heparin appropriate for managing hyperkalemia in a patient with CKD and impaired renal function?

Assessment of the Proposed Plan of Care

This plan is inappropriate and potentially dangerous—the proposed interventions will not adequately address severe hyperkalemia (K⁺ 6.4 mEq/L) and may worsen the patient's condition. The plan fundamentally misunderstands hyperkalemia management and makes critical errors regarding both torsemide dosing and anticoagulation switching.

Critical Problems with the Current Plan

Problem 1: Torsemide Will Not Lower Potassium Effectively

• Loop diuretics like torsemide are only effective for potassium elimination in patients with adequate renal function 1
• With an eGFR of 30 mL/min/1.73 m², this patient has Stage 3b-4 CKD, where loop diuretics have markedly reduced efficacy for potassium excretion 1, 2
• The FDA label for torsemide confirms that in renal impairment, "a smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action of any given dose of diuretic is reduced" 3
• Increasing torsemide from 20 mg to 40 mg will primarily cause volume depletion and hypotension, not meaningful potassium lowering 3

Problem 2: The Anticoagulation Switch is Dangerous and Illogical

• Switching from enoxaparin to unfractionated heparin (UFH) 5,000 units SQ q12h is grossly inadequate for treating active DVT/PE 4
• The dose of 5,000 units q12h is a prophylactic dose, not a therapeutic dose for established thromboembolic disease 4
• UFH also causes hyperkalemia through aldosterone suppression—this switch will not resolve the hyperkalemia 5
• A case report documents heparin-induced hyperkalemia in a patient with similar renal function (CrCl 23-27 mL/min), where discontinuation of heparin led to resolution as plasma aldosterone increased sixfold 5
• The clinical note's assertion that "guidelines recommend discontinuation or switching to UFH in CKD" is not supported by the evidence provided and misrepresents anticoagulation management

Problem 3: Failure to Address the Immediate Cardiac Risk

• K⁺ 6.4 mEq/L represents moderate-to-severe hyperkalemia with significant arrhythmia risk 1
• The plan contains no mention of obtaining an ECG to assess for hyperkalemic changes (peaked T waves, widened QRS, prolonged PR interval) 1, 6
• There is no provision for cardiac membrane stabilization with IV calcium if ECG changes are present 1, 6
• The plan relies entirely on interventions that will take days to work (if they work at all), leaving the patient at ongoing cardiac risk 1

What Should Actually Be Done

Immediate Management (First 24 Hours)

• Obtain a 12-lead ECG immediately to assess for hyperkalemic cardiac changes 1, 6
• If ECG changes are present, administer IV calcium gluconate (10%): 15-30 mL over 2-5 minutes for cardiac membrane stabilization 1, 6
• Administer insulin 10 units IV with 50 mL D50W to shift potassium intracellularly (onset 15-30 minutes, duration 4-6 hours) 1, 6
• Consider nebulized albuterol 10-20 mg over 15 minutes as adjunctive therapy to augment intracellular potassium shift 1, 2
• Recheck potassium within 1-2 hours after acute interventions to assess response 1

Addressing the Root Causes

• Discontinue enoxaparin entirely—do not switch to UFH 7, 5

  • Both enoxaparin and UFH suppress aldosterone synthesis and contribute to hyperkalemia 5
  • The patient has Factor V Leiden with history of DVT/PE, but hematology must be consulted urgently to determine if anticoagulation can be safely interrupted or if alternative agents (warfarin, direct oral anticoagulants) are appropriate 7
  • Enoxaparin is particularly problematic in CKD due to accumulation and increased bleeding risk 4

• Initiate a newer potassium binder immediately 7, 8, 9

  • Patiromer or sodium zirconium cyclosilicate (SZC) are the preferred agents for chronic hyperkalemia management in CKD 7, 9
  • These agents have been shown to maintain normokalemia for up to 52 weeks in patients with CKD on RAAS inhibitors 8
  • Do not rely on sodium polystyrene sulfonate (Kayexalate) alone—the patient has already refused it, and newer binders are safer and more effective 7, 9

Torsemide Considerations

• Do not increase torsemide to 40 mg daily 3
• The patient has "only trace edema" and is "not volume overloaded"—there is no indication for increased diuresis 3
• In hepatic disease (if present) or advanced CKD, torsemide can cause "sudden alterations of fluid and electrolyte balance" and worsen azotemia 3
• Maintain torsemide at 20 mg daily and focus on other interventions for hyperkalemia management 3

Monitoring Protocol

• Recheck BMP within 4-6 hours after acute interventions, not "tomorrow" 1, 6
• Once stabilized, check potassium and renal function every 5-7 days until stable, then weekly 7
• Monitor for rebound hyperkalemia, as temporary measures (insulin/glucose, albuterol) only last 2-4 hours 1, 2

Special Considerations for Long-Term Care Setting

• This patient's non-compliance and refusal of Kayexalate makes newer potassium binders even more critical 8, 9
• Patiromer has demonstrated efficacy in maintaining normokalemia in long-term care populations with CKD and HF 8
• Dietary potassium restriction must be reinforced, though newer binders may reduce the need for highly restrictive diets 7, 9
• The palliative care context requires balancing aggressive intervention with patient goals of care, but K⁺ 6.4 mEq/L poses immediate life-threatening risk that cannot be ignored 7, 1

Common Pitfalls Being Made in This Plan

• Overestimating the potassium-lowering effect of loop diuretics in advanced CKD 1, 3, 2
• Switching anticoagulation without addressing that all heparins cause hyperkalemia 5
• Using subtherapeutic anticoagulation dosing for active thromboembolic disease 4
• Delaying potassium rechecks for 24 hours when acute interventions are needed 1, 6
• Failing to obtain an ECG in a patient with moderate-severe hyperkalemia 1, 6
• Not utilizing newer potassium binders that would allow safer long-term management 7, 8, 9