# Situation: A 54-year-old man weighing 60 kg is on post-operative day 2 after a bowel resection complicated by bleeding. On the day of surgery, his blood pressure fell to 82/50 mmHg for about 20 minutes until blood transfusion and intravenous fluids restored it. His creatinine before surgery was 1.0 mg/dL (88 µmol/L), and he has no history of kidney disease. He has received no contrast dye and no nephrotoxic drugs, and a bladder scan shows an empty bladder. Today his blood urea nitrogen (BUN) is 46 mg/dL (16.4 mmol/L), his creatinine is 1.8 mg/dL (159 µmol/L), and his urine output has averaged 22 mL/h over the last 14 hours. The team is managing him for acute kidney injury (AKI). On post-operative day 4, he has passed no urine for 8 hours although his blood pressure is normal, and his serum potassium is 6.8 mEq/L (normal 3.5–5.0 mEq/L) with peaked T waves. Calcium gluconate and insulin with dextrose were given, and his electrocardiogram (ECG) has returned to his baseline. Two hours later, his potassium is still 6.8 mEq/L. Which treatment should the nurse prepare for to remove the excess potassium?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629712  
> language: ko  
> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: A 54-year-old man weighing 60 kg is on post-operative day 2 after a bowel resection complicated by bleeding. On the day of surgery, his blood pressure fell to 82/50 mmHg for about 20 minutes until blood transfusion and intravenous fluids restored it. His creatinine before surgery was 1.0 mg/dL (88 µmol/L), and he has no history of kidney disease. He has received no contrast dye and no nephrotoxic drugs, and a bladder scan shows an empty bladder. Today his blood urea nitrogen (BUN) is 46 mg/dL (16.4 mmol/L), his creatinine is 1.8 mg/dL (159 µmol/L), and his urine output has averaged 22 mL/h over the last 14 hours. The team is managing him for acute kidney injury (AKI).

On post-operative day 4, he has passed no urine for 8 hours although his blood pressure is normal, and his serum potassium is 6.8 mEq/L (normal 3.5–5.0 mEq/L) with peaked T waves. Calcium gluconate and insulin with dextrose were given, and his electrocardiogram (ECG) has returned to his baseline. Two hours later, his potassium is still 6.8 mEq/L. Which treatment should the nurse prepare for to remove the excess potassium?

## 보기

1. Furosemide intravenously to increase potassium excretion
2. A second dose of calcium gluconate intravenously
3. Salbutamol (albuterol) 10 mg by nebulizer
4. Hemodialysis through a temporary dialysis catheter **✔ 정답**

**정답: 4**

## 해설

Hyperkalemia is treated in three steps: calcium stabilizes the heart, insulin with dextrose or salbutamol shifts potassium into cells, and potassium is then removed from the body. Shifting is temporary, and in an anuric client a loop diuretic cannot remove potassium because no urine is formed. Refractory hyperkalemia in kidney failure is an indication for kidney replacement therapy, so the nurse prepares for hemodialysis.

## 심화 해설

Why the answer is hemodialysis
Hyperkalemia management follows a three-step sequence: first stabilize the myocardium with calcium, then shift potassium into cells with insulin plus dextrose or a beta-2 agonist, and finally remove potassium from the body. In this patient, calcium gluconate and insulin with dextrose were already given and the ECG normalized, but the potassium remained at 6.8 mEq/L two hours later. That means the shifting step did not lower the serum level enough, and the definitive removal step is now required.

In an anuric patient, potassium cannot be excreted through the kidneys, so a loop diuretic such as furosemide is ineffective. The bladder scan was empty, urine output has been minimal, and the patient has now passed no urine for 8 hours despite a normal blood pressure. This is not a prerenal volume problem that diuresis can fix; the kidney is not making urine. Therefore furosemide cannot remove potassium.

A second dose of calcium gluconate would only re-stabilize the cardiac membrane. It does not lower serum potassium at all. Salbutamol by nebulizer would shift potassium into cells temporarily, but the potassium has already proven refractory to a shifting strategy, and shifting does not remove potassium from the body. Key point! Calcium protects the heart; it never removes potassium. Insulin, dextrose, and salbutamol move potassium into cells; they do not eliminate it.

Refractory hyperkalemia with kidney failure and anuria is an indication for kidney replacement therapy. Hemodialysis through a temporary dialysis catheter directly removes potassium from the blood and is the definitive treatment when shifting measures fail and urine output is absent. The ISPD guideline supports dialysis as a suitable modality for AKI when kidney function is inadequate to manage metabolic complications such as severe hyperkalemia [1]. In low-resource and high-resource settings alike, kidney replacement therapy is a cornerstone of supportive care for severe AKI when life-threatening electrolyte abnormalities cannot be controlled by medical management alone [2].

Why this AKI is likely intrinsic, not prerenal
The patient had a hypotensive episode on the day of surgery with a systolic pressure around 82 mmHg for about 20 minutes. That degree of hypotension can reduce renal perfusion enough to cause acute tubular injury, even after blood pressure is restored. The preoperative creatinine was 1.0 mg/dL, and it has risen to 1.8 mg/dL by post-operative day 2. The BUN is also elevated at 46 mg/dL. The urine output of 22 mL/h over 14 hours is oliguric for a 60 kg adult, and by post-operative day 4 the patient is anuric. This pattern of rising creatinine with oliguria progressing to anuria after a hypotensive insult is consistent with acute tubular injury rather than simple dehydration. AKI is increasingly understood as a systemic syndrome in which the injured kidney cannot clear metabolites and electrolytes, leading to complications beyond the kidney itself, including hyperkalemia and cardiac dysrhythmia .

Why potassium is so dangerous here
A potassium of 6.8 mEq/L is a life-threatening emergency because the resting membrane potential of cardiac cells becomes less negative, making them more excitable initially and then paradoxically depressed. Peaked T waves are the earliest ECG sign. If untreated, this can progress to widened QRS, sine wave, ventricular fibrillation, or asystole. Calcium gluconate works within minutes to stabilize the cardiac membrane, but its effect lasts only 30 to 60 minutes and it does not change the serum potassium. Insulin with dextrose shifts potassium into cells within 15 to 30 minutes, but the effect also wears off. When the potassium remains at 6.8 mEq/L after these measures, the potassium burden is too large for temporary shifting to control, and removal is mandatory.

Comparing the options

| Intervention | Mechanism | Can it remove potassium in anuria? | Role in this case |
| --- | --- | --- | --- |
| Furosemide IV | Inhibits Na-K-2Cl cotransporter in thick ascending limb; increases urinary potassium excretion | No; requires urine output | Ineffective because the patient is anuric |
| Calcium gluconate repeat | Stabilizes cardiac membrane; no effect on serum potassium | No; does not remove or shift potassium | Only for ECG protection; potassium unchanged |
| Salbutamol nebulized | Beta-2 agonist; shifts potassium into cells via Na-K ATPase | No; temporary shift only | May lower potassium briefly but does not eliminate it |
| Hemodialysis | Removes potassium across a semipermeable membrane | Yes; independent of urine output | Definitive treatment for refractory hyperkalemia in AKI |

Watch out! Do not confuse membrane stabilization with potassium removal. Calcium gluconate is given first when ECG changes are present, but it is not a treatment for the potassium level itself. Key point! The sequence is stabilize, shift, remove. When shifting fails and the patient is anuric, removal by dialysis is the only effective option.References (research sources)

- [1]ISPD guidelines for peritoneal dialysis in acute kidney injury: 2020 update (adults).GuidelineCullis B, Al-Hwiesh A, Kilonzo K, McCulloch M, Niang A, Nourse P (2021) · DOI: 10.1177/0896860820970834

- [2]Kidney replacement therapy for acute kidney injury in low-resource settings: Lessons from Africa.Research articleAbdelhamid YM, Fayed A, Mayamba Nlandu Y, Ghosh S. (2026) · DOI: 10.5527/wjn.122148

## 임상 시나리오

Refractory Hyperkalemia in Anuric AKIWhen shifting fails, remove the potassium
Hyperkalemia management follows three steps: stabilize the myocardium with calcium, shift potassium into cells with insulin/dextrose or beta-2 agonists, then remove potassium from the body. If serum potassium remains 6.8 mEq/L after stabilization and shifting, definitive removal is required.

In an anuric patient, loop diuretics cannot excrete potassium because no urine is formed. Hemodialysis through a temporary dialysis catheter is the definitive treatment for refractory hyperkalemia in kidney failure.

CautionCalcium protects the heart but never lowers potassium. Insulin, dextrose, and salbutamol only shift potassium temporarily; they do not eliminate it. Repeating these agents does not replace the need for dialysis when potassium remains critically elevated.

## 핵심 개념

- **Refractory hyperkalemia** — Serum potassium that remains elevated despite stabilization and shifting treatments, requiring definitive removal via dialysis
- **Anuria** — Urine output less than 100 mL/day or no urine for 8-12 hours, indicating kidney failure
- **Peaked T waves** — Early ECG sign of hyperkalemia reflecting altered cardiac repolarization
- **Kidney replacement therapy** — Dialysis modalities that remove potassium and other solutes when kidneys cannot
- **Three-step hyperkalemia management** — Stabilize myocardium with calcium, shift potassium into cells, then remove potassium from body

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