Hyperkalemia due to renal failure case file

Hyperkalemia due to renal failure case file

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 52

A 54-year-old man is brought to the emergency department with complaints of generalized weakness, nausea, and an overall sense of illness. The patient symptoms have progressed insidiously over the past 2 to 3 days. His past medical history is remarkable for longstanding diabetes and poorly controlled hypertension. He is currently taking many medications that include a sulfonylurea, a diuretic, and an angiotensin-converting enzyme (ACE) inhibitor. On physical examination, the patient appears lethargic and ill. His temperature is 36.0°C (96.8°F), pulse rate is 70 beats per minute, blood pressure is 154/105 mm Hg, and the respiratory rate is 22 breaths per minute. His head and neck examination shows normal conjunctiva and mucous membranes. There is moderate jugular venous distention. The lungs have minor bibasilar rales. The cardiac examination reveals normal rate, no murmurs or rubs, and a positive S4. The abdomen is soft and nontender to palpation, with hypoactive bowel sounds and no organomegaly. The rectal examination is normal. Skin is cool and dry. Extremities demonstrate pitting edema to the knees bilaterally. On neurologic examination the patient moans and weakly localizes pain. He is oriented to person and place but cannot provide any further history. The initial rhythm strip is shown in Figure 52–1.

⯈ What is the most likely diagnosis?

⯈ What is the next step?

Figure 52–1. ECG rhythm strip.

ANSWER TO CASE 52:

Hyperkalemia Due to Renal Failure

Summary: A 54-year-old man with hypertension and diabetes complains of weakness, nausea, and a general sense of illness. His symptoms have progressed slowly over 3 days. His medications include a sulfonylurea, a diuretic, and an ACE inhibitor. On examination, he appears lethargic and ill. His BP is 154/105 mm Hg, HR 70 bpm, temperature 36.0°C (96.8°F), and respiratory rate 22 breaths per minute. The physical examination reveals moderate jugular venous distension, some minor bibasilar rales, and lower extremity edema. He is oriented to person and place but is not able to give further history. The ECG confirms a wide complex rhythm (Figure 52–2).

• Most likely diagnosis: Hyperkalemia
• Next step: Management of the ABCs, including immediate vascular access and continuous cardiac monitoring, rapid stepwise administration of medication to reverse the effect of excess potassium (calcium), shift potassium into cells (insulin, sympathomimetics, possibly sodium bicarbonate), and remove potassium from the body (sodium polystyrene sulfonate or diuretics). Arrange for emergency dialysis and admit to the hospital.

ANALYSIS

Objectives

1. Recognize the clinical settings, the signs and symptoms, and complications of hyperkalemia.
2. Understand the diagnostic and therapeutic approach to suspected hyperkalemia.

Figure 52–2. ECG.

Considerations

This patient has developed end-stage renal failure (also referred to as chronic kidney disease, stage 5), due to his longstanding hypertension and diabetes. His damaged kidneys have very little capacity to excrete potassium. ACE inhibitor therapy contributes to his potassium retention. Acidosis and blunted insulin response both lead to potassium shifts into the extracellular space. His cardiac cell membranes are destabilized by the high potassium level and he is at high risk of death by arrhythmia. His weakness and general sense of illness, while nonspecific, are very typical of untreated renal failure. Weakness can also be a prominent feature of severe hyperkalemia. It is important to suspect this condition from the history and ECG, because laboratory test results may be delayed and the patient could die before those test results become available.

Laboratory studies should be performed and in this patient case, the leukocyte count is 9000 cells/L, and the patient is mildly anemic with hemoglobin 10.5 and hematocrit 32%. Electrolytes show sodium of 134 mEq/L, potassium 7.8 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. BUN is 114 mg/dL and creatinine is 10.5. The serum glucose is 180 mg/dL (10 mmol/L). The serum amylase, bilirubin, AST, ALT, and alkaline phosphatase are within normal limits. A 12-lead ECG confirms the wide-complex rhythm shown previously. His CXR shows mild cardiomegaly and pulmonary vascular congestion.

This patient clinical presentation is fairly representative of hyperkalemia in renal failure. Hyperkalemia is a common complication of end-stage chronic kidney disease, though it can occur in many other clinical conditions. Symptoms of hyperkalemia may be nonspecific or even nonexistent, and are most often dominated by whatever illness has predisposed the patient to elevated potassium. Morbidity and mortality may result from delayed or inadequate treatment, since severe hyperkalemia may rapidly progress to arrhythmia and cardiac arrest. Early suspicion, prompt recognition of associated ECG changes, and prompt resuscitation with effective agent, are essential. Once resuscitated, the patient will require prompt consultation for emergent hemodialysis.

Approach To:

Suspected Hyperkalemia

CLINICAL APPROACH

Hyperkalemia is a severe metabolic emergency. A delay in treatment may lead to significant mortality. Up to one-quarter of patients with end-stage chronic kidney disease will have at least one episode of life-threatening hyperkalemia. Hyperkalemia can occur from many other conditions, including medication side effects, ingestion of potassium-containing supplements, crush injuries and burns, and redistribution resulting from acidotic states such as diabetic ketoacidosis. Many cases of hyperkalemia are discovered as an incidental laboratory finding. Clinical findings associated with hyperkalemia are summarized in Table 52–1.

Potassium Homeostasis

The average diet contains about 100 mEq of potassium per day, and most is excreted in the urine, with a smaller component excreted in the stool. Long-term balance is regulated in large part by the aldosterone system. Renal excretion can be markedly affected by any impairment of kidney function, and by a wide variety of medications. Two common and potent inhibitors of renal potassium excretion are the angiotensinconverting enzyme inhibitors and the potassium-sparing diuretics. The body has a very large intracellular store of potassium, with the serum potassium representing only about 2% of the total body store of approximately 3500 mEq. The serum level is tightly regulated to maintain appropriate gradients across cell membranes. Potassium is actively transported into cells in exchange for sodium by the Na-K-ATPase. Na-K-ATPase is a target of digitalis glycosides, so hyperkalemia is a prominent feature

of severe digoxin poisoning. Potassium uptake into cells is stimulated by insulin and beta-adrenergic drugs. In states of increased hydrogen ion concentration (acidosis), potassium may shift out of cells. Also, potassium follows osmotic gradients, so hyperosmolar states such as DKA may cause increased serum potassium.

Classification of Hyperkalemia

From a laboratory perspective, the normal range for serum potassium is 3.5 to 5.0 mEq/L. Levels from 5.1 to 5.5 mEq/L are generally not significant elevations. The range from 5.5 to 6.0 mEq/L is mild hyperkalemia and significant ECG changes would be unusual. Levels of 7.0 mEq/L or greater constitute severe hyperkalemia; prompt aggressive treatment is almost always warranted even if ECG changes are not severe. Although pseudohyperkalemia can result from hemolysis of the blood specimen prior to measurement, most clinical laboratories are attuned to this problem and will note hemolysis when it is detected.

ECG Changes of Hyperkalemia

One of the earliest ECG changes of hyperkalemia is a “peaked” appearance to the T wave. Unfortunately, there is no widely accepted scientific definition of a peaked T wave, though some authors have suggested imagining the T wave as a seat. If it is too pointed to sit upon comfortably, then it is likely peaked. Other described changes of hyperkalemia include widening of the QRS, prolongation of the PR interval, QT prolongation, ST changes (which may mimic myocardial infarction), wide P waves or the disappearance of P waves. Severe hyperkalemia generally causes a very wide QRS, which may progress to a sine wave pattern and asystole. A variety of blocks and dysrhythmias may also be seen.

Many textbooks describe a classic progression of ECG changes, and attempt to correlate those changes with usual levels of potassium. It is vitally important to understand that this correlation is poor. Patients may have severe hyperkalemia with minimal ECG changes, and prominent ECG changes with mild hyperkalemia. It is well described that patients with mild ECG changes may suddenly progress to severe changes, and a stepwise progression cannot be counted upon. Despite these caveats, the ECG remains the best available guide to the initial therapy of hyperkalemia.

Therapy

Calcium given intravenously is first-line lifesaving treatment. Calcium stabilizes cardiac cell membranes and can counteract hyperkalemia within seconds to minutes. Unfortunately the effect is not sustained and fades within 10 to 20 minutes, so additional agents are required. Because of the short-lived effect and potential downsides of hypercalcemia, this author reserves calcium for patients who demonstrate ECG changes suggestive of hyperkalemia. Calcium should be given to all dialysis patients who are in cardiac arrest, as hyperkalemia is very frequently a contributing cause of the arrest. Historically it was believed that calcium was contraindicated in potential digoxin toxicity, because the heart might undergo a tetanic contraction from which the patient could not be resuscitated. This historical concern has not been supported by current science (see Table 52–2).

Calcium is available in two forms, as calcium chloride and calcium gluconate. Calcium chloride contains approximately three times as much elemental calcium per unit volume, and is considerably more caustic to soft tissue. Thus, general practice is to use calcium chloride for patients in cardiac arrest or near-arrest situations, and calcium gluconate for patients with less severe ECG changes.

Sodium bicarbonate given intravenously is a traditional second-line agent for hyperkalemia. It is thought to shift K into cells by reversing acidosis. It also raises extracellular sodium levels, which may have beneficial effects on membrane potentials. Some research has called into question the benefit of sodium bicarbonate. In animal studies, no consistent K-lowering effect could be demonstrated. However, this may not be an adequate model of academic renal-failure patients, and even some nephrologists who have questioned the efficacy of bicarbonate continue to recommend it.

Insulin therapy is a mainstay in the acute management of hyperkalemia. Five to ten units of regular insulin given IV can reliably lower serum potassium approximately 0.5 mEq/L for 1 to 2 hours. Of course this therapy can cause hypoglycemia, so the insulin is usually given with 25 g or 50 g of 50% dextrose. Some have advocated giving just the D50, expecting the patient endogenous insulin stores to lower the potassium. However, many patients who experience hyperkalemia will be diabetic and may have impaired or absent insulin release. Furthermore, it has been shown in animal studies that large osmolar loads may transiently increase serum potassium.

Albuterol, administered as an aerosol in doses of 10 to 20 mg, reliably lowers the serum potassium by an average of 0.5 mEq/L for 1 to 3 hours. The effect is additive with the effect of insulin. Albuterol also reduces the incidence and severity of rebound hypoglycemia often seen after glucose and insulin therapy. Albuterol has the advantage of requiring no IV access, and therefore can be started quickly. Side effects of tremor and tachycardia may limit its use in some patients, especially those with severe cardiovascular disease. Note that this is a substantially higher dose than typically used for the initial treatment of asthma.

Sodium polystyrene sulfonate or SPSS (Kayexelate and others) is an ion-exchange resin that is usually administered orally. It can also be given rectally as an enema, but this is generally less effective and carries some risk of colonic injury. SPSS exchanges sodium for potassium across the gut, so patients who are severely volume overloaded may not tolerate this therapy. Onset of action takes several hours. This medication is contraindicated in cases of ileus or suspected bowel obstruction or perforation. It is more effective for maintenance therapy than for acute management.

If the patient is not completely anuric, diuresis is a remarkably effective way to excrete large quantities of potassium. This will not be effective for the end-stage kidney disease patient who has been on dialysis for years, but it is appropriate for many patients with acute hyperkalemia due to dehydration, rhabdomyolysis, or medication effects. Once intravascular volume is restored with crystalloid, loop diuretics such as furosemide can be given to promote potassium excretion.

Dialysis is the ultimate treatment of choice for all kidney disease patients with significant hyperkalemia. However, it is time-consuming and not always immediately available. Reliable vascular access and reasonably stable vital signs are prerequisites for hemodialysis, while the less-common peritoneal dialysis requires a peritoneal catheter.

COMPREHENSION QUESTIONS

52.1 A 55-year-old man presents in cardiac arrest. A dialysis fistula is present in the right arm. In addition to standard ACLS therapies, which of the following is most appropriate for this patient?

A. 25 g of 50% dextrose, IV push

B. Sodium bicarbonate, 50-mL IV push

C. Begin immediate hemodialysis

D. Calcium chloride, 20-mL slow intravenous push

52.2 A 45-year-old man is brought into the emergency center due to significant dehydration and weakness. His potassium level is noted to be 7.2 mEq/L. Which of the following statements is most accurate regarding his potassium level?

A. Hyperkalemia can usually be diagnosed by symptoms alone.

B. An ECG showing peaked T waves means the patient is stable and treatment can safely wait until laboratory results are obtained.

C. Hyperkalemia can mimic a myocardial infarction on the ECG.

D. Hyperkalemia is synonymous with kidney disease.

52.3 Which of the following statements regarding treatment of hyperkalemia in patients with some renal function is incorrect?

A. Administration of normal saline may hasten the excretion of potassium.

B. Administration of furosemide can hasten the excretion of potassium.

C. The combination of saline with a diuretic is often indicated because hyperkalemic patients are frequently dehydrated.

D. Patients with some renal function do not need dialysis even for severe hyperkalemia.

52.4 A patient with severe renal disease is found to have hyperkalemia, with tall, peaked T waves on ECG. Vascular access cannot be readily obtained, but vital signs are stable. Which of the following would be appropriate temporizing measures?

A. Inhaled albuterol 2.5 mg in 3 mL saline

B. Oral sodium bicarbonate with rectal sodium polystyrene sulfonate

C. Inhaled albuterol 20 mg, with oral or rectal sodium polystyrene sulfonate, 30 g

D. Oral dextrose 25 g

ANSWERS

52.1 D. Calcium is the only agent with rapid and reliable enough onset to potentially help this patient. Bicarbonate might be appropriate, but its onset is slower than calcium and its effect is more disputed. Dialysis requires a hemodynamically stable patient.

52.2 C. The ST-segment and T-wave changes of hyperkalemia may mimic the ECG appearance of myocardial infarction. The nonspecific symptoms typical of hyperkalemia are also often seen in patients with MI, particularly elderly patients. Peaked T waves indicate that the heart is significantly affected by hyperkalemia and the patient should not be considered stable. Many conditions and medications may cause hyperkalemia, not just renal failure.

52.3 D. Dialysis is definitive therapy for hyperkalemia. Patients who have some residual kidney function can sometimes be managed without resorting to dialysis, but it should always be available for those who fail to respond quickly.

52.4 C. High-dose inhaled albuterol (10-20 mg) can reliably lower serum potassium with reasonable safety. SPSS can remove potassium through the GI tract, but its effect is slow. Oral dextrose and oral bicarbonate have no role. Standard doses of albuterol have too slight an effect on potassium levels.

CLINICAL PEARLS

⯈ In a patient with known or suspected renal failure, ECG changes consistent with hyperkalemia should be treated immediately as a life-threatening emergency. Do not await laboratory confirmation.

⯈ The ECG findings of hyperkalemia can progress very rapidly, and do not reliably pass through all the stages of the “typical” textbook presentation.

⯈ Intravenous calcium is the antidote of choice for life-threatening arrhythmias related to hyperkalemia, but its effect is brief and additional agents must be used.

⯈ Symptoms of renal failure and hyperkalemia are usually nonspecific, so risk factors must be used to suspect the diagnosis.

REFERENCES

Evans KJ, Greenberg A. Hyperkalemia: a review. J Intensive Care Med. 2005;20(5):272-290. 

Kamel KS, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol Dial Transplant. 2003;18:2215-2218. 

Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med. 2011;40(1):41-46. 

Mahoney BA, Smith WA, Lo DS, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. 

Sood MM, Sood AR, Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc. 2007;82(12):1553-1561. 

Watson M, Abbott KC, Yuan CM. Damned if you do, damned if you don’t: potassium binding resins in hyperkalemia. Clin J Am Soc Nephrol. 2010;5(10):1723-1726.

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