CE - LETTER TO THE EDITOR

The emergency physician and the prompt management of severehyperkalemia

Alessandro Riccardi • Franco Tasso •

Luca Corti • Maria Panariello • Roberto Lerza

Received: 15 June 2012 / Accepted: 14 July 2012 / Published online: 29 July 2012

� SIMI 2012

Dear Editor,

We report a case that gives an opportunity to discuss the

importance of a faster approach to hyperkalemia, a poten-

tially lethal electrolyte disturbance because of threatening

dysrhythmias (asystole, ventricular fibrillation) that can

occur at any moment [1]. The availability of an immediate

measure of serum potassium is crucial, because the patient’s

ECG abnormalities are not often specific and significant

enough to give a clear indication to start a timely therapy [2].

Time of laboratory analysis or the lack of specific indications

especially in outpatient settings can cause a true therapeutic

delay and a risk for the patient’s life.

Case report

At 8:50 a.m., an 80-year-old woman was brought by

ambulance to our emergency department (ED) because of

dyspnea. The patient was immediately assisted. Vital

parameters showed a marked hypotension (80/? mmHg),

a heart rate of 90 beats per minute, a respiratory rate of 28

breaths/min, pulse oximetry 97 %, GCS 14, and capillary

blood glucose [500 mg/dL. She had a history of diabetes,

hypertension, and ischemic heart disease. She was taking

daily furosemide 60 mg, spironolactone 25 mg, bisoprolol

5 mg, ramipril 5 mg, glibenclamide and metformine, ace-

tylsalicylic acid. Supplemental oxygen and infusion of

NaCl 0.9 % were started immediately, and blood samples

were obtained. The patient was placed on a multiparameter

monitor that noted a very wide QRS complex. Arterial

blood gas analysis was quickly available, and showed a

metabolic acidosis with pH 7.22, pCO2 20 mmHg, pO2

130 mmHg, HCO3- 8.2 mmol/L, Lact 3.6 mmol/L, Na

116 mmol/L and K? 9.2 mmol/L. Immediately after a

standard electrocardiogram, two vials of calcium gluconate

were infused in 10 min, and in a second venous access a

slow infusion of sodium bicarbonate was started. The

sequences of the ECG changes induced by the therapy are

shown in Fig. 1a–c. In the first ECG, (Fig. 1a) a wide QRS

complex is present at the rate of 89/bpm. There is no

evidence of a P wave, and the QRS assumes a sine-wave

configuration. Fifteen minutes later the QRS complex has

markedly narrowed (Fig. 1b), and subsequently there is a

reappearance of the P wave (Fig. 1c). The laboratory

analysis results were available 30 min later, and confirmed

a severe metabolic derangement with a potassium 10 mEq/

L, corrected sodium 138 mEq/L, glucose 1,251 mg/dL, and

a creatine phosphokinase 3,233 U/I. The renal function

tests showed a serum creatinine of 4.04 mg/dL and a BUN

336 mg/dL. Two months prior to admission, the patient

had normal renal function. She progressively improved

with further therapy, including i.v. insulin and a protocol of

hydration with normal saline.

Discussion

The case described is a clear example of a time-dependent

treatment of extreme hyperkalemia, and documents how

the timing of therapy can dramatically change the clinical

picture. Hyperkalemia is a true emergency and a challenge

for physicians [1, 2]. Cardiac complications may not relate

to precise serum potassium levels [2], and it is possible to

observe ventricular fibrillation as the primary event of

A. Riccardi (&) � F. Tasso � L. Corti � M. Panariello � R. Lerza

S.C. Medicina e Chirurgia d’Accettazione e d’Urgenza,

Ospedale San Paolo, Via Genova c/o, Savona 17100, Italy

e-mail: dottriccardi@yahoo.it

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Intern Emerg Med (2012) 7 (Suppl 2):S131–S133

DOI 10.1007/s11739-012-0838-1

Fig. 1 The sequences of the

ECG changes induced by the

therapy: a a wide sine wave

QRS complex without a P wave;

b 15 min later the QRS complex

markedly narrowed; c finally,

we observe the reappearance of

the P wave

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hyperkalemia or even a normal ECG in cases of marked

hyperkalemia [1–3]. In fact, the known correlation between

ECG changes and serum potassium levels may be influ-

enced by various other metabolic disturbances [2, 3] and by

potassium growth rate. Therefore it is often not advisable

to wait for the results of the laboratory before treating

patients, because lengthening the time to treatment can be

very dangerous.

In a retrospective study, Freeman et al. [4] report that

the beginning of an appropriate therapy for this disorder is

frequently delayed. Nevertheless, how can emergency

physicians draw a definite diagnosis before having blood

tests results? This is the real problem in an emergency.

Two aspects can help the physician evaluation, and they

are the patient history and the ECG changes, but they are

not always expressive [1, 2]. It is relatively easy to think of

hyperkalemia when faced with a patient on dialysis or with

known kidney problems. Therefore, the spectrum of

hyperkalemia is very broad, so it is less common to think of

a threatening hyperkalemia due to iatrogenic effects, dia-

betic ketoacidosis, severe dehydration, hypoadrenalism, or

rhabdomyolysis [3]. Sometimes, as in our case, the situa-

tion is so urgent that there is no time to investigate the

patient history, or alternatively, it may happen to have an

inexpressive history. The more classical findings on ECG

are generally well known to emergency physicians, but

severe hyperkalemia may occur also in presence of atypical

or minimal ECG findings [1–3]. For example, in the study

of Freeman et al. [4], peaked T waves at presentation are

only seen in 35 % of patients with potassium values

[6 mEq/L. Considering our case, how many physicians

would treat the patient before knowing their potassium

values in spite of the ECG findings? Moreover, many sit-

uations with a potential threat for the patient’s life are

probably underestimated. For this reason, in some cases we

believe that the expert physician should start the appro-

priate treatment for hyperkalemia before receiving labo-

ratory results.

Several medical textbooks and algorithms usually rec-

ommend a therapy relating to different measures of

potassium level. However, the real problem in emergency

medicine is the need to treat the patient as soon as possible,

sometimes without knowing the serum potassium value.

On the other hand, the rapid availability of the serum

potassium value is certainly a comfort in our treatment

decisions. In settings outside the hospital, in the ambulance

or in the ED of small hospitals, the lack of instrumentation

systems for blood gas analysis, or the rapid point-of-care

ability to check electrolytes can lead to a lack of useful

information and delay treatment decisions. So we believe

that today the adoption of technologic advancements

should be recommended in any context, because hyperka-

lemia is a relatively common condition.

Another important aspect of the therapeutic approach is

the hope that the medical literature will emphasize more

strongly the relevance and safety of empirical treatment

with intravenous calcium that, to date, is not found in many

resuscitation algorithms. For example, in Resuscitation

Council Guidelines 2010, intravenous calcium chloride is

recommended in the presence of hyperkalemia or hypo-

calcaemia, but it is not clearly stated that intravenous cal-

cium should be administered empirically in an attempt to

avoid the possibility to underestimate a life-threatening

condition as hyperkalemia [5]. Calcium chloride or cal-

cium gluconate can be also given safely at therapeutic

doses to patients who are normocalcemic. Calcium directly

antagonizes the myocardial effects of hyperkalemia on the

excitable cell membranes, it acts quickly in few minutes,

and it must be considered the first step of therapy in severe

hyperkalemia in an emergency [1]. In any patient who

might be hyperkalemic, instead of taking time to prove it, it

is advisable to initiate life saving therapy with a dose of

calcium, that will last 20 min, while you set about proving

the entity, and initiating other longer lasting therapy. This

could be done for any patient with known or unknown

renal failure who is a candidate for being hyperkalemic.

Many such patients will show ECG changes, when the

serum potassium is greater than 6.5 mEq/mL, but not all,

and sometimes the calcium therapy will simply be empir-

ical prudence while the exact details of the history and

magnitude of the hyperkalemia are being elucidated.

Conflict of interest None.

References

1. Pepin J, Shields C (2012) Advances in diagnosis and management

of hypokalemic and hyperkalemic emergencies. Emerg Med Pract

14:1–17

2. Wrenn KD, Slovis CM, Slovis BS (1991) The ability of physicians

to predict hyperkalemia from the ECG. Ann Emerg Med

20:1229–1232

3. Weisberg LS (2008) Management of severe hyperkalemia. Crit

Care Med 36:1–6

4. Freeman K, Feldman JA, Mitchell P et al (2008) Effects of

presentation and electrocardiogram on time to treatment of

hyperkalemia. Acad Emerg Med 15:239–249

5. Deakin CD, Nolan JP, Soar J, Sunde K, Koster RW, Smith GB,

Perkins GD (2010) European Resuscitation Council Guidelines for

Resuscitation 2010 Section 4. Adult advanced life support.

Resuscitation 81(10):1305–1352

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