Case Report

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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 32 (2014) 286.e1-286.e4

Hypokalemia-induced pseudoischemic electrocardiographic changes and quadriplegia?

Abstract

Hypokalemia is a common biochemical abnormality. Severe hypokalemia can produce cardiac rhythm alterations and neuro- logic manifestations. Early detection and treatment allow clini- cian to prevent morbidity and mortality from cardiac arrhythmias and respiratory failure. Here, we describe a case of severe hypokalemia inducing pseudoischemic electrocardiograph- ic (ECG) alterations and quadriplegia, in a patient affected by chronic diarrhea. Electrocardiographic alterations and Neurologic manifestations completely disappeared after potassium replace- ment; however, prolonged potassium supplementation was required to achieve the normalization of plasmatic Potassium levels. Consecutive figures show ECG improvement until normal- ization of ECG findings.

Hypokalemia is a common biochemical abnormality in approx- imately 11% of patients admitted to the emergency department (ED) [1]. Early detection and treatment allow clinician to prevent morbidity and mortality from cardiac arrhythmias and respiratory failure. Moreover, a relationship between hypokalemia and quadri- plegia has been reported in some cases [2]. Here, we describe a case of severe hypokalemia inducing pseudoischemic ECG alterations and quadriplegia.

A 77-year-old woman presented to the ED complaining of Epigastric pain, vomiting, generalized weakness, impossibility to walk, and dysphagia. Epigastric pain and vomiting acutely appeared 3 hours before to the ED arrival, whereas weakness and dysphagia progressively developed in 48 hours.

The patient had undergone duodenocephalopancreasectomy 6 weeks before because of duodenal adenocarcinoma. Few days after discharge from surgery clinic, diarrhea developed with approximately

6 to 8 stool emissions per day. The patient was also affected by diabetes mellitus and mild aortic stenosis (a preoperatory balloon valvuloplasty downstaged the stenosis from severe to mild). Her drug therapy included pantoprazole, metformin, insulin-detemir, aspirin, and Pancreatic enzymes.

At the ED, blood pressure was 110/60 mm Hg, pulse rate was 76 beats per minute, oxygen saturation was 94%, temperature was 36.0?C. At physical examination, the patient appeared bed ridden, weak, and dysphagic. Cardiac examination showed a regular S1 and S2 with a systolic 2/6 murmur. Thoracic examination was

? Authors’ contribution: All authors contributed in the clinical management of the patient as well as in the preparation and revision of the manuscript.

within normal limits. The abdomen was soft, with a diffuse tenderness at palpation; bowel sounds were hyperrepresented; and there was no hepatosplenomegaly. At neurologic examination, there were flaccid quadriplegia and hyporeflexia. Bilateral ankle swelling was present.

At the ED, electrocardiogram (ECG) (Fig. 1A) showed sinus rhythm, Right bundle-branch block (RBBB) pattern with diffuse ST- segment depression, mostly marked in V₂ to V₃ leads. Therefore, a troponin T assay showed raised plasmatic concentration (0.295 ng/mL, normal value b 0.014). To rule out signs of posterior myocardial ischemia or right ventricle overload, right leads were obtained (Fig. 1B), and an echocardiogram was performed, showing normal right and left ventricular kinetic without regional abnormalities. Brain computed tomographic scan excluded acute abnormalities. Blood tests showed extremely low potassium levels (1.3 mEq/L, n.v. 3.5-5.0 mEq/L). Potassium replacement was started, and the patient was admitted to our internal medicine inpatients unit for further evaluation and treatment. A central venous catheter (peripherally inserted central catheter) was placed, and because of dysphagia and malnutrition, total paren- teral nutrition was started. Because potassium levels were persistently low after 80 mEq KCl intravenous infusion, potassium supplementation of 200 mEq/d was started. Moreover, because of the presence of severe hypoproteinemia with swelling of lower limbs, intravenous spironolactone was prescribed. Because stool cultures revealed the presence of carbapenemic-resistant Pseudo- monas aeruginosa, probiotics were prescribed.

After 2 days, potassium levels were 1.8 mEq/L; dysphagia

disappeared, and stool emissions were reduced to 3 to 4 per day (Fig. 2). After 5 days of potassium administration, quadriplegia disappeared (Fig. 3). After 10 days, potassium levels returned within normal values, with a complete disappearance of ECG alterations and normalization of troponin T levels (Fig. 4). Intravenous potassium supplementation was stopped. Diarrhea progressively disappeared, and a personalized diet was pre- scribed. Patient was discharged in good clinical conditions after 15 days of hospitalization.

The present case shows the occurrence of pseudoischemic ECG changes, and quadriplegia, induced by severe hypokalemia, completely disappeared after potassium replacement.

The patient, affected by chronic diarrhea, came to ED because of an acute upper abdominal symptoms and neurologic symptoms. It is conceivable that diarrhea was due to pancreatic insufficiency and gut dismicrobism with Pseudomonas aeruginosa overgrowth. Chronic diarrhea leads to severe hypokalemia with subsequent cardiologic and neurologic manifestation.

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286.e2 A. Mirijello et al. / American Journal of Emergency Medicine 32 (2014) 286.e1–286.e4

A

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B

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Fig. 1. A, Twelve-leads ECG showing sinus rhythm, RBBB pattern with diffuse ST-segment depression, mostly marked in V₂ to V₃ leads. B, Right leads (V₃-V₆) with RBBB pattern (K+, 1.3 mEq/L).

Hypokalemia is a common biochemical abnormality in the ED and internal medicine patients [1]. The most frequent causes are diarrhea, vomiting, inappropriate Fluid replacement, and diuretics. The effect of hypokalemia on cell membrane is to increase the resting membrane potential and to increase the duration of the action potential and refractory period. Several electrolyte distur- bances are associated with specific or nonspecific ECG changes [3]. In particular, hypokalemia can produce PR prolongation, T-wave inversion, ST-segment depression, U wave (a positive deflection after the T wave best seen in leads V₂-V₃), T- and U-wave fusion, prolonged QT interval, a variety of tachyarrhythmias, and rarely atrioventricular block [4]. However, in the ED setting and in multimorbid patients attributing the causal role of ECG findings directly to electrolytes disturbances, excluding a priori an ischemic

etiology could be difficult. Severe hypokalemia (b 2.5 mEq/L) can also produce ascending muscle weakness that begins with the legs and progresses to the trunk and arms, mimicking Guillan-Barre syndrome [5].

In case of diffuse ECG abnormalities associated to troponin T elevation, hypokalemia must be considered. In our patient, both ECG alterations and neurologic symptoms dramatically improved after potassium replacement. However, a prolonged supplementa- tion (10 days) with high doses of intravenous potassium was required to normalize kalemia. Considering potassium distribution between intracellular (98%) and extracellular (2%) fluids, it is conceivable that clinical and laboratory manifestations in our patients were due to severe intracellular and extracellular potassium depletion [6].

A. Mirijello et al. / American Journal of Emergency Medicine 32 (2014) 286.e1–286.e4 286.e3

Fig. 2. Twelve-leads ECG showing sinus rhythm, diffuse ST-segment depression, U waves in V₂/V₄ (K+, 1.8 mEq/L).

Antonio Mirijello MD Emanuele Rinninella MD Francesca De Leva MD Alberto Tosoni MD Gabriele Vassallo MD Mariangela Antonelli MD Giovanni Addolorato MD Raffaele Landolfi MD Department of Medicine

Catholic University School of Medicine

Rome, Italy E-mail address: antonio.mirijello@gmail.com

http://dx.doi.org/10.1016/j.ajem.2013.09.033

References

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   G. Etiology and symptoms of severe hypokalemia in emergency department patients. Eur J Emerg Med 2013 in press.

   Gennari FJ. Hypokalemia. N Engl J Med 1998;339(7):451-8.

2. Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: classification, differential diagnosis, and caveats. Cleve Clin J Med 2011;78(6):404-14.
3. Glancy DL, Wilklow FE, Rochon BJ. Electrocardiogram after 2 weeks of diarrhea. Proc (Bayl Univ Med Cent) 2010;23(2):173-4.
4. Valtier B, Mion G, Pham LH, Brochard L. Severe hypokalemic paralysis from an unusual cause mimicking the Guillain-Barre syndrome. Intensive Care Med 1989;15(8):534-5.
5. Boddy K, King PC, Hume R, Weyers E. The relation of total body potassium to height, weight, and age in normal adults. J Clin Pathol 1972;25(6):512-7.

   

   Fig. 3. Twelve-leads ECG showing sinus rhythm, diffuse T inversion in V₁ to V₃ (K+, 2.9 mEq/L).

   286.e4 A. Mirijello et al. / American Journal of Emergency Medicine 32 (2014) 286.e1–286.e4

   I

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   V1

   V4

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   Fig. 4. Twelve-lead ECG showing normal findings (K+, 4.1 mEq/L).