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Case Report
Multiple Organ Dysfunction during Treatment of a Severe Hypokalemia in an Aged Female Patient: A Case Report
Zhao Xiaojing* MD, PhD, Gao Yanxia

Department of Emergency Medicine, the Second Affiliated Hospital of Xian Jiaotong University, China

*Corresponding author:  Dr. Zhao Xiaojing, Department of Emergency Medicine, the Second Affiliated Hospital of Xian Jiaotong University, Xian, 710004,China, Tel: 0086-029-87679403; Email: zxj47@aliyun.com

Submitted: 01-01-2016 Accepted: 02 -08-2016 Published: 02-18-2016 

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Hypokalemia is one of the most severe electrolyte imbalances in emergency which can lead to malignant arrhythmias and even cardiac arrest with serious consequences. Given that the aged patients with hypokalemia have been committed one or more chronic diseases, rapid reverse of hypokalemia with much amount of diluent administered in a short period might invoke multiple organ dysfunction. One 85-aged woman with severe hypokalemia and frequent ventricular fibrillation was treated with electrical cardioversion, anti-hypertension, and potassium infiltration orally and intravenously. Acute left heart failure, pneumonedema and respiratory failure were complicated. The patient died after further treatment had been refused by her family members. If the background of patients (age, gender, etc), the underlying disease, and aggregated effects of serial electrical cardioversion are neglected without delicate control of intravenous potassium supplement during the process of hypokalemia rebalance, the prognosis of patients would be very unacceptable and severe combinations, even multiple organ dysfunction and failure, could be complicated, although serum potassium concentration is rebalanced.

Keywords: Hypokalemia; Acute left Heart Failure; Respiratory Failure


Serum potassium is the vital ion maintaining the electrical activity of cardiac and skeletal muscle cells. Hypokalemia is one of the most common, emergent and severe electrolyte imbalance [1]. Hypokalemia can lower the excitability of skeletal muscle, resulting in myasthenia of limbs and even flaccid paralysis. Hypokalemia can also cause extended action potential duration, abnormal enhanced autonomy, decreased conductivity and contractility of cardiac muscle cell [2]. Severe hypokalemia can induce malignant arrhythmia  and even cardiac arrest [3]. Severe hypokalemia is defined with serum concentration of potassium ranging less than 2.5 mmol/L. There are a lot of potassium supplement method, such as taking pills, nasal feeding and intravenous. Concentration of potassium via peripheral venous is limited to 40 mmol/L with maxim rate of 60mmol/h, due to the side effect of potassium, such as complicated pain caused by spasticity of small vessels. Then solution of 5000 mL should be administered during potassium supplement in the case of severe hypokalemia. This volume might be acceptable for
young patients without underlying diseases. But it is totally unacceptable for aging patients, especially for those suffering  ypertension, coronary artery diseases and other critical underlying diseases. Special and safe protocols of potassium supplement and symptomatic treatment should be considered for this group of patients with hypokalemia in order to reduce the mortality of complications and improve the prognosis.

Case Presentation

An 85-year-old woman was hospitalized after suffering myasthenia in both legs for one day, with poor appetite, aggravating discomfort in upper abdomen and intermittent emesis for more than 2 months. The patient had once been administered with symptomatic treatment in a community clinic, but no instrumental inspection was conducted. The patient had a history of hypertension for more than 2 years with the highest blood pressure up to 200/105 mmHg. Nifedipine sustained release tablets had been administered orally with uncertain doses. No definite history of coronary artery disease or diabetes had been reported. Frequent ventricular premature beats were documented by electrocardiogram right after the hospitalization (Figure 1). Severe hypokalemia was reported with serum potassium concentration of 1.56 mmol/L one hour after hospitalization. Potassium chloride solution (10%, w/v) of 1.5g dissolved in glucose ringer’s solution of 500 mL was administered intravenously, immediately after hypokalemia was confirmed. Potassium chloride mixture (10%, w/v) was also administered orally alongside. Ventricular fibrillation occurred 1.5h after hospitalization (Figure 2), and disappeared after immediate electric defibrillation with dual-directional wave of 120J without anesthesia. A formal report of serum electrolyte test 2h after hospitalization was listed below: Na,134 mmol/L; K, 1.56 mmol/L; CL, 81.6 mmol/L;- Ca, 0.78 mmol/L; P, 0.56 mmol/L.

Figure 1. Electrocardiogram assay: frequent multifocal ventricular premature beat with high voltage of ventriculus sinister cordis.
case fig 27.1

Figure 2. Electrocardiogram assay: Torsades de Pointes.

case fig 27.2
The patient was admitted into the Emergency Intensive Care Unit 4h after hospitalization with the preliminary diagnosis of severe hypokalemia, arrhythmia (frequent ventricular premature beats), WHO/ISH High Risk hypertension of JNC8 Stage III (cardiac function of NYHA Class II). The vital signs of the patient were listed below: body temperature, 36.5°C; pulse, 70 beats per minute; breath, 20/ min; blood pressure, 160/90 mmHg, finger pulse oxygen saturation, 96% in room air. The patient was conscious. No dry rales or moist rales were heard in both lungs. Apex beat with arrhythmia located in the sixth intercostal space, 1.0 cm outside the left mid-clavicular line. No pathologic heart murmur was heard. No pathologic sign in abdomen was found. Muscle Strength Grading Scales of limbs (Oxford Scale) were all in 3/5. Tendon reflex was weaken in both sides while Babinski’s sign was negative.

Ventricular fibrillation was reported for four times and was stopped by electric defibrillation with dual-directional wave of 120J without anesthesia, accompanied by continuous intravenous pump of 2 mg/min lidocaine, during the first six hours after hospitalization. Meanwhile, potassium of 4.4 g was administered via peripheral intravenous, accompanied by oral potassium supplement with the rate of 0.5 g/h. The total volume of input liquid during this stage was 2600 mL, while the total output was 1300mL.

Ventricular fibrillation was reported for four times and was stopped by protocols mentioned above, during the 7h-30h after hospitalization. Meanwhile, potassium of 6g was administered via central intravenous (0.9g/h), accompanied by potassium supplement of 9g via peripheral intravenous and magnesium supplement of 2.5g. The total volume of input liquid during this stage was 3799 mL, while the total output was 1800 mL. Sinus rhythm was monitored by electrocardiogram (Figure 3). Unfortunately, acute left heart failure and pneumonedema rapidly developed during this stage (Figure 4). Anti heart failure treatment including diuretic was approached immediately but the therapeutic reaction was poor. Enlargement of left ventricle and atrium with ejection fraction of only 31% was monitored by bedside echocardiography.

Figure 3. Electrocardiogram assay: sinus rhythm with high voltage of ventriculus sinister cordis.

case fig 27.3
Figure 4. Chest X-ray study: Lobular pneumonia change along with both hilum pulmonis and lung markings, much with pulmones dexter.
case fig 27.4
The anti heart failure treatment was continued during the 31-34h after hospitalization, along with potassium supplement of 1.6g via central intravenous (0.4 g/h) and magnesium supplement. The total input volume of liquid during this stage was 500mL and the output was 200 mL.

The patient fell into superficial coma during the 35th h, with the finger pulse oxygen saturation of 66%, pH 7.15, PCO2 94 mmHg, PO2 49 mmHg in blood gas analysis. The patient was finally dead after the ventilator-assisted ventilation via endotracheal intubation was refused by her family members.

The results of laboratory test were listed below: white blood cell count, 10.67×109/L; red blood cell count, 3.47×1012/L; platelet count, 356×109/L; hemoglobin, 100g/L; total bilirubin, 3.40 μmol/L; direct bilirubin, 1.80 μmol/L; indirect bilirubin, 1.60 umol/L; alanine aminotransferase, 13 IU/L; aspartate aminotransferase, 34 IU/L; total protein, 49 g/L; albumin, 30 g/L; globulin, 19 g/Lμserum urea nitrogen, 3.42 mmol/L; serum creatinine, 117.97 umol/L; brain natriuretic peptide, 15641pg/ml; troponin I, 0.17ng/ml; myoglobin, 606.60 ng/ml; heart-fatty acid binding protein, positive; procalcitonin, <0.50 ng/ml. The dynamics of serum potassium concentration was showed in Table 1.
Table 1. Serum potassium concentrations before and after admission into the Emergency Intensive Care Unit.
case table 27.1

The patient was an aged woman, suffering severe hypokalemia caused by excessive loss and insufficient intake of potassium. This case was featured with the following characters: (1)age of 85 years old, malnutrition and hypoproteinemia, (2)underlying cardiac diseases, hypertension and chronic cardiac dysfunction, (3)increased serum troponin I and brain natriuretic peptide, (4)decreased ejection fraction, cardiac dysfunction complicated by repeated electric defibrillation, (5)hypokalemia complicated by acute left heart failure and respiratory failure. Considering albumin is the vital substance maintaining plasma colloid osmotic pressure, hypoproteinemia status in the patient might be an important factor to aggregate pneumonedema.

According to the Starling’s Law, the ventricular ejection fraction could be ameliorated by increased left ventricular end diastolic volume. But the ejection fraction could be deteriorated if the increased volume exceeds the limit of compensation [4]. The total volume of input liquid in this case was obviously more than that of output liquid, facilitating the latent advance of decompensation in cardiac function, malignant increasing of left ventricular end diastolic pressure, increased left atrial pressure, emergence of pneumonedema, poor reaction to anti heart failure treatment and diuretic, finally the emergence of hypoxemia, decreased contractility of respiratory muscles, and type II respiratory failure[5]. If the ventilator-assisted ventilation or intra-aortic balloon pump had not been adopted, the mortality rate for this kind of cases was very high. Several
important insights could be deduced from this case, including that (1)Q-T interval could be elongated by hypokalemia and lidocaine might be better than amiodarone when it was intravenously administered to control the advance of ventricular arrhythmia, (2)the input liquid volume of aged patient merited intensive attention when hypokalemia was rebalanced by intravenous supplement of potassium and the central venous pathway should be considered with priority over peripheral venous pathway given that the input volume could be limited in a range much less than peripheral pathway, (3) the cardiac and respiratory function should be continuously monitored as soon as possible in order that the sings of cardiac and respiratory dysfunction could be discovered as early as possible,(4)the cardiac function might be impeded by repeated electric defibrillation [6].

Hypokalemia is very common in Emergency Rooms. Although mild and moderate hypokalemia predominated the cases and potassium supplement orally or via peripheral venous could rebalance the potassium homeostasis [7], the rare severe  hypokalemia needs intensive attention, especially in aged patients, given that hypokalemia in aged patients was usually complicated with underlying cardiac diseases, respiratory diseases and innutrition. The case report might cast light on treatment of severe hypokalemia accompanied with recurrent malignant arrhythmia in aged patients, in order that the complicated multiple organ dysfunction might be avoided and the prognosis might be improved.

Declaration of conflicting interests

The authors declare that there are no conflicts of interest.

Cite this article: Zhao Xiaojing. Multiple Organ Dysfunction during Treatment of a Severe Hypokalemia in an Aged Female Patient: A Case Report. J J Clini Case Rep. 2016, 2(1): 027.

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