Abstract
Background:
Hypokalaemia (K+<3.5 mmol/L) is observed in 20% of hospitalised patients. Previous studies have often dealt with the symptoms, prevalence and risk factors in hospitalised patients. Very few studies have dealt with hospital-induced hypokalaemia. The aim was to determine the incidence, predisposing risk factors and prognosis of patients developing hypokalaemia after admission.
Materials and Methods:
A prospective observational study was performed for two months. Patients with at least two potassium values after admission and normal K values at admission were considered for inclusion. Clinical features, diagnoses, laboratory reports and treatment details, including antibiotics, were noted.
Results:
A total of 653 patients were studied; 138 (21.1%) developed hypokalaemia. Diabetes, ischaemic heart disease (IHD), heart failure, chronic kidney disease, hypertension, chronic liver disease and chronic obstructive pulmonary disease (COPD) were the most associated comorbidities. Urea, creatinine, transaminases and neutrophilia at admission differed significantly between those with and without hypokalaemia groups. Most patients developed mild hypokalaemia (78.2%). Hypokalaemia developed mostly on the second (22.4%) and third (24.6%) days of hospitalisation. Antibiotics were used in 60% of patients. The potassium values returned to normal within 2.5 ± 1.9 days. Three patients subsequently developed hyperkalaemia.
Conclusion:
Patients admitted under general medicine mostly developed mild hypokalaemia, even if they had multiple risk factors for developing hypokalaemia. Inpatient hypokalaemia had an incidence of 21%. An overwhelming majority (~88%) had at least one risk factor. Hypokalaemia was not attributed to causing mortality in any patient.
Keywords: Antibiotics, aetiology, hospital-induced hypokalaemia, hypokalaemia, inpatient hypokalaemia
INTRODUCTION
One of the most common electrolyte abnormalities in clinical practice is a low serum potassium (≤3.5 mmol/L) concentration.[1] Hypokalaemia is found in over 20% of hospitalised patients but is clinically significant only in 4–5%.[2] It is often well tolerated but can be life-threatening if severe. Even mild and moderate hypokalaemia increases the risk of morbidity and mortality in patients with cardiovascular disease. Hypokalaemia is either mild (3.0–3.5 mmol/L), moderate (2.5–3.0 mmol/L) or severe (<2.5 mmol/L).[3] The degree and duration of serum potassium reduction determine the severity of the clinical manifestations. Compared to other electrolytes, potassium is predominantly an intracellular ion, and extracellular fluid contains only 2% of all potassium in the body; therefore, a small decrease in serum potassium may demonstrate a significant decrease in intracellular potassium.[4] Patients with mild hypokalaemia usually have no symptoms. Moderate hypokalaemia causes minor complaints, such as fatigue, muscle weakness, muscle pain, cramps and constipation.[5] Severe hypokalaemia can cause potentially life-threatening complications such as cardiac dysrhythmias, respiratory failure, rhabdomyolysis, paralysis, urinary retention, paralytic ileus and diaphragmatic weakness.[5]
Hypokalaemia generally results from either increased potassium excretion or intracellular shifts and less frequently from reduced potassium intake.[6] Regulation of potassium homoeostasis is done by kidneys, gastrointestinal tract, hormones and cellular transports.[7] Hypokalaemia developing after hospitalisation is often due to ongoing newly initiated treatment or the disease process itself. Normokalaemia at presentation may lead to a delay in the diagnosis of newly developed hypokalaemia. A delay in diagnosis or correction can lead to significant morbidity and occasional mortality.[3] Most studies have investigated the aetiology and symptoms of hypokalaemia and its prevalence at the time of admission. Hypokalaemia in hospitalised patients who were normokalaemic at admission is not well established. To our knowledge, no such study has been performed among hospitalised patients in India. Therefore, we performed this study to determine the incidence of hypokalaemia in hospitalised patients following admission and its associated risk factors.
MATERIALS AND METHODS
This prospective cohort study was performed in the general medicine wards of a teaching government hospital under the Indian Council of Medical Research-Short term studentship (ICMR-STS) scheme (Reference ID: 2022-05095). This study was approved by the institutional ethics committee (No. JIP/IEC-OS/2022/241). We aimed to estimate the incidence of hypokalaemia in patients with normal potassium levels at admission and to determine the predisposing risk factors and outcomes in such patients. For two months, patients admitted to five wards with a total of 180 beds were monitored for serial potassium values that were available in the bedside charts. Patients with at least two potassium levels after admission (and admission values ≥3.5 mmol/L) were considered for inclusion in the study. Those with hypokalaemia (<3.5 mmol/L) observed in the second sample were included in the final analysis. Patients with K+<3.5 mmol/L in the first sample were excluded. The diagnosis, demographics, comorbidities, symptoms and signs, investigations and treatment details of these patients were recorded in an Epicollect 5 form created for this purpose. Attention was paid to drugs or conditions that could affect potassium balance through reduced oral intake, loss through urine or the gastrointestinal tract and redistribution. Gastrointestinal loss was considered when the patient experienced vomiting or diarrhoea. The renal loss was considered when the patient was on diuretics, had polyuria or had a documented urinary potassium level >20 mmol/L. Reduced oral intake pertained to vomiting, abdominal pain, reduced appetite, altered sensorium and nasogastric feeding, which caused reduced intake compared with the usual intake by >50%.
The IBM Statistical Package for the Social Sciences (SPSS) for Windows v22 was used for statistical analysis. Frequencies of categorical variables, such as comorbid illness and treatment details, were calculated and analysed using the Chi-square test. Continuous variables were compared between those with and without hypokalaemia using Student’s t-test. A paired t-test analysis was performed to compare potassium supplementation and treatment dosages of insulin and diuretics before and after the development of hypokalaemia. Statistical significance was set at P < 0.05.
The data set is available at 10.6084/m9.figshare. 21864507
RESULTS
Our study included 653 patients, among whom 138 developed hypokalaemia, with an incidence of 21.1% [Table 1]. Diabetes mellitus (DM) was the most common comorbidity (n = 115), followed by ischaemic heart disease (IHD) and heart failure (n = 147) and chronic kidney disease (CKD) (n = 98). Ninety-two patients with hypokalaemia were male. Most patients had mild hypokalaemia (n = 108), while moderate (n = 27) and severe (n = 3) hypokalaemia were observed in smaller numbers. Potassium, urea, creatinine, transaminases and neutrophilia at admission also differed significantly between the two groups. Cardiovascular symptoms were the most common in patients who developed hypokalaemia, while pallor was the most common clinical finding [Table 2].
Table 1.
Baseline characteristics of the study population
| Characteristics | Hypokalaemia (n=138) | No hypokalaemia (n=515) | P |
|---|---|---|---|
| Males | 92 (66.7) | 319 (61.9) | 0.30 |
| Age (y) | 44.6±15.7 | 44.9±15.1 | 0.86 |
| Hypothyroidism (n) | 10 (7.2) | 3 (0.6) | <0.001 |
| Diabetes mellitus (n) | 45 (32.6) | 70 (13.6) | <0.001 |
| Hypertension (n) | 39 (28.3) | 34 (6.6) | <0.001 |
| Chronic kidney disease | 27 (19.6) | 71 (13.8) | 0.09 |
| Chronic liver disease (n) | 7 (5.1) | 12 (2.3) | 0.08 |
| Chronic obstructive pulmonary disease (n) | 1 (0.7) | 9 (1.7) | 0.38 |
| Ischaemic heart disease (n) | 28 (20.3) | 119 (23.2) | 0.48 |
| Stroke (n) | 3 (2.2) | 25 (4.9) | 0.16 |
| Admission potassium (mg/dL) | 4.1±0.5 | 4.3±0.5 | 0.005 |
| Second potassium (mg/dL) | 3.8±0.6 | 4.3±0.5 | <0.001 |
| Serum sodium (mmol/L) | 135.0±0.7 | 136.1±0.7 | 0.92 |
| Urea (mg/dL) | 59.3±59.0 | 47.1±51.8 | 0.01 |
| Creatinine (mg/dL) | 2.8±4.3 | 2.0±3.7 | 0.02 |
| Corrected calcium admission (mg/dL) | 7.4±4.9 | 7.9±10.3 | 0.56 |
| Magnesium (mg/dL) | 2.0±0.4 | 2.8±11.8 | 0.48 |
| Aspartate transaminase (IU/L) | 1592.9±1246.7 | 126.5±5.7 | 0.05 |
| Alanine transaminase (IU/L) | 422.5±36.2 | 144.1±6.5 | <0.001 |
| Alkaline phosphatase (IU/L) | 94.0±8.15 | 186.5±8.5 | 0.35 |
| Phosphate (mg/dL) | 2.3±0.9 | 1.8±0.0 | 0.33 |
| Haemoglobin (g/dL) | 10.1±3.8 | 10.5±3.2 | 0.54 |
| Total leucocyte count (×109/L) | 16.1±45.3 | 11.3±11.2 | 0.03 |
Table 2.
Clinical characteristics of patients with hypokalaemia
| Characteristics | Means±SD/n (%) (n=138) |
|---|---|
| Age (y) | 44.6±15.7 |
| Duration of symptoms (d) | 22.8±37.6 |
| Fever (n) | 76 (55.1) |
| Gastrointestinal symptoms (n) | 69 (50) |
| Gastrointestinal loss (n) | 56 (40.6) |
| Renal symptoms (n) | 53 (38.4) |
| Neurological symptoms (n) | 42 (30.4) |
| Cardiovascular symptoms (n) | 89 (64.5) |
| Respiratory symptoms (n) | 42 (30.4) |
| Elevated JVP (n) | 28 (20.3) |
| Pallor (n) | 65 (47.1) |
| Pedal oedema (n) | 54 (39.1) |
| Clubbing (n) | 6 (4.3) |
| Icterus (n) | 19 (13.8) |
| Reduced skin turgor (n) | 2 (1.4) |
| Dry oral mucosa (n) | 7 (5.1) |
| Pulse rate (n) | 97.1±19.7 |
| Systolic blood pressure (mmHg) | 120.7±27.8 |
| Diastolic blood pressure (mmHg) | 75.6±15.9 |
| Respiratory rate (breaths/min) | 21.6±6.9 |
| Ascites (n) | 13 (9.4) |
| Focal neurological deficits (n) | 12 (8.7) |
| Infections (n) | 54 (39.1) |
| Haematological disorders (n) | 12 (8.6) |
None of the patients developed any cardiovascular complications or neuroparalysis. Most patients developed hypokalaemia on the second (n = 31) and third (n = 34) days of hospitalisation. Only 21 of 138 patients developed hypokalaemia beyond the 7th day after admission. The median pH and bicarbonate levels in arterial blood gas analysis were 7.34 and 17.6, respectively. Urinary electrolytes were measured in less than 10% of patients with hypokalaemia and revealed both potassium loss and sodium loss in urine [Table 3]. Antibiotics were used in 60% of patients with hypokalaemia, with 23% and 24.5% of patients receiving one and two antibiotics, respectively. The use of diuretics in two-fifth, laxatives in one-fifth, insulin in one-fourth and inhaled salbutamol in one-sixth of the study group was also observed [Tables 4 and 5]. Cephalosporins were administered to nearly half of the patients [Table 6]. Twenty-six per cent of the study population did not have traditional risk factors related to comorbid illnesses or treatment. The potassium values returned to normal with a mean of 2.5 ± 1.9 days. Three patients developed hyperkalaemia, one each with severe falciparum malaria, community-acquired pneumonia with diabetes and hypothyroidism and aplastic anaemia.
Table 3.
Other inpatient laboratory values in patients with hypokalaemia
| Values | Means±SD/n (%) (n=138) |
|---|---|
| First hypokalaemia value (mmol/L) | 3.1±0.2 |
| Hyponatraemia (n) | 60 (43.4) |
| Hypomagnesaemia at admission (n) | 5 (3.6) |
| Corrected calcium after hypokalaemia (mg/dL) | 9.0±0.7 |
| Magnesium after hypokalaemia (mg/dL) | 1.8±0.3 |
| Hypomagnesaemia after hypokalaemia (n) | 9 (6.5) |
| PTH (pg/mL) | 262.2±257.1 |
| TSH (mIU/mL) | 6.5±16.3 |
| Urine potassium (mmol/L) | 25.2±16.8 |
| Urine sodium (mmol/L) | 86.8±40.1 |
| Urine Ca/creatinine ratio | 2.68±3.7 |
| Urine pH | 5.5±0.5 |
| Urine osmolality (mOsm/kg) | 320.3±112.4 |
| ECG heart rate (per minute) | 101.0±23.9 |
| ECG PR interval (ms) | 147.6±29.1 |
| ECG QRS duration (ms) | 91.7±19.6 |
| ECG QTc interval (ms) | 454.3±70.0 |
Table 4.
Drugs affecting potassium levels in patients with hypokalaemia
| Treatment | n (%) | Admission potassium | P | |
|---|---|---|---|---|
|
| ||||
| With drug | Without drug | |||
| Frusemide (n) | 42 (30.3) | 4.0±0.5 | 4.3±0.5 | 0.002 |
| Frusemide + spironolactone (n) | 6 (4.3) | 4.3±0.6 | 4.1±0.5 | 0.7 |
| Mannitol (n) | 7 (5.1) | 3.7±0.3 | 4.1±0.5 | 0.02 |
| Laxatives (n) | 30 (21.7) | 4.2±0.6 | 4.1±0.5 | 0.56 |
| Salbutamol (n) | 11 (7.9) | 4.4±0.7 | 4.1±0.5 | 0.10 |
| Insulin (n) | 32 (23.1) | 4.1±0.5 | 4.1±0.5 | 0.64 |
| Steroids (n) | 23 (16.7) | 4.1±0.6 | 4.1±0.5 | 0.98 |
| Thyroxine (n) | 10 (7.2) | 4.0±0.4 | 4.1±0.5 | 0.32 |
| Digoxin (n) | 5 (3.6) | 4.1±0.3 | 4.1±0.5 | 0.95 |
| Beta-blockers (n) | 8 (5.7) | 4.3±0.5 | 4.1±0.5 | 0.27 |
| Enalapril (n) | 5 (3.6) | 3.8±0.3 | 4.1±0.6 | 0.21 |
Table 5.
Treatment before and after the development of hypokalaemia
| Treatment | Pre- hypokalaemia | Post- hypokalaemia | P |
|---|---|---|---|
| Frusemide dosage (mg) | 358.6±6 | 156.3±26.4 | <0.001 |
| Frusemide duration (d) | 2.6±0.2 | 1.4±0.1 | <0.001 |
| Spironolactone dosage (mg) | 250.0±273.8 | 212.5±103.1 | 0.88 |
| Spironolactone duration (d) | 1.0 ± ± 0.2 | 0.7±0.1 | 0.70 |
| Mannitol (mL) | 678.5±339.6 | 411.2±205.6 | 0.18 |
| Insulin dose (u) | 20.0±71.7 | 14.7±48.2 | 0.39 |
| Oral KCl supplementation (n) | 4 | 83 | 0.001 |
| Oral KCl (mEq) | 165.0±161 | 60.0±30.0 | 0.55 |
| Oral KCl duration (d) | 0.6±0.0 | 1.4±0.1 | 0.01 |
| IV KCl supplementation (n) | 0 | 20 | 0.05 |
| Intravenous KCl (mEq) | 0 | 97.43±25.9 | 0.004 |
| Intravenous KCl duration (d) | 0.1±0.0.0 | 0.4±0.1 | 0.08 |
| Juice (mL) | 46.7±234.2 | 504.3±559.2 | 0.001 |
Table 6.
Antimicrobials and other miscellaneous drugs affecting potassium
| Admission potassium | n (%) | With drug | Without drug | P |
|---|---|---|---|---|
| Antimicrobials (n) | 84 (60.8) | 4.1±0.5 | 4.1±0.6 | 0.88 |
| Linezolid (n) | 2 (1.4) | 3.5±0.1 | 4.1±0.5 | 0.01 |
| Amikacin (n) | 12 (8.6) | 4.2±0.7 | 4.1±0.5 | 0.86 |
| Acyclovir (n) | 4 (2.8) | 4.2±0.9 | 4.1±0.5 | 0.84 |
| Vancomycin (n) | 4 (2.8) | 4.4±0.7 | 4.1±0.5 | 0.34 |
| Piperacillin–tazobactam (n) | 20 (14.4) | 4.2±0.6 | 4.1±0.5 | 0.57 |
| Cephalosporins (n) | 61 (44.2) | 4.2±0.6 | 4.0±0.4 | 0.07 |
| Azithromycin (n) | 16 (11.5) | 4.4±0.6 | 4.1±0.5 | 0.06 |
| Doxycycline (n) | 17 (12.3) | 4.1±0.7 | 4.1±0.5 | 0.93 |
| Metronidazole (n) | 10 (7.2) | 4.0±0.4 | 4.1±0.5 | 0.34 |
| Amoxicillin/ampicillin (n) | 9 (6.5) | 4.1±0.9 | 4.1±0.5 | 0.95 |
| Cloxacillin (n) | 8 (5.7) | 4.3±0.9 | 4.3±0.5 | 0.35 |
| Phenoxymethyl penicillin (n) | 5 (3.6) | 4.3±0.8 | 4.1±0.5 | 0.54 |
| Rifampicin (n) | 8 (5.7) | 4.3±0.6 | 4.1±0.6 | 0.52 |
| Heparin (n)* | 24 (17.3) | 4.0±0.3 | 4.2±0.5 | 0.09 |
| Thiamine (n)# | 24 (17.3) | 4.0±0.6 | 4.1±0.5 | 0.40 |
| Vitamin B12 (n)# | 14 (10.1) | 4.1±0.4 | 4.1±0.5 | 0.86 |
| Second potassium | ||||
| Metronidazole (n) | 10 (7.2) | 3.3±0.3 | 3.8±0.7 | 0.02 |
| Azithromycin (n) | 16 (11.5) | 4.2±0.9 | 3.7±0.6 | 0.007 |
| Linezolid (n) | 2 (1.4) | 3.4±0.1 | 3.8±0.7 | 0.01 |
| Cyclosporine (n)* | 2 (1.4) | 3.8±0.7 | 4.2±0.1 | <0.001 |
DISCUSSION
One hundred and twenty-one (87.6%) patients had at least one risk factor, while 81 (58.6%) had ≥2 risk factors. Only 2% of our study population had K+ less than 3 mmol/L, which is similar to other studies.[4,6] Hypokalaemia is seen in 40% of patients taking diuretics and 17% of patients with cardiovascular conditions.[8] Elderly patients may be predisposed to the development of hypokalaemia as an independent risk factor.[9] All patients >60 years in this study had either mild (n = 19) or moderate (n = 3) hypokalaemia. Age was not correlated with the development of hypokalaemia (r = -0.163). Half of the elderly patients (7/15) were treated with diuretics.
Very few studies have been performed on hospitalised patients to detect incident hypokalaemia after admission.[10,11,12,13] In 1979, Lawson et al.[10] studied 58167 patients in a teaching hospital, with 292 patients with severe hypokalaemia (<2.5 mmol/L), giving an incidence of 0.5%. Patients were from multiple medical and surgical specialties, were more likely to be women and had malignancies such as acute myeloid leukaemia. In 1986, the same cohort showed 21% with hypokalaemia and 56% attributable to drug therapy or intravenous fluids.[14] In the current study, 84 (60.8%) patients received antimicrobials, followed by diuretics with 42, insulin with 32 and laxatives with 30, none of them being mutually exclusive. Seventeen did not have a single risk factor.
Janko et al.[11] studied 1177 patients with hypokalaemia; 592 developed hypokalaemia after hospitalisation (cut-off, 3 mmol/L). DM, polytrauma and gastrointestinal and urogenital diseases were associated with hypokalaemia. This study did not include mild hypokalaemia. In an Indonesian study (2006) of 105 patients with infectious diseases (dengue = 82), DM, hypertension or hepatobiliary disorder receiving replacement solutions such as normal saline, ringer lactate and ringer’s acetate, 39% (37/105) developed hypokalaemia. Most patients (91.4%) received Ringer’s lactate.[13] Patients with renal and cardiac failure, diarrhoea and diuretic use were excluded from the study. In Saudi Arabia, hypokalaemia during hospitalisation (17.2%) increased as compared to the time of admission in patients with infectious diseases.[15] In the Netherlands, there was an 8.4% (100/1178) incidence of hypokalaemia in the general hospital population. Sixteen patients developed hyperkalaemia.[12] The study population included patients from internal medicine and medical subspecialties, surgery and surgical subspecialties, and gynaecology.[12] Our study focused only on patients admitted to general internal medicine care.
Hypokalaemia was associated with both hyponatraemia (24%) and hypomagnesaemia (61%).[12] The corresponding figures for hyponatraemia and hypomagnesaemia in the current study were 62% and 9%, respectively. A triad consisting of hypomagnesaemia, hypokalaemia and hypophosphataemia has also been reported, which was observed in 8% of patients with hypomagnesaemia and 17% of patients with severe hypomagnesaemia (plasma magnesium < or = 0.50 mmol/L).[16] In the current study, six patients received oral magnesium supplements before hypokalaemia development. After the development of hypokalaemia, nine (6.5%) patients were found to have hypomagnesaemia. Hypophosphataemia was not associated with hypokalaemia.
Severe hypokalaemia in hospitalised patients is commonly the result of multiple iatrogenic factors, and medications such as insulin, beta-2 agonists, laxatives, diuretics, antibiotics and methylxanthines are generally known to induce hypokalaemia.[17] Most studies involving inpatient hypokalaemia have had shortcomings in treatment histories since they were retrospective in nature, or a computerised database was used instead of directly perusing patient files. Krogager et al.[18] studied a Danish hypertensive registry on combination antihypertensives containing diuretics. Thiazide combinations were associated with a high risk of hypokalaemia. Our study population had diuretic use (furosemide, spironolactone and mannitol) because of CKD, chronic liver disease (CLD), heart failure and stroke. Zhu et al.[19] studied 108 patients scheduled for laparoscopic colorectal resection and found hypokalaemia in two-thirds and a longer time to first faeces.[19] The use of ≥2 cathartics, restricted oral intake and hypertension were risk factors for hypokalaemia. The incidence of hypokalaemia was not reported. Falcone et al.[20] also utilised a single-study population of patients with bone and joint infections. Zhou et al.[21] retrospectively studied 4445 patients with traumatic brain injury and predicted the development of inpatient hypokalaemia using machine-based algorithms. An incidence of 46.5% was found that was associated with higher mortality. All these studies had a homogeneous population in contrast to the current study.
Hypokalaemia had a strong association in patients with severe coronavirus disease 2019 (COVID-19) infection and prolonged hospital stay in a study from China.[22] Antimicrobials commonly associated with hypokalaemia include piperacillin–tazobactam,[23] amphotericin B,[24] aminoglycosides,[24] ureidopenicillins,[24] vancomycin[25] and flucloxacillin.[26] In piperacillin–tazobactam-administered patients, the incidence rate of hypokalaemia was as high as 20%, and patients aged >80.5 years were considered a high-risk group.[23] Falcone et al.[20] reviewed 150 patients with recurrent admissions who used a few combinations of ciprofloxacin, vancomycin and rifampicin. Severe hypokalaemia (39%) was common, particularly in the elderly; this was associated with the simultaneous use of loop diuretics and thiazides.[20] We had a similar number of patients using 15 different antibiotics, three antivirals, two antifungals, three antiparasitic agents and one antituberculous drug along with a miscellaneous group, many of which have been associated with hypokalaemia. Other antimicrobials that have been reported to cause or be associated with hypokalaemia are cyclosporine,[27] fluconazole,[28] acyclovir,[29] azithromycin,[30] ceftriaxone,[30] ampicillin,[17] rifampicin,[20] colistin,[31] clindamycin,[32] meropenem,[32] ciprofloxacin[20] and entecavir.[33] Other drugs in hospitalised patients include thyroxine,[34] thiamine,[35] vitamin B12,[36] imatinib,[37] hydroxychloroquine,[38] valproate[39] and noradrenaline.[40] [Table 7].
Table 7.
Other antimicrobials and miscellaneous drugs that were administered
| Drug | No. of patients | Drug | No. of patients |
|---|---|---|---|
| Clindamycin (n)# | 1 | Imatinib (n)# | 1 |
| Colistin (n)# | 1 | Azathioprine (n) | 1 |
| Tigecycline (n) | 1 | Hydroxyurea (n)* | 2 |
| Meropenem (n)# | 1 | Allopurinol (n) | 2 |
| Amphotericin (n)# | 1 | Febuxostat (n) | 1 |
| Fluconazole (n)# | 2 | Hydroxychloroquine (n)# | 1 |
| Albendazole (n) | 1 | Noradrenaline (n)# | 2 |
| Ivermectin (n) | 1 | Diltiazem (n)# | 1 |
| Artesunate (n) | 1 | Valproate (n)# | 2 |
| Entecavir (n)# | 1 | Octreotide (n)* | 1 |
| Oseltamivir (n) | 1 |
#Studies report drug causation or association with hypokalaemia; *Drug usually causes hyperkalaemia
ECGs were available for only 113 patients after the development of hypokalaemia. Many of the changes, such as ST or T waves, could be explained by co-existing illnesses, such as IHD, heart failure, strokes, hypothyroidism, uraemic pericarditis and hypertension. As hypokalaemia was also mostly mild, electrocardiogram (ECG) was probably not very useful in this population.
Some studies have shown that the treatment of dyselectrolytaemia is often suboptimal. In a multiphasic ambispective Swiss educational programme in five hospitals over 10 years, only 60% of patients had normokalaemia before discharge and only 20% had serum magnesium levels checked and 1% developed hyperkalaemia.[41] The average length of stay, as well as the incidence of falls and mortality, is almost double in hypokalaemic patients compared with normokalaemic patients.[41] Magnesium levels were tested in 112 (81.1%) before hypokalaemia, and 108 (78.2%) had a repeat test after hypokalaemia. An Israeli study retrospectively observed the quality of care of patients with hypokalaemia from a computerised database.[42] Failure to stop drugs that led to hypokalaemia was considered inappropriate. Among patients admitted with severe hypokalaemia, about 30% were discharged from the hospital with a subnormal potassium level, and 6.4% had no subsequent serum K+ levels measured.[42] In our study, in fluid overload states such as CKD, CLD, heart failure and strokes, which necessitated diuretics, only the dose could be reduced but not discontinued. No in-hospital deaths were attributable to low potassium levels.
There were no deaths attributable to hypokalaemia in our study. The mean duration of hospital stay was 15.4 ± 8.4 days.
Strengths and limitations
The study had a large number of participants (n = 653) providing for the incidence rate. All patients were discharged only after the normalisation of potassium values. The study duration was two months, which precluded a longer follow-up of many patients who developed hypokalaemia beyond two weeks. Therefore, the number of patients with hypokalaemia may have been slightly higher. The time to repeat potassium testing (in hours) by the treating unit even after the admission K+ was found to be normal, and the reason for doing so was not documented. None of our patients underwent ECG after the development of hypokalaemia. Most patients also did not get completely worked up for the aetiology of hypokalaemia in the form of arterial blood gases, urine electrolytes, pH, osmolality and thyroid profiles, which could have helped in the diagnosis of other underlying disorders.
CONCLUSION
The incidence of hypokalaemia among hospitalised patients admitted under general medicine was comparable to other studies. DM, hypertension, hypothyroidism and treatment, such as diuretics and antibiotics, contributed to the development of hypokalaemia, which was mostly mild in nature without causing cardiovascular or neurological adverse events. Nearly 88% of the patients had at least one risk factor for developing hypokalaemia. The workup for hypokalaemia was less than optimal considering the obvious risk factors, rapid recovery and enhanced costs.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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