Displaying publications 1 - 20 of 28 in total

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  1. A Patient with Hypokalemia and Hypoxemia-What Is the Culprit?
    Lai YY, Lim CH, Nazli MS, Samsudin IN, Thambiah SC
    Clin Chem, 2023 Nov 02;69(11):1220-1225.
    PMID: 37932109 DOI: 10.1093/clinchem/hvad158
    Matched MeSH terms: Hypokalemia*
  2. Adverse drug event of hypokalaemia-induced cardiotoxicity secondary to the use of laxatives: A systematic review of case reports
    Khan S, Khan SU
    J Clin Pharm Ther, 2020 Oct;45(5):927-936.
    PMID: 32672366 DOI: 10.1111/jcpt.13204
    WHAT IS KNOWN AND OBJECTIVE: The imbalance in serum potassium caused by laxatives can negatively affect the cardiovascular system, leading to life-threatening consequences. Our objective was to evaluate the reported evidence of adverse events related to the cardiac system due to laxative-induced hypokalaemia from case reports.

    METHODS: A systematic electronic literature search of PubMed, Embase, the Cochrane Library and Science Direct was conducted for the period 1995-2019. In these databases, search terms describing hypokalaemia and cardiotoxicity were combined with the term laxative use.

    RESULTS AND DISCUSSION: Over the 23 years, 27 incidents were identified in 12 countries. There were 19 female and eight male patients, with ages ranging from 1 month to 93 years. The frequency of reported cases according to severity was the following: severe hypokalaemia 48%, moderate hypokalaemia 44.4% and mild hypokalaemia 7.4%. In 70% of patients, the effect of laxative on the heart was typical hypokalaemic electrographic changes, 7.4% showed abnormal changes in cardiac rhythm, whereas in 18.5%, the cardiotoxicity observed was a very serious kind. Two patients died due to severe cardiac effects.

    WHAT IS NEW AND CONCLUSION: The laxatives-along with the involvement of some other contributing factors-caused mild-to-severe hypokalaemic cardiotoxicity. These factors were non-adherence of the patient to the recommended dosage, laxative abuse, drug-drug and drug-disease interactions, non-potassium electrolyte imbalances and the use of herbal laxatives. We recommend that laxatives and aggravating factors should be taken into account in the assessment of patients with suspected hypokalaemic cardiotoxicity.

    Matched MeSH terms: Hypokalemia/chemically induced*; Hypokalemia/complications; Hypokalemia/physiopathology
  3. Fulltext Drug utilization review of potassium chloride injection formulations available in a private hospital in kuching, sarawak, malaysia
    Melissa MH, Azmi S
    Malays J Med Sci, 2013 Jul;20(4):47-55.
    PMID: 24043996 MyJurnal
    The concentrated potassium chloride injection is a high-alert medication and replacing it with a pre-mixed formulation can reduce the risks associated with its use. The aim of this study was to determine the clinical characteristics of patients receiving different potassium chloride formulations available at a private institution. The study also assessed the effectiveness and safety of pre-mixed formulations in the correction of hypokalaemia.
    Matched MeSH terms: Hypokalemia
  4. Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting
    Birkhahn RH, Gaeta TJ, Melniker L
    J Emerg Med, 2000 Feb;18(2):199-202.
    PMID: 10699522
    A 27-year-old male of Malaysian descent presented to the Emergency Department (ED) with rapidly progressive flaccid paralysis that quickly compromised his respiratory effort. The patient was found to have a serum potassium of 1.9 meq/L, and was diagnosed as having an acute paralytic episode secondary to thyrotoxic periodic paralysis. The paralytic attack was aborted with a combination of potassium replacement and parenteral propranolol in large doses. We report the use of a rarely described, yet possibly more effective, therapy for an acute attack of thyrotoxic periodic paralysis.
    Matched MeSH terms: Hypokalemia/complications; Hypokalemia/diagnosis
  5. Fulltext Rhabdomyolysis associated with hypokalaemic periodic paralysis of renal tubular acidosis
    Hanip MR, Cheong IK, Chin GL, Khalid BA
    Singapore Med J, 1990 Apr;31(2):159-61.
    PMID: 2371581
    Two cases of hypokalaemia with serum potassium levels of 1.4 mmol/L and 1.9 mmol/L causing severe periodic paralysis since childhood are presented. There were associated with muscular aches and markedly raised muscle enzymes suggesting massive rhabdomyolysis. These abnormalities were due to renal tubular acidosis with markedly acidic arterial pH. The hypokalaemia and rhabdomyolysis responded to potassium and bicarbonate replacement. We postulate these patients had sporadic distal type of renal tubular acidosis and that the hypokalaemia and acidosis had caused the rhabdomyolysis.
    Matched MeSH terms: Hypokalemia/complications*; Hypokalemia/physiopathology
  6. Fulltext Two cases of pseudohyperkalemia that occurred after emergency splenectomy: what goes up, will come down
    Tan, G.H., Nor Faezan, A.R., Hairol, A.O., Bong, J.J.
    Journal of Surgical Academia, 2011;1(1):32-34.
    MyJurnal
    Pseudohyperkalemia is a spuriously high serum potassium measurement in a patient with no clinical evidence of hyperkalemia. It has been reported to occur in patients with leukocytosis and thrombocytosis. Only a few cases of pseudohyperkalemia have been reported in patients after splenectomy. Two cases of pseudohyperkalemia occurring after emergency splenectomy for abdominal trauma are presented to highlight their clinical presentation and sequalae. Consecutive patients who underwent emergency splenectomy for trauma and subsequently developed pseudohyperkalemia were monitored in Universiti Kebangsaan Malaysia Medical Centre for their clinical sequalae. Both the patients developed leukocytosis, thrombocytosis and high serum potassium level within 2-weeks of their splenectomies. They did not demonstrate any symptoms and signs of hyperkalemia. Their conditions resolved spontaneously without any specific treatment. Pseudohyperkalemia should be suspected in a similar clinical scenario to avoid unnecessary treatment that could lead to severe hypokalemia.
    Matched MeSH terms: Hypokalemia
  7. Fulltext Refractory hypokalemia during barbiturate coma therapy used for treating refractory intracranial hypertension in traumatic brain injury
    Wan Hassan WM, Najid NM, Muslim HS, Izaini Ghani AR
    Asian J Neurosurg, 2015 3 15;10(1):59.
    PMID: 25767595 DOI: 10.4103/1793-5482.151528
    Barbiturate coma therapy (BCT) is a choice treatment for refractory intracranial hypertension after all surgical or medical managements have failed to control the intracranial pressure (ICP). It helps to reduce cerebral blood flow, cerebral metabolic rate of oxygen consumption and ICP. However, this therapy can also cause many complications. One of the underreported, but life-threatening complications is refractory hypokalemia, which can lead to subsequent rebound hyperkalemia after sudden cessation. We report our experience of managing unusual complication of refractory hypokalemia during BCT with thiopentone in postdecompressive craniectomy patient.
    Matched MeSH terms: Hypokalemia
  8. Fulltext Life-Threatening Dyskalaemia after Barbiturate Coma Therapy: The Strategy of Management
    Tat YB, Hassan WMNW, Chuen TY, Ghani ARI
    Malays J Med Sci, 2017 Mar;24(2):100-105.
    PMID: 28894410 MyJurnal DOI: 10.21315/mjms2017.24.2.13
    Barbiturate coma therapy (BCT) is a treatment option that is used for refractory intracranial hypertension after all other options have been exhausted. Although BCT is a brain protection treatment, it also has several side effects such as hypotension, hepatic dysfunction, renal dysfunction, respiratory complications and electrolyte imbalances. One less concerning but potentially life-threatening complication of BCT is dyskalaemia. This complication could present as severe refractory hypokalaemia during the therapy with subsequent rebound hyperkalaemia after cessation of the therapy. Judicious potassium replacement during severe refractory hypokalaemia and gradual cessation of the therapy to prevent rebound hyperkalaemia are recommended strategies to deal with this complication, based on previous case series and reports. In this case report, we show that these strategies were applicable in improving severe hypokalaemia and preventing sudden, life-threatening rebound hyperkalaemia. However, even with use of these strategies, BCT patients could still present with mild, asymptomatic hyperkalaemia.
    Matched MeSH terms: Hypokalemia
  9. Primary aldosteronism: from bench to bedside
    Sukor N
    Endocrine, 2012 Feb;41(1):31-9.
    PMID: 22042487 DOI: 10.1007/s12020-011-9553-3
    Primary aldosteronism is now thought to be the commonest potentially curable and specifically treatable form of hypertension. The detection of primary aldosteronism is of utmost importance not only because it provides an opportunity for a targeted treatment, but also because it has been demonstrated that patients with primary aldosteronism are more prone to cardiovascular events and target organ damage than essential hypertensives. Normalization of blood pressure and hypokalemia should not be the only goal of treatment. Normalization of circulating aldosterone or mineralocorticoid blockade is necessary to prevent aldosterone-induced tissue damage that occurs independent of blood pressure. This review will focus on the current understanding and comprehensive management review of primary aldosteronism, highlighting the new evidence that has become recently available.
    Matched MeSH terms: Hypokalemia/etiology
  10. Fulltext A young woman with hypogonadism, hypertension and hypokalaemia
    Toh VK, Yung CH
    Med J Malaysia, 2009 Sep;64(3):242-3.
    PMID: 20527279 MyJurnal
    We report a case of a 16 years old girl who presented sequentially with primary amenorrhoea, hypertension and hypokalaemia. Eight years later, she was finally diagnosed with 17alpha-hydroxylase deficiency congenital adrenal hyperplasia. Previous antihypertensive medications were stopped. Hydrocortisone alone successfully maintained normotension and normokalaemia.
    Matched MeSH terms: Hypokalemia/etiology
  11. Pregnancy outcome in hyperemesis gravidarum and the effect of laboratory clinical indicators of hyperemesis severity
    Tan PC, Jacob R, Quek KF, Omar SZ
    J Obstet Gynaecol Res, 2007 Aug;33(4):457-64.
    PMID: 17688612
    To determine pregnancy outcome in hyperemesis gravidarum and the effect of metabolic, biochemical, hematological and clinical indicators of disease severity on outcome.
    Matched MeSH terms: Hypokalemia/blood
  12. Fulltext Torsade de pointes and sudden death associated with diabetic autonomic diarrhoea--a case report
    Quek DK, H'ng PK
    Singapore Med J, 1993 Jun;34(3):266-70.
    PMID: 8266190
    A 68-year-old diabetic and hypertensive woman presented with chronic autonomic diarrhoea, syncope and palpitations which were associated with QT prolongation and recurrent episodes of torsade de pointes. She was on glibenclamide, indapamide and probucol (for type V hyperlipidaemia). Despite intravenous infusions of potassium, lignocaine and amiodarone, the unstable rhythm persisted. However, intravenous magnesium sulphate with small doses of intravenous propranolol terminated the torsade de pointes. She was stabilised but following discharge she relapsed, and upon re-admission, succumbed to intractable ventricular fibrillation. Early recognition and aggressive treatment of this condition is emphasised. Multiple aggravating factors ie autonomic diarrhoea resulting in severe potassium and magnesium depletion, kaliuretic effect of indapamide, probable QT prolongation associated with diabetic autonomic neuropathy and probucol; probable underlying coronary artery disease and heightened emotional and sympathetic discharge could have contributed to this very unstable ventricular arrhythmia and sudden death.
    Matched MeSH terms: Hypokalemia/complications
  13. Fulltext Potassium and massive blood transfusion
    Reddy SV, Sein K
    Singapore Med J, 1991 Feb;32(1):29-30.
    PMID: 2017701
    Sixty patients who received massive blood transfusion intraoperatively and/or in the immediate post-operative period were analysed. Six patients had hypokalemia and two had hyperkalemia. The multifactorial changes leading to electrolyte disturbances especially involving potassium are discussed in relation to hypotension, hypothermia, acidosis, pH, and release of catecholamine. Potassium changes in relation to anaesthesia are discussed. The danger of routine administration of calcium during massive blood transfusion is stressed.
    Matched MeSH terms: Hypokalemia/etiology
  14. High prevalence of hypokalemia after acute acetaminophen overdose: impact of psychiatric illness
    Zyoud SH, Awang R, Syed Sulaiman SA, Al-jabi SW
    Hum Exp Toxicol, 2010 Sep;29(9):773-8.
    PMID: 20144962 DOI: 10.1177/0960327110361759
    Hypokalemia is not an isolated disease but an associated finding in a number of different diseases. It is also a commonly neglected condition among patients with acute acetaminophen overdose.
    Matched MeSH terms: Hypokalemia/blood; Hypokalemia/complications*; Hypokalemia/epidemiology*; Hypokalemia/prevention & control
  15. Fulltext Transient hyperthyroidism of hyperemesis gravidarum
    Tan JYL, Loh KC, Yeo GSH, Chee YC
    BJOG, 2002 Jun;109(6):683-8.
    PMID: 12118648
    OBJECTIVE: To characterise the clinical, biochemical and thyroid antibody profile in women with transient hyperthyroidism of hyperemesis gravidarum.
    DESIGN: Prospective observational study.
    SETTING: Hospital inpatient gynaecological ward.
    POPULATION: Women admitted with hyperemesis gravidarum and found to have hyperthyroidism.
    METHODS: Fifty-three women were admitted with hyperemesis gravidarum and were found to have hyperthyroidism. Each woman was examined for clinical signs of thyroid disease and underwent investigations including urea, creatinine, electrolytes, liver function test, thyroid antibody profile and serial thyroid function test until normalisation.
    MAIN OUTCOME MEASURES: Gestation at which thyroid function normalised, clinical and thyroid antibody profile and pregnancy outcome (birthweight, gestation at delivery and Apgar score at 5 minutes).
    RESULTS: Full data were available for 44 women. Free T4 levels normalised by 15 weeks of gestation in the 39 women with transient hyperthyroidism while TSH remained suppressed until 19 weeks of gestation. None of these women were clinically hyperthyroid. Thyroid antibodies were not found in most of them. Median birthweight in the infants of mothers who experienced weight loss of > 5% of their pre-pregnancy weight was lower compared with those of women who did not (P = 0.093). Five women were diagnosed with Graves' disease based on clinical features and thyroid antibody profile.
    CONCLUSIONS: In transient hyperthyroidism of hyperemesis gravidarum, thyroid function normalises by the middle of the second trimester without anti-thyroid treatment. Clinically overt hyperthyroidism and thyroid antibodies are usually absent. Apart from a non-significant trend towards lower birthweights in the infants of mothers who experienced significant weight loss, pregnancy outcome was generally good. Routine assessment of thyroid function is unnecessary for women with hyperemesis gravidarum in the absence of any clinical features of hyperthyroidism.
    Matched MeSH terms: Hypokalemia/etiology; Hypokalemia/metabolism
  16. Fulltext Primary Hyperaldosteronism in End-Stage Renal Disease: Diagnostic Challenges and Treatment Considerations
    Chand R, Tandukar S, Asmil S, Chico M
    Cureus, 2020 Aug 07;12(8):e9599.
    PMID: 32923203 DOI: 10.7759/cureus.9599
    An adrenal incidentaloma is defined as an adrenal mass measuring at least 1 cm that is discovered surreptitiously in an imaging study done for reasons other than the evaluation of adrenal disease. The increase in the prevalence of adrenal incidentalomas has paralleled the increase in diagnostic imaging done for evaluation of other abdominal pathologies. However, most of these adrenal incidentalomas are benign non-hyperfunctioning adenomas. When an adrenal incidentaloma is discovered, the simultaneous presence of hypokalemia, metabolic alkalosis, mild hypernatremia, and mild to severe drug-resistant hypertension may alert a clinician to underlying primary hyperaldosteronism. We present a case of adrenal incidentaloma noted in a patient with end-stage renal disease on hemodialysis which presented a diagnostic challenge due to the correction of metabolic parameters with hemodialysis. The patient was found to have an aldosterone-producing adenoma based on an elevated aldosterone-to-renin ratio and was started on a mineralocorticoid antagonist.
    Matched MeSH terms: Hypokalemia
  17. Fulltext Neuropsychiatric manifestations of osmotic demyelination syndrome secondary to overcorrection of severe hyponatraemia in hyperemesis gravidarum: a case report
    Sim Mervyn Ian, Nor Zuraida Zainal, Aili Hanim
    Malaysian Journal of Psychiatry, 2018;27(2):0-0.
    MyJurnal
    Osmotic demyelination syndrome (ODS) may occur as a consequence of a
    rapid change in serum osmolality. We report a case of a 32-year-old woman
    who presented to the hospital with symptoms suggestive of severe
    hyperemesis gravidarum. Blood investigation results showed that patient had
    severe hyponatraemia (serum sodium 109 mmol/L) and hypokalaemia
    (serum potassium 1.7 mmol/L). Active and vigorous corrections to these
    electrolyte imbalances had led to an overly increased of serum sodium levels
    within a short duration of time. Four days after the rapid correction, patient
    started exhibiting neuropsychiatric manifestations. Radiological findings
    were consistent with the diagnosis of ODS. The neuropsychiatric symptoms
    experienced by patient gradually worsened with time. Subsequently,
    intravenous methylprednisolone was administered to patient. Patient showed
    marked response to the steroid given. At the time of discharge, twenty-seven
    days later, patient had recovered from most of the neuropsychiatric sequelae;
    but still required assistance during ambulation. In conclusion, correction of
    electrolyte imbalances should be done in a more judicious manner. Prudent
    corrections of electrolyte alterations could have possibly prevented the onset
    of ODS and its’ devastating neuropsychiatric sequelae in this patient.
    Matched MeSH terms: Hypokalemia
  18. Fulltext The invisible evil twin of an adrenal adenoma
    Aimi Fadilah M, Fatimah MS, Nor Aisyah Z, Nur’Aini EW, Nazimah AM, Effat O, et al.
    Journal of Clinical and Health Sciences, 2019;4(1):58-63.
    MyJurnal
    Primary aldosteronism (PA) causes a persistently elevated blood pressure (BP) due to
    excessive release of the hormone aldosterone from the adrenal glands. Classically, it is called
    Conn’s syndrome and is described as the triad of hypertension and hypokalemia with the
    presence of unilateral adrenal adenoma. It can be cured with surgical resection of the
    aldosterone-secreting adenoma leading to resolution of hypertension, hypokalemia and
    increased cardiovascular risk associated with hyperaldosteronism. We present a case of a man
    with previous ischemic heart disease (IHD) who presented with resistant hypertension.
    Investigations for secondary causes of hypertension revealed an elevated aldosterone level
    and saline suppression test confirmed the diagnosis of PA. Radiological examination revealed
    a left adrenal adenoma and a normal right adrenal gland. However, adrenal venous sampling
    showed lateralization of aldosterone secretion towards the right. He subsequently underwent
    a laparoscopic right adrenalectomy which improved his BP control promptly. This case
    highlights the importance of recognizing the need to investigate for secondary causes of
    hypertension. It also underscores the importance of dynamic tests, which may not be easily
    accessible to most clinicians but should pursue, to allow a definitive diagnosis and effective
    treatment.
    Matched MeSH terms: Hypokalemia
  19. Fulltext Hartman's solution or normal saline in the treatment of hyperemesis gravidarum among South East Asian population: a randomised controlled trial
    Adibah, I., Khursiah, D., Ahmad, A.I., Zaki, N.N.M.
    International Medical Journal Malaysia, 2008;7(2):21-24.
    MyJurnal
    Introduction: The aim of treatment for hyperemesis gravidarum is to stop vomiting, correction of dehydration, starvation and electrolytes imbalance. The common types of fluid used for fluid replacement are isotonic solutions like normal saline and hartman's solutions. The absence of potassium in normal saline makes hartman's solution superior but there is a possibility that the lactate component in hartman's solution could worsen the starvation state of the patients. This study is to evaluate which of these two solutions is more effective for fluid replacement in hyperemesis gravidarum. The objectives are to compare which solution corrects dehydration, hypokalaemia and acetonuria faster and to evaluate whether the ketosis state is aggravated by lactate component in hartman's solution. Materials and Methods: Patients with hyperemesis gravidarum were randomised to receive either Hartman's solution or normal saline at the rate of 125mls/hour. Blood urea and serum electrolytes, haematocrit, lactate and urine acetone were taken during admission and repeated every 12 hours. The volume of fluid required to correct dehydration, hypokalaemia and acetonuria were compared. Comparison of the pre and post treatment level of serum lactate were also done. Results: Both hartman's solution and normal saline are both effective in correcting dehydration (11.52±3.28 pints versus 11.94 ± 2.30pints respectively) and acetonuria (11.64 ± 2.75 pints versus 11.64 ± 2.54 pints respectively).
    A lower volume of hartman's solution was needed to correct hypokalaemia (8.34 ± 2.44 pints versus 8.88 ± 2.63 pints) but was not statistically significant. Ketonaemia was not made worse after treatment with hartman's solution. Conclusion: Normal saline and hartman's solution are equally effective in treating complications of hyperemesis gravidarum.
    Matched MeSH terms: Hypokalemia
  20. Fulltext Renin dependent hypertension caused by accessory renal arteries
    Chan PL, Tan FHS
    Clin Hypertens, 2018;24:15.
    PMID: 30410790 DOI: 10.1186/s40885-018-0100-x
    Background: Hypokalemia in the presence of hypertension is often attributed to primary hyperaldosteronism as a cause of secondary hypertension, however secondary hyperaldosteronism may present similarly. Accessory renal arteries are variants in the vascular anatomy which are often thought to be innocuous but in some circumstances can cause renovascular hypertension leading to secondary hyperaldosteronism.

    Case presentation: We report 2 cases of hypertension with secondary hyperaldosteronism associated with accessory renal arteries. Both patients presented with hypokalemia and further investigations revealed hyperaldosteronism with unsuppressed renin levels. Imaging studies showed the presence of accessory renal artery.

    Conclusion: Accessory renal arteries are a potential cause renovascular hypertension which can be detected via CT angiography or magnetic resonance angiography. Hormonal evaluation should be undertaken to determine whether its presence contributes to hypertension in the patient as targeted treatment such as aldosterone antagonist can be initiated. Surgical intervention or renal denervation may be considered in resistant cases.

    Matched MeSH terms: Hypokalemia
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