Glyphosate poisoning - a case report.

Glyphosate is the most commonly used broad-spectrum, non-selective herbicide in the world. The toxicity is supposed to be due to uncoupling of oxidative phosphorylation and the surfactant polyoxyethylene amine (POEA)- mediated cardiotoxicity. Clinical features of this herbicide poisoning are varied, ranging from asymptomatic to even death. There is no antidote and aggressive supportive therapy is the mainstay of treatment for glyphosate poisoning. We present a 69-year-old female patient with suicidal consumption of around 500 ml of Glycel®. Initially, gastric lavage was done and intravenous fluids were given. Within two hours of presentation, the patient developed respiratory distress needing intubation, hypotension needing vasopressor support, and severe lactic acidosis. She also developed acute respiratory distress syndrome, hypokalemia, hypernatremia, and aspiration pneumonia. Our patient was critically ill with multiple poor prognostic factors, but with timely aggressive supportive management, the patient gradually recovered.

Promoting oral potassium administration in a tertiary care hospital: An eleven-year study.

INTRODUCTION: Potassium is used to treat or prevent hypokalemia and exhibits all the characteristics of an intravenous to oral therapy conversion program. Despite this, the intravenous route for potassium replacement seems frequently unjustified. OBJECTIVES: To determine the impact of a conversion program on the use of intravenous and oral galenic forms in a university tertiary care hospital. METHODS: Two promotion campaigns were conducted in 2006 and 2009. The following years this was completed by pharmacist interventions during prescription analysis and face-to-face discussions with physicians during ward rounds. The consumption of products containing potassium was obtained by analyzing the hospital's financial database. RESULTS: The proportion of the oral route increased from 18% in 2006 to 22% in 2011, and from 25% in 2012 to 44% in 2016; the increase was significantly greater in the second period (P<0.0001). In 2016, in emergency, pulmonology, infectious diseases, and cardiology departments, the proportion of oral use ranged from 57% and 82%. The greatest progression from 2006 to 2016 was found for intensive care (4% vs. 12%) and visceral surgery departments (9% vs. 34%) that increased approximately four-fold, followed by the emergency department (28% vs. 57%) that increased approximately two-fold. CONCLUSION: Promoting the oral route for potassium replacement modifies prescriber habits and is followed by a notable increase in the proportion of potassium administered orally irrespective of department type.

Plasma exchange successfully treats central pontine myelinolysis after acute hypernatremia from intravenous sodium bicarbonate therapy.

BACKGROUND: Osmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy. CASE PRESENTATION: A 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren's syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer's test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride. CONCLUSION: This case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.

Recurrent ventricular fibrillation related to hypokalemia in early repolarization syndrome.

We describe a case of early repolarization syndrome in which augmented J waves were documented during an electrical storm associated with hypokalemia. The patient was referred to our hospital for therapy to treat recurrent ventricular fibrillation (VF). The 12-lead electrocardiogram showed giant J waves associated with hypokalemia during multiple episodes of VF. Although antiarrhythmic agents or deep sedation were not effective for the VF, an intravenous supplementation of potassium completely suppressed the VF with a reduction in the J-wave amplitude. Our report discusses the possible relationship between hypokalemia and VF in early repolarization syndrome.

[45-year-old woman with muscle weakness and hypopotassemia]. / 45-jährige Patientin mit Muskelschwäche und Hypokaliämie.

We report a 45-year-old female patient with muscle weakness. We diagnosed renal tubular acidosis type I by laboratory findings of hypopotassemia, hypopotassuria, metabolic acidosis and basic urine. The muscle weakness improved rapidly by substitution of potassium and an alcalescent substance. Searching for associated autoimmune diseases we diagnosed primary biliary cirrhosis and initiated a therapy with ursodeoxycholic acid.

A case of nephrotic syndrome with Gitelman's syndrome.

Nephrotic syndrome, though common in children, association of it with Gitelman's syndrome (GS) is a rare occurrence. Very few cases have been reported in the medical literature so far. Here we report a case of nephrotic syndrome with frequent relapses and remissions on intermittent steroid and diuretic therapy. Patient was restarted on steroids and frusemide. Puffiness of face, bipedal edema and oliguria improved but patient developed tingling numbness in both limbs, perioral numbness and carpopedal spasm. On investigation she was found to have proteinuria, metabolic alkalosis, hypokalemia, hypocalcemia, hypomagnesemia and hyperreninemia with normal blood pressure.

Hypokalemic paralysis as an initial presentation of Sjogren syndrome.

Sjogren syndrome (SS) is a systemic autoimmune disorder with predominant exocrine gland involvement leading to sicca symptoms. Among extraglandular manifestations, renal disease is the most common. Tubular interstitial nephritis and renal tubular acidosis (RTA) are the common presentations. Mild hypokalemia associated with distal RTA is common in SS, however, severe hypokalemia causing paralysis is unusual. We report the case of a 26-year-old female who presented with hypokalemic paralysis. On evaluation, distal RTA was diagnosed. Further evaluation showed positive SS-a/SS-b antibodies in high titer, which confirms the diagnosis of primary SS. Our report illustrates that SS is a rare but important cause of hypokalemic paralysis.

Résumé syndrome de Sjogren (SS) est une maladie auto-immune systémique avec une atteinte prédominante des glandes exocrines entraînant des symptômes de sicca. Parmi manifestations extraglandulaires, la maladie rénale est la plus courante. La néphrite interstitielle tubulaire et l'acidose tubulaire rénale (RTA) sont les présentations. Une hypokaliémie légère associée à un RTA distal est courante dans les SS, cependant, une hypokaliémie sévère provoquant une paralysie est inhabituelle. Nous rapportons le cas d'une femme de 26 ans qui présentait une paralysie hypokaliémique. À l'évaluation, un RTA distal a été diagnostiqué. Plus loin l'évaluation a montré des anticorps SS-a / SS-b positifs à titre élevé, ce qui confirme le diagnostic de SS primaire. Notre rapport montre que SS est un cause rare mais importante de paralysie hypokaliémique.

Ureterosigmoidostomy[corrected]-associated quadriparesis, non-traumatic rhabdomyolysis, and tetany in an adult.

We report an adult case of ureterosigmoidostomy-associated quadriparesis, rhabdomyolysis, and tetany which may be the first such case in the literature. A 32-year-old female patient was brought to the emergency room of our hospital, having been unable to walk or use her arms for 24 h. Neurological examination revealed quadriparesis. She had severe hypokalemia (1.27 mmol/l) and metabolic acidosis (pH=7.05). Creatine kinase value was 2,590 U/l on the third day. She received intensive therapy to correct the hypokalemia and acidosis. On the third day of hospitalization tetany was detected in her upper extremities. The patient regained full muscle power after intravenous potassium chloride, bicarbonate, and calcium replacement therapy.

[Study on safety and efficacy of concentrated potassium chloride infusions in critically ill patients with hypokalemia].

OBJECTIVE: To explore the safety and clinical efficacy of intravenous infusion of concentrated potassium chloride using micro-pumps in critically ill patients with hypokalemia. METHODS: One hundred and twenty-eight critically ill patients with hypokalemia, the endogenous creatinine clearance rate over 0.5 ml/second and the urine output over 50 ml/hour were randomly divided into the therapy group (n=64) and the control group (n=64). Patients in therapy group received 1,208 mmol/L (9%) KCl, while those in the control group received 201 mmol/L (1.5%) potassium chloride, intravenously with the aid of a micro-pump, with hourly equal quantity of KCl in both groups. Patients in both groups were monitored strictly, and the potassium infusion was stopped whenever the serum potassium exceeded or equal to 3.5 mmol/L. RESULTS: It took (15.55+/-3.22) hours and (14.18+/-4.93) hours for the therapy group and the control group to correct the hypokalemia respectively, and there was no significant difference (P>0.05). Potassium infusion brought larger amount of fluid in the control group than the therapy group [(124.36+/-25.79) ml vs. (680.83+/-236.70) ml, P<0.01]. All patients tolerated the infusion without evidence of hemodynamic change, hyperkalemia or acute heart dysfunction. For all the patients, renal function did not throw significant influence on the potassium infusion time. An inverse correlation was observed between preinfusion potassium concentration and the quantity of potassium infused (r= -0.259, P<0.01). CONCLUSION: Under meticulous monitoring, it is safe and effective to infuse concentrated potassium for the critically ill patients with hypokalemia. This strategy can also be followed in patients with mild renal dysfunction but without oliguria or anuria under careful monitoring.

Life-Threatening Hypokalemic Quadriplegia in a Postoperative Patient.

Acute hypokalemic paralysis is a reversible but potentially lethal clinical condition. We report a case, who developed rapidonset quadriparesis in immediate postoperative period after undergoing right percutaneous nephrolithotomy for bilateral renal stones. On evaluation, she was found to have hypernatremic, hyperchloremic, hypokalemic acidosis. This severe hypokalemia-induced quadriparesis was precipitated by repeated furosemide injections, use of potassium-free fluid as maintenance, intracellular shift due to free water administration in this patient, who had pre-existing distal renal tubular acidosis.

Expanding the differential: toluene-induced toxicity.

A 31-year-old woman presented to the hospital with generalised weakness and lower back and abdominal pain. The only significant finding on physical examination was the weakness of the legs. Laboratory analysis in the emergency department revealed that she was hypokalaemic with metabolic acidosis. She was treated with oral and intravenous potassium, which resolved her weakness. During the search for an explanation for her renal tubular acidosis, she said she was exposed to paint exposure while working on a friend's house. She was discharged on correction of her hypokalaemia, and a subsequent test revealed elevated blood toluene level.

Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Hyperaldosternoism: A Case Report.

BACKGROUND Thyrotoxic periodic paralysis (TPP) is commonly observed in patients with acute paralysis and hyperthyroidism. However, there is a possibility of secondary causes of hypokalemia in such a setting. CASE REPORT Herein, we present the case of a 38-year-old woman with untreated hypertension and hyperthyroidism. She presented with muscle weakness, nausea, vomiting, and diarrhea since one week. The initial diagnosis was TPP. However, biochemistry tests showed hypokalemia with metabolic alkalosis and renal potassium wasting. Moreover, a suppressed plasma renin level and a high plasma aldosterone level were noted, which was suggestive of primary aldosteronism. Abdominal computed tomography confirmed this diagnosis. CONCLUSIONS Therefore, it is imperative to consider other causes of hypokalemia (apart from TPP) in a patient with hyperthyroidism but with renal potassium wasting and metabolic alkalosis. This can help avoid delay in diagnosis of the underlying disease.

Thyrotoxic periodic paralysis as an initial presentation of Graves' disease in a Saudi patient.

Thyrotoxic periodic paralysis (TPP) is a well-known complication of hyperthyroidism, characterised by recurrent flaccid paralysis with hypokalaemia. To date, only five cases of this rare disorder have been reported in Saudi Arabia. Here, we report an additional case involving a 25-year-old Saudi man who presented with lower limb paralysis and severe hypokalaemia. Clinically, he showed symptoms and signs suggestive of Graves' disease, which was confirmed by laboratory investigations. Carbimazole, a beta-blocker and potassium replacement were administered, resulting in dramatic improvement of the TTP. This case emphasises the importance of considering TPP in patients with acute muscle weakness and the importance of promptly initiating treatment and preventing relapse of TPP.

Celiac crisis with hypokalemic paralysis in a young lady.

Celiac crisis presents as severe acute diarrhea with life-threatening metabolic derangement in a patient with celiac disease. We report a 30-year-old lady who was admitted with one-month history of worsening small bowel-type diarrhea. She developed acute quadriparesis due to refractory hypokalemia. Celiac disease was diagnosed on the basis of positive serology and histological features. She improved with aggressive correction of hypokalemia and gluten-free diet. Celiac crisis is a rare presentation of this heterogeneous disease in adulthood.

SFE/SFHTA/AFCE consensus on primary aldosteronism, part 6: Adrenal surgery.

Treatment of primary aldosteronism (PA) aims at preventing or correcting hypertension, hypokalemia and target organ damage. Patients with lateralized PA and candidates for surgery may be managed by laparoscopic adrenalectomy. Partial adrenalectomy and non-surgical ablation have no proven advantage over total adrenalectomy. Intraoperative morbidity and mortality are low in reference centers, and day-surgery is warranted in selected cases. Spironolactone administered during the weeks preceding surgery controls hypertension and hypokalemia and may prevent postoperative hypoaldosteronism. In most cases, surgery corrects hypokalemia, improves control of hypertension and reduces the burden of pharmacologic treatment; in about 40% of cases, it resolves hypertension. However, success in controlling hypertension and reversing target organ damage is comparable with mineralocorticoid receptor antagonists. Informed patient preference with regard to surgery is thus an important factor in therapeutic decision-making.

SFE/SFHTA/AFCE consensus on primary aldosteronism, part 7: Medical treatment of primary aldosteronism.

Spironolactone, which is a potent mineralocorticoid receptor antagonist, represents the first line medical treatment of primary aldosteronism (PA). As spironolactone is also an antagonist of the androgen and progesterone receptor, it may present side effects, especially in male patients. In case of intolerance to spironolactone, amiloride may be used to control hypokaliemia and we suggest that eplerenone, which is a more selective but less powerful antagonist of the mineralocorticoid receptor, be used in case of intolerance to spironolactone and insufficient control of hypertension by amiloride. Specific calcic inhibitors and thiazide diuretics may be used as second or third line therapy. Medical treatment of bilateral forms of PA seem to be as efficient as surgical treatment of lateralized PA for the control of hypertension and the prevention of cardiovascular and renal morbidities. This allows to propose medical treatment of PA to patients with lateralized forms of PA who refuse surgery or to patients with PA who do not want to be explored by adrenal venous sampling to determine whether they have a bilateral or lateralized form.

Diuretic-induced hypokalemia in uncomplicated systemic hypertension: effect of plasma potassium correction on cardiac arrhythmias.

Sixteen patients with diuretic-induced hypokalemia underwent 24-hour ambulatory electrocardiographic monitoring during and after correction of hypokalemia. Plasma potassium averaged 2.83 +/- 0.08 mEq/liter before and 3.73 +/- 0.06 mEq/liter after correction with potassium chloride, triamterene or both. Premature atrial contractions decreased in 6 patients, increased in 6 and remained unchanged in 4. There was no improvement in ventricular ectopic activity after plasma potassium correction. Ventricular ectopic activity improved in 5 patients, worsened in 10 and remained unchanged in 1. Ventricular tachycardia was not observed in either phase. Plasma magnesium remained normal throughout. The investigators conclude that in patients with uncomplicated hypertension, correction of diuretic-induced hypokalemia does not significantly reduce the occurrence of spontaneous atrial or ventricular ectopic activity.

Thiazide treatment of systemic hypertension: effects on serum magnesium and ventricular ectopic activity.

Clinical and investigational evidence has proved an association between thiazide-induced electrolyte imbalances and ventricular arrhythmias. It is hypothesized that this increases the potential for sudden unexplained death. Elderly hypertensive patients are at particular risk because of their tendency to have significantly depressed serum magnesium levels, which decrease even further when treated with thiazide diuretics. Potassium supplementation does not effectively restore electrolyte balance unless accompanied by magnesium. Therefore, concomitant administration of potassium and magnesium supplementation appears to be an approach to reducing the risk of arrhythmias and death in thiazide-treated hypertensive patients.