Acute poisoning by a barium chloride burn

A 62-year-old man sustained a barium chloride burn after his jackhammer penetrated a pocket of molten barium chloride. He subsequently developed signs of systemic barium poisoning including bigeminy and hypokalemia. Treatment consisted of early thorough debridement and intravenous potassium supplementation. Serum barium levels were determined. In a review of the literature these appeared to be the first toxic barium levels to be reported. The literature concerning barium poisoning and its complications is reviewed and related to the clinical presentation and treatment of this chemically burned patient.     

Cibenzoline-induced respiratory muscular paralysis in a hemodialysis patient

A 69-year-old man was admitted to our kidney center with endstage renal failure. We started intermittent peritoneal dialysis immediately because of severe azotemia, hyperkalemia, and metabolic acidosis. Two weeks after admission, he developed uremic pericarditis with frequent ventricular premature contractions and supraventricular premature contractions. The intermittent peritoneal dialysis was then replaced by intensive hemodialysis, and oral administration of 300 mg/d of cibenzoline was started. Four days later, he developed thirst, weakness, and dyspnea due to respiratory muscular paralysis. We initiated respiratory support with a respirator because analysis of his blood gases revealed marked hypercapnia and hypoxia. He also developed hypoglycemia and prolonged PQ and QRS intervals on the electrocardiogram, which we believed were due to cibenzoline intoxication; we discontinued the cibenzoline immediately. All symptoms improved, and he was extubated 5 days later. After 2 months, his pericardial effusion disappeared. He now continues maintenance hemodialysis as an outpatient. We suspect that the cibenzoline induced the respiratory muscular paralysis for 2 reasons: 1) the patient experienced the respiratory muscular paralysis, at the same time he also experienced thirst, weakness, hypoglycemia, and prolonged PQ and QRS intervals on electrocardiogram, and all of these symptoms improved after the discontinuation of cibenzoline, and 2) his plasma concentration of cibenzoline became remarkably elevated, to 20 times above the standard therapeutic level. This patient's clinical course indicates that hemodialysis might be superior to intermittent peritoneal dialysis for treatment of cibenzoline intoxication.     

Atypical electrolyte kinetics during an emergency dialysis session in a patient with Leriche syndrome

A hemodialysis patient suffered from circulation failure due to a low output syndrome caused by a hyperkalemia (9.9 micromol/l) with typical ecg signs. An emergency hemodialysis was started. After 2 h ecg signs of hypokalemia (2.1 micromol/l) were detectable. Hemodialysis was stopped. 2 h later, serum potassium rose to 6.2 micromol/l. An obturation of the aorta and the inferior caval vein with perfusion through collateral vessels of the lower body side was obvious, resulting into a faster electrolyte correction in the upper and a delayed correction in the lower body side with a rebound in the upper compartment. Dialysis time and dialysate potassium (4.0 micromol/l) were increased. Furthermore no potassium problems occurred.     

Case of distal renal tubular acidosis complicated with renal diabetes insipidus, showing aggravation of symptoms with occurrence of diabetes mellitus

We report herein a 27-year-old male case of inherited distal renal tubular acidosis complicated with renal diabetes insipidus, the symptoms of which were aggravated by the occurrence of diabetes mellitus. At 2 months after birth, he was diagnosed as having inherited distal renal tubular acidosis and thereafter supplementation of both potassium and alkali was started to treat his hypokalemia and metabolic acidosis. At the age of 4 years, calcification of the bilateral renal medulla was detected by computed tomography. Subsequently his urinary volume gradually increased and polyuria of approximately 4 L/day persisted. At the age of 27 years, he became fond of sugar-sweetened drinks and also often forgot to take the medicine. He was admitted to our hospital due to polyuria of more than 10 L day, muscle weakness and gait disturbance. Laboratory tests disclosed worsening of both hypokalemia and metabolic acidosis in addition to severe hyperglycemia. It seemed likely that occurrence of diabetes mellitus and cessation of medications can induce osmotic diuresis and aggravate hypokalemia and metabolic acidosis. Consequently, severe dehydration, hypokalemia-induced damage of his urinary concentration ability and enhancement of the renin angiotensin system occurred and thereby possibly worsened his hypokalemia and metabolic acidosis. As normalization of hyperglycemia and metabolic acidosis might have exacerbated hypokalemia further, dehydration and hypokalemia were treated first. Following intensive treatment, these abnormalities were improved, but polyuria persisted. Elevated plasma antidiuretic hormone (12.0 pg/mL) and deficit of renal responses to antidiuretic hormone suggested that the polyuria was attributable to the preexisting renal diabetes insipidus possibly caused by bilateral renal medulla calcification. Thiazide diuretic or nonsteroidal anti-inflammatory drugs were not effective for the treatment of diabetes insipidus in the present case.     

Pseudoaldosteronism due to the concurrent use of two herbal medicines containing glycyrrhizin: interaction of glycyrrhizin with angiotensin-converting enzyme inhibitor

A 77-year-old man with a history of hypertension and hyperuricemia was admitted to our hospital complaining of limb weakness, persistent constipation, and worsening hypertension. He had been taking a Chinese herbal remedy for allergic rhinitis for the past 10 years, together with an angiotensin-converting enzyme inhibitor (ACE-I; enalapril, 20 mg daily). After the dosage of enalapril had been reduced to 10 mg daily about 1(1/2) years before the current admission, he had developed persistent constipation. Therefore, he had started taking another traditional Chinese herbal remedy, a laxative, for the constipation, about 4 months prior to this hospitalization. Laboratory data on admission demonstrated marked metabolic alkalosis with severe hypokalemia associated with urinary wasting of potassium and chloride. A diagnosis of pseudoaldosteronism was made based upon his past history of exposure to various traditional Chinese medicines containing glycyrrhizin. Discontinuation of the Chinese remedies and supplementation of potassium successfully normalized the electrolyte imbalance and relieved all symptoms within a short time. The present case describes the occurrence of pseudoaldosteronism induced by a patient taking two traditional Chinese herbs, both containing glycyrrhizin, resulting in an overdose of this causative chemical agent. The development of pseudoaldosteronism appeared to be of particular interest with regard to the interaction of the renin-angiotensin-aldosterone (RAA) system with glycyrrhizin, in which an ACE-I retarded the development of pseudoaldosteronism.     

Hypokalemic paralysis mimicking Guillain-Barré syndrome and causing acute respiratory failure

A 33-year-old female patient admitted to the ICU with ascending muscle weakness leading to acute hypercapneic respiratory failure. She gave a 10-day history of severe diarrhea and vomiting. Laboratory work up revealed severe hypokalemia, mixed metabolic and respiratory acidosis, and renal impairment. Continuous potassium replacement produced rapid and complete recovery from quadriplegia and respiratory failure without requirement for mechanical ventilation.     

Gitelman’s syndrome associated with chondrocalcinosis: a case report

Abstract

Gitelman’s syndrome (GS) is a rare disease with autosomal recessive trait, characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria and hyperkinemic hyperaldosteronism. While muscle weakness, tetany, stomachache, nausea and fever are very common, it could sometimes be completely asymptomatic as is the case in our patient. It is generally benign, but some severe complications like growth retardation and, though rare, paralysis and cardiac arrest could also be seen. A 57-year-old male patient sent to our hospital for further examination because of hypokalemia was diagnosed with GS as a result of clinical and laboratory assessments. Potassium and magnesium replacement was started. We are presenting our case seeing that GS is not a syndrome to be overlooked as it bears a risk of severe complications, although it might be asymptomatic until advanced ages.     

A physiologic-based approach to the treatment of a patient with hypokalemia

Hypokalemia is common and can be associated with serious adverse consequences, including paralysis, ileus, cardiac arrhythmias, and death. As a result, the body maintains serum potassium concentration within very narrow limits by tightly regulated feedback and feed-forward systems. Whereas the consequences of symptomatic hypokalemia and severe potassium depletion are well appreciated, chronic mild hypokalemia can accelerate the progression of chronic kidney disease, exacerbate systemic hypertension, and increase mortality. Persistent hypokalemia may reflect total-body potassium depletion or increased renal potassium clearance. In a patient with simple potassium depletion, potassium replacement therapy should correct serum potassium concentration, but may have little effect when renal potassium clearance is abnormally increased from potassium wasting. In such cases, the addition of potassium-sparing diuretics might be helpful. Serum potassium concentration is an inaccurate marker of total-body potassium deficit. Mild hypokalemia may be associated with significant total-body potassium deficits and conversely, total-body potassium stores can be normal in patients with hypokalemia due to redistribution. The speed and extent of potassium replacement should be dictated by the clinical picture and guided by frequent reassessment of serum potassium concentration(.) The goals of therapy should be to correct a potassium deficit, if present, without provoking hyperkalemia. Oral replacement is preferred except when there is no functioning bowel or in the setting of electrocardiogram changes, neurologic symptoms, cardiac ischemia, or digitalis therapy.     

Severe hyperkalemic type 4 renal tubular acidosis after kidney transplantation: a case report

BACKGROUND: Hyperkalemia after transplantation is a common event, occurring in up to 70% of patients. It is usually asymptomatic but sometimes manifests as muscle weakness or cardiac arrhythmias. METHODS: Case report. RESULTS: At 102 days after a second cadaveric kidney transplantation, a 15-year-old boy, was admitted to the emergency room with severe muscle weakness. His examinations showed a serum potassium of 9.8 mEq/L; blood pH 7.1; serum bicarbonate 7.6 mmol/L; and creatinine 2.5 mg/dL. He was initially treated with sodium bicarbonate, calcium gluconate, and furosemide. Subsequent investigation showed hyperchloremic metabolic acidosis, urinary pH <5.5, positive urinary anion gap, reduced transtubular potassium gradient (TTKG, 1.5) and low levels of aldosterone (0.7 ng/mL), suggesting the presence of type 4 renal tubular acidosis (RTA). Other causes of hyperkalemia were excluded in the present case. Serum levels of potassium returned to normal when fludrocortisone was added to the bicarbonate supplementation. This case of severe hyperkalemic secondary to type 4 RTA after kidney transplantation only responded to the combination of alkali and mineralocorticoid therapies.     

Severe metabolic acidosis and hypokalemia in a patient with enterovesical fistula

We report a case of a 59-year-old woman who had severe metabolic acidosis and hypokalemia due to an enterovesical fistula. The patient came to our hospital complaining of systemic weakness and numbness of the fingers. She was found to have hyperchloremic metabolic acidosis (arterial bicarbonate, 2.8 mEq/l) and hypokalemia (serum potassium, 1.9 mEq/l) and was admitted for treatment. Following the correction of metabolic acidosis and hypokalemia, the patient was examined for the underlying cause of these electrolyte and acid-base disorders. She had a history of total hysterectomy followed by radiotherapy due to uterine cancer 30 years previously. After the surgery, she had suffered postoperative neurogenic bladder dysfunction, necessitating intermittent self-catheterization. Two years before admission, she had begun to experience watery diarrhea. A radiographic study after recovery from the acid-base and electrolyte disorders revealed the presence of an enterovesical fistula. The fistula was surgically resected and the metabolic acidosis completely cleared. Unexplained hyperchloremic metabolic acidosis with hypokalemia may suggest the presence of an enterovesical fistula in patients with a surgical history of malignant pelvic tumor and neurogenic bladder dysfunction.     

Temporal profile of serum potassium concentration in nondiabetic and diabetic outpatients on chronic dialysis

We analyzed routine serum potassium concentration measurements and conditions temporally associated with abnormalities in potassium concentration in outpatients on chronic hemodialysis (136 nondiabetics, 36 diabetics) and continuous ambulatory peritoneal dialysis (16 nondiabetics, 10 diabetics). The following potassium concentration frequencies were found: prehemodialysis, nondiabetics: normal 51.3%, severe hyperkalemia (greater than 6.0 mmol/l) 10%, severe hypokalemia (less than 3.0 mmol/l) 0.3%; diabetics: normal 57.8%, severe hyperkalemia 8.7%, severe hypokalemia 0.5%. Peritoneal dialysis, nondiabetics: normal 73.7%, severe hyperkalemia 0.6%, severe hypokalemia 4.9%; diabetics: normal 72.5%, severe hyperkalemia 0.9%, severe hypokalemia 2.9%. Normokalemia and severe hypokalemia were significantly (chi 2 test) more frequent in peritoneal dialysis than in prehemodialysis, whereas severe hyperkalemia was more frequent in prehemodialysis serum samples. No difference was found between nondiabetics and diabetics for either form of dialysis. 50% of prehemodialysis episodes of hyperkalemia were diet-induced. Hyperkalemic drugs and anuria were not associated with a higher risk of prehemodialysis hyperkalemia, but each one of 3 abnormalities, very high BUN (greater than 40 mmol/l), metabolic acidosis (TCO2 less than 15 mmol/l) and, in diabetics, severe hyperglycemia (serum glucose greater than 30 mmol/l), was associated with a statistically higher risk of hyperkalemia.     

A case of fatal caffeine poisoning

Caffeine is a natural alkaloid methylxanthine that is found in various plants such as coffee or tea. Symptoms of a severe overdose may present with hypokalemia, hyponatremia, ventricular arrhythmias, hypertension followed by hypotension, respiratory failure, seizures, rhabdomyolysis, ventricular fibrillation and finally circulatory collapse. A 21‐year‐old woman called for the ambulance herself soon after the ingestion of about 10,000 mg of caffeine. At the arrival of the ambulance, the patient went into cardiac arrest almost immediately. After a total resuscitation period of 34 min including seven counter‐shocks and 2 mg epinephrine, the patient was stable enough to be transferred to the hospital. The patient soon went into VF again and received two more counter‐shocks and 1 mg epinephrine and finally an intravenous bolus dose of 300 mg amiodarone. The initial arterial blood gas showed pH at 6.47, lactate at 33 mmol/l and potassium level at 2.3 mmol/l. Unfortunately, no blood samples for caffeine analysis were taken. Three days after hospital admission, the patient developed myoclonus, which did not respond to medical treatment. Excessive intake of caffeine may produce arrhythmias and pronounced hypokalemia and ensuing ventricular fibrillation. In case of counter‐shock‐resistant VF, it can be necessary to give an early loading dose of amiodarone. Furthermore, it may be beneficial to replace the potassium as early as possible. Epinephrine and buffer solutions used during resuscitation may further decrease blood potassium levels and should be administrated cautiously. Epinephrine can be replaced by other vasopressor drugs, such as vasopressin without effects on β‐receptors.     

Does magnesium play a role in the hypokalemia of Bartter's syndrome?

A patient with Bartter's syndrome manifested hypomagnesemia in addition to hypokalemia. Under conditions of maximal free water production, he had a fractional distal solute reabsorption of 0.65, a value consistent with a renal defect in sodium chloride reabsorption in the thick ascending limb of the loop of Henle. This is also the site of 65% to 70% of urinary magnesium reabsorption. With magnesium supplementation and amiloride, the urinary potassium decreased and the serum potassium increased. Atrial natriuretic peptide concentrations in the plasma were low. Evaluation of family members showed five of nine offspring had hypokalemia with no disorder in the parents, an apparent autosomal recessive mode of inheritance. This is a US government work. There are no restrictions on its use.     

Mechanism and prevention of cardiac arrhythmias in chronic hemodialysis patients

We monitored, by the Holter method, 23 clinically stable maintenance hemodialysis patients for 5 +/- (SEM) 2 hours before hemodialysis, 5.0 +/- 0.5 hours during hemodialysis, and 13 +/- 3 hours after hemodialysis. Of 23 patients, 9 (39%) had unexpected frequent or complex ventricular arrhythmias recorded and after hemodialysis with a potassium dialysate bath concentration of 2.0 mEq/liter. Patients with ventricular arrhythmias were more likely to be using digoxin (8/9 vs. 1/4) and to have evidence of left ventricular hypertrophy (9/9 vs. 7/4 than were those patients without arrhythmias. Of these 9 patients with arrhythmias, 6 underwent repeat Holter monitoring during multiple dialysate protocols. Of the 6 patients, 4 had a significant reduction in the frequency of ventricular ectopy when a dialysate of 3.5 mEq/liter potassium was used (P < 0.05), but of these 6, 3 still had complex arrhythmias. The use, however, of a 3.5 mEq/liter potassium dialysate plus the administration of a 400-mg dose of quinidine sulfate orally 45 min prior to hemodialysis was successful in reducing ventricular ectopic frequency and complexity in all the patients studied. Conclusion. Maintenance hemodialysis patient using digoxin and with left ventricular hypertrophy have an unexpectdly high indicence of occult, potentoial serious, ventricular arrhythmias during and after hemodialysis, revealed by Holter monitoring. There is preliminary evidence that a low-potassium bath concentration may play a role in predisoposing patients to these arrhythmias. Further prospective studies with largaer number of patients will be needed, however, to evaluate the significance of these findings.     

Ectopic ACTH syndrome revealed as severe hypokalemia and persistent hypertension during the perioperative period: a case report

Both severe hypokalemia and persistent hypertension are clinical symptoms of hyperaldosteronism. Hyperaldosteronism may occur as a primary or secondary syndrome. Excess ACTH produced ectopically by tumors may induce hyperaldosteronism through the mineralocorticoid activity of glucocorticoids that are upregulated by ACTH. Licorice, with the active ingredient glycyrrhiza, is also a well-known inducer of hyperaldosteronism under specific conditions. In this report, we describe a case of severe hypokalemia caused by ectopic ACTH syndrome (EAS) elicited by an intrathoracic carcinoid tumor, which had transformed to produce ACTH during the 6-year clinical course, and was modulated by licorice ingestion. Hypokalemia was not clearly recognized preoperatively but became obvious within 3 h of general anesthesia with epidural blockade. At the end of anesthesia, arterial blood gas analysis indicated severe hypokalemia ([K⁺] = 1.7 mEq/l) and metabolic alkalosis (pH 7.56, PaCO₂ = 54.9 mmHg, HCO₃ ⁻ = 44.5 mmol/l, BE = 21.8 mmol/l), without any typical symptoms such as muscle weakness or ECG abnormalities. The hypokalemia was resistant to potassium supplementation and persisted for 4 days. Perioperative imbalance between the administration and elimination of potassium and surgical stress might contribute to the rapid exacerbation and induce the clinical manifestation of EAS.     

Hypokalemic myopathy. Our experience at an intensive care unit]

Disturbances of potassium homeostasis are frequently iatrogenic: some drugs, especially diuretics, are sometimes taken without proper electrolyte control and replacement; this can lead to more or less severe hypokalemic states. After some physiopathologic remarks, the Authors report their experience with four patients admitted for severe hypokalemia; the clinical picture was always quite typical: severe muscle weakness (even quadriparesis), cardiac rhythm abnormalities, metabolic alkalosis. A reliable diagnostic tool is muscle biopsy that shows aspects of vacuolar myopathy.     

Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman

The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. Triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.     

Obstructive uropathy by total uterine prolapse leading to end-stage renal disease

A 74-year-old woman was admitted to our emergency room complaining of general weakness and anorexia that started 20 days earlier. She denied other underlying diseases that might have provoked chronic renal disease. Her serum creatinine was 12.35 mg/dL. A pelvic examination and computed tomography revealed severe bilateral hydroureteronephrosis with marked cortical thinning induced by total uterine prolapse. She was started on emergency hemodialysis due to her uremic symptoms and severe metabolic acidosis. Despite Foley catheter insertion and manual reduction of uterus for 1 month, renal function was not recovered. The department of gynecology was strongly opposed to performing a procedure to reverse the hydroureteronephrosis due to the irreversibility of her renal function. She is undergoing chronic maintenance hemodialysis. This is a case report of rare end-stage renal disease (ESRD) caused by obstructive uropathy due to pelvic organ prolapse (POP). We should consider POP as a cause of ESRD.     

A case of hypokalemia-induced fatal arrhythmia caused by indapamide in an anorexic elderly patient

An 84-year-old man was referred to our hospital for atrioventricular block and severe hypokalemia. He had been treated for hypertension since 2007 with indapamide, a thiazide-like diuretic. His laboratory data had not been tested for a long time. One week before his first visit, he suffered from a common cold and anorexia. He was admitted to our hospital because his electrocardiogram showed ventricular flutter, and pulmonary arrest occurred at the time of his visit. Cardiopulmonary resuscitation was successfully performed. Hypokalemia (K, 1.7 mEq/L) was considered as the cause of acute cardiopulmonary failure. His oral intake of potassium decreased, but potassium loss from the kidney persisted (urinary potassium, 14.0 mEq/L; transtubular potassium gradient, 5.00). These results suggested that although hypokalemia was suspected to have been present for a long time due to indapamide, severe hypokalemia was induced during the period of anorexia. After discontinuation of indapamide and intravenous administration of potassium l-aspartate for potassium supplementation, the patient’s serum potassium levels increased and his general condition improved. Although it is well known that hypokalemia is caused by indapamide, the incidence is not frequent and if observed is not severe. However, we experienced an unusual case of hypokalemia-induced fatal arrhythmia caused by indapamide. Hence, the serum potassium concentration of patients under the drug, especially anorexic elderly patients, should be monitored.     

Ectopic adrenocorticotropic hormone syndrome in a case of small cell carcinoma of the bladder manifesting as severe muscle weakness

Ectopic adrenocorticotropic hormone syndrome is a paraneoplastic syndrome associated with small cell carcinoma. However, ectopic adrenocorticotropic hormone syndrome is rare in association with small cell carcinoma of the bladder. We report what we believe to be the first case of ectopic adrenocorticotropic hormone syndrome associated with small cell carcinoma of the bladder that manifested as severe muscle weakness due to hypokalemia. An early diagnosis and aggressive potassium replacement is essential for retaining muscle strength. The patient died of pneumonia less than 2 months after the diagnosis. Severe immunosuppression by excess cortisol production was suspected. Control of cortisol levels before chemotherapy might be beneficial in preventing infective complications.