Hypokalemic rhabdomyolysis in a patient with a laparoscopic adjustable gastric banding.
A GrandeV GiustolisiV TabitaClemente GiuffridaS RiccobeneC. Le MoliValentina CannoneE MairaG NarboneFrancesca NigroR. ParadisoC Tramontana
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Abstract:
Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells. It can be related to a variety of factors: muscular trauma, muscle enzyme deficiencies, infections, drugs, toxins, alcohol ingestion, endocrinopathies and electrolyte imbalances such as hypokalemia. We report the case of a 46-year-old woman admitted to the Emergency Department for frequent episodes of vomiting associated with food intake in the last two weeks, general muscular weakness and myalgia. Physical examination on admission was unremarkable, except for a symmetrical and dominantly proximal muscular weakness of all four extremities. Blood pressure was 116/70 mmHg with a sinus bradycardia (53 beats/min) on the electrocardiogram. Laboratory tests showed a metabolic alkalosis with marked hypokalemia (K+= 1.9 mEq/l) and elevation of muscular enzymes (myglobin= 993 ng/ml, troponin T= 0,10 ng/ml e CK= 1113 U/l). No symptoms of recurrent rhabdomyolysis were reported, patient denied alcohol consumption and there was not clinical evidence of hyperthyroidism. A iatrogenic etiology could not be excluded for certain because patient was in therapy with lansoprazole (Naranjo algorithm 3/13) but, revealing medical history that she underwent a laparoscopic adjustable gastric banding for the treatment of a severe obesity, we focused our attention on hypokalemia, due to persistent vomiting. Fasting, administration of metoclopramide and infusion of potassium chloride resulted in steady improvement of clinical conditions and normalization of electrolyte imbalance. At the clinical follow-up of three months, after partial deflation of the gastric banding, the patient was asymptomatic with muscular enzymes and potassium levels in the normal range. Authors discuss the pathophysiologic mechanisms of these alterations.Keywords:
Muscle cramp
myalgia
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Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study
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Background: Hypokalemia (serum potassium below 3.5 mmol/L) may be caused by several mechanisms. Severe hypokalemia must be immediately managed, as it can have important cardiac repercussions. Clinical case: A previously healthy eight-year-old female, with normal growth and normal-to-low blood pressure, was observed due to persistent abdominal pain, anorexia, and fever two days after overcoming a mild gastroenteritis episode. Serum biochemistry revealed severe hypokalemia (1.8 mmol/L), hypomagnesemia, and metabolic alkalosis. The patient was admitted to the Pediatric Intensive Care Unit for correction of electrolyte imbalance, cardiac monitoring, and investigation. Complementary studies included a spot urine ionogram that revealed inappropriate potassium wasting. Ionic correction was achieved by both intravenous and oral supplementation plus spironolactone. Genetic testing was positive for Gitelman syndrome. Discussion/Conclusion: Suspicion of complex causes should be raised and a comprehensive approach undertaken upon a discrepancy between clinical history and hypokalemia severity.
Alkalosis
Triamterene
Metabolic disorder
Anion gap
Electrolyte Disorder
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Hypokalemiaperiodic paralysis (HPP) is a rare disorder characterized by acute muscle paralysis. Basedon its etiology, HPP can be classified as primary and secondary types. One of the most common causes ofsecondary HPP is renal tubular acidosis (RTA) which may be also present in thyroid disease. We observed acase of a 48-year-old female, with complaints of weakness in both lower extremities for two days. Difficultiesin walking and weakness in both arms were also present. Patient also experienced nausea, vomiting, anddiarrhea 4 days before coming to the hospital. She had a history of thyroidectomy in 2009 and in 2019 wasadmitted for similar symptoms. Medication consumed by the patient were Euthyrox 100 mg one time dailyand KSR 600 mg three times daily. In the last week, Euthyrox was discontinued by the patient due to herdiarrhea. The patient’s general condition was weak and vital signs were BP 120/80 mmHg, pulse 84 bpm, RR18 times per minute and temperature was 36.6°C. Motoric strength was 4/4 in both arms and 3/3 in both legs.No pathological neurological reflexes were found during examination. Inverted T wave and prominent Uwave were seen on electrocardiogram (ECG) results.Laboratory results showed hypokalemia (2.0 mmol/L),Blood Gas Analysis: Metabolic Acidosis (pH 7.42, pCO2 32 mmHg, HCO3 20.8 mmol/L, BE -3.7 mmol/L)with anion gap of 14.2 meq/L. Urinalysis results were pH 8, urinary anion gap 18.29 mmol/h. Decreasedthyroid function was also shown in the endocrine laboratory panel FT4 0.57 ng/dl and TSH 32.097 IU/mL.HPP is a disorder characterized by muscle weakness and may be present in distal type RTA. Clinicalsymptoms of distal type RTA are hypokalemia, hyperchloremic metabolic acidosis, urinary pH <5.5. Distaltype RTA can be caused by endocrine disorder i.e., hypothyroidism. Observation of patient condition andlaboratory results lead to the conclusion that the patient is diagnosed with hypokalemic periodic paralysisand renal tubular acidosis based on hypokalemia, metabolic acidosis with normal anion gap, and alkalineurine with positive urinary anion gap.
Anion gap
Renal tubular acidosis
Etiology
Hypokalemic periodic paralysis
Periodic paralysis
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A 55-year-old Japanese man was admitted to our hospital with severe weakness. Without measurement of serum electrolyte concentrations, diuretic therapy for hypertension was started 2 weeks prior to admission. Laboratory findings showed profound hypokalemia (1.4 mEq/L), and extreme elevation of the serum creatinine phosphokinase levels (15,760 IU/L), suggesting that the patient had hypokalemic paralysis and hypokalemia-induced rhabdomyolysis. Further evaluations, including adrenal venous sampling strongly suggested that he had primary aldosteronism. He was treated successfully by laparoscopic adrenalectomy. This case provides an important lesson that serum electrolyte concentrations should be measured in hypertensive patients before the administration of antihypertensive agents.
Primary Aldosteronism
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Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells and can be caused by a variety of factors whose nature is not necessarily traumatic. Hypokalemia is one of the most common metabolic causes, accounting for about 14-28% of rhabdomyolytic syndromes. We report and discuss three cases of hypokalemia caused by diuretic treatment with hydrochlorothiazide: the main clinical features were muscle symptoms following massive rhabdomyolysis.
Thiazide
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Rhabdomyolysis is a syndrome characterised by muscle necrosis and dispersing its intracellular content in the circulation. Clinical symptoms are usually presented by muscle pain and muscle weakness. Rhabdomyolysis could be produced, among other causes, by diabetic ketoacidosis and hypothyroidism. We report a case of a 36 years old female patient who was admitted to the medical intensive care unit (MICU) because of rhabdomyolysis. At her admission we found compensated diabetic ketoacidosis with normal serum osmolarity and mild hypothyroidism. The patient was treated by rehydration, urine alkalinisation, forced augmentation of diuresis, correction of blood glucose levels, and levothyroxine substitution therapy. After 17 days, she was completely recovered and discharged home. We believe that rhabdomyolysis in our patient developed as a summary of two important factors, uncontrolled diabetes mellitus and hypothyroidism. Hypothyroidism, possibly fueled by bad regulate diabetes, may amplify the symptoms. Each considered factor separately may not be cause a muscle breakdown, but their combination can lead to serious and severe clinical symptoms associated with high levels of creatine kinase (CK) enzyme.
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Background: Profound hypokalemia, accompanied by rhabdomyolysis, often makes rapid and accurate differential diagnosis challenging. Methods: We used the potassium-to-creatinine ratio in freshly voided urine to differentiate the etiology of hypokalemia. Results: A 27-year-old man with a 5-year history of hypertension presented with an initial biochemistry indicating marked hypokalemia (1.8 mmol/L) and metabolic alkalosis with low urinary potassium excretion. The patient did not have a history of abusing alcohol or diuretics. Persistent hypokalemia (3.0 mmol/L) continued despite aggressive potassium supplementation. Hyperaldosteronism was confirmed, and computed tomography revealed a 2.4-cmdiameter mass over the left adrenal gland. After undergoing laparoscopic left adrenalectomy, the patient's condition improved without further medication. Discussion: It is feasible to use the potassium-to-creatinine ratio in freshly voided urine for the differential diagnosis of hypokalemia. However, this case highlights that the initial kaliuretic effect of aldosterone may be restricted in severe hypokalemia.
Kaliuresis
Hyperaldosteronism
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Hypokalemia is a common electrolyte abnormality. Generally being asymptomatic, muscular fatigue, paresis and arrhythmia can be seen as the severity of hypokalemia increases. Severe rhabdomyolysis and neuromuscular findings can be seen in severe hypokalemia cases. Presence of hypokalemia can be a precursor of secondary hypertension in hypertensive patients, and also should bring hyperaldosteronism into consideration. Mild hypokalemia is usually seen in primary hyperaldosteronism. However, deficient potassium levels are also seen in some cases. We have shared the case of a hypertensive patient, who presented to the emergency department with findings of rhabdomyolysis and neuromuscular findings secondary to severe hypokalemia. The potassium level of our patient was 1.3 mmol, and it was one of the lowest potassium levels reported up to today.
Hyperaldosteronism
Electrolyte Disorder
Potassium deficiency
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Hypokalemia is a common electrolyte abnormality. Generally being asymptomatic, muscular fatigue, paresis and arrhythmia can be seen as the severity of hypokalemia increases. Severe rhabdomyolysis and neuromuscular findings can be seen in severe hypokalemia cases. Presence of hypokalemia can be a precursor of secondary hypertension in hypertensive patients, and also should bring hyperaldosteronism into consideration. Mild hypokalemia is usually seen in primary hyperaldosteronism. However, deficient potassium levels are also seen in some cases. We have shared the case of a hypertensive patient, who presented to the emergency department with findings of rhabdomyolysis and neuromuscular findings secondary to severe hypokalemia. The potassium level of our patient was 1.3 mmol, and it was one of the lowest potassium levels reported up to today.
Hyperaldosteronism
Electrolyte Disorder
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Objective To explore the pathogenic factors,clinical characteristics and treatment method of the hypokalemia related to acute upper respiratory tract infection.Methods The clinical data of 572 patients with hypokalemia admitted and treated during the period from Jan.2004 to Jun.2009 were analyzed retrospectively.Results 112(19.58%) cases of hypokalemia patients had acute upper respiratory infection symptoms before the occurrence of disease.18 cases were of mild hypokalemia,67 cases of moderate hypokalemia,and 27 cases of severe hypokalemia.The symptoms of all hypokalemia patients were relieved after oral or intravenous administration of kalium supplement.Conclusion The main cause of hypokalemia was possibly related t o the virus infection and misuse of drug(dexamethas,antibiotics,antifebrile) and insufficient intake and loss from the gastrointestinal tract.On the basis of routine kalium supplement,the safe and effective treatments with spironolactone and potassium magnesium aspartate should be supplemented.
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