Cases reported "Paralysis"

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1/62. Renal tubular acidosis, hypokalemic paralysis, rhabdomyolysis, and acute renal failure--a rare presentation of Chinese herbal nephropathy.

    We encountered a 66-year-old Chinese man presented with hypokalemic paralysis, rhabdomyolysis and acute renal failure after administration of mixed Chinese herbs. Proximal renal tubular acidosis and selective glucosuria were the main tubular dysfunctions. The renal failure recovered smoothly and rapidly after resuscitation and the tubular function abnormalities regained spontaneously after medicine withdrawal. It should be recognized that renal tubular acidosis with hypokalemic paralysis, rhabdomyolysis and subsequent acute renal failure may develop after taking Chinese mixed herbal medicine.
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2/62. caffeine-induced hypokalemic paralysis in pregnancy.

    BACKGROUND: Excessive ingestion of caffeine can induce hypokalemia, which affects the neuromuscular system and can lead to paralysis. CASE: A 24-year-old woman, gravida 3, para 2-0-0-2 at 33 weeks' gestation presented with muscular paralysis and hypokalemia secondary to drinking 6 to 7 L of cola per day with little other oral intake. After potassium replacement and stopping caffeine ingestion, the symptoms resolved quickly. CONCLUSION: The physiologic changes of pregnancy might potentiate the effect of caffeine on serum potassium concentration.
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3/62. Hypopotassemic paralysis: a rare presentation of proximal renal tubular acidosis.

    neurologic manifestations can accompany systemic diseases, and primary disease can be identified with a careful history, physical examination, and laboratory investigations. A 14-year-old girl with paraplegia and absence of deep tendon reflexes in the lower extremities after 2 days of vomiting and diarrhea was referred to our pediatric neurology department with a diagnosis of guillain-barre syndrome. Short stature, dehydration, motor and mental retardation, bilateral cataracts, glaucoma, and band keratopathy were detected on physical examination. Hypopotassemia and severe metabolic acidosis were found on biochemical examination. Her paraplegia improved after appropriate fluid and electrolyte replacement, but metabolic acidosis persisted after cessation of intravenous therapy, and isolated proximal renal tubular acidosis was detected. Because she had isolated proximal renal tubular acidosis and other abnormalities, she was diagnosed with Donckerwolcke-Winsnes syndrome.
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keywords = diarrhea
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4/62. Aristolochic acid-induced Fanconi's syndrome and nephropathy presenting as hypokalemic paralysis.

    Hypokalemic paralysis rarely is seen as the presenting feature in patients with Fanconi's syndrome. We describe a 60-year-old man who presented with the inability to ambulate on awakening in the morning. The pertinent history revealed he had consumed Chinese herbs for leg edema for 5 months. physical examination was unremarkable except for extracellular fluid volume depletion and total paralysis of both lower extremities. Laboratory investigation showed hypokalemia (1.8 mEq/L), hyperchloremic metabolic acidosis (Cl-, 111 mEq/L, and HCO3-, 14.0 mEq/L), hypophosphatemia (0.9 mg/dL) with hyperphosphaturia, hypouricemia (1.3 mg/dL) with hyperuricosuria, and glycosuria, consistent with Fanconi's syndrome. Mild renal insufficiency (serum creatinine, 1.7 mg/dL) also was noticed. Blood and urine screens for heavy metals, autoantibodies, and monoclonal gammopathy were negative. A renal biopsy specimen revealed typical findings of aristolochic acid-associated nephropathy. aristolochic acids were detected in the consumed Chinese herbs. This case highlights that consumption of Chinese herbs containing aristolochic acids may cause Fanconi's syndrome and should be considered as a cause of hypokalemic paralysis.
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5/62. Thyrotoxic hypokalemic periodic paralysis in a Hispanic male.

    We report a case of a Hispanic male presenting with acute onset of bilateral lower extremity weakness, without any antecedent viral or bacterial illness, dietary changes, infiltrative orbitopathy, diffuse goiter, infiltrative dermopathy, and family history of periodic paralysis, who was later found to have Graves' disease. This demonstrates a rare case of periodic paralysis as the initial presentation of hyperthyroidism. Thyrotoxic hypokalemic periodic paralysis is common in Asian and Hispanic individuals and uncommon in whites and african americans.
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6/62. Hypokalaemia and paralysis.

    A patient with a severe degree of hypokalaemia (1.8 mmol/l) and paralysis was brought to the emergency department. Hypokalaemic periodic paralysis was an unlikely diagnosis, because an acid-base disorder (metabolic alkalosis) and a high rate of potassium (K( )) excretion were present. During an imaginary consultation with Professor McCance, the combination of emphasis on principles of integrative physiology, a deductive analysis, common sense, and clinical skills led to an obvious diagnosis. Nevertheless, a surprise was in store, because renal K( ) wasting persisted for almost 2 weeks after removal of the causative agent. Possible explanations for the continued kaliuresis, as well as therapeutic strategies to avoid potential complications, were considered. This case illustrates the value of applying principles of physiology in a quantitative fashion at the bedside.
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ranking = 0.0003091698816178
keywords = alkalosis
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7/62. An unusual cause of hypokalemic paralysis: chronic licorice ingestion.

    Long-term licorice ingestion is a well-known cause of secondary hypertension and hypokalemia. Nevertheless, its initial presentation with a very severe degree of hypokalemia and paralysis is exceedingly rare. We report an elderly Asian man who presented to the emergency department with marked muscle weakness that progressed to paralysis. His blood pressure was 160/96 mm Hg. The major biochemical abnormalities were hypokalemia (plasma K concentration, 1.8 mmol/L) and metabolic alkalosis (HCO - 3 , 36 mmol/L). His renal potassium excretion was higher (transtubular potassium gradient of 9). plasma renin activity and aldosterone concentration were suppressed and cortisol concentration was normal. A detailed history revealed that he had ingested tea flavored with 100 g of natural licorice root containing 2.3% glycyrrhizic acid daily for 3 years. Note that renal potassium wasting and hypertension persisted for 2 weeks after discontinuing licorice consumption along with KCl supplement and spironolactone. Long-term licorice ingestion should be kept in mind as a cause of paralysis with an extreme degree of hypokalemia to avoid missing this recognizable and curable medical disorder.
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keywords = hypokalemic, alkalosis
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8/62. Licorice consumption causing severe hypokalemic paralysis.

    Hypokalemic paralysis due to licorice consumption is extremely rare, with only 40 cases in the English literature describing paralysis secondary to exposure to licorice in candies, medications, chewing tobacco, and herbal preparations. We describe a patient who suffered life-threatening hypokalemic paralysis caused by consumption of licorice in the form of a tea sweetener superimposed on long-term consumption of licorice candy. Aggressive fluid and potassium replenishment produced complete and lasting recovery. To our knowledge, this is the first report of hypokalemic paralysis due to exposure to licorice as a tea sweetener, a common custom among the Arab population. The case emphasizes the importance of considering patients' cultural backgrounds and local customs, which often may lead the treating physician to the correct clinical diagnosis.
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9/62. Muscle pathology correlates with permanent weakness in hypokalemic periodic paralysis: a case report.

    We present a morphological follow-up in a case of familial hypokalemic periodic paralysis with progressive weakness. At age 12 years muscle biopsy revealed mild vacuolar changes. Seventeen years later, after the patient had developed permanent weakness, light and electron microscopy disclosed tubular aggregates in about 15% of the fibers and medium-grade myopathic alterations. We describe correlation of muscle pathology with permanent weakness in hypokalemic periodic paralysis.
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10/62. Improvement of the exercise test after therapy in thyrotoxic periodic paralysis.

    The diagnosis of periodic paralysis (PP) can be aided by demonstrating a decrease in compound motor action potential (CMAP) amplitude after several minutes of exercise. We report a case of secondary hypokalemic PP due to thyrotoxicosis in which the decrease in the CMAP amplitude after exercise dramatically improved after treatment, when a euthyroid state was achieved. The exercise test is a useful electrophysiologic means of monitoring the neuromuscular status of patients with thyrotoxic periodic paralysis prior to, and after treatment of the thyrotoxicosis.
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