6/21/2023 0 Comments Chest pain caffeine overdose![]() ![]() Two months later, a third event occurred with the same symptoms and signs. In the second event, the 24-hour urine potassium excretion was measured at 57.4 mEq/24-hours while intravenous potassium replacement was performed. When the patient visited the emergency room at the first event, symptoms improved rapidly after intravenous potassium replacement and were discharged without a 24-hour urine test. Serum and urine laboratory test results were similar to those of the first event: serum potassium, 2.9 mmol/L serum renin, 0.48 ng/mL/hr and aldosterone, 7.39 pg/mL. Sixteen months after the first event, he visited the emergency room again with the same symptoms and signs. When he visited an outpatient clinic a few days later, the potassium level was within the normal range (4.3 mmol/L). His potassium level was 4.4 mmol/L and he refused to be admitted for evaluation of the cause of hypokalemia. He was discharged from the emergency room after the muscle weakness improved by 40 mEq of intravenous potassium replacement. The spot urine potassium/creatinine ratio was 16 mEq/gCr. The transtubular potassium gradient (TTKG) was 2.43, but it was not valid because the urine osmolality was less than plasma osmolality. His laboratory examination data demonstrated considerable hypokalemia (2.6 mmol/L as K +), decreased serum renin (0.14 ng/mL/hr, reported 8 days after testing) and aldosterone (11.81 pg/mL, reported 8 days after testing), metabolic acidosis with respiratory compensation, and diluted urine (decreased urine osmolality, 130 mOsm/kg H 2O) (Table 1). First he felt progressive generalized muscle weakness and fatigue after a few hours, the muscle weakness and numbness became intolerable. He felt no discomfort for several years before the symptoms presented. He had no symptoms such as fever, dyspnea, chest pain, palpitations, abdominal pain, or diarrhea. No documented endocrinal dysfunction was noted. The patient was not under medication with herbal medicines (such as licorice), diuretics, or laxatives. Blood pressure was within normal range and no other abnormalities were found on his physical examination. His motor power values were 3 of 5 in all four extremities with normal reflexes and sensation. He had no specific family history including diabetes mellitus and hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.Ī 29-year-old man without a significant past medical history visited our hospital emergency room with severe generalized muscle weakness and bilateral leg numbness that continued for several hours. ConclusionsĪn increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. The patient was not under medication with laxatives, diuretics, or herbal remedies. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. Laboratory tests revealed low serum potassium concentration (2.6–2.9 mmol/L) and low urine osmolality (100–130 mOsm/kgH 2O) in three such prior episodes. Case presentationĪ 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. ![]() However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. ![]()
0 Comments
Leave a Reply. |