Cases reported "Acidosis"

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1/9. Hypokalaemic, hyperchloraemic metabolic acidosis requiring ventilation.

    A 16-year-old patient required intermittent positive pressure ventilation for hypokalaemic muscle weakness resulting from metabolic complications of combined colonic bladder augmentation and incomplete voiding via a prosthetic sphincter. Catheter re-establishment of urinary flow and electrolyte replacement produced dramatic metabolic and clinical improvement allowing the return of adequate spontaneous respiration.
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2/9. Metabolic acidosis and coma following a severe acetaminophen overdose.

    OBJECTIVE: To report a case of metabolic acidosis and coma in a severe acetaminophen overdose. CASE SUMMARY: A 29-year-old white woman was admitted to the emergency department with a diminished level of consciousness and metabolic acidosis. The toxicology screen revealed a serum acetaminophen concentration of 1072 microg/mL, and she was consequently treated with intravenous acetylcysteine. Despite the elevated concentration, the patient did not manifest signs of hepatotoxicity. DISCUSSION: Metabolic acidosis and coma are rare manifestations in acetaminophen overdoses. In published case reports, severe acetaminophen ingestion independently causes metabolic acidosis and coma in the absence of hepatotoxicity. The mechanism by which metabolic acidosis occurs is not clearly defined. Studies conducted on animals demonstrated that in severe overdoses, acetaminophen may cause lactic acidosis by inhibiting mitochondrial respiration. The mechanism by which acetaminophen can cause coma is still unknown. CONCLUSIONS: Severe acetaminophen overdoses can independently cause metabolic acidosis and coma in the absence of hepatotoxicity.
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3/9. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema.

    BACKGROUND: Toxicity secondary to rectally administered hypertonic phosphate solution in patients with normal renal function is rarely reported in the literature. We report a case of electrolyte disturbance and seizure secondary to the rectal administration of 2 Fleet pediatric enemas. CASE REPORT: A 4-year-old white female with spinal muscular atrophy and chronic constipation was brought to the emergency department with complaints of lethargy and difficulty breathing following the administration of 2 Fleet pediatric enemas. In the emergency department, physical examination was significant for a depressed level of consciousness and shallow respirations. A basic metabolic profile was significant for a calcium of 3.3 mg/dL, phosphate of 23 mg/dL, and sodium of 153 mEq/L. Arterial blood gases revealed a pH of 7.24, Pco2 of 38 mm Hg, Po2 of 220 mm Hg. Electrocardiogram revealed a prolonged QT interval of 340 milliseconds with a corrected QT interval of 498 milliseconds. Sixteen hours postexposure, she experienced a generalized seizure unresponsive to multiple doses of lorazepam and responsive only to 100 mg of intravenous calcium chloride. Two days after presentation, the patient experienced complete resolution of symptoms. CONCLUSION: Osmotically acting hypertonic phosphate enemas can result in severe toxicity if retained. This is true even in patients without predisposing risk factors.
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4/9. A case of supercarbia following pneumoperitoneum in an infant.

    A 4-month-old healthy male infant underwent left herniotomy under general anesthesia with caudal block. carbon dioxide (CO2) pneumoperitoneum was created through the left hernial sac for inspection of the right processus vaginalis. Episodes of desaturation associated with significant reduction in chest compliance were noted intraoperatively. This was overcome by increasing the inspired oxygen concentration (FiO2). The infant failed to regain consciousness and spontaneous respiration at the end of surgery. The chest compliance deteriorated further and clinically a CO2 pneumothorax (capnothorax) was suspected. The endtidal carbon dioxide (P(E)CO2) was initially low in the immediate postoperative period. Subsequent to the readministration of sevoflurane and manual ventilation with a Jackson Rees circuit, a sudden surge in P(E)CO2 with improvement of chest compliance was observed. At that time arterial blood gas (ABG) analysis revealed a PCO2 of 17.5 kPa (134 mmHg) and pH of 6.9. The causes of severe hypercarbia and the physiological changes observed in this infant are discussed.
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keywords = respiration
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5/9. Bialaphos poisoning with apnea and metabolic acidosis.

    A 64-year-old man with ethanol intoxication, ingested a bottle of Herbiace (100 ml, 32 w/v% of bialaphos, CAS #35597-43-4, Meiji Seika Kaisha, tokyo, japan). He had severe metabolic acidosis and was treated with infusions of sodium bicarbonate and furosemide, plus gastric lavage and enema. The metabolic acidosis improved 15 hours after treatment but nystagmus, apnea and convulsions were progressive. Although his sensorium was clear, spontaneous respirations were not observed for 64 hours. The electroencephalographic findings of atypical triphasic waves and slow waves suggest a unique response to bialaphos poisoning. His clinical course indicates that the management of apnea is critically important to recovery from bialaphos poisoning.
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keywords = respiration
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6/9. Defective intramitochondrial NADH oxidation in skin fibroblasts from an infant with fatal neonatal lacticacidemia.

    A small-for-gestational-age female infant born at term developed severe lactic acidosis and died on day 13 of life. Two previous sibs had also died of overwhelming lactic acidosis in the neonatal period. The lactate-to-pyruvate and 3-hydroxybutyrate-to-acetoacetate ratios were elevated at 136 and 42 to one, respectively. The activities of the pyruvate dehydrogenase complex and pyruvate carboxylase in cultured skin fibroblasts were normal but a defect in respiration was indicated by the low rates of conversion of 1-[14C]pyruvate, glutamate, and lactate to 14CO2 in these cells. skin fibroblast cultures also displayed an elevated lactate-to-pyruvate ratio (72:1) when incubated with glucose as substrate compared to control cell cultures (20:1). When mitochondrial preparations of skin fibroblasts (prepared by digitonin extraction) were tested for their ability to synthesize ATP from a variety of substrates, it was found that those of the patient made adequate amounts of ATP with either succinate or ascorbate/tetramethyl-phenylenediamine as substrate but not with the nad-linked substrates pyruvate, isocitrate, and palmitoyl carnitine. We propose that this is indicative of a defect in the respiratory chain between NADH and coenzyme Q, for the first time demonstrable in cultured skin fibroblasts.
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keywords = respiration
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7/9. Alcoholic ketoacidosis presenting with extreme hypoglycemia.

    A 66-year-old man with a history of chronic alcoholism presented with Kussmaul respirations following several days of fasting accompanied by vomiting, in the presence of continued ethanol intake. He was subsequently found to have a serum glucose level of <20 mg/dL and an anion gap of 36. Despite his profound hypoglycemia, he was fully alert with no obvious neurological deficits. He recovered without incident with intravenous saline, dextrose, thiamine, and antibiotics for a bacteremic pneumonia. He had no evidence of hypoxemia, hypotension, or other features of sepsis. Alcoholic ketoacidosis in the setting of hypoglycemia is discussed. If the serum glucose level is less than the anion gap, the diagnosis of alcoholic ketoacidosis should be considered.
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8/9. A confused man with rapid respiration.

    A 71-year-old man presented with incoherent, slurred speech, auditory hallucinations, and tachypnea. According to the neighbor who called for emergency medical service, the man had appeared to be in good health the day before. On admission, his blood pressure was normal.
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keywords = respiration
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9/9. Alcoholic ketoacidosis in pregnancy.

    The presence of severe ketoacidosis in the absence of hyperglycemia and glucosuria is reported in a young pregnant chronic alcohol abuser. The clinical presentation included an arterial pH of 7.15, a base deficit of 23 mEq/liter, a bicarbonate of less than 10 m Eq/liter, larger serum and urinary ketone levels, and hyperpnea with Kussmual-type respiration. Corrective therapy consisted of rapid fluid, electrolyte, bicarbonate, and glucose replacement with insulin supplementation. The ability of the fetus to tolerate the maternal metabolic derangements of "alcoholic ketoacidosis" as well as the stress of uterine contractions is discussed and contrasted with diabetic ketoacidosis.
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keywords = respiration
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