Cases reported "Acidosis"

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1/603. Induction of a critical elevation of povidone-iodine absorption in the treatment of a burn patient: report of a case.

    A critical elevation of povidone-iodine absorption which occurred in a burn patient who was topically treated with 10% povidone-iodine (PI) gel is herein reported. A 65-year-old man was admitted to our hospital for deep second- and third-degree burns covering 26% of his total body surface area. The intravenous administration with lactated Ringer's solution and topical treatment with silver sulfadiazine were applied in addition to such treatments as debridement and skin grafting. However, wound infection occurred due to pseudomonas aeruginosa. Topical treatment with PI gel was effective for this condition. Persistent nodal bradycardia with hypotension, metabolic acidosis, and renal failure occurred 16 days after the start of PI gel treatment. Iodine toxicosis caused by PI gel was suspected with a serum iodine level of 20600 microg/dl (normal range 2-9 microg/dl). The PI gel treatment was therefore discontinued immediately, and hemodialysis was scheduled. However, the patient's family refused hemodialysis and he died 44 days after admission. To our knowledge, only eight patients with iodine toxicosis have been reported in burn patients treated with PI gel. ( info)

2/603. Familial enteropathy: a syndrome of protracted diarrhea from birth, failure to thrive, and hypoplastic villus atrophy.

    We have studied 5 infants with persistent severe diarrhea from birth and marked abnormalities of absorption associated with failure to thrive leading to death in 4 infants. Three had siblings who died and a sibling of a 4th is ill at present, all with a similar illness; 2 were the products of consanguinous marriages. Exhaustive investigation failed to identify a recognized disease entity in any patient. steatorrhea, sugar malabsorption, dehydration, and acidosis were severe in all patients, whatever the diet fed. Total parenteral nutrition was used, but excessive stool water and electrolyte losses persisted even when nothing was fed by mouth. There was no evidence of a hematological or consistent immunological defect in any infant and no abnormalities of intestinal hormones were noted. In the duodenal mucosa of all infants we saw similar abnormalities characterized by villus atrophy, crypt hypoplasia without an increase in mitoses or inflammatory cell infiltrate in the lamina propria and in villus enterocytes absence of a brush border, increase in lysosome-like inclusions, and autophagocytosis. In 3 infants studied by marker perfusion of the proximal jejunum we found abnormal glucose absorption and a blunted response of Na absorption to actively transported nonelectrolytes; in 2 there was net secretion of Na and H2O in the basal state. Our patients evidently suffered from a congenital enteropathy which caused profound defects in their capacity to assimilate nutrients. The similar structural lesion seen in the small intestinal epithelium of all of our cases undoubtedly contributed to their compromised intestinal function, but the pathogenesis of this disorder, if indeed it is a single disease, remains obscure. ( info)

3/603. Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases.

    Severe hyperkalemia with minimal or nonspecific electrocardiographic (ECG) changes is unusual. We report data on seven patients with renal failure, metabolic acidosis, and severe hyperkalemia (K > or =8 mmol/L) without typical ECG changes. Initial ECGs revealed sinus rhythm and PR and QT intervals in the normal range. QRS intervals were slightly prolonged in two patients (110 ms), and incomplete right bundle branch block was evident in one. Thus, the absence of typical ECG changes does not preclude severe hyperkalemia. ( info)

4/603. Recovery from prolonged metabolic acidosis due to accidental ethylene glycol poisoning.

    In this report, we describe a case of accidental ethylene glycol poisoning in a 90-year-old woman. Despite a delay in diagnosis and treatment of over 24 hours, this patient recovered completely from profound and lengthy metabolic acidosis. She is therefore the oldest known survivor of severe ethylene glycol intoxication. We review 79 additional cases of ethylene glycol intoxication reported in the literature since 1976 and comment on diagnostic, therapeutic and prognostic features of this form of poisoning. ( info)

5/603. Metabolic acidosis and thiamine deficiency.

    We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly thiamine. After thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement. Clinicians must be aware that thiamine is essential for normal glucose metabolism and that thiamine deficiency can lead to lactic acidosis. thiamine deficiency should be included in the differential diagnosis of lactic acidosis. The recent shortage of intravenous multivitamin preparations has led to documented cases of lactic acidosis as a result of thiamine deficiency, and a previous shortage led to several deaths due to lactic acidosis as a consequence of thiamine deficiency. All patients receiving parenteral nutrition must also receive adequate vitamin supplementation. ( info)

6/603. Metabolic acidosis in restraint-associated cardiac arrest: a case series.

    The mechanism of death in patients struggling against restraints remains a topic of debate. This article presents a series of five patients with restraint-associated cardiac arrest and profound metabolic acidosis. The lowest recorded pH was 6.25; this patient and three others died despite aggressive resuscitation. The survivor's pH was 6.46; this patient subsequently made a good recovery. Struggling against restraints may produce a lactic acidosis. Stimulant drugs such as cocaine may promote further metabolic acidosis and impair normal behavioral regulatory responses. Restrictive positioning of combative patients may impede appropriate respiratory compensation for this acidemia. Public safety personnel and emergency providers must be aware of the life threat to combative patients and be careful with restraint techniques. Further investigation of sedative agents and buffering therapy for this select patient group is suggested. ( info)

7/603. High anion gap metabolic acidosis associated with aminocaproic acid.

    OBJECTIVE: To report a case of high anion gap metabolic acidosis related to infusion of aminocaproic acid (ACA) that temporarily corrected during hemodialysis and resolved upon ACA discontinuation. CASE SUMMARY: A 65-year-old white woman with staphylococcal sepsis complicated by acute renal failure was treated with ACA to control a hemorrhagic coagulopathy. After receiving an initial 5-g bolus of ACA, she received a continuous intravenous infusion of 500 mg/h for just over 5 days, then 250 mg/h for a final 12 hours. Immediately after beginning ACA therapy, she developed a severe anion gap metabolic acidosis that briefly improved after hemodialysis. The condition resolved completely only after the discontinuation of ACA and therapy with a systemic alkalinizer. DISCUSSION: ACA is not among the previously identified causes of high anion gap metabolic acidosis. The temporal profile relating anion gap to ACA initiation, hemodialysis treatment, and ACA discontinuation supports causality in this case. The magnitude of increase in the anion gap appears to have been proportional to the dose of ACA. CONCLUSIONS: In patients with renal impairment, ACA administration may produce a dose-related, high anion gap metabolic acidosis that might be reversible during hemodialysis. Insufficient data are available, but when ACA must be used in such patients, a more conservative dosing of ACA should be coupled with close monitoring. ( info)

8/603. Abnormal ductus venosus blood flow: a clue to umbilical cord complication.

    We report a case of umbilical cord complication causing, fetal hypoxemia and acidemia. At 30 weeks of gestation, the patient was referred because of slightly increased amniotic fluid volume and a non-reactive cardiotocogram. biometry was appropriate for gestational age. Umbilical artery and fetal aortic Doppler findings were normal, whereas diastolic blood flow velocities in the middle cerebral artery were increased and the ductus venosus showed severely abnormal flow velocity waveforms with reversal of flow during atrial contraction. Since other reasons for fetal hypoxemia could be excluded, careful examination of the umbilical cord was performed. traction of the hypercoiled umbilical cord due to its course around the fetal neck and shoulders was suspected. cesarean section confirmed the sonographic findings and fetal blood gases revealed fetal acidemia. This case indicates that investigation of fetal venous blood flow may also help to identify fetal jeopardy due to reasons other than increased placental vascular resistance. ( info)

9/603. methemoglobinemia after axillary block with bupivacaine and additional injection of lidocaine in the operative field.

    methemoglobinemia may occur after the administration of various drugs, including some local anesthetics. We report a patient with chronic renal failure and ischemic heart disease who developed clinically significant methemoglobinemia after an axillary block with bupivacaine and additional injection of lidocaine in the operative field. Although the two local anesthetics usually do not cause methemoglobinemia, we suspect that the displacement of lidocaine from protein binding by bupivacaine, in combination with metabolic acidosis and treatment with other oxidants, was the reason for the development of methemoglobinemia. ( info)

10/603. Acute myopathy after status asthmaticus: steroids, myorelaxants or carbon dioxide?

    Acute myopathy complicating treatment of status asthmaticus has been increasingly recognized since its original description in 1977. We report a case of an 11-year-old boy with severe asthma requiring mechanical ventilation. He was given high doses of parenteral steroids and neuromuscular blockade with non-depolarizing agents in order to achieve controlled hypoventilation with an ensuing hypercapnoea. He developed rhabdomyolysis with elevated creatinine kinase and renal impairment secondary to myoglobinuria. Electrophysiological studies revealed myopathic abnormalities. The aetiology for this myopathy appears to be related to therapy with parenteral steroids, muscle-relaxant agents and respiratory acidosis. patients treated with steroids and neuromuscular blocking agents should be regularly monitored for development of myopathy. ( info)
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