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David L Burns

Publications and source records attributed to David L Burns.

5 recordsLinked to original sources
PubMed2002

Recurrent Clostridium difficile colitis. Tackling a tenacious nosocomial infection.

C difficile infection recurs in about 20% of previously treated hospitalized patients. The elderly and patients with underlying colonic disease who have recently used antibiotics are at high risk. Signs and symptoms include diarrhea, abdominal pain, and leukocytosis. Diagnosis is dependent on a high degree of clinical suspicion and ELISA testing of a stool sample for toxins. Recurrence is thought to be due to the persistence of C difficile spores. Treatment can be difficult. Oral vancomycin or metronidazole for 10 to 14 days may be helpful as first-line therapy. Tapering the dose over 1 month helps destroy the spores while enabling the normal colonic flora to regrow. Probiotics, such as lactobacillus GG and S boulardii, are being developed to help restore normal colonic flora. Immunization may help prevent C difficile infection in the first place.

Clostridioides difficile↗
PubMedDate not supplied

Recurrent Clostridium difficile colitis.

Clostridium difficile is the most common cause of nosocomial infectious diarrhea that is usually treated adequately with standard treatment of metronidazole or vancomycin. Relapse or recurrent infection can occur in certain patients and this can be very difficult to treat.

Anion Exchange Resins↗
PubMedDate not supplied

Severe ataxia, myelopathy, and peripheral neuropathy due to acquired copper deficiency in a patient with history of gastrectomy.

BACKGROUND: In animal studies, copper absorption has been demonstrated to occur in the proximal gut via duodenal enterocytes. Acquired copper deficiency is known as "swayback" in ruminant animals and Menkes' disease in humans. Copper is an essential micronutrient necessary for the hematologic and neurologic systems. Acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B(12) deficiency. METHODS: This is a single case report. Our patient developed a neurologic constellation of ataxia, myelopathy, and peripheral neuropathy similar to vitamin B(12) deficiency many years after gastrectomy for severe peptic ulcer disease. The patient was maintained for decades with enteral feedings via jejunostomy that provided the recommended dietary allowance (RDA) for copper. RESULTS: Copper deficiency was suspected, identified, and treated. Over 3 months of follow-up, serum copper levels increased from 4 microg/dL to 20 microg/dL (70-150 microg/dL), and ceruloplasmin increased from 6 mg/dL to 8 mg/dL (14-58 mg/dL). During this short time of follow-up, the patient has had no further progression of his neurologic symptoms. CONCLUSIONS: Ataxia and myelopathy secondary to acquired copper deficiency are rare complications of major gastric resection. This is quite similar to the syndrome of vitamin B(12) deficiency. Vitamin B(12) repletion does not improve symptoms. Bariatric procedures such as gastric bypass surgery result in a similar functional anatomy of the proximal gut and may place more patients at increased risk. Early recognition and therapy with oral or parenteral copper may lead to a decrease in both neurologic and hematologic consequences.

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