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C Ackermann

Publications and source records attributed to C Ackermann.

63 records · Page 4Linked to original sources
PubMed1987

[Hiatal hernia and reflux disease--long-term results following fundoplication and consequences in therapeutic failures].

UNLABELLED: 10 to 20 years (median 15.1 years) after fundoplication for primary reflux disease 257 patients were questioned about their symptoms. Data of 163 patients could be analyzed. RESULTS: 21.4% of the patients have persistent or recurrent reflux symptoms, about half of them (9.8%) need medical treatment. Adverse side-effects of the fundoplication are frequent: dysphagia in 28.2%, gas-bloat in 50.3%. Using the Visick criteria for classification we found Visick grade I and II for 75.5%, grade III for 17.2%, and IV for 7.4%. Diagnostic and therapeutic concepts in case of failed reflux control are discussed.

Esophagogastric Junction↗
PubMed1987

The stability of parenteral fat emulsions in nutrition mixtures.

The effect of dilution, dextrose, amino acids and electrolytes on the stability of two parenteral fat emulsions (Travamulsion and Intralipid) were investigated. It was found that dilution of intravenous emulsions with water for injection had a different influence on the stability of the two emulsions. In addition, a dextrose concentration of 15-20% and higher, in the absence of amino acids caused coagulation of the fat droplets after storage (4 degrees C for 24 h followed by 24 h at room temperature). The addition of amino acids increased the stability of emulsions in the presence of dextrose. The differences found in the particle size distribution of the different emulsions investigated were reflected in their stability in the presence of electrolytes. Critical aggregation concentrations (monovalent cation) of 240 mmol/l for Travamulsion 10% and 156 mmol/l for Intralipid 10% were determined.

Amino Acids↗
PubMed1980

[Long-term results of thoracic truncal vagotomy and pyloroplasty in complicated reflux disease].

In advanced cases of esophagitis with acquired short esophagus and stricture, operative treatment to eliminate gastroesophageal reflux may be difficult or impossible. 24 such patients were treated by transthoracic truncal vagotomy and pyloroplasty. In a long-term follow-up 9--11 years later 12 patients were examined by X-ray and esophagoscopy. In 9 patients symptoms due to reflux or obstruction had improved, 5 of them were symptom-free. At endoscopy and barium-swallow 2 patients showed back-formation of their stricture, the other patients had generally unchanged findings. Transthoracic truncal vagotomy with drainage seems to be able to prevent progression of severe esophagitis and to improve its symptoms.

Esophageal Stenosis↗
PubMedDate not supplied

Necrosis of intraabdominal esophagus and proximal third of the stomach after proximal gastric vagotomy and fundoplication.

Lesser curve necrosis is a rare but known complication of proximal gastric vagotomy (PGV). Incidence seems to increase when PGV is combined with fundoplication. In reports of this complication, the necrosis was of various sizes, but generally limited to the lesser curve. We report a 54-year-old patient with hiatus hernia, severe peptic esophagitis, and increased acid output who developed necrosis of the whole intraabdominal esophagus, cardia, and proximal third of the stomach after PGV and fundoplication with division of several short gastric vessels. A proximal gastric resection with intrathoracic esophagogastric anastomosis had to be performed. After drainage of a subphrenic abscess, the patient made a complete recovery. When combining PGV with a fundoplication, an increased risk of necrosis of the stomach must be considered. Division of the short gastric arteries should be avoided and the original Nissen fundoplication is preferred.

Esophagus↗
PubMedDate not supplied

Relationship of hairless mouse skin surface temperature to wound severity and maturation time.

Skin surface temperature (SST) changes measured on live hairless mice are presented as a simple means of following wound healing. SST is generally determined by 3 factors which are the ambient temperature, the rate of water loss from the surface of the skin and the diffusion of thermal energy from the body's core. The SST increase immediately after a burn injury reflects the amount of thermal energy absorbed by the skin surface. For burns and other injuries, the drop in SST following injury, but after thermal equilibrium has been established, provides an early indication of the degree of impairment of the skin's barrier. Three kinds of mouse skin wounds, mechanical (tape stripping), thermal and chemical (phenol application), were investigated. SST nadirs ranged from 2.1 to 4.4 degrees C with mild to full-thickness burns, respectively. Except for the earliest moments after wounding, striking parallels were noted between SST and transepidermal water loss profiles for these injuries. The SST profile over the full course of wound healing clearly indicates the severity of the injury, the stages of wound maturation and the time to complete skin healing.

Animals↗