Surgical removal of intestinal foreign bodies using a laparotomy-assisted endoscopic approach in dogs and cats and comparison with enterotomy.

OBJECTIVES: To describe a novel surgical technique for intestinal foreign body removal without enterotomy using a laparotomy-assisted endoscopic approach and compare short-term outcomes to enterotomy. MATERIALS AND METHODS: Medical records of dogs and cats with intestinal foreign bodies that underwent attempted treatment with a laparotomy-assisted endoscopic approach between June 2019 and July 2021 were extracted. The approach consisted in manoeuvring the intestinal foreign body into the stomach during laparotomy and then removing it via a gastroscopy. If the foreign body was unmovable, an enterotomy was performed. RESULTS: Fifty-eight cases were enrolled and foreign bodies were successfully removed in 25 cases using a laparotomy-assisted endoscopic approach. The median distance between the pylorus and the proximal part of the foreign body was 55 cm (range: 0 to 300). The mean surgical time and median endoscopic time were 49 minutes (±sd 12.8) and 5 minutes (range: 2 to 28), respectively. All but two cases were discharged 1 day postoperatively. In 20 cases, the foreign body was not easily movable, and an enterotomy was performed. In three of these cases, conversion to enterotomy was required due to serosal tears that occurred as a consequence of the attempted retrograde manipulation of the foreign body. Foreign body width, length and distance to pylorus were not significantly different between the two techniques. Mean surgical time was significantly shorter for laparotomy-assisted endoscopic approach compared to enterotomy: 49 minutes (±SD 12.8) versus 61.7 minutes (±SD 14.6). CLINICAL SIGNIFICANCE: Surgical removal of intestinal foreign bodies through a laparotomy-assisted endoscopic approach is a feasible technique that offers satisfactory outcomes and shorter surgical time than enterotomy. Retrograde manipulation of the intestinal foreign body may result in serosal tears.

Citric acid ingestion: a life-threatening cause of metabolic acidosis.

We present a case that illustrates the acute (<6 hours) metabolic and hemodynamic effects of the ingestion of a massive oral citric acid load. The principal findings included metabolic acidosis accompanied by an increase in the plasma anion gap that was not caused by L -lactic acidosis, hyperkalemia, and the abrupt onset of hypotension. A unique feature was a dramatic clinical improvement when ionized calcium was infused. The case illustrates the importance of considering the properties of the conjugate base (anion) of the added acid because, in this instance, the citrate anion had a unique and life-threatening consequence (lower ionized calcium level) that was rapidly reversible.

Procoagulant activity after exposure of monocyte-derived macrophages to minimally oxidized low density lipoprotein. Co-localization of tissue factor antigen and nascent fibrin fibers at the cell surface.

The role of tissue factor (TF) as an initiator of the thrombotic complications secondary to atherosclerosis has been acknowledged, and in situ expression of TF activity by monocyte-derived macrophages and lesion-associated macrophage foam cells has been documented. Macrophages express TF activity upon exposure in vitro to either oxidized low density lipoprotein LDL (Ox-LDL) or endotoxin (lipopolysaccharide). This activity has been associated with membrane vesicles that apparently are shed after procoagulant expression. The present study based upon the correlative use of an enzyme-linked coagulant assay and three-dimensional multi-antigen, immunogold electron microscopy, reports the ultrastructural localization of TF antigen and spatially correlates TF with OX-LDL binding and the presence of nascent fibrin polymers on the plasma membrane of cultured macrophages. Pigeon monocyte/macrophages, after a 4-hour induction with lipopolysaccharide (2 micrograms/ml) or minimally oxidized LDL (50 micrograms/ml; thiobarbituric acid reducing substance, 5 to 8 nmol/mg protein) were incubated for 40 minutes in a Tris-buffered medium containing factors VII, V, X, II, and I before either assaying for coagulant activity or processing for gold-colloid cytochemistry. TF activity, as measured by enzyme-linked coagulant assay peaked 6 hours after agonist exposure with lipopolysaccharide and Ox-LDL giving, respectively, 115- and 60-fold stimulation as compared with control. This activity corresponded to the elaboration of membrane ruffles and microvilli on the cell surfaces. Through correlative immunogold cytochemistry (15-nm-diameter colloid) and gold-ligand cytochemistry (30-nm-diameter colloid), TF antigen (83%) and Ox-LDL (78%) were primarily associated with the membrane ruffles and microvilli. Multi-antigen immunogold cytochemistry when used in conjunction with ligand-gold cytochemistry documented co-localization of Ox-LDL (22-nm gold), TF antigen (15-nm gold) and a delicate three-dimensional network of short fibrin fibers that were decorated in a linear fashion with the immunogold probes (30-nm gold). These results provide evidence that TF antigen is located at selected regions on the cell surfaces. Furthermore, these same regions provide binding sites for agonist uptake and organization sites for fibrin polymerization. Hypothetically, the localized membrane regions could be shed from the cell surface as a means for regulating coagulation potential.