Etiology

• Etiology is usually unknown, however a variety of factors can predispose to the development of torsions.

Predisposing factors

General

• Rolling of cattle to correct uterine torsion or left displaced abomasum Non-surgical correction of LDA.
• Association between ad-lib milk substitute feeding of calves, particularly loose housed machine fed calves where it is thought intake can be high enough to facilitate milk over-flow into ileum: leading to rapid fermentation of lactose in the ileum, leading to gas production/distension and dilatation, which may result in torsion. Milk feeding systems
• Causes of small intestinal obstruction may predispose to torsion, including:
  • Abomasal/intestinal impaction Abomasal bloat and impaction.
  • Intussusceptions - the most common cause of small intestinal obstruction in cattle.
  • Internal hernias/prolapse of intestines through mesentery - more common in adult cattle than root of mesentery torsion.
  • Adhesions (iatrogenic, inflammatory).

Pathophysiology

• Rotation of sections of small intestine through up to 180° along the long axis of the mesenteric root results in loss of blood supply to sections of bowel, as well as obstruction of the gut lumen.
• Rotation of the mesenteric root itself causes obstruction and ischemia to the whole of the small intestine.
• Pain results due to stretching of the obstructed bowel, to mesenteric traction, and, within hours, to bowel compromise and toxin leakage.
• Bowel compromise due to ischemia results in circulatory compromise via release of bacteria and toxins into the bloodstream. Bacteria and toxins are also released into the peritoneum causing fluid and white blood cell sequestration to this area. Hypovolemic and endotoxic shock result.
• Collapse and death due to endotoxemia or visceral rupture.
• Vascular compromise is more serious, and the severity depends on the extent:
  • Venous drainage of the area is impaired → increase swelling, edema, and congestion.
  • There is progressive arterial obstruction → cyanosis and ischemia of the affected bowel → gut spasm.
  • Intraluminal distension → progressive ischemia and disruption of the mucosal layers → necrosis and cell sloughing. Within 4-5 hours the mucosal epithelium is necrotic, after 6-7 hours the necrosis has extended to the external muscular layer.
  • Protein-rich fluid leaks into the gut lumen, as well as the peritoneal cavity.
  • Endotoxins and bacteria leak into the bloodstream and peritoneal cavity.
  • Hypovolemia, endotoxic shock, electrolyte and acid/base abnormalities develop.
• Pain caused by bowel wall distension and gut / vascular compromise is continuous, and shows no, or only temporary response to analgesics.
• Cardiovascular compromise is reflected by tachycardia, a decrease in pulse quality, mucous membrane congestion or cyanosis, and an increase in capillary refill time. Secondary increases in packed cell volume (PCV) and plasma proteins (TPP) are seen, and metabolic acidosis causes tachypnea.
• Peritoneal fluid is sero-sanguinous, and contains increased protein and leukocyte levels, as the disease progresses, these levels rise further, and the fluid takes on a turbid appearance.

Timecourse

• This depends on the degree of vascular obstruction, but within 2-4 hours vascular compromise will cause bowel wall damage, and endotoxic shock and death can follow this within hours.