Gross anatomy of the portal vein and hepatic artery ramifications in dogs: corrosion cast study.

The anatomical variations of the portal vein and the hepatic artery ramifications were analysed on liver corrosion casts in 20 dogs as a possible aid in the surgical management of the organ. The portal vein ramified similarly in all dogs. It divided into the smaller right portal branch from which vessels for the caudate process and both right lobes arose and the substantial left portal branch, which supplied the remaining liver portions and in 12 cases also the dorsal part of the right lateral lobe. Right lateral, right medial and left branches are the major arteries originating from the hepatic artery; however, their origin and course varied among individual animals. In 10 livers, the right lateral and the left branches originated from the hepatic artery, while the right medial branch arose from the left branch and usually supplied the right medial lobe solely. In nine livers, the right medial branch arose directly from the hepatic artery and supplied quadrate lobe and gallbladder as well, while in one liver the common artery, which subsequently divided into lobar branches, branched away from the hepatic artery. An additional branch for the caudate process, originating directly from the hepatic artery, was observed in 10 livers. Certain liver portions received the arterial blood from two major branches, which was particularly characteristic for the right medial lobe (six livers) and caudate process (10 livers). The course of the major arterial branches was also variable, although they proceeded in close anatomical relationship with the portal vein branches. The left arterial branch accompanied the left portal branch on its dorsal aspect (15 cases) or crossed it from the caudal aspect (five cases). The right lateral branch crossed the initial parts of the left and right portal branches either from cranial (12 cases) or caudal aspects (eight cases), while the right medial branch always crossed the left portal branch from its caudal aspect.

Is early enteral nutrition a risk factor for gastric intolerance and pneumonia?

BACKGROUND: Early enteral nutrition (EN) after injury reduces septic complications, but upper digestive intolerance (UDI) occurring immediately post-trauma is a risk factor for pneumonia. Our study aimed to determine whether early intragastric feeding may lead to gastric intolerance and subsequent pneumonia in ventilated multiply injured patients. METHODS: This prospective study involved two groups of patients randomized either to immediate intragastric EN, or to delayed intragastric EN started later than 24 h after admission. UDI was diagnosed when gastric residual volume, measured with a 50-ml syringe after stopping the feeding for 2 h, exceeded 200 ml at least at two consecutive measurements, and/or when vomiting occurred. RESULTS: Out of 52 patients, 27 were included in the early EN group, and 25 in the delayed-EN group. On day 4, the early EN group received a greater amount of feeding because of intolerance problems occurring in the delayed-EN group (1175 +/- 485 ml vs. 803 +/- 545 ml). Twenty-five subjects--33% of the early EN patients and 64% of the delayed-EN patients--met the criteria for pneumonia (P = 0.050). On average, patients with pneumonia were older, more severely injured, and therefore required more ventilator days and a longer stay in the intensive care unit than patients without pneumonia. CONCLUSIONS: If properly administered, early enteral nutrition can decrease the incidence of upper intestinal intolerance and nosocomial pneumonia in patients with multiple injuries.