Intra-abdominal hypertension (IAH) contributes to organ dysfunction and leads to the development of the abdominal compartment syndrome (ACS). IAH and ACS are relatively frequent fi ndings in patiens with severe acute pancreatitis (SAP) and are associated with deterioration in organ functions. The most affected are cardiovascular, respiratory and renal functions. The incidence of IAH in patients with SAP is approximately 60-80%. There is an accumulating evidence in human and animal studies that changes of perfusion, particularly to the microvasculature, are crucial events in the progression of acute pancreatitis (AP). The perfusion of the small and large intestine is impaired due to reduced arterial pressure, increased vascular resistence and diminished portal blood fl ow. Bacterial translocation has been described in patients with ACS, and this may apply to patients with SAP. Approximately 30-40% of SAP patients develop ACS because of pancreatic (retroperitoneal) infl ammation, peripancreatic tissue edema, formation of fl uid collections or abdominal distension. Surgical debridement was the preferred treatment to control necrotizing pancreatitis in the past. However, the management of necrotizing pancreatitis has changed over the last decade. The main objective of this article is to describe the association between IAH and AP and to emphasize this situation in clinical praxis as well (Fig. 1

Giant inguinoscrotal hernia is defined as an inguinal hernia extending below the midpoint of inner thigh in standing position. The authors describe giant inguinoscrotal hernia and small umbilical hernia with 12 years history of this uncommon disease. After preoperative evaluation, US and CT examination he was operated on. It was very difficult to return the hernia sac contents back to the abdomen and additional infraumbilical incision was needed. Hernioplasty suo modo without mesh was done. Patient recovered uneventfully. In the discussion the authors present the newer classification of giant inguinal hernia, the current treatment options and known serious complications of surgery. Finally, it indicates that good treatment results can only be achieved by close cooperation of concerned professionals in the treatment and intensive intraoperative and postoperative patient monitoring (Fig. 9, Ref. 31).

BACKGROUND: Various authors defi ned three patterns of the posterior part of the circulus arteriosus cerebri Willisi (CW) according to the diameter of the posterior communicating artery (PCoA) and the precommunicating segment of the posterior cerebral artery (P1). In the adult pattern, the P1 has a diameter larger than the nonhypoplastic PCoA. In the transitional pattern, the diameter of the PCoA is equal to that of the P1. In the fetal pattern, the diameter of the P1 is smaller than the diameter of the PCoA. The study was aimed to evaluate the confi gurations and calibers of the posterior part of the CW. METHODS: The work was conducted on 185 adult post-mortem brains. The CW and its branches were photographed by a digital camera. We used the software Image J to evaluate and process the gained images. RESULTS: The fetal pattern was found unilaterally in 8.37 %, and bilaterally in 4.86 %. The transitional pattern was observed unilaterally in 6.47 %, and bilaterally in 1 %. The prevalence of the unilateral and bilateral adult patterns was equal (21.62 % for each confi guration). The hypoplastic PCoA was found unilaterally in 17.57 %, and bilaterally in 16.76 %. CONCLUSION: Various factors including genetic and environmental may affect the development of the cerebral vessels and their dimensions. The distinguishing of the vascular dimensions in vivo can help in the expectation and may be the avoidance of possible cerebrovascular disturbances in the future. Correlation and interdisciplinary cooperation of the studies dealing with morphology, radiology, and hemodynamics of the cerebral vessels are becoming an urgent need. The assumed results of this cooperation can be used in tabulating the calibers of the cerebral vessels and determining the threshold dimensions under which failure of hemodynamics and collateral function may appear (Tab. 2, Fig. 5, Ref. 28). Text in PDF www.elis.sk. . KrishnamurthyA, Nayak SR, Ganesh Kumar C. Morphometry of posterior cerebral artery: embryological and clinical signifi cance. Roman J Morphol Embryol 2008; 49 (1): 43-45. 27. Chuang YM, Liu CY, Pan PJ, Lin CP. Posterior com municating artery hypoplasia as a risk factor for acute ischemic stroke in the absence of carotid artery occlusion. J Clin Neurosci 2008; 15 (12): 1376-1381. 28. Sahni D, Jit I, Lal V. Variations and anomalies of the posterior communicating artery in northwest Indian brains. Surg Neurol 2007; 68 (4): 449-453.