To prevent infections, the incision is covered with a sterile bandage or surgical adhesive. Laparoscopic appendectomy
Laparoscopic appendectomy was introduced in 1983 and has become an increasingly prevalent intervention for acute appendicitis. This surgical procedure consists of making three to four incisions in the abdomen, each 0.25 to 0.5 inches (6.4 to 12.7 mm) long. This type of appendectomy is made by inserting a special surgical tool called a laparoscope into one of the incisions. The laparoscope is connected to a monitor outside the persons body, and it is designed to help the surgeon to inspect the infected area in the abdomen. The other two incisions are made for the specific removal of the appendix by using surgical instruments. Laparoscopic surgery requires general anesthesia, and it can last up to two hours. Laparoscopic appendectomy has several advantages over open appendectomy, including a shorter post-operative recovery, less post-operative pain, and lower superficial surgical site infection rate. However, the occurrence of an intra-abdominal abscess is almost three times more prevalent in laparoscopic appendectomy than open appendectomy. Laparoscopic-assisted transumbilical appendectomy
In pediatric patients, the high mobility of the cecum allows externalization of the appendix through the umbilicus, and the entire procedure can be performed with a single incision. Laparoscopic-assisted transumbilical appendectomy is a relatively recent technique but with long published series and very good surgical and aesthetic results. Pre-surgery
The treatment begins by keeping the person who will be having surgery from eating or drinking for a given period, usually overnight.
Diagnosis is difficult, as pathognomonic signs on MRI such as cortical ribboning or hockey stick sign, periodic sharp wave complexes on EEG, and tests for 14-3-3 protein and tau protein are usually not helpful, and no mutations have been observed in the coding region of the PrP gene, unlike CJD and Variant CJD. The diagnosis can be made on pathological examination. There are unique microscopic and immunohistochemical features, and the prions cannot be digested using proteases. Because 8 out of 10 patients had a positive family history of dementia in the original study, a genetic cause was suspected. Some have suggested the disease may be a sporadic form of Gerstmann–Sträussler–Scheinker syndrome (GSS).In 2013, Zou W.Q. and coworkers revealed that the peculiar protease-resistant PrP (PrPres) originally found in VPSPr is also detectable in the brain of patients with a genetic CJD linked to PrP Valine (V) to isoleucine (I) mutation at residue 180 (PrPV180I); moreover, they found that the pathological PrP from both VPSPr and gCJDPrPV180I shares a similar glycoform-selective prion formation mechanism. [8,9] Interestingly, the authors further demonstrated that the protease-resistant PrPres from both VPSPr and gCJDV180I lacks the PrP species glycosylated at the first N-linked glycosylation site at residue 181 and they proposed that the deficiency in PrP glycosylation may be involved in the pathogenesis of the two conditions.