The abdomen
Peter Kopelman, Dame Jane Dacre in Handbook of Clinical Skills, 2019
Ascites Ascites is caused by free fluid in the abdominal cavity. It causes abdominal distension, which is often more prominent in the flanks. There are two commonly used methods of detection: percussion, and the detection of a fluid thrill. Percussion for ascites depends on eliciting shifting dullness. This is done by percussing the abdomen from the midline towards the flanks, until the note becomes dull. Keep the hand in the same position and ask the patient to roll towards you; then continue to percuss in that position. If the area where the dullness was confirmed has become resonant, this suggests free fluid in the abdominal cavity. To elicit a fluid thrill, ask an assistant (or the patient) to place their hand longitudinally along the midline. Then flick the flank beneath the area of dullness with the other hand on the opposite side, as if at the other end of a diameter of a circle (Fig. 4.13). If there is a fluid thrill, it will be felt shortly after the flick, as a flutter.
Management of Conditions and Symptoms
Amy J. Litterini, Christopher M. Wilson in Physical Activity and Rehabilitation in Life-threatening Illness, 2021
Progressive liver failure, associated with diagnoses such as cirrhosis, hepatitis, and primary or metastatic liver cancer (see Chapter 9, malignant neoplasms), often results in ascites. Ascites is the accumulation of fluid within the abdominal cavity, which in advanced cases, distends the abdomen causing discomfort, pressure, nausea, and bloating for the patient. Shortness of breath can also occur due to increased pressure on the diaphragm; if fluid migrates across the diaphragm, ascites can also cause pleural effusion. Bilateral lower extremity swelling, as well as umbilical hernia are possible with significant ascites. The severe sense of fullness, and tightness in the abdominal cavity and chest, often restricts comfortable range of motion and functional mobility. The diagnosis is typically made by physical exam, ultrasound, and/or MRI or CT scanning. When associated with disseminated cancer, it is referred to as malignant ascites.
Ascites and Peritonitis
John F. Pohl, Christopher Jolley, Daniel Gelfond in Pediatric Gastroenterology, 2014
The most common cause for ascites in children is portal hypertension resulting from chronic liver disease (55.2, 55.3) or, less commonly, obstruction of hepatic vein outflow (as in Budd–Chiari syndrome) (Table 55.1). Other more common causes include pancreatitis, lymphatic obstruction, or trauma. Lymphatic disruption either from abdominal surgery, trauma, or neoplasms leads to chylous ascites (55.4, 55.5). Older children may also have traumatic extrahepatic perforation of the bile tree causing biliary ascites (55.6, 55.7). There have also been patients with ascites secondary to the following causes: right heart failure, constrictive pericarditis, intestinal necrosis (55.8), ventriculoperitoneal shunts (55.9, 55.10), intra-abdominal neoplasms such as lymphoma (55.11), Henoch–Schönlein purpura, Crohn disease (55.12, 55.13), and vitamin A toxicity.
Acute pelvic inflammatory disease as a rare cause of acute small bowel obstruction
Published in Acta Chirurgica Belgica, 2019
Alexandre Haumann, Sarah Ongaro, Olivier Detry, Paul Meunier, Michel Meurisse
Abdominal ultrasound showed ascites and indirect signs of inflammation of the right iliac fossa. Neither the appendix nor the ovaries and the uterine tubes were visualized. Abdominal computed tomography (CT) described a proximal SBO with transition point under the umbilicus, small bowel dilatation at 37 mm and feces sign. No associated local complications as perforation/necrosis were described, but there was moderate intraperitoneal fluid. ICD was in the right place and there was no visible gynecological complication (Figure 1). In view of important abdominal pain, abdominal CT findings and the lack of clear diagnosis, an explorative laparoscopy was performed. Abdominal cavity was full of clear ascites. Proximal small bowel was dilated and whirled. An exploration of the bowel was performed with a total revision from the terminal ileum to the proximal jejunum. The transition point was in the jejunum, corresponding to a 360° loop around a fresh adherence. In fact, dissection showed three new scars that consisted of fibrotic bridge between the small bowel and the omentum. Pelvic cavity was very inflammatory and bulky. There was no abscess, no clear ductal infection and no appendicitis. Upper abdomen was normal despite free fluid. All the adhesions were split and normal anatomy was restored. Abdominal cavity was washed with 3 liters of water and one pelvic 24Fr silastic drain was left. Bacterial analysis and sexually transmitted infection tests were conducted (Figure 2).
Validity of administrative codes associated with cirrhosis in Sweden
Published in Scandinavian Journal of Gastroenterology, 2020
Bonnie Bengtsson, Johan Askling, Jonas F. Ludvigsson, Hannes Hagström
The ICD code for ascites was, as defined above, validated for ascites due to liver disease and not the presence of ascites in general. Of the 129 cases, ascites was present in 128 (99%). Of noteworthy is that only 56/129 (PPV = 43%, 95%CI: 35–52) of the cases had ascites related to liver disease. Typically, in cases not considered caused by liver disease, gynaecologic cancers (27/129) and GI tumours (20/129) were the causes of ascites. Other non-liver causes included heart failure, nephrotic syndrome and other cancers. Some 54/129 patients had coding for a chronic liver disease within 2 years of the date of ascites (defined in Table 1). When the ICD-10 code for ascites was combined with a code for chronic liver disease, the diagnosis was correct in 50/54 cases (PPV = 93%, 95%CI: 82–98). PPVs for validated ICD-codes are also presented in Figure 2.
The impact of portal vein thrombosis on the prognosis and liver function of nonmalignant cirrhotic patients
Published in Scandinavian Journal of Gastroenterology, 2018
Kei Endo, Takayoshi Oikawa, Keisuke Kakisaka, Akio Tamura, Shigeru Ehara, Yasuhiro Takikawa
A total of 137 medical containing the words ‘portal vein thrombosis,’ and ‘cirrhosis’ reports that were registered between June 2009 and June 2017 were identified from the electronic system. A total of 110 patients were excluded based on the exclusion criteria. The details of the patient selection are shown in Figure 1. Ultimately, 27 patients met the inclusion criteria. The clinical characteristics of the patients at registration are shown in Table 1. The location of PVT was the portal trunk in nine patients (33.3%), portal trunk to SMV in nine patients (33.3%), right main portal vein in three patients (11.1%), left main portal vein in four patients (14.8%) and SMV in two patients (7.4%). Fourteen patients (52%) complained of the new onset of symptoms when PVT was recognized. The symptoms were as follows: new or worsening ascites (n = 7), variceal bleeding (n = 4) and abdominal pain (n = 3). Thirteen patients had no new symptoms, and their PVT was diagnosed at routinely scheduled imaging studies.
Related Knowledge Centers
- Cirrhosis
- Shortness of Breath
- Spontaneous Bacterial Peritonitis
- Abdomen
- Peritoneal Cavity
- Tuberculosis
- Cancer
- Pancreatitis
- Shortness of Breath
- Heart Failure
- Budd–Chiari Syndrome