DOCSLIB.ORG

Malignant Ascites Ascites Fluid Analysis: Mandatory Tests

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Malignant Ascites Ascites Fluid Analysis: Mandatory Tests Approach to Ascites Paul Martin MD, FRCP,FRCPI Division of Hepatology, University of Miami. • 62 year old man referred with abdominal distension. • Remote icteric illness during college • Describes himself as social drinker • P/E mild muscle wasting, BP 110/70, Pulse 90/minute, afebrile • Mild flank distension, diminished liver span with splenic dullness ? Shifting dullness, no fluid wave • Initial Labs: Bilirubin 1.9 mgs/dl, AST 70, ALT 23, alk phos 135, platelet count 110 k, INR 1.2 • Ultrasound perfomed ULTRASOUND IS THE MOST SENSITIVE METHOD TO DETECT ASCITES Ultrasound is the Most Sensitive Method to Detect Ascites Ascites Liver Ascites Initial workup DIAGNOSTIC PARACENTESIS Diagnostic Paracentesis Indications New-onset ascites Admission to hospital Symptoms/signs of SBP Renal dysfunction Unexplained encephalopathy Contraindication s None INITIAL WORKUP OF ASCITES: DIAGNOSIS PARACENTESIS Initial Workup of Ascites Diagnostic Paracentesis Optional Glucose, LDH Amylase Protein/Albumin Routine ? secondary ? infection cirrhotic ? pancreatic ascites PMN count ascites Cytology Culture ? SBP ? malignant ascites Ascites Fluid Analysis: Mandatory Tests • Cell count – WBC & RBC – Purple top tube • Serum albumin - ascites albumin gradient (SAAG) – Terms exudate & transudate – Should no longer be used – Apply to only pleural effusions • Cultures – 10-20 ml in blood culture bottles ASCITES CAN BE CHARACTERIZED BY SERUM-ASCITES ALBUMIN GRADIENT (SAAG) AND ASCITES PROTEIN Ascites Can Be Characterized by Serum- Ascites Albumin Gradient (SAAG) and Ascites Protein Source of ascites Hepatic sinusoids Peritoneum SAAG > 1.1 SAAG < 1.1 “Capillarized” sinusoid Normal “leaky” sinusoid Peritoneal lymph Ascites protein < 2.5 Ascites protein > 2.5 Ascites protein > 2.5 Sinusoidal Post-sinusoidal Peritoneal pathology hypertension hypertension - Malignancy -Cirrhosis - Cardiac ascites - Tuberculosis -Late Budd- - Early Budd-Chiari Chiari - Veno-occlusive disease Etiology of Ascites TB Other Malignancy CHF Cirrhosis 5% Mixed Ascites Fluid Analysis: Optional Tests • Infected ascites – Total protein, LDH & glucose – Gram stain – To R/O free perforation of the gut – Not for SBP (10% sensitive) • Milky ascites – TG > 200 mg/ml – Occasionally high WBC count • Malignant ascites – LDH (ascites > serum) – Cytology Ascites Classification: High Gradients • Serum albumin - ascites albumin (SAAG) > 1.1 • Portal hypertension present (90-95%) • Causes – Liver – Cirrhosis – Very severe, acute hepatitis – Cancer: massive liver mets – Venous – Budd-Chiari syndrome – Veno-occlusive disease – Portal vein thrombosis – Cardiac (R-CHF, constrictive pericarditis) Ascites Classification: Low Gradients • Serum albumin - ascites albumin (SAAG) < 1.1 g/dL • Causes (every other organ in the abdomen) – Perforated gastric ulcer – Ruptured gallbladder / biliary leak – Infarcted bowel – Pancreatitis – Renal – Nephrotic syndrome – Ruptured urinary bladder – Peritoneum – Infectious – Cancer • 62 year old man with ascites • Ascites tapped: albumin 1.1 g/dl, wbc < 250,serum albumin 3.1 g/ dl • SAAG: 2 consistent with portal hypertension • HCV antibody positive,: diagnosis cirrhosis • Describes himself as social drinker Ascites Initial management MANAGEMENT OF UNCOMPLICATED ASCITES Management of Uncomplicated Ascites Definition: Ascites responsive to diuretics in the absence of infection and renal dysfunction Sodium restriction Effective in 10-20% of cases Predictors of response: mild or moderate ascites, Urine Na excretion > 50 mEq/day Diuretics Should be spironolactone-based A progressive schedule (spironolactone furosemide) requires fewer dose adjustments than a combined therapy (spironolactone + furosemide) DEFINITION AND TYPES OF REFRACTORY ASCITES Definition and Types of Refractory Ascites Occurs in ~10% of cirrhotic patients Diuretic-intractable ascites 80% Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications Diuretic-resistant ascites 20% No response to maximal diuretic therapy (400 mg spironolactone + 160 mg furosemide/day) Arroyo et al. Hepatology 1996; 23:164 Ascites Beyond diuretics Ascites: Other Options • Repeated Large Volume Paracentesis: inconvenient, if required < every 2 weeks suggests non-compliance with salt and fluid restriction • TIPS: used to manage ascites, recurrent variceal hemorrhage, hepatic hydrothorax etc. May worsen liver disease TIPS Blood Flow Changes COMPARED TO LVP, TIPS IS ASSOCIATED WITH LESS ASCITES RECURRENCE BUT MORE ENCEPHALOPATHY Compared to LVP, TIPS Reduces Ascites Recurrence But Increases Risk of Encephalopathy LVP TIPS p (n=35) (n=35) Recurrent ascites 11.7± 2.7* 3.6 ± 1.7 0.003 TIPS obstruction - 40% - Grade 3-4 PSE 0.5 ± 0.02 1.1 ± 0.02 0.02 Death 51% 57% ns * Episodes/patient Gines et al., Gastroenterology 2002; 123:1839 Ascites: Other Options • Peritoneovenous shunt: largely replaced by TIPS • Pleurx catheter; left in situ, used in malignant ascites PERITONEO-VENOUS SHUNT (PVS) IS USEFUL IN THE TREATMENT OF REFRACTORY ASCITES Peritoneo-Venous Shunt (PVS) is Useful in the Treatment of Refractory Ascites Use of jugular vein will hinder TIPS placement One-way valve Intraabdominal adhesions may complicate liver transplant surgery Ascites: Survival & OLT 100 80 After Liver Transplant Survival 60 (%) 40 20 1 2 3 4 5 6 Onset Years Cirrhosis Background HISTOLOGICAL IMAGE OF CIRRHOSIS Fibrosis Regenerative nodule PATHOGENESIS OF LIVER FIBROSIS Normal Hepatic SInusoid Retinoid droplets Fenestrae Hepatic stellate cell Space of Disse Sinusoidal endothelial cell Hepatocytes PATHOGENESIS OF LIVER FIBROSIS Alterations in Microvasculature in Cirrhosis Activation of stellate cells Collagen deposition in space of Disse Constriction of sinusoids Defenestration of sinusoids IN CIRRHOSIS, NITRIC OXIDE ACTIVITY IS REDUCED AND THE ACTIVITY OF VASOCONSTRICTORS IS INCREASED In Cirrhosis, Nitric Oxide (NO) Activity is Reduced and Vasoconstrictors (VC) are Increased Cirrhosis Prognosis Stable cirrhosis in absence of complications (Fattovich, Gastroenterology 1997) No complications Complications Platelets <115,000 > predictor Stable Cirrhotic • Routine Health Maintenance • Surveillance for HCC • Screening and prophylaxis of varices • SBP prophylaxis Management of the stable cirrhotic: HCC surveillance • Cirrhosis is high risk factor for HCC: 23 fold risk after 3.5 years (Chalasani, Amer J Gastr 1999) • If presenting with symptoms, median survival is 4 months • Surveillance: – AFP sensitivity 64%/specificity 91% – UTZ sensitivity 59-74%/specificity 94% – Optimal frequency unknown Cirrhosis Complications NATURAL HISTORY OF CIRRHOSIS Development of Complications in Compensated Cirrhosis 100 80 Probability of 60 Ascites Jaundice developing event Encephalopathy 40 GI hemorrhage 20 0 0 20 40 60 80 100 120 140 160 Months Gines et. al., Hepatology 1987; 7:122 SURVIVAL TIMES IN CIRRHOSIS Decompensation Shortens Survival 100 80 Median survival 60 All patients~ 9 years with cirrhosis Probability of survival 40 20 Decompensated Median cirrhosis survival 0 ~ 1.6 years 0 20 40 60 80 100 120 140 160 180 Months Gines et. al., Hepatology 1987;7:122 COMPLICATIONS OF CIRRHOSIS Complications of Cirrhosis Result from Portal Hypertension or Liver Insufficiency Portal hypertension Variceal hemorrhage SBP Ascites Cirrhosis HRS Liver insufficiency Encephalopathy Jaundice Cirrhosis Varices Prevalence and Size of Esophageal Varices in Patients with Newly-Diagnosed Cirrhosis 100 80 Large % 60 Patients with 40 Medium varices 20 Small 0 Overall Child A Child B Child C n=494 n=346 n=114 n=34 Mortality 20%-30% at 6 weeks Pagliaro et al., In: Portal Hypertension: Pathophysiology and Management, 1994: 72 Large Varices are more Likely to Rupture No Varices 100 Small Varices p<0.01 * 75 % Patients 50 Large Varices * * without bleeding 2-year probability of first 25 bleed: Small varices: 7% Large varices: 30% 0 60 0 12 24 36 48 52 Time (months) *Merli et al., Hepatol 2003; 38:266, **Conn et al., Hepatology 1991; 13:902 VARICES INCREASE IN DIAMETER PROGRESSIVELY Varices Increase in Diameter Progressively No varices Small varices Large varices 7-8%/year 7-8%/year Merli et al. J Hepatol 2003;38:266 PROGNOSTIC INDICATORS OF FIRST VARICEAL HEMORRHAGE Variceal hemorrhage Varix with red signs Predictors of hemorrhage: Variceal size Red signs Child B/C NIEC. N Engl J Med 1988; 319:983 TREATMENT OF ACUTE VARICEAL HEMORRHAGE Treatment of Acute Variceal Hemorrhage General Management: IV access and fluid resuscitation Do not overtransfuse (hemoglobin ~ 8 g/dL) Antibiotic prophylaxis Specific therapy: Pharmacological therapy: terlipressin, somatostatin and analogues, vasopressin + nitroglycerin Endoscopic therapy: ligation, sclerotherapy Shunt therapy: TIPS, surgical shunt PROPHYLACTIC ANTIBIOTICS PREVENT EARLY VARICEAL REBLEEDING Probability of Remaining Free of Recurrent Variceal Hemorrhage 1.0 Prophylactic antibiotics (n=59) 0. 8 0. No antibiotics (n=61) % 6 free of 0. variceal 4 hemorrh 0. age 2 0 0 1 2 3 12 18 24 30 Follow-up (months) Hou M-C et al., Hepatology 2004; 39:746 Prophylaxis of Variceal Hemorrhage Diagnosis of Cirrhosis Endoscopy No Varices Small Varices Medium/Large Varices Follow-up EGD in 2-3 years* Follow-up EGD in 1-2 years* *EGD every year in decompensated cirrhosis Beta-blocker therapy No Contraindications •Stepwise increase until maximally tolerated dose Contraindications •Continue beta-blocker (life-long) or Beta-blocker intolerance Endoscopic Variceal Band Ligation CLASSIFICATION OF GASTRIC VARICES Classification of
Load more

Recommended publications
  • Atypical Abdominal Pain in a Patient with Liver Cirrhosis
    IMAGE IN HEPATOLOGY January-February, Vol. 17 No. 1, 2018: 162-164 The Official Journal of the Mexican Association of Hepatology, the Latin-American Association for Study of the Liver and the Canadian Association for the Study of the Liver Atypical Abdominal Pain in a Patient With Liver Cirrhosis Liz Toapanta-Yanchapaxi,* Eid-Lidt Guering,** Ignacio García-Juárez* * Gastroenterology Department. National Institute of Medical Science and Nutrition “Salvador Zubirán”. Mexico City. Mexico. ** Interventional Cardiology. National Institute of Cardiology “Ignacio Chávez”. Mexico City. Mexico. ABSTRACTABSTABSTABSTRACT The causes of abdominal pain in patients with liver cirrhosis and ascites are well-known but occasionally, atypical causes arise. We report the case of a patient with a ruptured, confined abdominal aortic aneurysm. KeyK words.o d .K .Key Liver cirrhosis. Abdominal aortic aneurysm. INTRODUCTION CASE REPORT Abdominal pain in cirrhotic patients is a challenge. A 47-year-old male with the established diagnosis of Clinical presentation can be non-specific and the need for alcohol-related liver cirrhosis, presented to the emer- early surgical exploration may be difficult to assess. Coag- gency department for abdominal pain. He was classified ulopathy, thrombocytopenia, varices, and ascites need to as Child Pugh (CP) C stage (10 points) and had a model be taken into account, since they can increase the surgical for end stage liver disease (MELD) - sodium (Na) of 21 risk. Possible differential diagnoses include: Complicated points. The pain was referred to the left iliac fossa, with umbilical, inguinal or postoperative incisional hernias, an intensity of 10/10. It was associated to low back pain acute cholecystitis, spontaneous bacterial peritonitis, pep- with radicular stigmata (primarily S1).
    [Show full text]
  • High Risk Percutaneous Endoscopic Gastrostomy Tubes: Issues to Consider
    NUTRITIONINFLAMMATORY ISSUES BOWEL IN GASTROENTEROLOGY, DISEASE: A PRACTICAL SERIES APPROACH, #105 SERIES #73 Carol Rees Parrish, M.S., R.D., Series Editor High Risk Percutaneous Endoscopic Gastrostomy Tubes: Issues to Consider Iris Vance Neeral Shah Percutaneous endoscopy gastrostomy (PEG) tubes are a valuable tool for providing long- term enteral nutrition or gastric decompression; certain circumstances that complicate PEG placement warrant novel approaches and merit review and discussion. Ascites and portal hypertension with varices have been associated with poorer outcomes. Bleeding is one of the most common serious complications affecting approximately 2.5% of all procedures. This article will review what evidence exists in these high risk scenarios and attempt to provide more clarity when considering these challenging clinical circumstances. INTRODUCTION ince the first Percutaneous Endoscopic has been found by multiple authors to portend a poor Gastrostomy tube was placed in 1979 (1), they prognosis in PEG placement (3,4, 5,6,7,8). This review Shave become an invaluable tool for providing will endeavor to provide more clarity when considering long-term enteral nutrition (EN) and are commonly used these challenging clinical circumstances. in patients with dysphagia following stroke, disabling motor neuron diseases such as multiple sclerosis and Ascites & Gastric Varices amyotrophic lateral sclerosis, and in those with head The presence of ascites is frequently viewed as a and neck cancer.They are also used for patients with relative, if not absolute, contraindication to PEG prolonged mechanical intubation, as well as gastric placement. Ascites adds technical difficulties and the decompression in those with severe gastroparesis, risk for potential complications (see Table 1).
    [Show full text]
  • Dysphagia to Liver Failure Vincent Ting Fung Cheung,1 Jey Singanayagam,2 Angus Molyneux,3 Neil Rajoriya1
    Images in… BMJ Case Reports: first published as 10.1136/bcr-2015-212522 on 26 November 2015. Downloaded from Dysphagia to liver failure Vincent Ting Fung Cheung,1 Jey Singanayagam,2 Angus Molyneux,3 Neil Rajoriya1 1Department of DESCRIPTION Gastroenterology, Milton A 54-year-old man presenting with dysphagia, Keynes University Hospital, Milton Keynes, UK weight loss, epigastric pain and cervical lymphaden- 2Department of Radiology, opathy was referred directly to endoscopy. The Milton Keynes University medical history included hypertension and hyper- Hospital, Milton Keynes, UK 3 cholesterolaemia. Blood tests showed normal biliru- Department of bin, aspartate transaminase (AST) 490 iu/L, Histopathology, Milton Keynes γ University Hospital, Milton -glutamyl transferase (GGT) 535 iu/L, alkaline Keynes, UK phosphatase (ALP) 829 iu/L and prothrombin time (PT) 13 s. Correspondence to Gastroscopy showed a lower oesophageal lesion Dr Vincent Ting Fung Cheung, fi [email protected] ( gure 1) with biopsies showing high-grade dyspla- sia. A CT scan showed lower oesophageal wall Accepted 19 September 2015 thickening and multiple lymphadenopathy in the chest/abdomen but no liver metastases (figure 2). The local multidisciplinary team meeting outcome was for repeat oesophageal biopsies and supraclavi- cular lymph node biopsy to exclude a lymphoma. The patient thereafter clinically deteriorated over Figure 2 CT scan showing oesophageal cancer (red a 4-week period, developing jaundice. On admis- arrow) but no obvious liver lesions. sion, he became overtly encephalopathic within 48 h, with a suggestion of acute liver failure. Bloods revealed: bilirubin 238 μmol/L, AST 1034 iu/L, GGT 569 iu/L, ALP 887 iu/L, albumin 20 g/L, PT 27.2 s and lactate 4.7 mmol/L.
    [Show full text]
  • 5. Guidelines for the Management of Malignant Ascites in Palliative Care
    5. GUIDELINES FOR THE MANAGEMENT OF MALIGNANT ASCITES IN PALLIATIVE CARE 5.1 GENERAL PRINCIPLES Ascites is the accumulation of fluid in the peritoneal cavity. 1, 2 Malignancy is the underlying cause in approximately 10% of all cases of ascites. About 15- 50% of patients with malignancy will develop ascites. 3 Cancers commonly associated with the development of ascites include breast, colorectal, endometrial, gastric, ovarian and pancreatic. 3 Non-malignant causes of ascites include liver disease, congestive cardiac failure, nephrotic syndrome, pancreatitis, tuberculosis and bowel perforation. 2, 3 Several different pathophysiological mechanisms are implicated in the development of malignant ascites. These include: 4 − peritoneal lymphatic obstruction. − hypoalbuminaemia leading to a reduction in oncotic pressure. − increased capillary permeability. − increased portal vein pressure with activation of the renin-angiotensin pathway. Symptoms resulting from an accumulation of ascitic fluid include abdominal bloating / swelling, pain, nausea and vomiting, anorexia, fatigue, peripheral oedema, heartburn and dyspnoea. 5 Malignant ascites carries a poor prognosis. Management should be aimed at maximising patient comfort and quality of life. 7 Management options for malignant ascites include diuretic therapy, therapeutic paracentesis and peritoneovenous shunts. 8 Oncological interventions may be helpful in ovarian carcinoma and lymphoma. Hormonal therapy may be useful in hormone sensitive malignancies such as some breast cancers. 2, 7 9 There is no evidence that any particular therapeutic option is more effective than another. 5.2 GUIDELINES 5.2.1 Diuretic therapy Diuretic therapy should be considered in every patient with malignant ascites particularly those with a prognosis of greater than 4 weeks. Urea and electrolytes should be checked before starting treatment and during treatment as appropriate.
    [Show full text]
  • Pulmonary Vascular Complications of Liver Disease
    American Thoracic Society PATIENT EDUCATION | INFORMATION SERIES Pulmonary Vascular Complications of Liver Disease People who have advanced liver disease can have complications Jaundice that affect the heart and lungs. It is not unusual for a person (yellow tint to skin with severe liver disease to have shortness of breath. Breathing and eyes) problems can occur because the person can’t take as big a breath due to large amounts of ascites (fluid in the abdomen) or pleural effusions (fluid build-up between the tissues that line the lung and chest) or a very large spleen and liver that pushes the diaphragm up. Breathing problems can also occur with Hepatomegaly liver disease from changes in the blood vessels and blood flow in the lungs. There are two well-recognized conditions that can result from liver disease: hepatopulmonary syndrome and portopulmonary hypertension. This fact sheet will review these Breathing two conditions and how they relate to liver disease. problems What is liver disease? the rest of your body. These toxins can damage blood vessels The liver is the second largest organ in the body and has many in your lungs leading to dilated (enlarged) or constricted important roles within the body including helping with digestion, (narrowed) vessels. Two different conditions can be seen in the metabolizing drugs, and storing nutrients. Its main job is to lungs that arise from liver disease: hepatopulmonary syndrome filter blood coming from the digestive tract and remove harmful and portopulmonary hypertension: CLIP AND COPY AND CLIP substances from it before passing it to the rest of the body.
    [Show full text]
  • Ascites ইংরাজী যিদ আপনার .থম ভাষা না হয় এবং আপনার সাহােয9র .েয়াজন হয় তেব অনু=হ কের ?দাভাষী এবং অনুবাদ পিরেষবা@েত ?যাগােযাগ কBন an Information Guide
    If English is not your first language and you need help, please contact the Interpretation and Translation Service Jeśli angielski nie jest twoim pierwszym językiem i potrzebujesz pomocy, skontaktuj się z działem tłumaczeń ustnych i pisemnych ا رﮔ ا یزﯾرﮕﻧ پآ ﯽﮐ ﮩﭘ ﯽﻠ ﺑز نﺎ ںﯾﮩﻧ ﮯﮨ روا پآ وﮐ ددﻣ ﯽﮐ ترورﺿ ﮯﮨ وﺗ ، هارﺑ مرﮐ ﯽﻧﺎﻣﺟرﺗ روا ہﻣﺟرﺗ تﻣدﺧ تﻣدﺧ ہﻣﺟرﺗ روا ﯽﻧﺎﻣﺟرﺗ مرﮐ هارﺑ ، وﺗ ﮯﮨ ترورﺿ ﯽﮐ ددﻣ وﮐ پآ روا ﮯﮨ ںﯾﮩﻧ ﮯﺳ ر ا ﺑ ط ہ ﮐ ر ﯾ ںﯾرﮐ ﮯ Dacă engleza nu este prima ta limbă și ai nevoie de ajutor, te rugăm să contactezi Serviciul de interpretare și traducere Ascites ইংরাজী যিদ আপনার .থম ভাষা না হয় এবং আপনার সাহােয9র .েয়াজন হয় তেব অনু=হ কের ?দাভাষী এবং অনুবাদ পিরেষবা@েত ?যাগােযাগ কBন An information guide إ ذ ا مﻟ نﻛﺗ ﻠﺟﻧﻹا ﺔﯾزﯾ ﻲھ كﺗﻐﻟ ﻰﻟوﻷا ﺗﺣﺗو جﺎ إ ﻰﻟ ةدﻋﺎﺳﻣ ، ﻰﺟرﯾﻓ لﺎﺻﺗﻻا ﺔﻣدﺧﺑ ا ﻟ ﺔﻣﺟرﺗ ا ﺔﯾوﻔﺷﻟ او ﻟ ﺔﯾرﯾرﺣﺗ وﺔوﺷ ﻣر ﻣﺧ ﺎﺗاﻰرﻓ،ةﻋﺳ ﻟإج ﺣوﻰواكﻐ ھﺔز ﺟﻹ ﻛ ﻟ : 0161 627 8770 : [email protected] To improve our care environment for Patients, Visitors and Staff, Northern Care Alliance NHS Group is Smoke Free including buildings, grounds & car parks. For advice on stopping smoking contact the Specialist Stop Smoking Service on 01706 517 522 For general enquiries please contact the Patient Advice and Liaison Service (PALS) on 0161 604 5897 For enquiries regarding clinic appointments, clinical care and treatment please contact 0161 624 0420 and the Switchboard Operator will put you through to the correct department / service The Northern Care Alliance NHS Group (NCA) is one of the largest NHS organisations The Northern Care Alliance NHS Group (NCA) is one of the largest NHS organisationsin the country, employingin the country 17,000 bringing staff and together providing two a NHS range Trusts, of hospital Salford and Royalcommunity NHS Foundationhealthcare services Trust and to around The Pennine 1 million Acute people Hospitals across Salford, NHS Trust.
    [Show full text]
  • FDA Warns About Rare Occurrence of Serious Liver Injury with Use of Hepatitis C Medicines Mavyret, Zepatier, and Vosevi in Some Patients with Advanced Liver Disease
    FDA Drug Safety Communication FDA warns about rare occurrence of serious liver injury with use of hepatitis C medicines Mavyret, Zepatier, and Vosevi in some patients with advanced liver disease Safety Announcement [08-28-2019] The Food and Drug Administration (FDA) has received reports that the use of Mavyret, Zepatier, or Vosevi to treat chronic hepatitis C in patients with moderate to severe liver impairment has resulted in rare cases of worsening liver function or liver failure. All these medicines contain a hepatitis C virus (HCV) protease inhibitor and are not indicated for use in patients with moderate to severe liver impairment. In most patients, symptoms resolved or new onset worsening of liver function improved after stopping the medicine. These medicines have been widely used and are safe and effective in patients with no or mild liver impairment. In many of the reported cases, liver failure occurred in patients who had signs and symptoms of moderate to severe liver impairment (Child-Pugh B or C) or other serious liver problems and should not have been treated with these medicines. In some cases, patients were reported to have no cirrhosis or compensated cirrhosis with mild liver impairment (Child-Pugh A) despite having evidence of decreased platelets at baseline or an increase in the pressure within the portal vein that carries blood from the digestive organs to the liver. In addition, some cases had other significant pre-existing risk factors such as liver cancer, alcohol abuse, or serious medical illnesses associated with serious liver problems. These factors may have contributed to clinical worsening of liver function or liver failure during treatment with these hepatitis C medicines.
    [Show full text]
  • Canine Ascites W
    Volume 44 | Issue 1 Article 3 1982 Canine Ascites W. Michael Peden Iowa State University R. D. Zenoble Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Gastroenterology Commons, and the Small or Companion Animal Medicine Commons Recommended Citation Peden, W. Michael and Zenoble, R. D. (1982) "Canine Ascites," Iowa State University Veterinarian: Vol. 44 : Iss. 1 , Article 3. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol44/iss1/3 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Canine Ascites by W. Michael Peden, DVM R. D. Zenoble, DVM* INTRODUCTION cirrhosis, and cholangitis. Most of the cardiac Canine ascites is an infrequently seen and hepatic diseases are associated with por­ clinical sign which is often the primary com­ tal hypertension as the direct cause of ascites. plaint for presentation of an animal to a vet­ Another cause of fluid accumulation in the erinarian. As in all cases a good history is a peritoneal cavity is hypoproteinemia due to priority as further questions may reveal renal loss of protein. Diseases such as behavioral changes, vomiting, anorexia, and amyloidosis and glomerulonephritis may other clinical signs which may be important cause massive proteinuria. Other causes of in defining the primary problem. Ascites itself abdominal fluid accumulation include can physically interfer with respiration, cause neoplasia of an abdominal organ, ruptured general discomfort, and disturb fluid and urinary bladder, and hemorrhage from electrolyte metabolism.
    [Show full text]
  • Episode 77 –Fever in the Returning Traveler
    Case 1 General approach to fever in the returning traveler A 60 year-old male, presents with a fever to your ED. He recently returned from India, where he spent 3 weeks visiting Episode 77 –Fever in the Returning relatives. He has no significant past medical history. Traveler Immunizations are up to date. He did id not receive any travel immunizations or malaria prophylaxis. The fever started 2 With Dr. Matthew Muller & Dr. Nazanin Meshkat days ago, and is associated with cough and chills. In the ED his vital signs are: Temp 38.4°C, BP 135/85, HR 120 bpm, RR Prepared by Dr. Keerat Grewal and Dr. Anton Helman, March 2016 22 and O2 saturation 94% on RA. Every year an increasing number of people travel abroad, and Key historical elements for fever in the returning travelers to tropical destinations are often immunologically traveler naïve to the regions they’re going to. It’s very common for travelers to get sick. In fact, about 2/3 of travelers get sick While it seems obvious here, one of the common errors that while they’re traveling or soon after their return, and emergency providers make in assessing fever is simply somewhere between 3 and 19% of travelers to developing forgetting to ask a travel history and thus missing the deadly countries will develop a fever. tropical disease diagnosis that has a vague presentation. Fever in the returning traveler is usually not caused by a Ask about travel in every patient who presents with fever dangerous tropical disease. These patients are much more The following areas are important to ask about in fever in the likely to have typical viral illnesses as a cause for their fever.
    [Show full text]
  • Ascites and Right Pleural Effusion: Demonstration of a Pentoneo-Pleural Communication
    Case Reports Ascites and Right Pleural Effusion: Demonstration of a Pentoneo-Pleural Communication Jean Verreault, Serge Lepage, Guy Bisson, and Andre Plante Departments ofNuc/ear Medicine and Internal Medicine, Centre Hospitalier Universitaire, University ofSherbrooke, Sherbrooke, Québec,Canada A 54-yr-oldfemale with known livercirrhosis presented with a right transudative pleural effusion and ascites. To findthe source of pleural fluid,[@“TcJsuIfurcolloidwas injected intraperitoneallyand a serial imagingstudy revealed its passage to the right pleural space on 2-hr and 24-hr images. Mechanisms proposed in the formation of pleural effusion in liver cirrhosis are (a) lymphatic drainage and (b) diaphragmatic defect. Radioisotope migration speed may be a clue for differentiating these two mechanisms, being more rapid in the presence of a diaphragmatic defect. J NucIMed 27:1706—1709,1986 leural effusions occur in 5% to 10% of patients with cluded enlarged liver and evidence of free liquid in the pen cirrhosis of the liver (1 ). In these patients, ascites is toneal cavity. usually evident but a pleural effusion may develop in a The chest x-ray demonstrated a large right pleural effusion. cirrhotic patient in the absence ofdetectable ascites (2). Other laboratory tests were compatible with liver cirrhosis and The effusions are usually right-sided, but may be bilat toxic effects ofalcohol. Thoracentesis revealed a fluid that had the characteristics ofa transudate as did a sample of pentoneal eral or left-sided. The precise mechanism of fluid ac fluid. Forty-eight hours after the thoracentesis of 1,800 cc, the cumulation is not clear. right pleural space was completely refilled (Fig.
    [Show full text]
  • Causes of Eosinophilic Ascites – a Systematic Review
    Causes of eosinophilic ascites – A systematic review LARISA PINTE1, CRISTIAN BAICUŞ1, 2 1Internal Medicine Department, “Colentina” Clinical Hospital, Bucharest, Romania 2“Carol Davila” School of Medicine, Bucharest, Romania Background. In the last years an uprising interest for a relatively unknown entity, eosinophilic ascites (EA), has been recorded. Our aim is to investigate the potential causes of EA development, as well as clinical, laboratory, endoscopic and radiologic features, management and outcome in these patients. Methods. The following research was performed on PubMed (MEDLINE) database using the medical subject headings [Mesh] terms “Ascites” AND “Eosinophils”. Results. A total of 284 results, dating from 1962 onwards, were found and abstracts were examined. 131 papers were excluded and the remaining 153 publications, consisting in case reports and series of cases, were analyzed. From 171 patients with EA, 127 subjects (74%) had EGE, 17 (10%) parasitic and fungal infections, 11(7%) Hypereosinophilic syndrome and 16 patients (9%) less common diseases (eosinophilic pancreatitis, chronic eosinophilic leukemia, myelofibrosis, T-cell lymphoma, Churg Strauss Syndrome, Systemic lupus erythematosus, Familial paroxysmal polyserositis and Ménétrier’s disease). High eosinophil blood count and IgE levels as well as gastrointestinal symptoms are frequent. The diagnosis is based on ascitic fluid analysis, imaging and endoscopic biopsies. Therapy with corticosteroids results in resolution of eosinophilic ascites in almost all patients. Conclusion. In most cases, in the absence of allergy, parasitic infections, malignancy, hematological disorders, peritoneal tuberculosis, inflammatory bowel disease or autoimmune disease, EA develops as a manifestation of eosinophilic gastroenteritis. Key words: Ascites, Hypereosinophilia, Eosinophilic ascites, Eosinophilic gastroenteritis, Hyper- eosinophilic syndrome, parasitic infection, systematic review.
    [Show full text]
  • ​Clinical Guideline Xifaxan (Rifaximin)
    Clinical Guideline ​ Guideline Number: PG022, Ver. 1 Xifaxan (rifaximin) Disclaimer Clinical guidelines are developed and adopted to establish evidence-based clinical criteria for utilization management decisions. Oscar may delegate utilization management decisions of certain services to third-party delegates who may develop and adopt their own clinical criteria. The clinical guidelines are applicable to all commercial plans. Services are subject to the terms, conditions, limitations of a member’s plan contracts, state laws, and federal laws. Please reference the member’s plan contracts (e.g., Certificate/Evidence of Coverage, Summary/Schedule of Benefits) or contact Oscar at 855-672-2755 to confirm coverage and benefit conditions. Summary Xifaxan (Rifaximin) is an intestinal antibiotic that comes in two different formulation strengths - 200 mg tablets and 550 mg tablets. It works by inhibiting bacterial and mycobacterial RNA synthesis. It is FDA indicated for use in hepatic encephalopathy, irritable bowel syndrome with diarrhea, and traveler’s diarrhea. The 200 mg formulation is used for treatment of traveler’s diarrhea and the 550 mg formulation is used for treatment of hepatic encephalopathy and irritable bowel syndrome with diarrhea. The most common potential adverse reactions associated with drug administration are gastrointestinally related (i.e. abdominal pain, nausea, ascites). Definitions “Hepatic encephalopathy” is a reversible impairment of neuropsychiatric function associated with ​ impaired hepatic function. “Irritable bowel syndrome” is a chronic functional disorder of the gastrointestinal tract characterized by ​ chronic abdominal pain and altered bowel habits in the absence of an organic disease. “Small Intestinal Bacterial Overgrowth (SIBO)” is a condition in which the small bowel is colonized by ​ excessive aerobic and anaerobic microbes that are normally present in the colon.
    [Show full text]