A Nurse Is Reviewing the Laboratory Results of a Client Who Has Cirrhosis

Continuing Education Activity

Ascites is the pathologic aggregating of fluid within the peritoneal cavity. Information technology is the most common complication of cirrhosis and occurs in about 50% of patient with decompensated cirrhosis in 10 years. The development of ascites denotes the transition from compensated to decompensated cirrhosis. Mortality increases from complications such as spontaneous bacterial peritonitis and hepatorenal syndrome. Mortality ranges from 15% in a year to 44% in 5 years. This activity describes the evaluation, diagnosis, and management of ascites and highlights the role of team-based interprofessional care for affected patients.

Objectives:

• Identify the etiology of ascites.

• Review the workup of a patient with ascites.

• Outline the treatment and management options bachelor for ascites.

• Describe interprofessional squad strategies for improving care coordination in the evaluation and handling of ascites to improve outcomes.

Access complimentary multiple choice questions on this topic.

Introduction

Ascites is the pathologic accumulation of fluid within the peritoneal cavity. It is the well-nigh common complication of cirrhosis and occurs in about 50% of patient with decompensated cirrhosis in 10 years. The evolution of ascites denotes the transition from compensated to decompensated cirrhosis. Mortality increases from complications such as spontaneous bacterial peritonitis and hepatorenal syndrome. Bloodshed ranges from 15% in a year to 44% in 5 years.[ane][ii][three]

In most healthy individuals, there is very little free intraperitoneal fluid; some women may take about xx ml during the menstrual cycle.

Etiology

In the Us, the almost common disease that causes patients to get ascites is cirrhosis, which accounts for approximately 80% of cases. Other causes of ascites include cancer, ten%; heart failure, three%; tuberculosis, 2%; dialysis, 1%; pancreatic disease, one%; and others, 2%. Upwardly to 19% of patients with cirrhosis will have hemorrhagic ascites; this may develop spontaneously with 72% of the cases most likely due to encarmine lymph and 13% due to hepatocellular carcinoma. It can also develop following paracentesis.[4][5]

Other causes of asictes include:

• Chronic alcohol use

• IV drug apply

• Obesity

• Hypercholesterolemia

• Type ii diabetes

• Nephrotic syndrome

• Severe malnutrition

• Pancreatic ascites

• Ovarian lesions

Epidemiology

Patients with cirrhotic ascites have a 3-yr mortality rate of approximately 50%. Refractory ascites carries a poor prognosis, with a one-year survival charge per unit of less than 50%. Males have petty intraperitoneal fluid, females take approximately 20 mL, depending on the phase of their menstrual cycle.

Pathophysiology

The first abnormality that develops is portal hypertension in the example of cirrhosis. Portal pressure increases above a disquisitional threshold and circulating nitric oxide levels increase, leading to vasodilatation. Equally the land of vasodilatation becomes worse, the plasma levels of vasoconstrictor sodium-retentive hormones elevate, renal function declines, and ascitic fluid forms, resulting in hepatic decompensation.

Through the production of proteinous fluid past tumor cells lining the peritoneum, peritoneal carcinomatosis also tin can cause ascites. In loftier-output or low-output heart failure or nephrotic syndrome, effective arterial blood volume is decreased, and the vasopressin, renin-aldosterone, and sympathetic nervous systems are activated, leading to renal vasoconstriction and sodium and water retention.[6]

History and Physical

Patients typically written report progressive abdominal distension that may exist painless or associated with intestinal discomfort, weight gain, early satiety, shortness of breath, and dyspnea resulting from fluid accumulation and increased intestinal pressure level. Symptoms such every bit fever, intestinal tenderness, and confusion tin can be seen in spontaneous bacterial peritonitis.

Patients with cancerous ascites tin have symptoms related to malignancy, which may include weight loss. On the other hand, patients with ascites due to centre failure may study dyspnea, orthopnea, and peripheral edema, and those with chylous ascites report diarrhea, steatorrhea, malnutrition, edema, nausea, enlarged lymph nodes, early satiety, fevers, and night sweats.

Patients with ascites typically will have flank dullness on test, shifting dullness, a fluid moving ridge, testify of pleural effusions, and findings related to the underlying cause of the ascites, such every bit stigmata of cirrhosis (cirrhosis includes spider angioma, palmar erythema, and abdominal wall collaterals.

Spider angiomata, jaundice, muscle wasting, gynecomastia, and leukonychia are present in patients with advanced liver affliction.

An umbilical nodule that is not bowel or omental, such as a Sis Mary Joseph nodule, provides evidence for cancer equally the cause of ascites. In eye failure, concrete examination findings may include jugular venous distension, pulmonary congestion, or peripheral edema.

Evaluation

Diagnostic abdominal paracentesis with the appropriate ascitic fluid analysis is probably the about rapid and cost-effective method of diagnosing the cause of ascites.[7][8]

The initial tests that should be performed on the ascitic fluid include a claret cell count, with both a total nucleated cell count and polymorphonuclear neutrophils (PMN) count, and a bacterial culture by bedside inoculation of blood civilization bottles.

Ascitic fluid protein and albumin are measured simultaneously with the serum albumin level to calculate the serum-ascites albumin gradient (SAAG).

The presence of a gradient greater or equal to 1.1 g/dL (greater or equal to 11 g/Fifty) predicts that the patient has portal hypertension with 97% accuracy. This is seen in cirrhosis, alcoholic hepatitis, center failure, massive hepatic metastases, middle failure/pericarditis, Budd-Chiari syndrome, portal vein thrombosis, and idiopathic portal fibrosis. A gradient less than i.ane thousand/dL (less than 11 k/Fifty) indicates that the patient does not have portal hypertension and occurs in peritoneal carcinomatosis, peritoneal tuberculosis, pancreatitis, serositis, and nephrotic syndrome.

Additional tests may be performed simply if a specific diagnosis is suspected clinically. LDH and glucose level should be adamant in suspected cases of secondary peritonitis. Other tests to consider include amylase (greater than 1000 U/Fifty suggests pancreatic ascites). Mycobacterial culture should exist performed only if tuberculosis is strongly suspected. Other ascitic fluid indices such as lactate and pH offer little to no additional information.

Chest x-ray may reveal elevated diaphragm.

Ultrasound is the most sensitive test to discover ascites. It will reveal homogenous freely mobile anechoic collection in the peritoneal cavity. The smallest amount of fluid is commonly seen in Morison pouch.

CT scan can likewise exist used to observe ascites and may also help decide for presence of any masses.

Treatment / Management

Advisable treatment of ascites depends on the cause of fluid retention. The goals of therapy in patients with ascites are to minimize the ascitic fluid volume and decrease peripheral edema, without causing intravascular volume depletion.[nine][ten][11]

Sodium restriction and diuretics form the basis of treatment

In cases of  high-albumin-slope ascites which occurs in cirrhosis, the treatment of ascites in these patients  includes abstinence from booze, restricting dietary sodium to 88 mEq (2000 mg)  per twenty-four hour period, and treating with diuretics (spironolactone and furosemide in a ratio of 100:xl mg/solar day)

Patient with a treatable liver condition, such as autoimmune hepatitis, chronic hepatitis B with reactivation, hemochromatosis, or Wilson disease, should receive specific therapy for these diseases. Occasionally, cirrhosis due to causes other than booze or hepatitis B is reversible; still, these diseases are commonly less reversible than in alcoholic liver illness, and by the fourth dimension ascites is present, these patients may be better candidates for liver transplantation than for protracted medical therapy.

Low-albumin-gradient ascites commonly occurs in not-ovarian peritoneal carcinomatosis. These patients often benefit from an outpatient therapeutic paracentesis. Patients with ovarian malignancy may benefit from surgical debulking and chemotherapy.

TB peritonitis is treated with anti-tuberculous medications, while pancreatic ascites and postoperative lymphatic leak from a distal splenorenal shunt or radical lymphadenectomy may resolve spontaneously.

Chlamydia peritonitis is cured with antibiotics using doxycycline and ascites caused by lupus serositis may reply to glucocorticoids.

Over the years many types of active and passive pumps accept been adult simply none works reliably. They are prone to obstacle, mechanical failure, and leaks.

Therapeutic paracentesis is ofttimes washed for symptom relief or in patients with tense ascites. Supplements of albumin should be administered at the aforementioned time to prevent hypotension. Terlipressin is recommended instead of albumin, if available.

Transjugular intrahepatic portosystemic shunt is an effective treatment for patients who do not respond to diuretics.

Differential Diagnosis

• Liver Failure

• Biliary disease

• Alcoholic liver illness

• Cirrhosis

• Dilated Cardiomyopathy

• Liver cancer

• Portal hypertension

• Viral hepatitis

• Nephrotic syndrome

Prognosis

The prognosis of patients with ascites depends on the crusade and chronicity. Disorders that are astute and respond to treatment accept a much favorable prognosis, compared to disorders that practise not respond.

Complications

Spontaneous bacterial peritonitis

Complications related to paracentesis

• Infection

• Electrolyte imbalance

• Bowel perforation

• Bleeding

• Leak of fluid through abdominal wall

• Injury to the kidneys

Postoperative and Rehabilitation Care

Patients with ascites demand long-term monitoring to assess the effectiveness of treatment. The body weight and urinary sodium levels should be monitored in all patients treated with furosemide.

The goal of treatment is to ensure in that location is minimal edema and the patient is able to perform some daily living activities.

A low sodium nutrition is recommended.

Consultations

• Gastroenterologist

• Hepatologist

• General Surgeon

Deterrence and Patient Pedagogy

• Limit alcohol intake

• Hepatitis B vaccination

• Sodium restriction is recommended (2000 mg/d)

Pearls and Other Issues

Transfusion of blood products (fresh frozen plasma or platelets) routinely earlier paracentesis in patients with cirrhosis and coagulopathy, presumably to prevent hemorrhagic complications, is non supported by data

Contraindications to paracentesis include coagulopathy in the presence of DIC, massive ileus with bowel amplification unless the procedure is epitome-guided to guarantee that the bowel is non entered.

Complications of ascites may include simply are non limited to the post-obit: Spontaneous bacterial peritonitis, cellulitis, tense ascites, pleural effusion, and intestinal wall hernias.

Enhancing Healthcare Team Outcomes

While information technology may appear that ascites is a GI related problem, the pathology affects nearly all organ systems and has very loftier morbidity and mortality. Ascites is non a benign disorder and depending on the cause tin have a mortality exceeding 20%. [12]To prevent complications and improve the quality of life, a streamlined protocol for management is vital.[3][13] (Level V)

Countless articles on an interprofessional approach have been published so that the morbidity and mortality tin can be improved. Besides the gastroenterologist the post-obit interprofessional group of health professionals is highly recommended:

• Pharmacist to oversee all medications and exist warning for drugs that cause liver injury

• Nurses to monitor body weight, abdominal girth, prevent deep vein thrombosis, encourage airing and educate the patient and family about the importance of a low sodium diet

• Internist to monitor coagulation parameters and full general health of the patient

• Surgeon in example the patient needs decompression of the portal organization or a liver transplant

• Nephrologist to monitor renal part

• Dietitian to promote diet

• Neurologist to appraise mental status

• Radiologist to perform TIPS in patients resistant to diuretics

• Physical therapist to encourage ambulation

Outcomes and Prove-based Medicine

Overall the prognosis is much worse for patients who have decompensated cirrhosis compared to those with compensated cirrhosis. Fifty-fifty patients who are ambulatory and have cirrhotic ascites have a 3-twelvemonth bloodshed rate of 50%. Patients with refractory ascites have a 1-year survival of less than l%. There are many show-based studies on managing patients with ascites.[14] (Level V). The bottom line is that aggressive intendance of these patients is disquisitional if 1 wants to avoid the high mortality. Ascites patients are circuitous to manage and thus the need for an interprofessional team to ensure that the patient gets the correct handling, including a liver transplant.

Review Questions

Effigy

Intestinal ascites. Contributed by Elisa M. Aponte

Figure

Paracentesis, bowel, ascites. Contributed by MyPhuong Mitarai

Figure

Pocket of ascites ideal for paracentesis. Contributed by Maria O'Rourke

References

one.

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2.

Privitera Chiliad, Figorilli F, Jalan R, Mehta G. Portosystemic Shunt Embolization and Recurrent Ascites: A Single-Center Case Series. Gastroenterology. 2018 Nov;155(5):1649-1650. [PubMed: 30118744]

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Szkodziak PR, Czuczwar P, Wrona Westward, Paszkowski T, Szkodziak F, Woźniak S. Ascites Alphabetize - a novel technique to evaluate ascites in ovarian hyperstimulation syndrome: a concept-proof study. Ginekol Pol. 2018;89(4):182-8. [PubMed: 29781072]

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Storni F, Stirnimann K, Banz V, De Gottardi A. Treatment of Malignant Ascites Using an Automated Pump Device. Am J Gastroenterol. 2018 Jul;113(vii):1060-1061. [PubMed: 29867179]

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Strunk H, Marinova M. Transjugular Intrahepatic Portosystemic Shunt (TIPS): Pathophysiologic Nuts, Bodily Indications and Results with Review of the Literature. Rofo. 2018 Aug;190(8):701-711. [PubMed: 30045395]

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Siddique SM, Lane-Fall One thousand, McConnell MJ, Jakhete Northward, Crismale J, Porges Due south, Khungar V, Mehta SJ, Goldberg D, Li Z, Schiano T, Regan L, Orloski C, Shea JA. Exploring opportunities to forbid cirrhosis admissions in the emergency department: A multicenter multidisciplinary survey. Hepatol Commun. 2018 Mar;two(3):237-244. [PMC gratuitous commodity: PMC5831018] [PubMed: 29507899]

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Ede CJ, Nikolova D, Brand M. Surgical portosystemic shunts versus devascularisation procedures for prevention of variceal rebleeding in people with hepatosplenic schistosomiasis. Cochrane Database Syst Rev. 2018 Aug 03;8:CD011717. [PMC free commodity: PMC6524620] [PubMed: 30073663]

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Source: https://www.ncbi.nlm.nih.gov/books/NBK470482/

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