Assessment and management

A new minor surgical procedure for ascites has been devised wherein a specially designated one way pressure activated valve is implanted to create a permanent peritoneo-venous shunt. The normally closed valves opens only when the peritoneal pressure rises 3-5 cm higher than the intrathoracic venous pressure thus preventing backflow of blood and closing the valve should the venous pressure rise from the over-infusion of ascitic fluid. The procedure has been performed on 45 patients but nine were terminal at the time of surgery. Prolonged relief of ascites occurred in 28 of 37 cases.

Peritoneo-venous shunting for ascites.

Studies on the Epidemiology of Adverse Drug Reactions: V. Clinical Factors Influencing Susceptibility

The liver is the major site of biotransformation for most opioids. Thus, the disposition of these drugs may be affected in patients with liver insufficiency. The major metabolic pathway for most opioids is oxidation. The exceptions are morphine and buprenorphine, which primarily undergo glucuronidation, and remifentanil, which is cleared by ester hydrolysis. Oxidation of opioids is reduced in patients with hepatic cirrhosis, resulting in decreased drug clearance [for pethidine (meperidine), dextropropoxyphene, pentazocine, tramadol and alfentanil] and/or increased oral bioavailability caused by a reduced first-pass metabolism (for pethidine, dextropropoxyphene, pentazocine and dihydrocodeine). Although glucuronidation is thought to be less affected in liver cirrhosis, and clearance of morphine was found to be decreased and oral bioavailability increased. The consequence of reduced drug metabolism is the risk of accumulation in the body, especially with repeated administration. Lower doses or longer administration intervals should be used to remedy this risk. Special risks are known for pethidine, with the potential for the accumulation of norpethidine, a metabolite that can cause seizures, and for dextropropoxyphene, for which several cases of hepatotoxicity have been reported. On the other hand, the analgesic activity of codeine and tilidine depends on transformation into the active metabolites, morphine and nortilidine, respectively. If metabolism is decreased in patients with chronic liver disease, the analgesic action of these drugs may be compromised. Finally, the disposition of a few opioids, such as fentanyl, sufentanil and remifentanil, appears to be unaffected in liver disease.

Pharmacokinetics of opioids in liver disease.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs in both acute and chronic liver failure. Although the precise pathophysiologic mechanisms responsible for HE are not completely understood, a deficit in neurotransmission rather than a primary deficit in cerebral energy metabolism appears to be involved. The neural cell most vulnerable to liver failure is the astrocyte. In acute liver failure, the astrocyte undergoes swelling resulting in increased intracranial pressure; in chronic liver failure, the astrocyte undergoes characteristic changes known as Alzheimer type II astrocytosis. In portal-systemic encephalopathy resulting from chronic liver failure, astrocytes manifest altered expression of several key proteins and enzymes including monoamine oxidase B, glutamine synthetase, and the so-called peripheral-type benzodiazepine receptors. In addition, expression of some neuronal proteins such as monoamine oxidase A and neuronal nitric oxide synthase are modified. In acute liver failure, expression of the astrocytic glutamate transporter GLT-1 is reduced, leading to increased extracellular concentrations of glutamate. Many of these changes have been attributed to a toxic effect of ammonia and/or manganese, two substances that are normally removed by the hepatobiliary route and that in liver failure accumulate in the brain. Manganese deposition in the globus pallidus in chronic liver failure results in signal hyperintensity on T1-weighted Magnetic Resonance Imaging and may be responsible for the extrapyramidal symptoms characteristic of portal-systemic encephalopathy. Other neurotransmitter systems implicated in the pathogenesis of hepatic encephalopathy include the serotonin system, where a synaptic deficit has been suggested, as well as the catecholaminergic and opioid systems. Further elucidation of the precise nature of these alterations could result in the design of novel pharmacotherapies for the prevention and treatment of hepatic encephalopathy.

Hepatic encephalopathy: An update of pathophysiologic mechanisms.

https://www.gastrojournal.org/article/S0016-5085(61)80071-1/pdf

Morphine tolerance in hepatic cirrhosis.

Neuropsychiatric complications following chlorothiazide therapy in patients with hepatic cirrhosis: possible relation to hypokalaemia.

Ascites in cirrhosis of the liver is associated with a raised portal venous pressure and a lowered serum albumin level. Sodium is retained in the body as ascites accumulates, and urinary sodium is extremely low, most of the dietary intake passing into the peritoneal cavity. The urinary sodium/potassium ratio is reduced ; this probably reflects the effects of aldosterone, increased amounts of which may be found in the urine of some cirrhotics with ascites (Wolff et al., 1956). Ascites can often be controlled by rigid restriction of sodium intake and the use of diuretics (Eisenmenger, 1952; Atkinson et al., 1954). The organic mercurials have been consistently useful, their only drawback being the necessity for parenteral administration; toxic effects are rare. An equally powerful but oral diuretic with no toxic properties would be of great value. The new oral diuretic, chlorothiazide (6-chloro7-sulphamyl-1-1,2,4-benzothiadiazine-1,1-dioxide; \"6 saluric,\" \" chlotride,\" \"diuril \") has been successfully used in patients with chronic cardiac failure (Moyer et al., 1957; Bayliss et al., 1958; Slater and Nabarro, 1958), and this prompted us to give it to patients with cirrhosis complicated by ascites. Chlorothiazide is chemically an aromatic sulphonamide derivative. Experimentally, in dogs, intravenous administration results in increased sodium and potassium excretion (Ford et al., 1957). Its primary action, like that of the mercurial diuretics, seems to be potent inhibition of tubular reabsorption of sodium with no significant effect on renal blood flow

/pdf/chlorothiazide-in-control-of-ascites-in-hepatic-cirrhosis-3xereyhwy2.pdf

Chlorothiazide in control of ascites in hepatic cirrhosis.

Colloid osmotic pressure and hydrostatic pressure relationships in the formation of ascites in hepatic cirrhosis.

Chlorothiazide in liver disease

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Read Ae

Author Tools

Chat about Author