SAVED
File name .JPG
File alt. text
Image should be px wide x px tall.
Select Image
home - Liver - Liver Failure - Varices Development Written by Dr Sebastian Zeki
Knowledge


Assesses the severity of liver dysfunction and its prognostic
significance following haemorrhage

Knows importance of correcting hypovolaemia preventing
complications of GI bleeding and deterioration of liver function and
stopping bleeding

Knows the potential use of blood & clotting factors the role of
antibiotics the use of vasoconstrictors therapeutic endoscopy the
indication for transjugular intra-hepatic portosystemic shunt (TIPS) or
surgical shunt surgery

Aware of the specific complications of bleeding in cirrhotic patients –
including hepatic encephalopathy need for airway protection
nutrition identification of alcohol withdrawal

Skills
Shows proficiency in endoscopy – including emergency endoscopic
techniques of variceal band ligation endoscopic sclerotherapy
injection of cyanoacrylate glues for gastric varices

Can place safely and manage a Sengstaken tube in refractory
variceal bleeding

Can prevent and treat complications including hepatorenal failure
ascites spontaneous bacterial peritonitis and hepatic encephalopathy

Behaviours
Appreciates criteria for referral to specialist centre when appropriate –
such as with bleeding gastric or ectopic varices or consideration of
TIPS

Appreciates need to treat patients using a multi–disciplinary approach
Shows understanding of an empathic approach which may involve


Also....

Knowledge
Knows risks and prognosis of recurrent variceal bleeding in cirrhotic
patients

Aware of role of secondary prophylaxis with either non–selective ?-
blockers endoscopic ligation or both

Skills
Can select suitable endoscopic therapy and perform the appropriate
procedure competently

Behaviours
Appreciates the potential role of other specialists e g interventional
radiologists and nurse specialists

Also...

Knowledge


Understands the mechanisms of biliary metabolism the various
abnormalities that lead to hyperbilirubinaemia and knows and
recognises the causes of the various forms of jaundice

Skills
Selects and interprets appropriate investigations and formulate
management plans

Behaviours
Approaches patients presenting with jaundice in a logical and
methodical manner

Also...
Knowledge


Can define the different types (I and II) of hepatorenal
syndrome(HRS)

Knows the differential diagnosis of different types of renal
failure/impairment in liver disease

Understands the major and minor criteria in diagnosis of HRS and be
able to differentiate between HRS and acute kidney injury

Appreciates the prognostic significance of renal impairment in
patients with chronic liver disease

Knows the options for management and treatment of HRS the role of
colloids and vasoconstrictors as well as renal supportive treatment by
dialysis

Skills
Uses and interprets result of sometimes complex investigations
appropriately

Behaviours
Can judge when to involve other specialists especially nephrologists
radiologists and intensivists

Also...

Knowledge


Understands the pathogenesis of hepatic encephalopathy (HE)
Knows the differential diagnosis of HE including the existence of risk
factors for its causation including metabolic disorders and intracranial
structural disorders (such as subdural haematomas)

Knows factors that may precipitate HE including bleeding electrolyte
disturbance drugs or other organ failure

Knows the various treatment options appropriate for grade of severity

Skills
Can grade the mental state (Glasgow coma score and West Haven
Criteria)

Shows ability to differentiate between acute and acute on chronic liver
injury

Can identify the patient at risk of raised intracranial pressure and
cerebral oedema

Selects and use investigations appropriately and determine timing of
airway protection

Behaviours
Appreciates the role of other specialists and interacts in a
professional manner with intensivists neurologists
neurophysiologists radiologists and other specialists

Makes referral where appropriate to specialist centre for liver
transplantation

Also...

Knowledge


Understands the causes of acute hepatitis including viral druginduced alcohol-induced and auto-immune liver disease

Knows the appropriate plan of investigation and management of
specific diseases including the role of serological investigations and
liver biopsy

Skills
Takes an accurate history from patients with acute liver disease and
performs detailed clinical examination

Utilises investigation in a structured manner
Behaviours
Considers all therapeutic modalities and preparedness to refer to
specialist centre where diagnosis remains in doubt or appropriate
management cannot be performed

Also...

Knowledge
Assessment
Methods GMP
Recognises and knows how to diagnose acute and chronic drug
induced liver injury and dysfunction
SCE 1,2
Aware of methods of diagnosis, role of liver biopsy and therapy
including role of steroids in treatment in selected cases
SCE, CbD 1
Skills
Understands the role of both prescription and recreational drugs and
the aetiology of a wide variety of liver disease and dysfunction often
requiring prompt intervention or involvement of specialist services
SCE, CbD 1,2,3
Has awareness of the range of iatrogenic liver dysfunction SCE, CbD 1,2,3
Behaviours
Able to interact with specialist pharmacy services. Can use yellow
card reporting system of potential adverse effects of drugs.

Also....

Knowledge


Understands the causes and pathophysiology of acute liver failure
Can plan appropriate investigation evaluate prognosis and construct
a detailed management plan

Identifies those potentially suitable for emergency liver transplantation
Skills
Develops ability to make accurate evaluation of patients with liver
failure at the stage of initial presentation

Can deliver management plan appropriately evaluate changes in
patient’s condition and react accordingly

Utilises the range of medical interventions necessary to support
critically ill patients

Behaviours
Demonstrates ability to identify patients at risk of developing acute
liver failure and understand the criteria for referral to specialist centres

Works collaboratively with nurses and all ITU staff as well as
colleagues in other clinical disciplines to deliver the highest standard
of clinical care

Communicates effectively and relates with empathy to family and
close friends of patients

Varices Development

Endoscopic Variceal LigationRole of beta blockers if had EVL for primary prophylaxis unkown (no dec. in rebleed rate but less likely to get recurrent varices)Surgical Portal Decompression—Abandoned as medical treatment does better and high encephalopathy ratesNitrates — Not recommended for primary prophylaxisCombination Therapy: Beta blockers lead to unopposed alpha adrenergic activity, which inc. splanchnic arterial pressure (with reduced portal pressure) but also causes inc. portohepatic outflow resistance (reducing net benefit on portal pressure)- this can be counteracted with nitrates Nitrates alone may be non-inferior to beta-blocker alone.Endoscopic Sclerotherapy- Not recommendedTIPS should not be used for primary prophylaxis of variceal hemorrhageBeta blockers: Block dilation in mesenteric arteries - hepatoportal venous gradient reduced by 15%Only used for prophylaxis against a first variceal hemorrhageReduces the risk of first variceal bleeding by 50 %.Reduces the likelihood of progression of small to large varices.Death due to variceal bleed lessFailure of beta blocker to prevent bleeding was associated with younger age, large variceal size, advanced liver failure, and lower doses of propranolol Monitoring response —Ideally monitor HVPG to <12 mmHg/ resting heart rate 55- 60 bpm Beta blockers can decrease renal blood flow; thus, renal function should be monitoredIn those patients in whom the pulse rate remains high despite large doses of beta blockers, measurement of the HVPG should be considered to guide further therapyConsider poor compliance in these individualsSide effects —In cirrhosis- bronchoconstriction, heart failure, and impotenceBeta blockers rarely induce liver failure from decreased portal blood flow because total hepatic blood flow is usually maintained by an increase in hepatic arterial flow Formation Of VaricesPortal hypertension (= hydrostatic pressure >5 mmHg) due to obstructed portal venous outflow which can be presinusoidal (portal vein thrombosis, portal fibrosis, or infiltrative lesions), sinusoidal (cirrhosis), or postsinusoidal (veno-occlusive disease, Budd Chiari syndrome)Most comon cause =cirrhosis.Varices occur when the pressure difference between portal and hepatic veins > 12 mmHg . Predictive factors For 1st BleedClinical features Child-Pugh scoreEndoscopic red wale signs1/3rd rebleed within 6wks (50% of these occur in the first 48 hours), 1/3rd after 6 weeksThe risk of early rebleeding is greatest in the first 48 hours after admission and declines subsequently Need OGD as soon as cirrhosis diagnosis made Cirrhotics without varices need 3 yearly OGD only and no beta-blockersIf decompensated, screening OGD yearly Secondary Prophylaxis Recommendations:-Use beta blockers if small varices present (<5mm) and increased risk of bleeding (Child-Pugh B/C, red whale marks). Consider using if not increased risk of bleeding.Dont need follow up OGD.-If the patient cant have beta blockers, repeat OGD every 2 years and annually if decompensated.-Medium/large varices with bleeding risk-can have either beta blocker or banding.-If not high risk for bleeding, give beta-blockers first, and band if beta blockers are contraindicated.-Patients on beta blockers dont need follow-up OGD.-If a patient is treated with EVL, it should berepeated every 1-2 weeks until obliteration with the first surveillance EGD performed 1-3 months after oblitera-tion and then every 6-12 months to check for variceal recurrence.-Nitrates (either alone/ in combination with Beta -blockers), shunt therapy, or sclerotherapy should not be used in primary prophylaxis of variceal haemorrhage. Small varices progressed in size at a rate of 12 % in year one, and 31 % at year three. Progression was predicted by:Child-Pugh scorePresence of red wale marks on the first examinationAlcoholic cause of cirrhosis. Increasing size of varix New varices developed in 5 % at year one, and 28 % at year three. Duration of cirrhosis New varices incidence once cirrhosis established Location of varicesOesophageal: Deep within the submucosa in the mid-esophagus; progressively more superficial in distal esophagus (more likely to bleed)Gastric: Location correlates risk of hemorrhage:Isolated gastric varices in the fundus (IGV1) less frequent than GOVs (10 v 90 %). IGV1 is the most likely to bleedSizeF1: Small straight varices F2: Enlarged tortuous varices that occupy less than one-third of the lumen F3: Large coil-shaped varices that occupy more than one-third of the lumen Appearance of varicesRed wale marks are longitudinal red streaks on varices that resemble red corduroy wales. Cherry red spots are discrete red cherry-colored spots that are flat and overlie varices. Hematocystic spots are raised discrete red spots overlying varices that resemble "blood blisters." GOV1: Continuous with oesophagus lesser curve GOV2: Continu-ous with oesophagus greater curve Isolated gastric varix 1 Isolated gastric varix 2 Varices Development Year 2 Year 1 Recommendations Recommendations Primary prophylaxis against variceal haemorrhage in patients with cirrhosis Portal v. SMV IMV Splenic vein Gastric v. Written by Dr Sebastian Zeki

Related Stories

Naringenin affords protection against lipopolysaccharide/D-galactosamine-induced acute liver failure: Role of autophagy

Percutaneous transhepatic treatment for biliary stricture after duct-to-duct biliary anastomosis in living donor liver transplantation: a 9-year single-center experience

Clinical use of N-acetyl cysteine during liver transplantation: Implications of oxidative stress and inflammation as therapeutic targets

Investigation of Inherited Chromosomally Integrated Human Herpesvirus-6A+ and -6B+ in a Patient with Ulipristal Acetate-Induced Fulminant Hepatic Failure

COVID-19: Multiorgan Dissemination of SARS-CoV-2 Is Driven by Pulmonary Factors