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home - Liver - Vascular Problems - Hepatic Infarction Written by Dr Sebastian Zeki
Knowledge


Understands the risk of variceal bleeding as a complication of with
portal hypertension


Knows risk of variceal haemorrhage in cirrhotics who have not bled

Knows risk of bleeding related to variceal size endoscopic findings
and severity of liver dysfunction


Knows range of therapeutic options (both endoscopic and
pharmacological).

Skills
Recognises and can treat portal hypertension.
Behaviours
Manages patients with oesophageal varices with skill and
compassion

Able to convey the serious risks to patients and their relatives.

Also...

Knowledge


Recognises and shows understanding of vascular liver disease
including Budd-Chiari syndrome veno-occlusive disease and
portomesenteric venous thrombosis; understands the underlying
anatomy and physiology of these often complex conditions

Aware of need for investigation for associated myeloproliferative and
procoagulant conditions

Understands the role of anticoagulation and indications for further
intervention including TIPS surgery or transplantation

Skills
Can make careful clinical of these conditions and has
heightened awareness of liver vascular disease in differential
diagnosis

Able to make a potentially difficult diagnosis of less common variants
of vascular conditions

Behaviours
Shows ability to keep patient and relatives informed and to refer
appropriately for specialist management

Hepatic Infarction

Hepatic Infarction(=focal ischemic injury of the liver. Ischaemic hepatitis is diffuse injury)Usually due to occlusion of a single intrahepatic branch of the hepatic artery and usually right lobeCan be detected on imaging/ transient rise in ALT with leukocytosis/ symptoms similar to cholangitis but not all need to be present Ca Ca Ca Ca zone 3 acinus Z o n e 2 a c i n u s ManagementManage cause and treat conservatively.Asymptomatic patients are managed conservatively.Patients who develop hepatic infarction after liver transplan-tation require urgent retransplantation. Serial CT scans may show resolution of the infarct over weeks, residual scarring, calcification, or atrophy of the involved lobe of liver PathologyCentral zone of complete coagulative necrosis involving hepatocytes, portal tracts, and central veins, surrounded by a zone of inflamm-tory reaction, surrounded by a zone of partial necrosis.The involvement of all three zones of the hepatic acinus is markedly different from the histologic pattern seen in ischemic hepatitis, in which necrosis is confined predominantly to zone 3. DiagnosisContrast enhanced CT: focal, wedge-shaped lesion of low attenuation, which may extend to the capsular surface of the liver (can be different shapes such as oval and can change shape).Characteristics:No gas; Doesn’t displace vessels; Can get other associated infarcts (splenic/ renal).MRI: Wedge-shaped region of diminished T1 signal and increased T2 signal, a finding that is relatively nonspecific.A Doppler ultrasound should be performed to assess the patency of the hepatic artery. Aetiologies: Iatrogenic ligation of usually the right hepatic artery post lap chole.Thrombosis due to atherosclerosis, a hypercoagulable state, or liver transplantation (at anastomosis between native and donor arteries).Embolization eg from infective endocarditis, tumor embolism, or therapeutic embolization or chemoembolization.RFA. Haemodynamic instability;Thrombosis Also described in severe respiratory failure, systemic hypoxemia, and obstructive sleep apneaUsually asymptomatic50% get reversible hepatopulmonary syndrome (from intrapulmonary hypertension) ManagementAim to restore haemodynamic stability. PathologyThe histologic hallmark of ischaemic hepatitis is necrosis of hepatocytes in zone 3 of the hepatic acinus with some architectural collapse around the central vein, depending upon the duration and extent of ischaemia.With severe prolonged ischaemia, necrosis may extend to the mid zonal hepatocytes.In rare patients, the necrosis is predominantly mid zonal.There are characteristically few inflammatory cells.There may also be signs of passive congestion.Despite extensive injury, hepatic architecture may return to normal after recovery from the ischaemic event. ALT rise peaks 2-3 days after insult usually returning to normal within 7-10 days.Bili < 4x ULN usually beginning its rise after aminotransferase levels have begun to decline.ALP < x2 ULNHepatic synthetic function usually remains normal or is only mildly impaired; the PT usually < 3s 7-10 days) Ischaemic hepatitis(hypoxic hepatitis) Features suggesting ischaemia rather than viral infection:An early rapid rise in the serum LDH level.A ratio of ALT: LDH of < 1.5 early on.A rapid fall in ALT after rapid rise.Accompanying ATN kidney (rise in creatinine). PrognosisThe prognosis is mostly related to the severity of the underlying systemic disease. Causes Hepatic artery damage due to..... Other causes: toxemia of pregnancy (with assoc hepatic bleed-ing), sickle cell anemia, polyarteritis nodosa, hepatic artery aneu-rysms, cocaine toxicity, and aortic dissection.) Clinical manifestations Written by Dr Sebastian Zeki

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