Liver Shrinkage (Cirrhosis): Complications

The following are the most important diseases or complications that may be contributed to by liver cirrhosis (liver shrinkage):

Respiratory system (J00-J99)

  • Hepatopulmonary syndrome (HPS) – vascular dilatation in the pulmonary circulation with development of a right-to-left shunt, resulting in arterial hypoxemia (lack of oxygen in the blood).

Blood, blood-forming organs – immune system (D50-D90).

  • Hemorrhagic diathesis (coagulation disorders).
  • Hypersplenism – complication of splenomegaly; leads to an increase in functional capacity beyond what is necessary; as a result, there is excessive elimination of erythrocytes (red blood cells), leukocytes (white blood cells), and platelets (blood platelets) from the peripheral blood, resulting in pancytopenia (synonym: tricytopenia; reduction of all three cell series in the blood)
  • Bone marrow suppression – reduction of bone marrow resulting in decreased synthesis of blood cells.

Endocrine, nutritional and metabolic diseases (E00-E90).

  • Diabetes mellitus (diabetes).
  • Hyperlipidemia/dyslipidemia (lipid metabolism disorders).
    • HDL cholesterol lowering
  • Hypogonadism (hypofunction of the gonads)
  • Hyponatremia (sodium deficiency)
  • Malnutrition
  • Metabolic acidosis

Cardiovascular system (I00-I99)

  • Fundus varices – outpouching of the veins in the area of the gastric dome (fundus gastricus).
  • Esophageal varices – bulging of the veins in the esophagus (esophagus) due to increased pressure in the venous system; there is a risk of esophageal variceal hemorrhage
  • Esophageal variceal hemorrhage; frequency of hemorrhage dependent on Child-Pugh stage:
    • Child A cirrhosis: 20-40%.
    • Child C cirrhosis: – 85 %
  • Cirrhotic cardiomyopathy (cirrhosis-related myocardial disease).

Liver, gallbladder, and bile ducts-pancreas (pancreas) (K70-K77; K80-K87).

  • Acute-on-chronic liver failure (ACLF) – acute hepatic decompensation of preexisting chronic liver disease with consecutive organ failure. Short-term survival is very poor and stage-dependent. Triggers are bacterial infections, which in this case lead to systemic inflammation (inflammation), It is a relatively new entity.
  • Acute liver failure (ALV):
    • Severe hepatic dysfunction with icterus (jaundice) and consecutive coagulopathy (INR > 1.5).
    • Hepatic encephalopathy (HE; see below).
    • Exclusion of preexisting chronic liver disease.
    • Symptom duration <26 weeks; fulminant: <7 days, protracted >4 weeks.
  • Acute hepatic decompensation of preexisting chronic liver disease.
  • Cholecystolithiasis (gallstones)
  • Chronic pancreatitis (inflammation of the pancreas).
  • Coma hepaticum (hepatic coma)
  • Hemorrhoidal disease (hemorrhoids)
  • Hepatorenal syndrome (HRS) – functional, in principle fully reversible decrease in glomerular filtration rate (total volume of primary urine at, which is filtered by all glomeruli (renal corpuscles) of both kidneys together, in a defined unit of time, is filtered) resulting in oliguric renal failure (in oliguric renal failure, the kidneys give < 500 ml of urine production / day) in patients with liver cirrhosis (irreversible damage to the liver and a pronounced remodeling of liver tissue) or fulminant hepatitis (liver inflammation) in the absence of evidence of other causes of renal failure (slowly progressive reduction in renal function).
  • Hepatic insufficiency (liver weakness).
  • Portal hypertension (portal hypertension; permanent increase in pressure in the portal vein > 10 mmHg); 15% of these patients develop spontaneous bacterial peritonitis/peritonitis
  • Terminal chronic liver failure (late stage of liver cirrhosis).

Mouth, esophagus (food pipe), stomach, and intestines (K00-K67; K90-K93).

  • Portal hypertension (portal vein hypertension) – clinically relevant when there is a permanent increase in pressure of > 10 mmHg in the vena portae (portal vein).
  • Portal hypertensive gastropathy (congestive gastritis → diffuse mucosal bleeding of the stomach) – gastric mucosal damage due to portal hypertension; may lead to oozing bleeding.
  • Spontaneous bacterial peritonitis (SBP)-infection of ascites without apparent cause; course in most cases asymptomatic, i.e., without symptoms; lethality (mortality related to the total number of people with the disease) approx. 50% [detection of > 250 segement-nucleated granulocytes/μL ascites and/or bacteria in ascites]Note: In any deterioration of the general condition of patients with liver cirrhosis and ascites, new complications or pathological blood findings, a diagnostic puncture must be performed early to exclude SBP!
  • Congestive enteropathy (congestive disease of the intestinal mucosa).
  • Stasis gastritis (inflammation of the stomach due to congestion of the gastric veins).

Musculoskeletal system and connective tissue (M00-M99).

  • Dupuytren’s contracture – flexion contracture of the fingers.
  • Muscular atrophy (muscle atrophy)

Neoplasms – tumor diseases (C00-D48)

  • Hepatocellular carcinoma (HCC; hepatocellular carcinoma) – liver cirrhosis is considered precancerous (precancerous); 15% develop hepatocellular carcinoma within 5 years; up to one-third of all patients with liver cirrhosis develop HCC

Psyche – Nervous System (F00-F99; G00-G99).

  • Hepatic encephalopathy (HE) – pathological, noninflammatory change in the brain due to severe liver dysfunction; most common complication of liver cirrhosis, with broad spectrum of neuropsychiatric disorders (impairment of: Consciousness; memory and cognition; motor ability; personality).

Symptoms and abnormal clinical and laboratory parameters, not elsewhere classified (R00-R99).

  • Ascites (abdominal fluid)
  • Icterus (jaundice), hepatocellular – see below jaundice/lab diagnostics.
  • Splenomegaly (splenomegaly).

Prognostic factors

  • Hyponatremia (sodium deficiency) – considered to be an extremely unfavorable prognostic marker.
  • Malnutrition