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    Home > Active Ingredient News > Digestive System Information > One article: chest complications of liver cirrhosis | Clinical Essentials

    One article: chest complications of liver cirrhosis | Clinical Essentials

    • Last Update: 2021-04-18
    • Source: Internet
    • Author: User
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    Cirrhosis is a slowly progressing disease characterized by the replacement of healthy liver parenchyma by scars and fibrotic tissue.

    Patients with liver cirrhosis may have different chest complications.
    This article will sort out these complications.

    Hepatopulmonary syndrome Hepatopulmonary syndrome (HPS) is seen in 4%-29% of patients with liver cirrhosis.
    It is caused by liver disease, increased alveolar-arterial oxygen gradient (hypoxemia) and lung The triad of vasodilatation.

    The disease is clinically manifested as progressive dyspnea, cyanosis and clubbing.

    Generally speaking, the long-term survival rate of HPS patients with PaO2<50 mmHg at baseline is lower.

    Regardless of the severity of hypoxemia, HPS is an indication for orthotopic liver transplantation (OLT).

    The pathogenesis of HPS has not yet been fully clarified.
    Most scholars believe that vasodilation/shunt in the lung is the main pathogenesis of HPS.

    In portal hypertension and liver dysfunction, vasoactive substances reduce fire extinguishing but increase production, the proportion of vasoconstrictor and vasodilator substances in the lung is imbalanced, or the sensitivity of pulmonary blood vessels to it changes; inflammation of macrophages and monocytes in the lungs Sex cells accumulate and release more inflammatory mediators.
    The above factors can cause vasodilation/shunt in the lungs, imbalance of alveolar ventilation-blood flow, and diffusion disorders, leading to hypoxemia.

    Portal pulmonary hypertension (POPH) is a disease characterized by increased mean pulmonary arterial pressure (mPAP) and increased pulmonary vascular resistance (PVR) on the basis of portal hypertension in patients with or without advanced liver disease.
    It is currently classified as a subtype of pulmonary arterial hypertension (PAH).

    About 2% -5% of patients with liver cirrhosis will develop POPH.

    The diagnostic criteria for POPH are: mPAP>25 mmHg and pulmonary capillary wedge pressure <15mmHg, and it has the characteristics of portal hypertension.

    The possible causes of POPH are: (1) the release of vasoactive substances (serotonin, interleukin-1, endothelin-1) can cause pulmonary artery vasoconstriction; (2) blood clots from the portal vein can be The portosystemic shunt to the pulmonary circulation leads to venous thromboembolism, leading to pulmonary hypertension; (3) The high cardiac output associated with liver cirrhosis exposes the pulmonary vascular bed to increased shear stress, which leads to hypertrophy and proliferation of pulmonary artery endothelial cells, and ultimately leads to vasoconstriction.

    Severe pulmonary hypertension in patients with liver cirrhosis is a sign of poor prognosis.

    Clinically, patients usually experience progressive dyspnea when exerting force.

    Other less common symptoms are fatigue, palpitations, fainting, or chest pain.

    Hepatic pleural effusion Hepatic pleural effusion is seen in 5%-10% of patients with liver cirrhosis.
    It is defined as patients with cirrhosis and portal hypertension.
    In the absence of heart, lung, kidney and other diseases, obvious pleural effusion occurs, which mostly occurs on the right side.
    Side (>500 ml).

    The etiology of hepatic pleural effusion is diverse, and may include: hypoalbuminemia caused colloidal osmotic pressure, ascites leakage through the diaphragm defect (congenital defect or diaphragmatic vesicle rupture), and increased lymphatic drainage.

    Most patients with hepatic pleural effusion have symptoms of ascites, portal hypertension, and end-stage liver disease.
    The most common symptoms are dyspnea, cough, nausea, and pleuritic chest pain.

    However, some patients may be asymptomatic.

    Pleural cavity infection-called spontaneous bacterial empyema (SBEM) or spontaneous bacterial pleurisy (SBPL)-is the main potential complication of hepatic pleural effusion.

    Spontaneous bacterial pleurisy As mentioned earlier, spontaneous bacterial pleurisy (SBPL) can occur in patients with hepatic pleural effusion and requires high clinical suspicion.

    Clinical manifestations include fever, pleuritic chest pain, deterioration of clinical status, or encephalopathy.

    After excluding the effusion around pneumonia, when the polymorphonuclear cell count is more than 500 cells/mm3, or the pleural fluid culture is positive and the cell count is more than 250 cells/mm3, SBPL can be diagnosed.

    Common pathogens are Escherichia coli, Streptococcus, Enterococcus, Klebsiella and Pseudomonas.

    Portal systemic collateral circulation in the thoracic cavity After the formation of portal hypertension in liver cirrhosis, part of the blood in the portal venous system flows back from the liver, and enters the lower-pressure systemic circulation through the collateral vessels between the portals, forming multiple portal circulation pathways, common portal pathways There are esophageal and (or) gastric varices caused by the left gastric and short gastric veins, umbilical veins and umbilical veins caused by abdominal wall veins and varicose and inferior mesenteric vein access caused by the formation of the lower rectal venous plexus.

    In addition, there are some rare collateral circulations, including: splenorenal venous shunt, gastro-renal venous shunt, retroperitoneal venous shunt, septal venous shunt, etc.

    Lung infections.
    Patients with chronic liver disease have poor immune status, which makes them more susceptible to various bacteria, fungi and viruses that cause lung infections.

    Patients with decompensated liver cirrhosis are more likely to develop infections than patients with compensated liver.

    The common infection in patients with liver cirrhosis is spontaneous bacterial peritonitis (25%), followed by urinary tract infection (20%), pneumonia (15%), postoperative sepsis, cellulitis, and spontaneous sepsis.

    The most common bacterial microorganism is Streptococcus pneumoniae.

    Other pathogens are Haemophilus influenzae, Pseudomonas aeruginosa, Klebsiella pneumoniae, Mycoplasma and Legionella.

    Hospital-acquired pneumonia is mainly caused by Gram-negative bacilli and Staphylococcus.

    Tuberculosis infection in patients with liver cirrhosis affects the outside of the lung more often than other infections.

    Due to low immune function, cytomegalovirus (CMV) infection in patients with liver cirrhosis can also lead to viral lung infections.

    Drug-induced pulmonary complication Sarcoidosis is a rare complication of interferon therapy, the exact mechanism of which is unclear.

    Although any organ system can be affected, the lungs and mediastinal lymph nodes are the most common sites of involvement.

    Inflammation and autoimmune-related complications Primary biliary cholangitis is an autoimmune liver disease characterized by cholestasis and bile duct fibrosis, which may eventually progress to liver cirrhosis.

    The possible related lung manifestations are pleural effusion, lymphocytic interstitial pneumonia, sarcoidosis, pulmonary fibrosis, intrapulmonary granuloma, cryptogenic organizing pneumonia, obstructive airway disease, pulmonary hypertension, liver Pulmonary syndrome and pulmonary hemorrhage.

    Muscular dystrophy/sarcopenia sarcopenia (or severe muscle atrophy) is one of the common but relatively insidious complications, which has a negative impact on the survival rate and quality of life of patients.

    Patients with advanced liver cirrhosis usually have severe protein consumption and muscle mass loss.
    This loss of muscle mass affects peripheral muscles and respiratory muscles, and may cause chronic dyspnea in patients with liver cirrhosis.

    Tension ascites dyspnea is a common symptom in patients with liver cirrhosis.
    Tension ascites causes dyspnea and shortness of breath due to restricted venous return of the lower extremities (inferior vena cava compression) and impaired lung expansion (elevated diaphragm and mechanical pressure) . References (slide down): [1] Sureka B, Bansal K, Patidar Y, Kumar S, Arora A.
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    Clinical characteristics of collateral circulation in rare cases of liver cirrhosis[J].
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