Journals / Haydarpaşa Numune Eğitim ve Araştırma Hastanesi Tıp Dergisi / 2011 / Cilt: 51 - Sayı: 1

Current approach to acute ischemic hepatitis

Akut iskemik hepatit güncel yaklaşım

Pages
41–45
Publication Date
2022-10-17
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Prognosis is usually associated with severity of the underlying systemic disease.

📌 3 Key Takeaways

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Objective & Hypothesis:Acute ischemic hepatitis, can occur due to sudden circulatory failure or hypoxia in the liver.
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Key Findings & Data:It regressed usually within 1 week and has subclinical course and a good prognosis, very rarely, fulminant course.
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Conclusion & Impact:Prognosis is usually associated with severity of the underlying systemic disease.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Acute ischemic hepatitis, can occur due to sudden circulatory failure or hypoxia in the liver. It regressed usually within 1 week and has subclinical course and a good prognosis, very rarely, fulminant course. The most common causes are systemic hypotension leading to cardiopulmonary collapse after myocardial infarction, decompensated congestive heart failure or pulmonary embolism. The hallmark finding of ischemic hepatitis is a massive increase in aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels 1 to 3 days after an episode of systemic hypotension. After obtaining hemodynamic stability, AST, ALT and LDH levels peak within 1 to 3 days and return to normal within 7 to 10 days. LDH level tends to rise quickly and ALT / LDH ratio is less than 1.5 in ischemic hepatitis unlike other causes of acute hepatitis. There is no specific treatment for ischemic hepatitis. In these patients our aim is to rectify cardiac output and underlying situation of hemodynamic deterioration. Prognosis is usually associated with severity of the underlying systemic disease.

Özet

Akut iskemik hepatit; karaciğerde ani gelişen dolaşım yetmezliği veya hipoksiye bağlı olarak gelişir. Genellikle 1 hafta içinde gerileyen, subklinik seyirli ve iyi prognoza sahiptir, çok nadir olarak fulminan seyredebilir. En yaygın nedenler sistemik hipotansiyona yol açan myokard enfarktüsü sonrası kardiyopulmoner kollaps, dekompanse konjestif kalp yetmezliği veya pulmoner embolidir. ‹skemik hepatitin ayırıcı özeliği aspartat aminotransferaz (AST), alanin aminotransferaz (ALT) ve laktat dehidrogenez (LDH) düzeyinin bir hipotansiyon atağından 1 ile 3 gün sonrasında aşırı artışıdır. Hemodinamik stabilite sağlandıktan sonra AST, ALT ve LDH düzeyleri 1 ile 3 gün içerisinde pik yapar ve 7 ile 10 gün içinde normale döner. LDH düzeyi hızlı şekilde artmaya eğilimlidir ve ALT/LDH oranı akut hepatitin diğer nedenlerinden farklı olarak iskemik hepatit de 1.5’in altındadır. İskemik hepatit için spesifik bir tedavi yoktur. Bu hastalarda amacımız kardiak outputu düzeltmek ve dolayısıyla hemodinamik bozukluğun altında yatan durumu düzeltmek olmalıdır. Prognoz çoğunlukla altta yatan sistemik hastalığın ağırlığı ile ilişkilidir.

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Cite This Article

KARATOPRAK, C., KAYATAŞ, K., TEPE, M., UYAR, S., DEMİRTUNÇ, R. (2022). Current approach to acute ischemic hepatitis. Haydarpaşa Numune Eğitim ve Araştırma Hastanesi Tıp Dergisi, Cilt: 51 - Sayı: 1, 41–45. https://ajindex.com/articles/535440

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References (1)

  1. Mandell, Douglas, and Bennett’s. Principles and Practice of Infectious Diseases, 7th ed. Churchill Livingstone, An Imprint of Elsevier 2009 2. Schafer DF, Sorrel MF. Vascular disease of the liver. Gastrointestinal and Liver Disease. Eds Feldman M, Fridman LS, Sleisenger MH, 7th ed. WB Saunders Co, Philadelphia 2002; 70: 1364-70. 3. Henrion J, Schapira M, Luwaert R, et al. Hypoxic hepatitis: clinical and hemodynamic study in 142 consecutive cases. Medicine (Baltimore) 2003;82: 392–406. 4. Giallourakis CC, Rosenberg PM, Friedman LS. The liver in heart failure. Clin Liver Dis 2002;6:947–67. 5. Seeto RK, Fenn B, Rockey DC. Ischemic hepatitis: clinical presentation and pathogenesis. Am J Med 2000;109:109–13. 6. Hickman PE, Potter JM. Mortality associated with ischaemic hepatitis. Aust N Z J Med 1990;20:32–4. 7. Fuchs S, Bogomolski-Yahalom V, Paltiel O, et al. Ischemic hepatitis: clinical and laboratory observations of 34 patients. J Clin Gastroenterol 1998;26:183–6. 8. Birrer R, Takuda Y, Takara T. Hypoxic hepatopathy: pathophysiology and prognosis. Intern Med 2007;46:1063–70. 9. Fuhrmann V, Madl C, Mueller C, et al. Hepatopulmonary syndrome in patients with hypoxic hepatitis. Gastroenterology 2006;131:69–75. 10. Cassidy WM, Reynolds TB. Serum lactate dehydrogenase in the differential diagnosis of acute hepatocellular injury. J Clin Gastroenterol 1994;19:118–21. 11. Anghern W, Schmid E, Althaus F, et al. Effect of dopamine on hepatosplanchnic flow. J Cardiovasc Pharmacol 1980;2:257–65. 12. Desai A, Kadleck D, Hufford L, et al. N-Acetylcysteine use in ischemic hepatitis. Am J Ther 2006;13:80–3. 13- Henrion J, Schapira M, Luwaert R, et al. Hypoxic hepatitis: clinical and hemodynamic study in 142 consecutive cases. Medicine (Baltimore) 2003;82: 392–406. 14. Fuhrmann V, Kneidinger N, Herkner H, et al. Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients. Intensive Care Med 2009;35:1397–405.