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acute fatty liver with pregnancy

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it is rare but catastrophic pregnancy related condition, know about it but get pleased not to meet it

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acute fatty liver with pregnancy

  1. 1. Acute Fatty Liver With Pregnancy Dr. Mohammed Abdalla Egypt, Domiat General Hospital
  2. 2. Historical points • (AFLP) was first identified by Sheehan in 1940 • Cc by microvascular steatosis in liver.
  3. 3. Incidence and Characteristics once in every 7,000 to 11,000 deliveries
  4. 4. • Acute fatty liver of pregnancy most frequently complicates the third trimester and is commonly associated (or complicated ) with preeclampsia (50 to 100 percent). Incidence and Characteristics
  5. 5. Incidence : 1/7000 -11,000 Age, (mean, range) 26 (16-39) Primiparous (%): 67 Male baby (%) :60 Onset week of pregnancy :33% (28-38) Mortality (%): ( Maternal )18% - ( Fetal) 47% Incidence and Characteristics
  6. 6. Liver Function Tests liver function tests” describes a panel of laboratory tests profiling discrete aspects of liver function No single liver function test is available to quantify liver disease
  7. 7. • Pregnancy causes very few alterations in the results of standard liver tests. The aminotransferases (AST and ALT), γ-glutamyl transpeptidase (GGTP), total bilirubin, and serum bile acid level remain within the normal range. • The alkaline phosphatase rises modestly in the third trimester. • The albumin level is lower than in nonpregnant women, and the cholesterol level higher Liver Function Tests
  8. 8. • aspartate aminotransferase (AST) • and alanine aminotransferase (ALT) evaluate Liver cell injury or necrosis Liver Function Tests •Marked ALT elevation (viral hepatitis) •Moderate ALT elevation (drug-induced hepatotoxicity, hyperemesis gravidarum, cholelithiasis, HELLP .AFLP.)
  9. 9. evaluate liver synthetic function (are depressed in cirrhosis or severe acute liver disease) Liver Function Tests albumin level prothrombin time
  10. 10. alkaline phosphatase,  bilirubin, gamma glutamyl transpeptidase Liver function tests In normal pregnancies, alkaline phosphatase levels may be elevated three- to fourfold, secondary to placental alkaline phosphatase levels evaluate Cholestasis and biliary obstruction
  11. 11. Pathogenesis The etiology is not known precisely.
  12. 12. •A genetic component has been suggested •Recent research suggests that AFLP is associated with a Glu474Gln mutation in the long-chain 3-hydroxy acyl-coenzyme A dehydrogenase (LCHAD), a fatty acid β oxidation enzyme. Pathogenesis This gene mutation is recessive; therefore, outside of pregnancy under normal physiological conditions, women have normal fatty acid oxidation.
  13. 13. • Recent studies document that infants born of affected pregnancies can be deficient in one of the enzymes of mitochondrial beta oxidation of fatty acids, long chain 3- hydroxyl-acyl CoA dehydrogenase (LCHAD) . Affected infants are at risk for developing nonketotic hypoglycemic coma, often with death Pathogenesis
  14. 14. Differential Diagnoses • Drug-Induced Hepatotoxicity • Eclampsia • HELLP Syndrome • Hepatitis, Viral • Preeclampsia • Toxicity, Acetaminophen
  15. 15. CLINICAL PRESENTATION Vomiting 80 Abdominal pain 52 Jaundice 93 Encephalopathy 87 Polydipsia 80 Pruritus 60 Ascitis 47 Symptoms/ Signs %
  16. 16. with or without polyuria, frequently is an early symptom in AFLP. polydipsia,
  17. 17. The patient may drink 2 or 3 liters of liquids overnight. it often exceeds the magnitude of vomiting. It has been interpreted as a transient diabetes insipidus. polydipsia,
  18. 18. jaundice Hyperbilirubinemia resulting in jaundice is rarely encountered in patients with severe preeclampsia. When jaundice is present in pregnancy, AFLP should be high on the differential.
  19. 19. • After hours or a few days, some patients become lethargic and may decline into hepatic coma, or milder degrees of mental impairment. Lethargy and encephalopathy
  20. 20. ascitis Usually transient and rarely prominent.
  21. 21. After delivery, most patients improve slowly, and a full clinical and laboratory recovery may take from 1 to 4 weeks. But marked deterioration after delivery has been observed
  22. 22. LABORATORY FEATURES • Liver test abnormalities  conjugated hyperbilirubinemia (usually between 5 and 15 mg/dL)  increased alkaline phosphatase (normal <170)  and modest increases in serum aminotransferases normal <50 (usually<1000 IU/L)  Leukocytosis occurs commonly  thrombocytopenia  decreased clotting factors  Hypoglycemia and renal dysfunction
  23. 23. Histopathology fatty metamorphosis by liver biopsy: •Sherlock S. Acute fatty liver of pregnancy and the microvesicular fat diseases. Gut 1983;24:265-9. The hepatic architecture is intact and the lobules are swollen with compressed sinusoids Centrilobular microvesicular fatty infiltration of hepatocytes ballooning of hepatocytes
  24. 24. In contrast with viral hepatitis and other common causes of fulminant hepatic failure, necrosis of hepatocytes is always minor . Vigil-De Gracia P, Lavergne JA. Acute fatty liver of pregnancy. Int J Gynaecol Obstet 2001;72:193-5. Histopathology
  25. 25. Complications cerebral edema, renal failure (60%), hypoglycemia (53%),  infections (45%) gastrointestinal hemorrhage (33%), coagulopathy (30%), fetal death severe postpartum hemorrhage
  26. 26. The upper gastrointestinal hemorrhage may be caused by Mallory-Weiss syndrome, acute gastric or duodenal lesions (e.g., gastritis, duodenitis, peptic ulcers), or it can be a manifestation of a coagulopathy. •Cano RI, Delman MR, Pitchumoni CS, et al: Acute fatty liver of pregnancy. Complication by disseminated intravascular coagulation •Killam AP, Dillard SH, Patton RC, et al: Pregnancy-induced hypertension complicated by acute liver disease and disseminated intravascular coagulation. Am J Obstet Gynecol 123:823, 1975
  27. 27. renal involvement is less severe than with toxemia (a mild proteinuria ,mild edema and a mild increase in blood urea nitrogen and creatinine).
  28. 28. When renal failure is aggravated, it usually is impossible to distinguish from toxemia.
  29. 29. A severe hypoglycemia often appears at any stage of the disease, or even during clinical recovery.
  30. 30. Ascites, detected clinically or by ultrasound, is transient and rarely prominent.
  31. 31. Maternal mortality (18%) usually is attributed to one of its complications (gastrointestinal hemorrhage, bleeding disorder, renal failure, acute pancreatitis) but not to liver failure alone.
  32. 32. It often is impossible to immediately perform a liver biopsy in pregnant patients with severe coagulation abnormalities. next
  33. 33. Therefore, in many cases, it is necessary to rely on the clinical and laboratory data and, in the physician's and obstetrician's experience, next
  34. 34. the emergency therapeutic decisions usually are made without waiting for a histologically proven diagnosis.
  35. 35. Liver biopsy is not indicated for diagnosis
  36. 36. • Ultrasound is most important in the exclusion of biliary tract disorders, but its value and the value of CT and MR imaging, has been considered limited and not helpful for the diagnosis and management of patients with AFLP.
  37. 37. The mild jaundice. and modest increase in serum aminotransferases are important signs the diagnosis of. fulminant hepatitis (viral or toxic).
  38. 38. Aspartate transaminase (AST) and alanine transaminase (ALT) • Aspartate transaminase (AST) and alanine transaminase (ALT) are not elevated in normal pregnancies. These can become elevated in many different conditions during pregnancy. Some are unique to pregnancy, such as preeclampsia/eclampsia, HELLP, and AFLP. High levels of ALT can be seen in patients with viral hepatitis; however, the highest levels are seen in patients with acute toxic liver injury, as can be seen in acetaminophen overdose . Both AST and ALT can be elevated due to the hepatic injury.
  39. 39. the mild increase in blood pressure, hyperuricemia, and the intense thirst are in fulminant hepatitis. and they favor the diagnosis of acute fatty liver of pregnancy.
  40. 40. No specific treatment
  41. 41. All patients should be hospitalized as soon as the diagnosis of AFLP is suspected
  42. 42. Moderate or severely affected patients (encephalopathic, deeply jaundiced, with a prothrombin time less than 40% of the control), or with any extrahepatic complications, should be attended in intensive care units.
  43. 43. it seems convenient to maintain glucose infusions . Because of the risk of a sudden hypoglycemia until a full metabolic recovery is obtained.
  44. 44. • Two laboratory tests: prothrombin time and blood glucose, should be repeated at least daily, Prothrombin time helps to assess the prognosis of liver failure, and blood glucose detects a severe hypoglycemia.
  45. 45. Pregnancy termination (yes OR no ) next
  46. 46. importance of interrupting pregnancy may seem questionable, next
  47. 47. As it noticed in some patients that the disease does not immediately improve after delivery next
  48. 48. But also that no patient has yet been reported with a recovery before delivery. next
  49. 49. • Regional anesthesia may be obtained if a coagulopathy is not evident. However, if a coagulopathy is present, it should be corrected prior to regional anesthesia as bleeding at the puncture site is a concern. With general anesthesia, the anesthesiologist should be careful not to use agents that have potential hepatotoxicity, such as halothane. Isoflurane has no hepatotoxicity and may improve hepatic blood flow.
  50. 50. AFLP should be suspected when persistent vomiting, malaise, encephalopathy or jaundice appear in the final weeks of pregnancy or in the early puerperium.
  51. 51. Diagnosis is mainly based on clinical and laboratory grounds. Liver biopsy is usually confirmatory,if done.. the emergency therapeutic decisions usually are made without waiting for a histologically proven diagnosis.
  52. 52. AFLP is a medical and obstetric emergency because of the metabolic alterations and complications and because of the impending need to interrupt pregnancy.
  53. 53. close surveillance of future pregnancies in patients affected previously by this disease is recommended.
  54. 54. an impaired fatty acid metabolism during childhood. may affect babies born of pregnancies with AFLP.
  55. 55. Thank You Dr. Mohammed Abdalla EGYPT, Domiat general hospital
  • MonaBabiker1

    Nov. 6, 2020

it is rare but catastrophic pregnancy related condition, know about it but get pleased not to meet it

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