Fulminant hepatic failure in pregnancy: challenges, management strategies, prognosis and outcomes

Fulminant hepatic failure is defined as a sudden, severe impairment of hepatic function leading to an encephalopathy, which occurs within eight weeks of appearance of first symptoms in the absence of pre-existing liver disease. The spectrum of liver disease in pregnancy may range from mild asymptomatic transaminitis to fatal and irreversible deterioration in liver function leading to significant morbidity and even mortality. Hepatic dysfunction in pregnancy may be categorized into Pre-eclampsia-associated liver diseases such as pre-eclampsia/eclampsia, the HELLP syndrome and Acute fatty liver of pregnancy (AFLP), and other causes of hepatic dysfunction namely Hyperemesis gravidarum (HG) and Intrahepatic cholestasis of pregnancy (IHCP). For this review, a search was conducted for published articles, case reports and clinical trials in MEDLINE/Pubmed from 1970 to 2020 with the keyword’s fulminant hepatic failure, acute liver failure in pregnancy, pre-eclampsia, HELLP and AFLP. We concluded that fulminant hepatic failure is one of the most dreaded complications in pregnancy in obstetrical units worldwide. Mandatory screening for etiology, early diagnosis and initiation of supportive management as soon as possible are absolutely essential to ensure better maternal and fetal outcomes. Effective communication with the obstetrician regarding timely delivery/termination of pregnancy ensures a favourable prognosis in the majority of cases. Liver transplant is a definitive life-saving option for cases of severe fulminant hepatic failure in pregnancy, and management has to be suited to each patient individually, keeping in mind the well-being of both the mother, and the child.

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Fulminant Hepatic Failure Possibly Related to Ciprofloxacin

Annals of Pharmacotherapy ◽

10.1177/106002809202600504 ◽

1992 ◽

Vol 26 (5) ◽

pp. 636-639 ◽

Cited By ~ 40

Author(s):

Bradford K. Grassmick ◽

Victoria Tutag Lehr ◽

Alistair S. Sundareson

Keyword(s):

Fulminant Hepatic Failure ◽

Hepatic Failure ◽

Case Reports ◽

Data Extraction ◽

Hepatic Function ◽

Data Synthesis ◽

The Past ◽

Serum Aspartate Aminotransferase ◽

History Of ◽

Oral Ciprofloxacin

OBJECTIVE: To report a case of hepatic failure in a patient who was receiving oral ciprofloxacin. DATA SOURCES: Case reports, review articles, and relevant laboratory studies identified by MEDLINE. DATA EXTRACTION: Data were abstracted from pertinent published sources by one author and reviewed by the remaining authors. DATA SYNTHESIS: A 66-year-old man was admitted for hip arthroplasty and developed fulminant hepatic failure during oral ciprofloxacin therapy. Ciprofloxacin was started on postoperative day 13 for treatment of a urinary tract infection. Over the next three days he became confused and hypoglycemic. His prothrombin time increased to >90 s. Serum aspartate aminotransferase and alanine aminotransferase concentrations were markedly elevated. The patient died on postoperative day 20. Postmortem examination of the liver revealed extensive centrilobular necrosis. A skin biopsy was consistent with a drug reaction. It is unknown whether the patient had received a quinolone compound in the past or had a history of exposure to hepatotoxins. CONCLUSIONS: It cannot be concluded that ciprofloxacin directly caused hepatic failure in this patient. It is possible that the drug evoked a hypersensitivity reaction or exacerbated a preexisting hepatotoxicity. A detailed patient history and evaluation of hepatic function should be obtained prior to initiating ciprofloxacin therapy. A nonquinolone antimicrobial may be a safer alternative for patients with hepatic dysfunction.

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Drug-induced fulminant hepatic failure in pregnancy

Obstetric Medicine ◽

10.1177/1753495x15598909 ◽

2015 ◽

Vol 8 (4) ◽

pp. 190-192 ◽

Cited By ~ 3

Author(s):

Tabassum Firoz ◽

Douglas Webber ◽

Hilary Rowe

Keyword(s):

Liver Disease ◽

Liver Failure ◽

Fulminant Hepatic Failure ◽

Hepatic Failure ◽

Liver Enzymes ◽

Abnormal Liver Function ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Elevated Liver Enzymes ◽

In Pregnancy

Liver disease in pregnancy can be classified as predating, co-incidental or unique to pregnancy. Medications are often overlooked as a significant cause of liver disease. We present the case of a 39-year-old patient who presented at 20 weeks with jaundice, elevated liver enzymes, and abnormal liver function progressing eventually to fulminant hepatic failure. The patient was on methyldopa and labetalol from 12 weeks’ gestational age. Liver biopsy was consistent with drug-induced liver injury. Both methyldopa and labetalol have been associated with hepatotoxicity including liver failure. This case highlights the importance of including medications as a cause of liver failure in pregnant patients.

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Hepatitis E Associated Fulminant Hepatic Failure in Pregnancy: Feasibility of LDLT

10.26226/morressier.58eb975dd462b80290b4fbe5 ◽

2017 ◽

Author(s):

Sonali Saraf

Keyword(s):

Fulminant Hepatic Failure ◽

Hepatic Failure ◽

Hepatitis E ◽

In Pregnancy

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The liver in pregnancy

Emergencies in Gastroenterology and Hepatology ◽

10.1093/med/9780199231362.003.0019 ◽

2013 ◽

pp. 309-318

Author(s):

Daniel Marks ◽

Marcus Harbord

Keyword(s):

Liver Disease ◽

Hyperemesis Gravidarum ◽

Gallstone Disease ◽

Liver Function Tests ◽

The Other ◽

Liver Disorders ◽

Hepatic Rupture ◽

Chiari Syndrome ◽

Acute Fatty Liver ◽

In Pregnancy

Liver disease in pregnancy Liver function tests in pregnancy Hyperemesis gravidarum Obstetric cholestasis Acute fatty liver of pregnancy Pre-eclampsia HELLP syndrome Spontaneous hepatic rupture Gallstone disease Pancreatitis Budd–Chiari syndrome Viral hepatitis Pre-existing cirrhotic liver disease A number of liver disorders are unique to, or more likely to occur in, pregnancy. These should be considered alongside the other causes of liver disease that occur in non-pregnant patients. Transient mild derangements of LFT are common and rarely require further assessment beyond repeat monitoring to ensure normalization. However, liver disorders in pregnancy often present non-specifically and, therefore. all patients merit formal clinical assessment....

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Inherited diseases of copper metabolism: Wilson’s disease and Menkes’ disease

Oxford Textbook of Medicine ◽

10.1093/med/9780198746690.003.0234 ◽

2020 ◽

pp. 2115-2120

Author(s):

Michael L. Schilsky ◽

Pramod K. Mistry

Keyword(s):

Liver Disease ◽

Fulminant Hepatic Failure ◽

Hepatic Failure ◽

Wilson’S Disease ◽

Menkes Disease ◽

Wilson's Disease ◽

Copper Transport ◽

Loss Of Function ◽

Copper Excretion ◽

P Type

Copper is an essential metal that is an important cofactor for many proteins and enzymes. Two related genetic defects in copper transport have been described, each with distinct phenotypes. Wilson’s disease—an uncommon disorder (1 in 30 000) caused by autosomal recessive loss-of-function mutations in a metal-transporting P-type ATPase (ATP7B) that result in defective copper excretion into bile and hence copper toxicity. Typical presentation is in the second and third decade of life with liver disease (ranging from asymptomatic to acute fulminant hepatic failure or chronic end-stage liver disease) or neurological or psychiatric disorder (dystonia, dysarthria, parkinsonian tremor, movement disorder, a spectrum of psychiatric ailments). While no single biochemical test or clinical finding is sufficient for establishing the diagnosis, typical findings include low serum ceruloplasmin, high urinary copper excretion, and elevated liver copper content. Corneal Kayser–Fleischer rings may be seen. Treatment is with copper chelating agents and zinc. Liver transplantation is required for fulminant hepatic failure and decompensated liver disease unresponsive to medical therapy. Menkes’ disease—a rare disorder (1 in 300 000) caused by X-linked loss-of-function mutations in a P-type ATPase homologous to ATP7B (ATP7A) that result in defective copper transport across intestine, placenta, and brain and hence cellular copper deficiency. Clinical presentation is in infancy with facial dimorphism, connective tissue disorder, hypopigmentation, abnormal hair, seizures, and failure to thrive, usually followed by death by age 3 years (although some variants with a milder phenotype result from milder mutations, e.g. occipital horn syndrome). Treatment, which is only effective when presymptomatic diagnosis is made in a sibling after florid presentation in a previous affected sibling, is with intravenous copper histidine.

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Endocrine disorders in pregnancy

Endocrinology (Oxford Desk Reference) ◽

10.1093/med/9780199672837.003.0010 ◽

2018 ◽

pp. 283-296

Author(s):

Helen E. Turner ◽

Richard Eastell ◽

Ashley Grossman

Keyword(s):

Thyroid Hormone ◽

Hyperemesis Gravidarum ◽

Post Partum ◽

Management Strategies ◽

Normal Pregnancy ◽

Endocrine Disorders ◽

Pituitary Diseases ◽

Pregnant State ◽

Pituitary Adrenal Axis ◽

In Pregnancy

This chapter discusses thyroid, adrenal, and pituitary diseases that occur during pregnancy. A series of changes in thyroid hormone economy take place in normal pregnancy. As a result of these changes, thyroid hormone levels in pregnancy differ from those in the non-pregnant state. This chapter includes a description of normal thyroid physiology and thyroid pathophysiology, including hyperemesis gravidarum, post-partum thyroiditis, hypothyroidism, and hyperthyroidism. Changes in the hypothalamo-pituitary–adrenal axis during normal and abnormal pregnancies are also described, with syndromes such as Cushing’s syndrome and Addison’s disease listed. Finally, pituitary adenomas in pregnancy, and their respective features and management strategies, are listed, including acromegaly, hypopituitarism, TSH-secreting adenomas, and prolactinoma.

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Reversible Fulminant Hepatitis Secondary to Cocaine in the Setting of β-Blocker Use

Journal of Investigative Medicine High Impact Case Reports ◽

10.1177/2324709620924203 ◽

2020 ◽

Vol 8 ◽

pp. 232470962092420 ◽

Cited By ~ 1

Author(s):

Rohan Sharma ◽

Nidhi Kapoor ◽

Kaustubh Suresh Chaudhari ◽

Robert Hal Scofield

Keyword(s):

Heart Failure ◽

Acute Heart Failure ◽

Fulminant Hepatic Failure ◽

Hepatic Failure ◽

Fulminant Hepatitis ◽

Viral Infections ◽

Hepatic Function ◽

Cocaine Use ◽

Β Blocker ◽

Acute Hypoglycemia

Background. Fulminant hepatitis is acute hepatic injury with severe decline in hepatic function manifested by encephalopathy, hypercoagulable state, jaundice, renal failure, hypoglycemia, or a constellation of these symptoms in patients without preexisting liver disease. Etiologies include viral infections, hepatotoxic drugs, autoimmune diseases, vaso-occlusive diseases, sepsis, and malignant infiltration. Case Report. A 56-year-old man presented with acute heart failure in the setting of cocaine use. The patient subsequently developed fulminant hepatic failure manifested by acute hypoglycemia, elevated liver enzyme, and worsening liver function, which resolved over 1 week with supportive care. The patient was on β-blocker, which was stopped during the admission. He was again admitted on several different occasion for cocaine-induced acute heart failure but did not develop hepatic failure as his β-blocker was discontinued. Discussion. Cocaine has been known to cause hepatotoxicity in humans. However, our patient developed fulminant hepatic failure in the setting of concomitant cocaine and β-blocker use likely secondary to unopposed α-adrenergic activity and ischemic hepatopathy. The patient did not develop hepatic failure on subsequent admissions with cocaine use after discontinuation of β-blockers.

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