Fulminant liver failure resulting from massive hepatic infarction associated with hemolysis, elevated liver enzymes, and low platelets syndrome

2016 ◽  
Vol 42 (10) ◽  
pp. 1375-1378 ◽  
Author(s):  
Masato Yoshihara ◽  
Michinori Mayama ◽  
Mayu Ukai ◽  
Sho Tano ◽  
Yasuyuki Kishigami ◽  
...  
2021 ◽  
pp. 175114372110254
Author(s):  
Evangelia Poimenidi ◽  
Yavor Metodiev ◽  
Natasha Nicole Archer ◽  
Richard Jackson ◽  
Mansoor Nawaz Bangash ◽  
...  

A thirty-year-old pregnant woman was admitted to hospital with headache and gastrointestinal discomfort. She developed peripheral oedema and had an emergency caesarean section following an episode of tonic-clonic seizures. Her delivery was further complicated by postpartum haemorrhage and she was admitted to the Intensive Care Unit (ICU) for further resuscitation and seizure control which required infusions of magnesium and multiple anticonvulsants. Despite haemodynamic optimisation she developed an acute kidney injury with evidence of liver damage, thrombocytopenia and haemolysis. Haemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome, a multisystem disease of advanced pregnancy which overlaps with pre-eclampsia, was diagnosed. HELLP syndrome is associated with a range of complications which may require critical care support, including placental abruption and foetal loss, acute kidney injury, microangiopathic haemolytic anaemia, acute liver failure and liver capsule rupture. Definitive treatment of HELLP is delivery of the fetus and in its most severe forms requires admission to the ICU for multiorgan support. Therapeutic strategies in ICU are mainly supportive and include blood pressure control, meticulous fluid balance and possibly escalation to renal replacement therapy, mechanical ventilation, neuroprotection, seizure control, and management of liver failure-related complications. Multidisciplinary input is essential for optimal treatment.


2019 ◽  
Vol 09 (01) ◽  
pp. e84-e87
Author(s):  
Jessica Morgan ◽  
Micaela Della Torre ◽  
Anna Whelan ◽  
Sophia Rodriguez ◽  
Laura DiGiovanni

Background Hepatic infarction is an exceedingly rare complication of hemolysis, elevated liver enzymes, and low platelets syndrome. Few cases have been described in the medical literature and the true incidence remains unknown. It can lead to fulminant liver failure, liver transplant, or death if not promptly addressed. Case Report A 22-year-old primigravida presented with right upper quadrant and epigastric pain at 28 weeks' gestation. She had severely elevated blood pressures requiring intravenous antihypertensives as well as proteinuria, thrombocytopenia, and mild transaminitis. Within 6 hours of admission, her rapidly rising liver function tests (LFTs) necessitated urgent delivery by primary cesarean section. Her liver enzymes continued to rapidly worsen postoperatively and immediate postpartum computed tomography of the abdomen and pelvis revealed massive hepatic infarction, 11 × 10 × 15 cm, of the right lobe of the liver. Her transaminases peaked at alanine transferase of 2,863 IU/L and aspartate transferase of 2,732 IU/L. She received supportive multidisciplinary intensive care, and LFTs returned to normal by postoperative day 20. Conclusion Hepatic infarction is an extraordinarily rare complication of pre-eclampsia. Early recognition and prompt multidisciplinary management are vital to prevent catastrophic bleeding, hepatic failure, and death.


2017 ◽  
Vol 33 (6) ◽  
pp. 375-379 ◽  
Author(s):  
Brittany D. Bissell ◽  
Jason E. Davis ◽  
Alexander H. Flannery ◽  
David A. Adkins ◽  
Melissa L. Thompson Bastin

Acute liver failure secondary to acetaminophen overdose can be a life-threatening condition, characterized by severe electrolyte derangements. Hepatocyte regeneration is associated with phosphorous utilization and is a known complication of liver recovery following injury. We report the case of profound, life-threatening hypophosphatemia following recovery from acute fulminant liver failure. As the liver enzymes normalized, serum phosphorous levels plummeted. Our patient required an aggressive, individualized phosphorus replacement regimen, which resulted in a continuous infusion of intravenous (IV) sodium phosphate, titrated to a maximum rate of 30 mmol/h or 0.5 mmol/kg/h. The patient required over 400 mmol of total IV and oral phosphorous over the course of 48 hours. An aggressive approach to phosphorous replacement was done safely and effectively. Traditional replacement protocols are not adequate to sustain patients with this degree of hypophosphatemia. This is the first report to utilize a continuous infusion of phosphate with a maximum reported rate (0.5 mmol/kg/h). Our report summarizes a novel and safe approach for clinicians to maximally support these patients through high-dose, continuous infusion phosphorous administration.


2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Jamshid Vafaeimanesh ◽  
Mohammad Bagherzadeh ◽  
Mahmoud Parham

Introduction. Many diseases and conditions can contribute to elevated liver enzymes. Common causes include viral and autoimmune hepatitis, fatty liver, and bile duct diseases, but, in uncommon cases like liver involvement in endocrine disorders, liver failure is also seen. Adrenal insufficiency is the rarest endocrine disorder complicating the liver. In the previously reported cases of adrenal insufficiency, mild liver enzymes elevation was seen but we report a case with severe elevated liver enzymes and liver failure due to adrenal insufficiency. Based on our knowledge, this is the first report in this field.Case Report. A 39-year-old woman was referred to emergency ward due to drowsiness and severe fatigue. Her laboratory tests revealed prothrombin time: 21 sec, alanine aminotransferase (ALT): 2339 IU/L, aspartate aminotransferase (AST): 2002 IU/L, and ALP: 90 IU/L. No common cause of liver involvement was discovered, and eventually, with diagnosis of adrenal insufficiency and corticosteroid therapy, liver enzymes and function became normal. Finally, the patient was discharged with good general condition.Conclusion. With this report, we emphasize adrenal insufficiency (primary or secondary) as a reason of liver involvement in unexplainable cases and recommend that any increase in the liver enzymes, even liver failure, in these patients should be observed.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Vinaya C. Maddukuri ◽  
Courtney D. Stephenson ◽  
Lon Eskind ◽  
William A. Ahrens ◽  
Preston Purdum ◽  
...  

Acute liver failure (ALF) during pregnancy is very uncommon. Pregnancy-specific liver conditions like hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome and acute fatty liver of pregnancy can cause ALF at term or postpartum, but, typically occur during the third trimester. Most of these patients recover spontaneously after delivery, but, on occasion, they require liver transplantation in the postpartum period. However, ALF during the first and second trimester of pregnancy requiring antepartum liver transplantation is rare. Only fifteen cases of liver transplantation during pregnancy have been reported, and very few occurred during the first trimester. We report a Woman who developed acute liver failure during the first trimester of pregnancy and underwent successful liver transplantation at 11-week gestation, followed by successful delivery of the fetus at 30 weeks. To our knowledge, this is the earliest case of successful liver transplantation during pregnancy followed by successful fetal outcome. We discuss management of the patient and fetus before, during, and after liver transplantation and review the literature on antepartum liver transplant in pregnancy.


2015 ◽  
Vol 8 (4) ◽  
pp. 190-192 ◽  
Author(s):  
Tabassum Firoz ◽  
Douglas Webber ◽  
Hilary Rowe

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.


2020 ◽  
Vol 13 (4) ◽  
pp. 163-170
Author(s):  
Chattip Prueksapraopong ◽  
Varisa Piriyakitpaiboon ◽  
Dissajee Lumbiganon

AbstractBackgroundAcute liver failure (ALF) is a rare condition during neonatal period.ObjectiveTo report a case of recipient twin with fulminant ALF secondary to hydrops fetalis caused by twin-to-twin transfusion syndrome (TTTS).MethodThe patient was admitted to the neonatal intensive care unit (NICU) for respiratory failure requiring mechanical ventilation and fulminant ALF with prolonged international normalized ratio (INR) and elevated liver enzymes with highest aspartate aminotransferase of 4,580 U/L.ResultsLaboratory investigation for secondary causes of liver failure was not revealing. Her liver enzymes and coagulation levels were dramatically normalized as the clinical symptoms of hypervolemia improved within 1 week.ConclusionTTTS can be a possible cause of neonatal ALF. Early detection with proper management of TTTS is important to avoid adverse outcomes. However, pathogenesis of hepatic dysfunction in TTTS is rarely described, and further studies are needed to help understanding the correlation between liver diseases and TTTS.


2018 ◽  
Vol 37 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Aline Gottlieb ◽  
Maren Kottmann ◽  
Paul Manka ◽  
Sotiria Bedreli ◽  
Johannes Hadem ◽  
...  

Background: The definition of acute liver failure (ALF) usually implies no previous liver injury. Though, some patients admitted to liver transplantation centers with the diagnosis of ALF are obese or have diabetes. Elevated liver enzymes were not recorded previously, and no signs of cirrhosis or prior decompensation of the liver function were ever present. Still, these patients differ from the “typical” ALF-patient. Goals: In this study, we aimed to confirm acute-on-chronic-liver failure (AOCLF) in patients diagnosed with ALF and to identify possible differences between ALF and AOCLF. Study: Patients were retrospectively recruited from all patients admitted to the University Hospital Essen with diagnosis of ALF between 2008 and 2015. Data of 163 patients were evaluated, resulting in a reclassification of 32 patients as AOCLF (remaining ALF: 131). Demographic and clinical data as well as serum parameters, including cell death markers, were correlated with clinical outcome. Results: Patients with AOCLF were significantly older, had a higher body mass index (BMI), and were more often male. The cause for liver failure in these patients differed significantly from patients who had an actual ALF. Significant differences were also found for serum liver enzymes. Outcome of patients did not differ between AOCLF and ALF. Though, lower BMI and MELD and higher AST and GLDH were predictors for a beneficial outcome. Conclusion: AOCLF is still commonly misdiagnosed as ALF. While clinical outcome does not significantly differ between ALF and AOCLF, risk factors for adverse outcome may significantly differ between these entities.


Author(s):  
D.R. Jackson ◽  
J.H. Hoofnagle ◽  
A.N. Schulman ◽  
J.L. Dienstag ◽  
R.H. Purcell ◽  
...  

Using immune electron microscopy Feinstone et. al. demonstrated the presence of a 27 nm virus-like particle in acute-phase stools of patients with viral hepatitis, type A, These hepatitis A antigen (HA Ag) particles were aggregated by convalescent serum from patients with type A hepatitis but not by pre-infection serum. Subsequently Dienstag et. al. and Maynard et. al. produced acute hepatitis in chimpanzees by inoculation with human stool containing HA Ag. During the early acute disease, virus like particles antigenically, morphologically and biophysically identical to the human HA Ag particle were found in chimpanzee stool. Recently Hilleman et. al. have described similar particles in liver and serum of marmosets infected with hepatitis A virus (HAV). We have investigated liver, bile and stool from chimpanzees and marmosets experimentally infected with HAV. In an initial study, a chimpanzee (no.785) inoculated with HA Ag-containing stool developed elevated liver enzymes 21 days after exposure.


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