The Incidence and Outcomes of Ischemic Hepatitis: A Systematic Review with Meta-analysis

Background

Ischemic hepatitis is a devastating cause of acute liver injury. Data are limited regarding its incidence and outcomes.

Methods

Systematic review and meta-analysis of studies from PubMed, EMBASE, and Web of Science with specific search terms. Inclusion criteria included case series with >10 patients and clear case definition (especially liver enzyme levels >10 times the upper limit of normal).

Results

Twenty-four papers met inclusion criteria. A total of 1782 cases were identified in these papers (mean 78 per paper, range 12-322). The pooled average age of the included patients was 64.2 years, and their mean peak aspartate aminotransferase level, alanine aminotransferase level, and total bilirubin were 2423 IU/L, 1893 IU/L, and 2.55 mg/dL, respectively. Ischemic hepatitis was present in 2 of every 1000 admissions; including 2.5 of every 100 intensive care unit admissions and 4 of 10 admissions associated with an aminotransferase level >10 times the upper limit of normal. The pooled proportions of patients with ischemic hepatitis who had a predisposing acute cardiac event or sepsis were 78.2% and 23.4%, respectively. The proportion of patients with a documented hypotensive event of any duration was 52.9%. Overall, the pooled rate of survival to discharge was 51% (range 23.1%-85.7%).

Conclusions

Ischemic hepatitis is a common cause of severe acute liver injury and is associated with a significant risk of in-hospital death. A major opportunity in the management of ischemic hepatitis is recognition of the condition without documented hypotension.     

Ischemic Hepatitis: Widening Horizons

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.     

Prolonged therapy of chronic hepatitis C with ribavirin

Summary. Therapy with ribavirin for 6–12 months is associated with decreases in serum aminotransferases in some patients with chronic hepatitis C. We have assessed the practicality and safety of prolonged therapy with ribavirin. Six patients with chronic hepatitis C were given 1000–1200mg of ribavirin daily for 24 months. Serum aminotranferases and hepatitis C virus (HCV) RNA levels were monitored during and after therapy. Liver biopsies were carried out before and at the end of treatment. With therapy, mean serum alanine aminotransferase (ALT) levels fell from 161 U/L to 45 U/L at 12 months and to 39 U/L at 24 months. HCV RNA levels did not change. Liver histology improved in five and was unchanged in one patient. When therapy was stopped, aminotransferases rose to pretreatment levels. Side effects included mild fatigue and headaches. Two patients developed gallstones during therapy, perhaps caused by the chronic haemolysis that occurred in all patients. In conclusion, prolonged therapy with ribavirin can result in sustained improvements in serum aminotransferases and hepatic histology in a proportion of patients with chronic hepatitis C. Ribavirin therapy does not cause decreases in viraemia and, therefore, probably must be continued indefinitely to provide lasting benefit. The advantages of such therapy must be weighed against possible long-term side-effects.     

ISCHEMIC HEPATITIS: CLINICAL FEATURES, DIAGNOSIS AND PROGNOSIS

Nineteen episodes of ischemic hepatitis were diagnosed by hepatitic liver function tests and characteristic liver pathology in 17 patients. All patients had an acute illness associated with a likely fall in cardiac output although only five episodes were associated with documented hypotension. Right ventricular failure was severe in only four, mild in six, and absent in nine whilst left ventricular failure was clinically apparent in 16. The hepatitic illness was usually mild. No patient died as a direct result of hepatic damage, prognosis depending on the underlying cardiac or systemic disease. Liver function tests were characterised by a marked rise in serum transaminase levels with a parallel increase in serum lactic dehydrogenase of hepatic origin and a short time course of the enzyme elevation lasting 3 to 11 days. It is concluded that ischemic hepatitis (a) is' caused by poor hepatic perfusion associated with an acute fall in cardiac output; (b) is usually a subclinical illness with little influence on prognosis, and (c) may be accurately differentiated from viral hepatitis on clinical and biochemical criteria alone.     

Refractory hypoglycemia secondary to topical salicylate intoxication

We describe a case of severe refractory hypoglycemia secondary to topical salicylate intoxication. A 72-year-old man with psoriasis and end-stage renal disease was treated with a topical cream containing 10% salicylic acid. The patient presented with encephalopathy and subsequently developed hypoglycemia refractory to infusions of large amounts of glucose. A serum salicylate concentration was elevated at 3.2 mmol/L. Emergent hemodialysis was accompanied by rapid lowering of serum salicylate concentration and resolution of refractory hypoglycemia. Salicylate is well absorbed across normal and diseased skin. Salicylate markedly impairs gluconeogenesis and increases glucose utilization, resulting in hypoglycemia. To our knowledge, this is the first article on hypoglycemia due to the application of topical salicylate.     

Cytomegalovirus hepatitis and myopericarditis

Cytomegalovirus （CMV） infection in inmunocompetent hosts generally is asymptomatic or may present as a mononucleosis syndrome but rarely can lead to severe organ complications. We report a case of simultaneous hepatic and pericardic CMV infection in a 36-year old immunocompetent man. He was admitted to coronary unit with fever, chest pain radiated to shoulders, changes on electrocardiogram with diffuse ST elevation and modest laboratory elevations in the MB fraction of creatine kinase （CK-MB） of 33.77 μg/L （0.1-6.73）, serum cardiac troponin T of 0.904 ng/mL （0-0.4）, creatine kinase of 454 U/L （20-195） and myoglobin of 480.4 μg/L （28-72）. Routine laboratory test detected an elevation of aminotransferase level： alanine aminotransferase 1445 U/L, aspartate aminotransferase 601 U/L. We ruled out other causes of hepatitis with normal results except IgM CMV. The patient was diagnosed with myopericarditis and hepatitis caused by cytomegalovirus and started symptomatic treatment with salicylic acid. In few days the laboratory findings became normal and the patient was discharged.     

Acute hepatitis after cutaneous application of an artisanal topical ointment with mercury

There is a risk of severe neurological disease, nephropathy and cutaneous complications during mercury poisoning. We report a case of acute generalized exanthematous pustulosis, associated with histologically confirmed acute cytolytic hepatitis without liver failure, after application of a topical home-made ointment containing mercury. The patient was previously sensitized with mercurothiolate. A high level of mercury was found in the blood (68 microg/L, normal < 5 microg/L). Clinical and biological features disappeared after the ointment was discontinued. Biological acute hepatitis was probably from type IV sensitization, like that seen in acute generalized exanthematous pustulosis, with no evidence of direct mercury poisoning and after lithiasis, viral, immune and drug side effects were excluded. Liver injury during acute generalized exanthematous pustulosis is uncommon and usually mild, but should be searched for.     

Relapsing hairy cell leukemia presenting as fulminant hepatitis.

PURPOSE: We report the first known case of fulminant hepatitis due to hairy cell infiltration. CASE REPORT: A 43-year-old woman with hairy cell leukemia returned 1 year after diagnosis with spider angiomata of the face and neck, palmar erythema, and diffuse telangiectasias. The liver span was normal. Laboratory studies included: aspartate aminotransferase, 56 U/L; alkaline phosphatase, 283 U/L; gamma-glutamyltransferase, 157 U/L; and normal bilirubin. A liver biopsy demonstrated modest infiltration of hairy cells with hemosiderosis and intact hepatocytes. RESULTS: The patient responded to interferon-alpha with resolution of the angiomata, decreased palmar erythema, and improved liver function tests. Five months later, she presented with right upper quadrant pain, anorexia, fatigue, and diffuse myalgias. The physical examination was unchanged. Laboratory studies included: aspartate aminotransferase, 299 U/L; alkaline phosphatase, 1,388 U/L; total bilirubin, 43 mumol/L; and direct bilirubin, 29 mumol/L. Two weeks later, she was admitted to the hospital. Her liver span was 15 cm. Laboratory studies showed the following values: aspartate aminotransferase, 618 U/L; alkaline phosphatase, 2,319 U/L; total bilirubin, 311 mumol/L; direct bilirubin, 233 mumol/L; and alanine aminotransferase, 462 U/L. Intensive investigation of contributing causes was not revealing. A subsequent liver biopsy demonstrated extensive portal and intralobular hairy cell infiltration with loss of normal architecture. Liver function deteriorated as shown by the following values: aspartate aminotransferase, 1,100 U/L; alkaline phosphatase, 3,645 U/L; bilirubin, 477 mumol/L; and ammonia, 47 mumol N/dL. The patient died 9 days after admission. CONCLUSIONS: Although liver infiltration is often present and mild elevations of liver function tests have been noted, evidence of such extensive hepatic injury caused by hairy cell leukemia has not been reported previously. Hairy cell infiltration of the liver can cause typical cutaneous changes of liver disease and even fulminant hepatitis.     

Left-sided heart failure presenting as hepatitis

Overt liver disease caused by left-sided heart failure is seldom recognized unless there is obvious hypotension. We now report 4 patients whose initial diagnosis was hepatitis but who were later shown to have central hepatic necrosis associated with left ventricular failure. Signs of right-sided heart failure were absent. Hepatitis was initially suspected in 3 patients because of striking transaminase elevations and in 1 patient because of jaundice and symptoms compatible with hepatitis. Liver biopsies performed on all patients revealed central hepatic necrosis without evidence of acute or chronic hepatitis. Left ventricular failure was documented in all 4 patients. One patient had coronary artery disease, and the other three patients had valvular heart disease. Liver function tests became normal or improved in all cases as the underlying heart disease was treated. We believe that liver dysfunction secondary to left ventricular failure is not uncommon and can be seen in the absence of right-sided heart failure or hypotension.     

Giant cell hepatitis: an unusual cause of fulminant liver failure

Giant cell hepatitis is a very rare disease of unknown origin. It has been hypothesized that drugs, viral infections, or autoimmune reactions may play a pathogenetic role. Here, we describe a 33 year old patient with bacterial bronchitis who was treated with doxycycline (100 mg/d) for one week. Furthermore the patient complained of malaise and a distinct jaundice. Liver parameters increased dramatically (AST 4670 U/l, ALT 5350 U/l, bilirubin 226 μmol/l) and liver function was impaired (INR = 1,45). The ultrasound scan showed a hepatomegaly with no signs of cirrhosis, normal spleen size and normal bile ducts; liver perfusion was normal. No evidence of Wilson's disease, hemochromatosis, autoimmune hepatitis, primary sclerosing cholangitis, primary biliary cirrhosis, hepatitis A, B, C and E, HIV, CMV, VZV, adenoviral infections, or paracetamol intoxication was found. Subsequently, the patient developed acute liver failure (AST 2134 U/l, ALT 2820 U/l, bilirubin 380 μmol/l, INR 3.0) and a beginning renal failure. Therefore, he was transferred to our transplant center. Due to increasing confusion and somnolence due to cerebral edema mechanical ventilation was needed. Because of an acute renal failure and severe hepatic encephalopathia MARS-hemodialysis was performed. Three weeks after the appearance of the jaundice he underwent liver transplantation (MELD 40). Surprisingly, in the explanted liver the diagnosis of giant cell hepatitis was made. Today--2 years after successful liver transplantation--the patient is in very good condition with normal liver function. In conclusion, giant cell hepatitis is a rare cause of acute liver failure that is often recognized only histologically.     

Lactic acidosis during telbivudine treatment for HBV: A case report and literature review

All oral nucleoside analogues against hepatitis B virus,with an exception of telbivudine,have been reported causing lactic acidosis(LA).Here we report the first case of chronic hepatitis B developing severe refractory LA during telbivudine monotherapy.A 36-year-old man of Chinese origin received telbivudine antiviral treatment for chronic hepatitis B.After 11 mo of therapy,he developed anorexia,nausea,and vomiting with mild muscle weakness.The patient was found with elevated serum creatine phosphokinase up to 3683 U/L(upper limit of normal 170 U/L)and marked LA.LA did not resolve immediately following discontinuation of telbivudine.His condition began to improve after hemodialysis treatment for 16 times and usage of glucocorticosteroid.The patient fully recovered after 16 wk of treatment.This is the first documented case with severe LA caused by telbivudine monotherapy.Besides serum creatine phosphokinase,blood lactate level should also be closely monitored in patients receiving telbivudine.     

Extreme Serum Elevations of Aspartate Aminotransferase

Objective : To determine the frequency, etiology, and associated mortality of extreme elevations of serum AST. Methods : The medical records were reviewed of all patients with a serum AST over 3000 U/L during 1 full calendar year at a large, tertiary-care hospital. Serum AST, with an upper limit of normal at 35 U/L, is included in the automated, 18-test chemistry profile run on virtually all clinically ill patients admitted to this hospital. Results : Of 23,125 admissions, 56 patients had or developed serum AST concentrations greater than 3000 U/L, an occurrence rate of approximately two per 1000 admissions. Either liver or skeletal muscle was the origin of virtually all such AST elevations. Acute hypotension (ischemic or hypoxic hepatitis) accounted for the majority (29/56) of the cases; toxic (seven) or viral (four) hepatitis together accounted for 11/56 cases. Overall mortality, on this admission, was 31/56 (55%). Conclusions : Extreme elevations of AST are most often attributable to hypoxic hepatitis. Patients with extreme AST due to hypoxic hepatitis had a 22/29 (75%) mortality compared with 9/27 (33%) for all other causes combined.     

Serial HBV DNA levels in patients with persistently normal transaminase over 10 years following spontaneous HBeAg seroconversion

Earlier studies addressing the hepatitis B virus (HBV) DNA cut-off level for inactive chronic HBV infection largely involved patients with normal alanine aminotransferase (ALT) for only 1-2 years and based on a single time HBV DNA assay. This study was conducted to address this issue using serial HBV DNA assays in patients with persistently normal ALT (PNALT) over 10 years following spontaneous hepatitis B e antigen (HBeAg) seroconversion. Serial serum specimens (mean 9 samples per patient) of 62 patients with PNALT and no disease progression over 10 years (median 18.1 years) after spontaneous HBeAg seroconversion were assayed for HBV DNA. Excluding assays within 1 year after HBeAg seroconversion, 21% and 82.3% of the patients with PNALT had HBV DNA levels persistently lower than 4 log(10) and 5 log(10) copies/mL, respectively, and only 8% had a level ≥ 5 log(10) copies/mL in at least two assays. Of the 27 patients with PNALT defined by ALT <30 U/L for male and <19 U/L for female, only 33% had serum HBV DNA level persistently <4 log(10) copies/mL. There was no significant difference in the serial HBV DNA changes among patients with different gender, HBV genotype or age at HBeAg seroconversion. Liver biopsy in nine patients invariably showed minimal necroinflammation and one showed Ishak fibrosis score 4. These results suggest that 5 log(10) copies/mL (20,000 IU/mL) is a more appropriate cut-off HBV DNA level for inactive chronic HBV infection in the setting of PNALT.     

Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% +/- 0.49% with significant elevations to 81.96% +/- 0.47% and 82.95% +/- 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2-9 mmHg and the range of peak values in galactosamine-treated rabbits was 18-55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.     

ACTIVE CHRONIC HEPATITIS WITH POSITIVE L.E. CELL TEST AND LUPUS NEPHRITIS

A case of active chronic hepatitis with a positive L.E. cell phenomenon and terminal acute renal failure secondary to lupus nephritis is reported in a Chinese girl of 10 years of age. This patient presented initially with an acute hepatitis which was associated with hypergammaglobulinæmia, raised immuno-globulin levels and evidence of renal involvement. Liver biopsy showed marked piecemeal necrosis with rosette formation, a picture of active chronic hepatitis. After seven months she developed acute renal failure, acute cardiac failure and severe anæmia. There was persistent jaundice and hepatomegaly. Tests for L.E. cells gave positive results on three separate occasions. She died in renal and liver failure. Necropsy material showed cirrhosis and the changes of lupus nephritis.     

Significance of hepatitis B core antigen in the liver in patients with chronic hepatitis B and its relation to hepatitis B virus DNA

Liver biopsies from 52 patients with chronic hepatitis B were investigated for the presence and distribution of HBcAg and the results were compared with the status of hepatitis B virus deoxyribonucleic acid (HBV-DNA). The patients consisted of 37 men and 15 women, aged 16-55 years (mean = 34 years). Serum alanine aminotransferase (ALT) was elevated in 50 patients (range: 18-969 U/L; mean = 290 U/L). Serological testing showed HBsAg in all, HBeAg in 45 (87%), and HBV-DNA in 28 (54%). Liver biopsies demonstrated HBcAg in 35 (67%) patients. HBcAg was not only present in 31 of 45 (69%) patients who were seropositive for HBeAg, but also in four of seven (57%) with antibody to HBeAg (anti-HBe). In 28 of 35 (80%) patients with HBcAg in the liver, serum HBV-DNA was detected. However, no serum HBV-DNA was detected in 17 patients who had no detectable HBcAg in the liver. The distribution of HBcAg in the liver was rather cytoplasmic and nuclear than nuclear alone. Among 33 patients with cytoplasmic HBcAg in the liver, 15 (45%) had an evidence of acute exacerbation of hepatitis with marked ALT elevation (range: 168-894 U/L; mean = 385 U/L) and nine patients showed severe chronic active hepatitis and confluent necrosis, histologically. These results indicate that the presence of HBcAg in the liver correlates with the amount of circulating hepatitis B virus as quantified by serum level of HBV-DNA. The predominant cytoplasmic HBcAg in the liver may suggest the possibility of multiple episodes of acute exacerbation and more severe ongoing hepatitis during the clinical course.     

A sweet tooth as the root cause of cardiac arrest

A 71-year-old woman was admitted with hypotension and bradycardia. An electrocardiogram showed flattened T waves and increased U wave prominence, resulting in a long QT(U) syndrome. Her initial serum potassium level was 1.6 mmol/L (all other electrolytes, including magnesium, were normal). She suffered recurrent ventricular tachycardia and ventricular fibrillation arrest requiring direct current cardioversion and high-dose intravenous potassium chloride replacement. Systematic enquiry revealed that she had been constipated for a number of months and had resorted to consuming large quantities of liquorice on a daily basis for its laxative effects. Endocrinology review identified no primary abnormality of the renin-angiotensin-aldosterone axis, and the patient was diagnosed with hypokalemia secondary to liquorice overindulgence. Liquorice has a mineralocorticoid effect. If chronically consumed in large quantities, this effect may lead to severe depletion of whole-body potassium stores. The present case highlights a rare but important cause of hypokalemic cardiac arrest of which all acute care physicians should be aware.     

Submassive hepatic necrosis associated with the use of progabide: A GABA receptor agonist

Progabide, a recently introduced gamma-aminobutyric acid mimetic, is currently undergoing clinical evaluation for a variety of convulsive disorders. We describe a patient in whom severe hepatic failure developed after four weeks of Progabide therapy. The patient's course was marked by encephalopathy, jaundice, hypoglycemia, markedly elevated serum aminotransferase levels, and prolongation of the prothrombin time. Liver biopsy showed extensive hepatocellular necrosis. The patient recovered slowly after discontinuation of the drug. The finding of eosinophilia and increased serum IgE suggests an immunologically mediated mechanism for the Progabide-induced hepatic injury. Alternatively, the lipophilic moiety of Progabide may interact with hepatocyte cell membrane lipids leading to toxic injury. We conclude that Progabide may occasionally cause severe hepatic injury.     

A comparative study of regression of jaundice in patients of malaria and acute viral hepatitis

BACKGROUND & OBJECTIVES: Jaundice is one of the common manifestations of severe malaria in adults. The purpose of this study is to compare the pattern of clinical and biochemical parameters such as serum bilirubin and liver enzyme levels in patients of malaria with jaundice and acute viral hepatitis. METHODOLOGY: The present study was conducted on 34 patients of malaria with jaundice and 15 patients of acute viral hepatitis. Estimation of serum bilirubin, aspartate amino transferase (AST), alanine amino transferase (ALT) and alkaline phosphatase was done daily using standard procedures in malaria patients and weekly in acute viral hepatitis patients. RESULTS: Mean level of serum bilirubin on first day in malaria and acute viral hepatitis patients was 7.07 +/- 3.94 and 10.38 +/- 7.87 mg%, whereas on Day 8 it was 1.19 +/- 1.43 and 7.88 +/- 7.02 mg% respectively. Mean level of AST on Day 1 in malaria and acute viral hepatitis patients was 158.47 +/- 120.35 and 1418.6 +/- 834.11 IU/L, whereas on Day 8 it was 41 +/- 28.33 and 775.3 +/- 399.01 IU/L respectively. Mean level of ALT on Day 1 in malaria and acute viral hepatitis patients was 220.14 +/- 145.61 and 1666.67 +/- 1112.77 IU/L, whereas on Day 8 it was 50.85 +/- 37.31 and 823.8 +/- 475.06 IU/L respectively. Mean level of serum alkaline phosphatase on Day 1 in malaria and acute viral hepatitis patients was 394.74 +/- 267.78 and 513.4 +/- 324.7 IU/L, whereas on Day 8 it was 84.76 +/- 68.50 and 369.27 +/- 207.75 IU/L respectively. INTERPRETATION & CONCLUSION: We observed that resolution of jaundice in malaria took 1-2 weeks in contrast 6 to 8 weeks in viral hepatitis. This difference in duration was statistically significant. Thus, jaundice not resolving in 1-2 weeks time in a patient of malaria requires serious consideration for presence of other concomitant diseases including viral hepatitis.     

Right ventricular failure following placement of a percutaneous left ventricular assist device

Right ventricular (RV) dysfunction following surgical implantation of a left ventricular assist device (LVAD) is a well-documented phenomenon, and it is associated with poor outcomes. We are reporting a 25-year-old male patient who presented to the hospital with flu-like symptoms, hypotension and acute hypoxic respiratory failure. The patient's Laboratory data was significant for elevated troponin, and his Chest X-ray showed acute pulmonary edema. Echocardiogram revealed reduced left ventricular (LV) ejection fraction and normal RV function. Coronary angiography was normal, and the cardiac index was 1.3?L/min/m². Impella 5.0 (Abiomed, MA) was placed through the left axillary artery graft and 4.5?L/min flow was achieved with an improvement in blood pressure. Thirty minutes later, he developed hypotension, the device flow dropped to 3.0?L/min, and right atrial pressure increased. The Pulmonary artery pulsatility index was consistent with RV failure. Possible causes of RV failure include unmasking of RV dysfunction with high LVAD flow and altered RV geometry due to ventricular septum shift. Impella RP (Abiomed, MA) was placed for RV support achieving a flow of 3.8?L/min with a significant improvement in impella LV flow, cardiac output and blood pressure (mean 90?mmHg). Ventricular support devices were weaned off on day 9. The patient was discharged on day 15. Conclusion: our case highlights the risk of RV failure following percutaneous LVAD placement. Early identification and appropriate mechanical support is imperative.