the liver receives nearly 30% of the total cardiac output with 70% of the total hepatic blood flow passing through the portal venous system and 30% passing through the hepatic arterial system .
more than half of the oxygen supply to the liver is delivered by hepatic arterial blood .
any process that substantially reduces arterial blood flow or arterial oxygen content to the liver can result in hypoxic hepatitis .
hypoxic hepatitis tends to be commoner in patients with systemic hypotension and other concomitant conditions which decrease the systemic or the hepatic circulation , and it occurs mostly in intensive care unit patients who are haemodynamically unstable .
the most common cardiac disorders responsible for ischaemic hepatitis are acute myocardial infarction and arrhythmias .
valvular heart disease , cardiomyopathy and pericardial tamponade also can result in arterial hypotension complicated by ischaemic hepatitis .
the rate of in - hospital mortality in hypoxic hepatitis is very high with studies reporting mortalities of 61.5% .
mortality tends to be higher in patients with septic shock ( 83.3% ) and cardiac arrest ( 77.7% ) .
cases of hypoxic hepatitis were also reported in relation to specific conditions such as obstructive sleep apnoea , profound anaemia , complicated aortic aneurysms , acute lower limb ischaemia , hereditary haemorrhagic telangiectasia   and grand mal seizures .
. diminished portal venous blood flow increases the susceptibility to hypoxic hepatitis during episodes of arterial hypotension or hypoxia .
furthermore , diminished hepatic venous outflow ( i.e. secondary to congestive heart failure , budd - chiari syndrome ) and biliary obstruction also increase an individual 's risk for ischaemic hepatitis with hypotension or hypoxia .
ischaemic hepatitis or  shock liver. liver ischaemia was until recently considered to be the only haemodynamic mechanism responsible for hypoxic hepatitis , and it was believed that a shock state was required .
however , other haemodynamic mechanisms of hypoxia , such as passive congestion of the liver , arterial hypoxaemia and dysoxia , have been shown to be important mechanisms in inducing hepatocyte damage with a shock state being observed in only 50% of cases of hypoxic hepatitis . accordingly , 
ischaemic hepatitis and  shock liver are misnomers and the term  hypoxic hepatitis better describes this condition .
the diagnosis should be suspected in patients who have evidence of past or present cardiac disease , in the presence of electrocardiographic abnormalities or radiographic pulmonary abnormalities ( found in about half of all patients with acute hypoxic hepatitis ) and in patients with marked increases in transaminase activity together with a degree of initial renal impairment .
the outcome of hypoxic hepatitis is influenced by the severity of liver impairment and the aetiology and severity of the underlying conditions .
peak aspartate transaminase , lactate dehydrogenase , inr and lactate levels are higher in intensive care unit patients with fatal hypoxic hepatitis
management involves treatment of the underlying conditions , with plenty of fluids in patients with hypotension and septic shock , maintaining adequate oxygenation in patients with underlying respiratory conditions and prompt management of cardiac disorders in order to restore haemodynamic stability .
we report here the case of a young healthy athlete who developed heat stroke associated with rhabdomyolysis and ischaemic hepatitis while he was running the final stages of a marathon .
the athlete was a 25-year - old hungarian gentleman who had been training for the malta marathon ( held over 42.2 km ) for several months .
he was fit , having had regular medical check - ups during his training and before the marathon .
the patient was feeling very well during the race , so much that he was improving on his usual time and towards the end of the race ( 41st km ) decided to sprint the last few metres towards the finish line .
he was noticed to collapse a few hundred metres from the finish and his next recollection was waking up in the intensive care unit at our centre . upon his collapse
a peripheral line was inserted and he was started on intravenous fluids . he was rushed to accident and emergency where he was found to be confused , with a glasgow coma score of 10 .
he had a temperature of 105.4f on admission and he was sweaty , tachycardic ( heart rate of 160 bpm ) and had a systolic blood pressure of 90 mm hg .
he was taken to the intensive care unit where he was resuscitated with plenty of fluids .
his blood pressure remained very low , requiring inotropic support with ephedrine for 6 h. a ct scan of his brain was normal .
repeat blood investigations the day after admission revealed an elevated creatinine phosphokinase ( cpk ) level ( 178,850 u / l ) , suggesting underlying rhabdomyolysis .
it was also noticed that the serum alanine aminotransferase ( alt ) had started rising with a level of 143 u / l on day one post admission .
the patient improved clinically , was responsive within a few hours and was transferred from intensive care to a general medical ward the following day . however , his alt peaked on the second day of admission ( table 2 ) . on examination
, there were no signs of chronic liver disease , no flap , and he was not jaundiced .
liver screen was normal with negative viral screen , autoimmune screen and mildly raised ferritin levels ( table 2 ) .
all non - essential treatment ( including the antibiotic ) was stopped and intravenous n - acetyl cysteine ( nac ) was started at a dose of 100 mg / kg 16-hourly .
he was discharged home with an early outpatients follow - up once both cpk and alt were improving progressively ( fig . 1 , fig .
graveling and frier   reported a similar case report of a young insulin - dependent diabetic patient who suffered an episode of nocturnal hypoglycaemia which provoked a tonic - clonic seizure the day before a marathon . despite this he ran in the marathon the following day during which he collapsed with severe hypoglycaemia and a further associated seizure .
he subsequently developed severe myalgia accompanied by a pronounced and persistent elevation of plasma cpk , indicating rhabdomyolysis , and deranged liver function , suggestive of hypoxic hepatitis .
the authors concluded that the rhabdomyolysis and hypoxic hepatitis occurred as a result of prolonged physical exercise following severe hypoglycaemia .
studies have shown that up to 11% of intensive care unit patients develop hypoxic hepatitis .
regression analysis has demonstrated a strong mortality risk for admissions with hypoxic hepatitis requiring vasopressor therapy , unlike hypoxic hepatitis in the absence of vasopressor therapy which does not appear to be significantly associated with mortality .
while it is relatively unexpected that a healthy , young athlete should develop hypoxic hepatitis , the vasopressors used for a short period in intensive care might have precipitated the hypoxic damage to the liver in our patient .
the relatively short period of vasopressor use might also explain this patient 's rapid recovery with rapid improvement in his alt levels .
nac has been shown to limit liver injury and improve prognosis in patients with acute liver failure secondary to paracetamol overdose .
nac limits liver injury by repleting hepatic glutathione and increasing oxygen delivery to peripheral tissues . while little evidence exists on the benefits of nac in hypoxic hepatitis , it has been tested as a treatment for acute liver failure not related to paracetamol overdose .
a placebo - controlled trial on 173 patients with acute liver failure that was not due to paracetamol overdose showed that patients treated with nac had more transplant - free survival and less orthotopic liver transplantation at 1 year when compared with those receiving placebo .
patients with grade 1 or 2 encephalopathy receiving nac also had better 1-year survival than those receiving placebo .
for this reason , nac may have an important therapeutic role in the management of acute hepatitis secondary to hypoxia .
 any process that substantially diminishes arterial blood flow or arterial oxygen content to the liver can result in hypoxic ( ischaemic ) hepatitis . 
 90% of hypoxic hepatitis occurs in unstable patients in intensive care units with haemodynamic failure secondary to heart failure , respiratory failure and toxic shock . 
 the rate of in - hospital mortality in hypoxic hepatitis is very high with studies recording mortalities of 61.5% . 
 it tends to be very uncommon in healthy , young patients with no underlying medical problems . 
 we report here the case of a young healthy athlete who developed heat stroke associated with rhabdomyolysis and hypoxic hepatitis while he was running the final stages of a marathon . 
 the patient required intensive care admission and inotropic support for a few hours after he was admitted with heat stroke . 
 he underwent a rapid recovery after he was resuscitated with fluids . 
 n - acetyl cysteine was also given during the acute stage of the hepatitis . 
 this case highlights an uncommon case of hypoxic hepatitis in a young , healthy patient secondary to hypotension and heat stroke . 
 inotropic support might have precipitated the hypoxic hepatitis in this young patient . 
Introduction
Case Report
Discussion