Journal of Dr. NTR University of Health Sciences

: 2013  |  Volume : 2  |  Issue : 4  |  Page : 282--284

Hyperglycemia in a child with hepatic encephalopathy

Aliyu Ibrahim, Akhiwu O Helen, Mustafa O Asani 
 Department of Paediatrics, Aminu Kano Teaching Hospital, Bayero University, Kano, Nigeria

Correspondence Address:
Aliyu Ibrahim
Department of Paediatrics, Aminu Kano Teaching Hospital, Kano


Hepatic encephalopathy is a serious life-threatening complication of liver disease. It is often associated with hypoglycemia in majority of cases. However, we report the case of a 3-year-old boy with hepatitis-B-virus-related chronic liver disease who presented with hepatic encephalopathy stage-three precipitated by malaria, who developed hyperglycemia while on admission. He was hepatitis B surface antigen positive and had two pluses (++) of Plasmodium falciparum malaria parasitaemia on peripheral film with deranged liver function tests and elevated serum lipase. He was managed conservatively; later, after recovering completely he was discharged home.

How to cite this article:
Ibrahim A, Helen AO, Asani MO. Hyperglycemia in a child with hepatic encephalopathy.J NTR Univ Health Sci 2013;2:282-284

How to cite this URL:
Ibrahim A, Helen AO, Asani MO. Hyperglycemia in a child with hepatic encephalopathy. J NTR Univ Health Sci [serial online] 2013 [cited 2020 Sep 21 ];2:282-284
Available from:

Full Text


Hepatic encephalopathy is a potentially reversible or progressive neuropsychiatric syndrome characterized by changes in cognitive function, behavior and personality, and also by transient neurologic symptoms with characteristic electroencephalographic patterns; it may be associated with acute or chronic liver failure. [1] They often present with hypoglycemia that results from impaired gluconeogenesis. But this case of a 3-year-old boy who had hyperglycemia with hepatic encephalopathy is a rare event. In this article, effort is made to identify and explain the cause of this bizarre association.

 Case Report

A 3-year-old boy presented with fever and altered sleep pattern, restlessness and two episodes of generalized tonic clonic seizure on the day of presentation. He was being followed for the last 9 months for chronic liver disease. He was also hepatitis B surface antigen positive.

On examination, he was febrile with temperature of 39.4°C, pale and jaundiced; he was not hydrated with peripheral edema. He was unconscious with a modified Glasgow coma score of 8/15 (for children less than 4 years), he had normal-sized pupils that were sluggishly reactive to light; he had no signs of meningeal irritation, normal muscle bulk with increased deep tendon reflexes (knees and ankles). His abdomen was full, soft, moved with respiration; the liver span was 5 cm; spleen was 6 cm along its longest axis, while the kidneys were not ballotable. The cardiovascular and respiratory systems examinations were not remarkable.

Urgent malaria parasite done was ++, packed cell volume was 24% and random blood sugar was 4.3 mmol/l. He was then placed on tabs neomycin, ampicillin + cloxacillin, cimetidine, I.V artesunate and mannitol, and was fed via nasogastric tube using plain pap. Eight hours on admission he was still unconscious with GCS of 10/15; his random blood sugar was 12 mmol/l. Bedsides urinalysis showed urobilinogen of +++, bilirubin ++, protein +, glucose +, and pH 6. The serum glucose was closely monitored. Ten hours on admission he had two episodes of generalized tonic clonic seizure each lasting about 1 min and aborted spontaneously. The repeat random blood sugar was 16.4 mmol/l. He also received phenytoin infusion at 10 mg/Kg. Eleven hours on admission repeat RBS was 18.3 mmol/l, urinalysis showed pH of 6, glucose +, bilirubin ++, urobilinogen of +++, protein +other parameters were negative. Urgent urea and electrolytes showed urea 4.2 mmol/l, Na 130 mmol/l, K 3.6 mmol/l, Cl 98 mmol/l that were essentially normal. Serum alkaline phosphatase was 29U/l with elevated alanine aminotransferase of 351U/l, asparte aminotransferase 256U/l; the total serum bilirubin was 139 mmol/l with conjugated fraction constituting 30%. He had normal serum proteins of 75 g/l, with reduced serum albumin of 27 g/l and elevated serum globulin of 48 g/l. Abdominal ultrasound scan showed increased echogenicity of the liver with irregular surface which was in keeping with a chronic liver disease, while the pancreas was essentially normal. He made 2.7 mls/kg/h of urine. Naso-gastric feeding was stopped and he was placed on normal saline. Twelve hours on admission the repeat serum glucose was 16 mmol/l. By 16 h on admission the serum glucose was 12.2 mmol/l and he had completed the prescribed normal saline. By the 18th hour on admission, the serum glucose was 7.4 mmol/l. Repeat urinalysis was unremarkable and no more convulsions. Twenty four hours on admission patient regained consciousness and had started communicating. His serum glucose at that point was 5.1 mmol/l. Clotting profile was within normal limits. Subsequent serum glucose results were within normal limit, temperature normalized, and full blood count was essentially normal. He steadily improved and by the tenth day of admission he was discharged home. The initial working diagnosis was hepatic encephalopathy with hyperglycemia precipitated by malaria rule-out septicaemia; however, 2 days before discharge results of serum pancreatic lipase, amylase, and blood culture showed; elevated serum lipase of 119.5 IU/L (two times above the upper limit of normal), normal serum amylase of 133 IU/L and a negative blood culture. Therefore, the possibility of an associated bacterial infection was excluded.


Currently there are four main theories explaining the pathogenesis of hepatic encephalopathy. These include accumulation of ammonia; false neurotransmitters in the brain; abnormal ligand(s) acting on g-amino butyric acid benzodiazepine (GABA-BDZ) receptors; deposition of Manganese in basal ganglia. [2] Hepatic encephalopathy is usually precipitated by infection, gastrointestinal bleeding, dehydration, constipation, electrolyte imbalances, and sedative use. [3] The precipitant of the hepatic encephalopathy in this case was considered to be malaria because the blood film showed ++ of ring forms of Plasmodium falciparum malaria while blood culture yielded no bacteria growth. Severe hepatic dysfunction in malaria is usually associated with coexisting viral hepatitis or underlying chronic liver disease [4] and malaria has also been reported to trigger pancreatitis. [5] Clinical features of hepatic encephalopathy are graded from 1 to 4 ranging from minimal changes in memory and intellect to coma without response to painful stimuli.

Hypoglycemia is common in children with hepatic encephalopathy and it is due to diminished gluconeogenesis. [6] Hence, the starting fluid of 10% dextrose in 0.25 N saline has been recommended. [6] Initial IV fluid should have at least 100 mg/ml of glucose (10%) and infusion should be titrated to maintain blood glucose between 120-240 mg/dl. [6] However, in the index case what was noticed was a raising serum glucose which lasted about 24 h despite not being on a dextrose containing infusion and the serum glucose only started to fall in response to normal saline infusion. Abnormalities of glucose homeostasis are common in chronic liver disease especially cirrhosis; hyperglycemia and glucose intolerance may be observed. Glucose intolerance is associated with normal or increased level of plasma insulin (except in patients with hemochromatosis), suggesting that insulin resistance rather than insulin deficiency may be responsible for cases of hyperglycemia. Patients with cirrhosis may also have elevated serum lactate levels. Hypoglycemia although commoner in acute fulminant hepatitis, may also be seen in patient with end stage liver disease with cirrhosis. The liver in children has limited glycogen store; therefore, it gets easily depleted during periods of fasting; hence, in end-stage liver disease, hypoglycemia may be due to decreased hepatic glycogen stores, diminished glucagon responsiveness, or decreased capacity to synthesize glycogen due to extensive parenchymal destruction. Although liver biopsy was not done in the index case to determine if he had cirrhosis, abdominal ultrasound showed evidence of hepatic parenchymal distortion. Furthermore, the hyperglycaemia might have been due to stressor response to infection (malaria). Again mannitol might have contributed to the progressive increase in the blood glucose noticed. Furthermore, the fact that the patient had convulsed several times could have raised the serum glucose due to the release of stress hormones resulting in hyperglycemia; however, hyperglycemia usually occurs within minutes of a convulsive episode and often resolve within an hour. [7] Moreover, this patient had convulsed before presentation and the serum glucose was normal on presentation. It was not until 8 h into the admission that the rising serum glucose was observed and the serum glucose did not return to normal until about 24 h after admission.

Acute pancreatitis has been reported in 14% of patients with hepatic coma, [8] though the exact mechanism is not completely understood; and pancreatitis may result in hyperglycemia. [9] Serum lipase is more specific for pancreatitis than serum amylase and the serum lipase levels are elevated for longer periods than the serum amylase. [10] Serum amylase may be within the reference range in up to 15% [10] of children with pancreatitis. Though the serum lipase was elevated in this case; it was not up to three times the upper limit; coupled with normal ultrasound of the pancreas and serum amylase the possibility pancreatitis was unlikely. Therefore, the cause of elevated serum lipase in this case is not clear.

This patient received phenytoin for his seizures; phenytoin and gabapentin are preferred anticonvulsants in hepatic encephalopathy. [11]


The presence of hyperglycemia in a child with hepatic encephalopathy is reported. This presentation though not common can occur. In this case, its exact cause is not clear but the possible roles of chronic liver disease with cirrhosis, infection, and stressors resulting in insulin resistance may all be contributory.


1Lizardi-Cervera J, Almeda P, Guevara L, Uribe M. Hepatic encephalopathy: A review. Ann Hepatol 2003;2:122-30.
2Riordan SM, Williams R. Treatment of hepatic encephalopathy. N Engl J Med 1997;337:473-9.
3Frederick RT. Current concepts in the pathophysiology and management of hepatic encephalopathy. Gastroenterol Hepatol (N Y) 2011;7:222-33.
4Bhalla A, Suri V, Singh V. Malarial hepatopathy. J Postgrad Med 2006;52:315-20.
5Mohapatra MK, Gupta MP. Falciparum malaria complicated with acute pancreatitis: A report of case series. J Vector Borne Dis 2011;48:177-9.
6Arya R, Gulati S, Deopujari S. Management of hepatic encephalopathy in children. Postgrad Med J 2010;86:34-41.
7Pillow MT, Doctor SU. Seizure assessment in the emergency department. Available from: th . [Last accessed on 2012 June 15].
8Pamperl H , Kleinberger G , Meryn S . Concomitant pancreatitis in hepatic coma. Leber Magen Darm 1982;12:213-6.
9Solomon SS, Duckworth WC, Jallepalli P, Bobal MA, Iyer R. The glucose intolerance of acute pancreatitis: Hormonal response to arginine. Diabetes 1980;29:22-6.
10Smith RC, Southwell-Keely J, Chesher D. Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis? . ANZ J Surg 2005;75:399-404.
11Prabhakar S , Bhatia R . Management of agitation and convulsions in hepatic encephalopathy. Indian J Gastroenterol 2003;22 Suppl 2:S54-8.