|Year : 2016 | Volume
| Issue : 2 | Page : 254-256
Reversible cortical blindness in a case of hepatic encephalopathy
Amlan Kanti Biswas1, Avinandan Banerjee2, Sanchaita Bala3
1 Department of Medicine, Medical College, Kolkata, West Bengal, India
2 Department of Nephrology, IPGME and R, Kolkata, West Bengal, India
3 Department of Dermatology, KPC Medical College, Kolkata, West Bengal, India
|Date of Web Publication||1-Mar-2016|
Amlan Kanti Biswas
C/O Hirendra Nath Kundu, No. 37, North Sreerampur, Garia, Kolkata - 700 084, West Bengal
Source of Support: None, Conflict of Interest: None
Hepatic encephalopathy is a frequent and often fatal manifestation of chronic liver disease. The pathogenesis of hepatic encephalopathy is believed to be multifactorial including impaired blood-brain barrier function, imbalance between the excitatory and inhibitory neurotransmitters in cortex, accumulation of various toxic and false neurotransmitters, and lack of nutrients like oxygen and glucose. Signs and symptoms of hepatic encephalopathy varies and commonly ranges from personality changes, disturbed consciousness, sleep pattern alternation, intellectual deterioration, speech disturbances, asterixis to frank coma and even death. Reversible or transient cortical blindness is rare manifestation of hepatic encephalopathy. It may even precede the phase of altered consciousness in such patients. Very few similar cases have been reported worldwide. Hence, we would like to report a case of transient cortical blindness in a patient of hepatic encephalopathy.
Keywords: Asterixis, cortical blindness, hepatic encephalopathy
|How to cite this article:|
Biswas AK, Banerjee A, Bala S. Reversible cortical blindness in a case of hepatic encephalopathy. Med J DY Patil Univ 2016;9:254-6
| Introduction|| |
Hepatic encephalopathy frequently occurs in patients with liver failure. Pathogenesis of hepatic encephalopathy is believed to include impaired blood-brain barrier (BBB) function, neurotoxic substance accumulation, alterations in the synthesis and catabolism of neurotransmitters, and a lack of nutrients (such as glucose). Signs and symptoms vary, but usually include disturbed consciousness, personality changes, intellectual deterioration, speech disturbance, and asterixis and sleep disturbance. Reversible cortical blindness has been described as a rare manifestation of hepatic encephalopathy and sometimes can precede the onset of altered sensorium. Van pesch et al. presented a case of cortical blindness associated with chronic liver faiture in 2006.  Ammar et al. in 2003 presented a case of permanent cortical blindness in fulminant hepatic failure.  So, patients with hepatic failure acute or chronic may have cortical blindness that may be transient or permanent and with appropriate treatment of hepatic failure cortical blindness in some occasion can be reversed. Here, we like to report a case of transient cortical blindness in a patient of hepatic encephalopathy.
| Case Report|| |
A 42-year-old nonalcoholic nondiabetic normotensive male patient was admitted with icterus, gradual onset abdominal swelling for 3 months followed by bipedal edema. Clinically, patient had positive shifting dullness in abdomen and mild splenomegaly.
Laboratory investigations revealed that the patient had an altered albumin globulin ratio (albumin −2.2 g/dl, globulin −4.6 g/dl, ratio −0.48:1), prolonged prothrombin time and international normalized ratio (INR) (P-time −24, control −13.8, INR −1.77), hyperbilirubinemia (total bilirubin −4.3 mg/dl, conjugated bilirubin −2.1 mg/dl), high SAAG ascites (Serum ascites albumin gradient −1.5). Patient was positive for hepatitis B surface antigen, hepatitis B e antigen and quantitative hepatitis B DNA copy came to be 1,93,900 IU/ml.
Ultrasonography whole abdomen with splenoportal Doppler study revealed shrunken liver with heterogenous coarse echotexture, 14 cm size spleen, portal vein of diameter of 15 mm and moderate ascites. Upper gastrointestinal endoscopy revealed few grade II varices and mild portohypertensive gastropathy. Hence, the patient was established as a case of hepatitis B-related chronic liver disease with portal hypertension and in decompensated state. The patient was put on conservative therapy and initiation of antiviral therapy in the form of entacavir was planned.
Until then the clinical course was uneventful on conservative therapy. However, on the afternoon of the 7 th day of admission, the patient was talking irrelevantly in a slurred speech and was in euphoric mood. His attendant informed that he had a disturbed sleep in the previous night. On the 8 th day morning the attendant told us that his patient is unable to see in both eyes after getting up from sleep.
The patient was immediately examined in the ward and was found to have absent finger counting and perception of light in both eyes. However, his papillary reflex was normal in both eyes. The patient was sent to ophthalmology department for further evaluation. Anterior segment of both eyes were normal and fundoscopy revealed healthy disc, macula and peripheral retina. With opthalmological advice patient was sent for magnetic resonance imaging (MRI) brain and retro-orbital area and visual evoked potential (VEP) of both eyes.
From that day evening patient became lethargic, drowsy and developed asterixis. The patient became comatosed that night onwards. He was put on aggressive management of hepatic encephalopathy. The patient responded to therapy and gradually regained consciousness and orientation in next 3-4 days. There was slow improvement of vision in both eyes. The patient became fully conscious in the next 5 days and regained vision in both eyes totally.
In the meantime the reports of MRI brain and VEP came. MRI brain and retro-orbital area revealed no significant abnormality. But VEP showed delayed P100 latencies in both eyes which is consistent with cortical blindness. Hence, it was concluded that the cortical blindness was accompanied by hepatic encephalopathy or a direct manifestation of it.
| Discussion|| |
Cortical blindness refers to loss of vision caused by unilateral or bilateral lesion in the occipital cortex in the presence of normal anterior segment. Neuroradiologic and/or electrophysiologic evidence of cortical abnormality is needed to establish diagnosis. Common etiology are cerebrovascular disease, hypertensive encephalopathy, postcardiac surgery, cerebral or coronary angiography, ecclampsia, other causes of raised intracranial tension, hyperammonemia. , Patient with significant neuroradiologic lesion has poor chance of complete recovery of vision and prognosis is much better in those case following vascular surgery, angiography and raised intracranial tension.
There have been few cases of transient cortical blindness in hepatic encephalopathy being reported. ,,] In all these cases, patient had chronic liver disease with recurrent hepatic encephalopathy. However in Miyata's case patient had recurrent transient cortical blindness with hepatic encephalopathy.  Ammar et al. in 2003 reported a case of permanent cortical blindness in fulminant hepatic failure. 
The probable reason for preferential damage of visual cortex may be due to the altered BBB function associated with hepatic encephalopathy that has allowed highly toxic neurotransmitter to accumulate to such a level that can temporarily damage the visual cortex. With treatment when the toxic level of neurotransmitters diminishes and the blindness improves. This phenomenon matches with what occurred in our patient.
Here, we present a case of temporary cortical blindness which may be a manifestation of hepatic encephalopathy in a case of the chronic liver disease. The damage to the visual cortex can be reversed with the treatment of hepatic encephalopathy.
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Conflicts of interest
There are no conflicts of interest.
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