Skip to main content

Alcoholic liver disease and bilateral multifocal central serous retinopathy: a case report

Abstract

Introduction

We present a unique case of a patient with bilateral, multifocal central serous retinopathy in a patient with alcoholic liver disease.

Case presentation

A 58-year-old Caucasian man with alcoholic liver disease, liver cirrhosis and ascites presented to the eye clinic. The ophthalmoscopic examination of both eyes revealed a symmetrical pattern of variably sized, slightly yellowish, translucent, raised lesions throughout the fundi which were confirmed to be caused by multifocal central serous retinopathy after optical coherence tomography and autofluoresence tests.

Conclusion

This case highlights the possible link between central serous retinopathy and end-stage liver disease, with potential implications for the pathogenesis of central serous retinopathy in these patients.

Peer Review reports

Introduction

Central serous retinopathy (CSR) is an exudative chorioretinopathy characterized by an exudative neurosensory retinal detachment with or without an associated detachment of the retinal pigment epithelium (RPE). It typically occurs in young, healthy adults and is usually idiopathic. The age range at the time of first diagnosis is generally from 22 to 83 years, and patients older than 50 years of age tend to have bilateral disease, systemic hypertension and a history of corticosteroid use [1]. Rare variants of CSR with chronic, bilateral, extrafoveal, multifocal and bullous retinal detachments have also been observed in patients undergoing cardiac transplantation [2]. Liver disease may be involved in sight-threatening eye diseases. The ophthalmic pathologies of cirrhosis in the literature include xerophthalmia, vitamin A deficiency and color blindness [3]. Abe et al. found retinopathy with hemorrhages and exudates in 31.8% of patients with hepatitis C, irrespective of liver cirrhosis [4]. According to Onder et al., retinopathy can be present not only in hepatitis C-positive patients but also in patients with other causes of liver cirrhosis, and soft exudates may develop in cirrhotic patients, probably due to loss of the synthetic function of the liver and the hemodynamic effects of portal hypertension [3]. Haimovici et al. showed a statistically significant relationship between alcohol intake and CSR [5]. Experimental studies have shown serous retinal detachment secondary to alteration of choroidal vascular permeability [6]. One of the studies suggests that ischemia at the level of the choroid can cause capillary and venous congestion with increased fluid transudation [7]. We report a unique case of bilateral multifocal CSR secondary to alcoholic chronic liver disease in a 58-year-old man.

Case presentation

A 58-year-old Caucasian man was referred to the eye clinic in view of multiple raised yellowish lesions in both fundi. He had originally visited his optician for occasional flashes and floaters. He had recently been diagnosed with diet controlled type 2 diabetes mellitus and was on a low dose of amlodipine (5mg/day) for well controlled hypertension. His other drug history included analgesics (paracetamol, dihydrocodeine) and omeprazole. He admitted to heavy alcohol consumption in the past and had chronic liver disease with ascites.

His examination revealed that he had hepatomegaly with a palpable liver edge three fingerbreadths below the right costal margin, but no splenomegaly. An ultrasound of the liver showed generally increased echogenicity suggestive of liver cirrhosis. A computed tomography (CT) scan confirmed the presence of liver cirrhosis and showed evidence of esophageal varices, in keeping with decompensated chronic liver disease.

There was no evidence of a localized lesion in the liver, ruling out the possibility of both hepatocellular carcinoma and metastatic disease as causes of decompensation. His liver function tests (LFTs), including alkaline phosphatase (ALP), alanine aminotransferase (ALT) and γ-glutamyl transferase (GGT), had been elevated for several years. Interestingly, he was also found to have a marginally elevated plasma viscosity of 1.81mPa/s (normal range 1.5 to 1.72mPa/s) with no evidence of paraprotein.

His ocular examination was within normal limits for the anterior segment. His visual acuity was 6/6 in both eyes. Ophthalmoscopic examination of both eyes revealed a symmetrical pattern of dozens of variably sized, slightly yellowish, translucent raised lesions throughout the fundi (Figures 1A and 1B). These lesions were confirmed as multiple neurosensory retinal detachments on optical coherence tomography (OCT) (Figure 2) and fundus autofluorescence (Figures 3A and 3B). The patient was followed-up in the eye clinic and was asymptomatic until his last follow-up. Visual acuity, fundus and OCT findings were unchanged. As the visual acuity was good and there was no evidence of choroidal neovascularization, conservative management was recommended.

Figure 1
figure 1

(A) and (B) Fundal images. Variably sized, slightly yellowish, translucent raised lesions throughout the fundi in both the right eye (A) and the left eye (B). Images were obtained at presentation.

Figure 2
figure 2

Optical coherence tomography image. Optical coherence tomography performed through the posterior pole demonstrated serous sensory detachment without any suggestion of retinal pigment epithelial detachment or retinal thinning. The image was obtained at presentation.

Figure 3
figure 3

(A) and (B) Fundus autofluorescence images. Fundus autofluorescence recorded using a confocal scanning laser ophthalmoscope showed autofluorescence, which corresponds with the detached sensory retina in the right eye (A) and the left eye (B). The images were obtained at presentation.

Discussion

From a pathophysiological aspect, we hypothesize that in our patient the damaged liver produced less blood protein. This may have disturbed the body’s fluid balance, leading to alteration of choroidal vascular permeability, increased fluid transudation, serous fluid accumulation in the neurosensory retina and thus multifocal CSR [6]. Ammonia dysmetabolism has also been noted in patients with liver cirrhosis. It is perhaps interesting to note that patients with minimal hepatic encephalopathy, despite their presenting with normal mental and neurological status upon clinical examination, have been found to demonstrate inflammation and raised levels of ammonia in the blood caused by diminished clearance by the liver [8]. The increased serum levels of inflammatory markers (such as C-reactive protein, white blood cell count and IL-6) found in patients with liver cirrhosis [8] have been implicated in the breakdown of the blood–brain barrier. IL-6 and TNF-α are known to enhance fluid-phase permeability of isolated brain endothelial cells in vitro[9], suggesting that these and other inflammatory markers could also potentially contribute to changes in the outer blood–retina barrier and to an increase in choroidal vascular permeability, leading to CSR. Moreover, alcohol has been shown to be associated with nitric oxide–related abnormalities of choroidal blood flow autoregulation [10], thus providing an additional mechanism for the change in choroidal vascular permeability and the associated fluid leakage in the sub-RPE space and CSR development. Oxidative stress has also been implicated in liver cirrhosis [11]. Enhanced production of reactive oxygen species is thought to be involved in the nitration of tyrosine residues in intracellular proteins, thus affecting transastrocytic substrate transport and selective degradation of the permeability of the blood–brain barrier and potentially the outer blood–retina barrier [12, 13].

Conclusion

To the best of our knowledge, this is the first case of multifocal CSR related to alcoholic liver disease to be reported in the literature and has potential implications for the pathogenesis of CSR in these patients. Our patient had no other risk factors for CSR [5], such as systemic steroid, antihistamine or antibiotic use; history of autoimmune disease; untreated hypertension; or tobacco use. The differential diagnoses of acute exudative polymorphous paraneoplastic vitelliform maculopathy [14] and acute exudative polymorphous vitelliform maculopathy [15] could not be excluded in the absence of fluorescein angiography and electroretinography, although the non-progressive nature of the lesions during follow-up in our patient, the absence of subretinal yellowish deposits gravitating as a meniscus below the macula, and the normal visual acuity were not supportive of these diagnoses.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Abbreviations

ALP:

Alkaline phosphatase

ALT:

Alanine aminotransferase

CSR:

Central serous retinopathy

CT:

Computed tomography

GGT:

γ-glutamyl transferase

IL:

Interleukin

LFT:

Liver function test

OCT:

Optical coherence tomography

RPE:

Retinal pigment epithelium

TNF:

Tumor necrosis factor.

References

  1. Spaide RF, Campeas L, Haas A, Yannuzzi LA, Fisher YL, Guyer DR, Slakter JS, Sorenson JA, Orlock DA: Central serous chorioretinopathy in younger and older adults. Ophthalmology. 1996, 103: 2070-2080.

    Article  CAS  PubMed  Google Scholar 

  2. Friberg TR, Eller AW: Serous retinal detachment resembling central serous chorioretinopathy following organ transplantation. Graefes Arch Clin Exp Ophthalmol. 1990, 228: 305-309. 10.1007/BF00920052.

    Article  CAS  PubMed  Google Scholar 

  3. Onder C, Bengur T, Selcuk D, Bulent S, Belkis U, Ahmet M, Eser P, Leyla AS: Relationship between retinopathy and cirrhosis. World J Gastroenterol. 2005, 11: 2193-2196.

    Article  PubMed  PubMed Central  Google Scholar 

  4. Abe T, Nakajima A, Satoh N, Koizumi T, Sakuragi S, Ono T, Komatsu M, Masamune O: Clinical characteristics of hepatitis C virus-associated retinopathy. Jpn J Ophthalmol. 1995, 39: 411-419.

    CAS  PubMed  Google Scholar 

  5. Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S: Central Serous Chorioretinopathy Case-Control Study Group. Risk factors for central serous chorioretinopathy: a case-control study. Ophthalmology. 2004, 111: 244-249. 10.1016/j.ophtha.2003.09.024.

    Article  PubMed  Google Scholar 

  6. Chon CH, Yao XY, Dalal R, Takeuchi A, Kim RY, Marmor MF: An experimental model of retinal pigment epithelial and neurosensory serous detachment. Retina. 1996, 16: 139-144.

    Article  CAS  PubMed  Google Scholar 

  7. Prünte C, Flammer J: Choroidal capillary and venous congestion in central serous chorioretinopathy. Am J Ophthalmol. 1996, 121: 26-34.

    Article  PubMed  Google Scholar 

  8. Shawcross DL, Wright G, Olde Damink SW, Jalan R: Role of ammonia and inflammation in minimal hepatic encephalopathy. Metab Brain Dis. 2007, 22: 125-138. 10.1007/s11011-006-9042-1.

    Article  CAS  PubMed  Google Scholar 

  9. Duchini A, Govindarajan S, Santucci M, Zampi G, Hofman FM: Effects of tumor necrosis factor-α and interleukin-6 on fluid-phase permeability and ammonia diffusion in CNS-derived endothelial cells. J Investig Med. 1996, 44: 474-482.

    CAS  PubMed  Google Scholar 

  10. Tittl MK, Spaide RF, Wong D, Pilotto E, Yannuzzi LA, Fisher YL, Freund B, Guyer DR, Slakter JS, Sorenson JA: Systemic findings associated with central serous chorioretinopathy. Am J Ophthalmol. 1999, 128: 63-68. 10.1016/S0002-9394(99)00075-6.

    Article  CAS  PubMed  Google Scholar 

  11. Wu D, Cederbaum AI: Oxidative stress and alcoholic liver disease. Semin Liver Dis. 2009, 29: 141-154. 10.1055/s-0029-1214370.

    Article  CAS  PubMed  Google Scholar 

  12. Murthy CR, Rama Rao KV, Bai G, Norenberg MD: Ammonia-induced production of free radicals in primary cultures of rat astrocytes. J Neurosci Res. 2001, 66: 282-288. 10.1002/jnr.1222.

    Article  CAS  PubMed  Google Scholar 

  13. Häussinger D, Schliess F: Pathogenetic mechanisms of hepatic encephalopathy. Gut. 2008, 57: 1156-1165. 10.1136/gut.2007.122176.

    Article  PubMed  Google Scholar 

  14. Grunwald L, Kligman BE, Shields CL: Acute exudative polymorphous paraneoplastic vitelliform maculopathy in a patient with carcinoma, not melanoma. Arch Ophthalmol. 2011, 129: 1104-1106. 10.1001/archophthalmol.2011.215.

    Article  PubMed  Google Scholar 

  15. Chan CK, Gass JD, Lin SG: Acute exudative polymorphous vitelliform maculopathy syndrome. Retina. 2003, 23: 453-462. 10.1097/00006982-200308000-00002.

    Article  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Despoina Gkotsi.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

DG conceived and wrote the manuscript. MG wrote and reviewed the manuscript and provided final approval of the manuscript for publication. GL reviewed the manuscript and collected the references with final approval. AS followed up the patient and reviewed the manuscript. BD suggested changes and gave final approval of the manuscript for publication. All authors read and approved the final manuscript.

Authors’ original submitted files for images

Rights and permissions

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Gkotsi, D., Gupta, M., Lascaratos, G. et al. Alcoholic liver disease and bilateral multifocal central serous retinopathy: a case report. J Med Case Reports 7, 43 (2013). https://doi.org/10.1186/1752-1947-7-43

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/1752-1947-7-43

Keywords