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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2019  |  Volume : 30  |  Issue : 3  |  Page : 715-718
Bilateral endophthalmitis and symmetrical peripheral gangrene in a patient with chronic kidney disease on maintenance hemodialysis

1 Department of Medicine, Chattogram Maa-O-Shishu Hospital Medical College, Chattogram, Bangladesh
2 Department of Nephrology, Chattogram Maa-O-Shishu Hospital Medical College, Chattogram, Bangladesh

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Date of Submission06-May-2018
Date of Decision09-Jul-2018
Date of Acceptance10-Jul-2018
Date of Web Publication26-Jun-2019


Dialysis patients have greater number of complications due to multiple comor-bidity and access-related infections as well as nosocomial infections due to reduced immunity and more frequent hospitalizations. Endogenous endophthalmitis is a potentially blinding ocular infection occurring in chronically debilitated patients and the use of invasive procedures. Symmetric peripheral gangrene (SPG) is defined as symmetrical distal ischemic damage in two or more sites in the absence of a major vascular occlusive disease. It carries a high mortality rate with a very high frequency of multiple limb amputations in the survivors. However, only a few case reports have described endogenous endophthalmitis in dialysis patients. Concomitant endophthalmitis and disseminated intravascular coagulation (DIC), presenting as SPG, is extremely rare and no such case was found in the literature survey. Herein, we report a very rare association of bilateral endophthalmitis with DIC and SPG in a patient with chronic kidney disease on maintenance hemodialysis.

How to cite this article:
Nath JD, Kashem A, Osman AM, Das T. Bilateral endophthalmitis and symmetrical peripheral gangrene in a patient with chronic kidney disease on maintenance hemodialysis. Saudi J Kidney Dis Transpl 2019;30:715-8

How to cite this URL:
Nath JD, Kashem A, Osman AM, Das T. Bilateral endophthalmitis and symmetrical peripheral gangrene in a patient with chronic kidney disease on maintenance hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Sep 25];30:715-8. Available from: http://www.sjkdt.org/text.asp?2019/30/3/715/261355

   Introduction Top

Bacterial endophthalmitis is an infection and inflammation of the posterior segment of the eye that can rapidly evolve into a sight-threatening situation. Endogenous endophthal-mitis usually presents with blurred vision and ocular pain, and only less than half of patients have signs of systemic infections such as fever. Many etiologic organisms (Gram-positive, Gram-negative, and fungal) have been reported to cause endogenous endophthalmitis.

During endophthalmitis, bacteria enter the posterior segment following trauma, surgery, or from spread into the eye through the bloodstream from a distant focus of infection. Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by widespread intravascular activation of coagulation that can be caused by any underlying pathology, such as severe infections, malignancies, trauma, or obstetric complications. DIC itself can be asymptomatic. It can also be associated with bleeding or the signs of systemic thrombosis that may lead to life-threatening multiple organ failure. Symmetrical peripheral gangrene (SPG) is very rare manifestation of DIC. Chronic dialysis patients have defects in both innate and adaptive immunity, thus predisposing them to infectious disease.

   Case Report Top

Informed consent was obtained from the immediate relatives of the patient before reporting the case.

A 57-year-old female with known chronic kidney disease (CKD) undergoing maintenance hemodialysis (MHD) twice weekly for the past seven months was admitted to a private hospital in Chattogram, Bangladesh, with complaints of high-grade intermittent fever with anuria and blurring of vision in both eyes for three days. She had previous history of diabetes and hypertension for 10 years. Initial examination showed that she was confused and febrile, mildly anemic, and had reduced blood flow in the arteriovenous fistula site. She was initially diagnosed with a case of acute kidney injury on CKD with bilateral endophthalmitis due to sepsis. She was treated with intravenous and ocular broad-spectrum antibiotics, and MHD was continuing with a jugular catheter. One day after admission, bluish discoloration followed by blackening of the distal left middle phalanx and swelling and blackening of the right hand and multiple hemorrhagic purpura appeared in soles of both feet [Figure 1] and [Figure 2]. At the same time, the patient complained of complete loss of vision in both eyes. Ocular examination showed no perception of light, projection of rays. Both radial and dorsalis pedis pulse were palpable. There was no past history of joint pain, hematuria, Raynaud’s phenomenon, and intake of B-blockers. Antibiotics were changed to intravenous piperacillin/tazobactam combination with metronidazole, and she was diagnosed further with bilateral panophthalmitis with SPG due to sepsis. Complete blood count showed neutrophilic leukocytosis, neutrophil was 95%, total count was 20.7 x 10[9]/L, hemoglobin (Hb) was 11 g/dL, and urine routine analysis and culture were normal. The serum creatinine was 9 mg/dL, fasting blood sugar and 2-h postprandial blood sugar were 119 and 198 g/dL, respectively, glycosylated Hb was 6.4%, serum albumin was 2.71 g/dL, and uric acid was 7 mg/dL. Serum electrolytes showed hyponatremia, sodium was 133 meq/ L, calcium was 6.1 mg/dL, and phosphate was 5.8 mg/dL. Blood culture showed the growth of Serratia species. The electrocardiogram showed nonprogression of R wave and left ventricular hypertrophy, echocardiography showed concentric hypertrophy, mild mitral and aortic regurgitation, and color Doppler imaging of both upper limbs showed no blood flow in the left 4th metacarpal artery, but sparing large arteries on both sides. Prothrombin time was >44 s, P-anti-nuclear cytoplasmic antibodies (ANCA) was 5.6 (<12, normal value), anti-nuclear antibody was 3.9 (<10, normal), C-ANCA was 10.2 U/mL, (<12, normal), Antidouble strand DNA was 14.2 U/mL (<20, normal), and D Dimer was initially 6.31 g/mL (<0.5, normal) which became progressively diminished to 4.1 g/mL and 2.3 g/mL later on, and APTT was 38 s (25–43 s). Unfortunately, the patient died 10 days later as her relatives were reluctant to subject him to any surgical procedure.
Figure 1: Multiple hemorrhagic purpuric lesions over soles of both feet.

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Figure 2: Blackening and gangrene of the distal right ring finger and dorsum of left hand and purpuric spots on right middle finger tips.

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   Discussion Top

CKD is associated with poor outcomes including an increased risk of cardiovascular disease and mortality.[1] These associations may result from the presence of traditional risk factors as well as biochemical abnormalities such as increased inflammatory factors, endothelial dysfunction, and enhanced coagulation. Increased risk for infections is linked to alterations in the immune system in CKD, since uremia is associated with a state of immune dysfunction characterized by immunodepression that contributes to the high prevalence of infections among these patients, as well as by immuno-activation resulting in inflammation.

Endogenous endophthalmitis (also known as metastatic endophthalmitis) results from the spread of the organism into the eye from an infection elsewhere in the body. Compared with endophthalmitis following trauma or surgery, endogenous endophthalmitis is relatively rare, accounting for only 2%–8% of all reported endophthalmitis cases.[2] The prevalence of endogenous endophthalmitis is higher than exogenous endophthalmitis in chronic dialysis patients. However, endogenous endophthalmitis carries with it the danger of bilateral infection in 15%–25% of cases. Fungal organisms account for at least 50% of all endogenous cases, with Candida albicans (75%–80% of fungal cases) being the leading causative agent. Gram-negative organisms cause 32%–37% of all cases of endogenous endophthalmitis and typically have poor visual outcomes because these infections are difficult to treat.[3]

Only a few case reports have described endogenous endophthalmitis among dialysis patients in the literature. These case reports highlight that vascular access should be considered as a possible and unique source of infection in the dialysis population. Serratia marcescens was earlier considered to be an innocuous, nonpathogenic organism, but over the past two decades, it has become an opportunistic pathogen causing nosocomial infections. A broad range of hospital-acquired infections caused by S. marcescens including respiratory tract infections, urinary tract infections, septicemia, meningitis, pneumonia, conjunctivitis, wound and eye infections, keratitis, endophthalmitis, and endocarditis have been reported.[4] Reports have shown rare cases of S. marcescens in nonhospital settings.

Severe systemic infections or sepsis are the most common causes of DIC. About 35% of cases of severe sepsis may be complicated by DIC. Classically, infection with Gram-negative microorganisms has been associated with DIC. Systemic infections with other microorganisms, including fungi or parasites, may lead to DIC as well. For example, high parasitemia, primarily of Falciparum malaria, may be associated with DIC and high mortality.[5]

The initiation and propagation of procoagulant pathways with simultaneous impairment of natural anticoagulant systems and suppression of endogenous fibrinolysis as a result of systemic inflammatory activation lead to platelet activation and fibrin deposition.[6],[7] Important mediators that regulate these processes are cytokines, such as interleukin-1 (IL-1) and IL-6 and tumor necrosis factor-α.

Purpura fulminans, a severe form of DIC, is characterized by diffuse microthrombi of the skin leading to hemorrhagic necrosis. This is classically seen in meningococcemia.

SPG is characterized by symmetric necrosis of the skin and distal extremities, following which two or more distal sites become gangrenous in the absence of large artery occlusion.[8],[9] SPG is described as multiple extremity ischemia at two or more sites in the absence of large vessel obstruction. It is well established that the digital perfusion will drop to zero in the presence of persistently low perfusion pressures of 35–60 mm Hg.[10]

SPG is known to present with pallor or cyanosis, coldness, and pain in the extremity in the initial phases. If appropriate care is not provided at this stage, the digits may progress to become erythematous with dusky discoloration of the skin followed by the development of bullae or blisters that subsequently result in the formation of gangrene.[11]

SPG is associated with a high rate of amputation (auto-amputation or surgical amputation) of the limbs in the survivors. In a prospective case series from Eastern India, six patients had amputation out of the nine survivors of SPG. In another retrospective case series from the USA, eight patients had amputation out of the nine survivors.[12] The mortality rate of SPG is also very high. About one-third of the patients of different case series had died.

Calciphylaxis is a serious, uncommon disease in which calcium accumulates in small blood vessels of the fat and skin tissues. Lesions begin characteristically as a livedo reticularis pattern of mottling with violaceous, superficial, tender nodules, and presentation can be mistaken for cellulitis. In this case, presentation was so florid with the lack of this discoloration. Hence, SPG was diagnosed clinically by the exclusion of calciphylaxis.[13]

   Conclusion Top

A high degree of suspicion is necessary to make an early diagnosis of endogenous endophthalmitis with patients commonly complaint of eye pain and blurring of vision. Surgical intervention is generally recommended for patients infected with virulent organisms. Even with aggressive treatment, outcome is very disappointing.

Conflict of interest: None declared.

   References Top

Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospital-lization. N Engl J Med 2004;351:1296-305.  Back to cited text no. 1
Okada AA, Johnson RP, Liles WC, D’Amico DJ, Baker AS. Endogenous bacterial endoph-thalmitis. Report of a ten-year retrospective study. Ophthalmology 1994;101:832-8.  Back to cited text no. 2
Jackson TL, Eykyn SJ, Graham EM, Stanford MR. Endogenous bacterial endophthalmitis: A 17-year prospective series and review of 267 reported cases. Surv Ophthalmol 2003;48:403-23.  Back to cited text no. 3
Hejazi A, Falkiner FR. Serratia marcescens. J Med Microbiol 1997;46:903-12.  Back to cited text no. 4
Levi M, van der Poll T. Coagulation and sepsis. Thromb Res 2017;149:38-44.  Back to cited text no. 5
Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013;369:840-51.  Back to cited text no. 6
Simmons J, Pittet JF. The coagulopathy of acute sepsis. Curr Opin Anaesthesiol 2015;28: 227-36.  Back to cited text no. 7
Goodwin JN. Symmetrical peripheral gangrene. Arch Surg 1974;108:780-4.  Back to cited text no. 8
Molos MA, Hall JC. Symmetrical peripheral gangrene and disseminated intravascular coagulation. Arch Dermatol 1985;121:1057-61.  Back to cited text no. 9
Roddie IC, Shepherd JT. Evidence for critical closure of digital resistance vessels with reduced transmural pressure and passive dilatation with increased venous pressure. J Physiol 1957;136:498-506.  Back to cited text no. 10
Davis MD, Dy KM, Nelson S. Presentation and outcome of purpura fulminans associated with peripheral gangrene in 12 patients at mayo clinic. J Am Acad Dermatol 2007;57:944-56.  Back to cited text no. 11
Ghosh SK, Bandyopadhyay D, Ghosh A. Symmetrical peripheral gangrene: A prospective study of 14 consecutive cases in a tertiary-care hospital in Eastern India. J Eur Acad Dermatol Venereol 2010;24:214-8.  Back to cited text no. 12
Wilmer WA, Magro CM. Calciphylaxis: Emerging concepts in prevention, diagnosis, and treatment. Semin Dial 2002;15:172-86.  Back to cited text no. 13

Correspondence Address:
Jishu Deb Nath
Department of Medicine, Chattogram Maa-O-Shishu Hospital Medical College, Chattogram
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DOI: 10.4103/1319-2442.261355

PMID: 31249239

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