British Journal of Ophthalmology, 1985, 69, 774-777

Clostridium septicum panophthalmitis with systemiccomplicationsMICHAEL S INSLER, ZEYNEL A KARCIOGLU, AND THOMAS NAUGLE JR

From the Department of Ophthalmology, Tulane University School of Medicine, 1430 Tulane Avenue,New Orleans, LA 70112, USA

SUMMARY A fulminant case of endophthalmitis due to Clostridium septicum is described. Thepatient presented with spontaneous gas gangrene panophthalmitis, with early visual loss and an airbubble in the anterior chamber. Death ensued, and necropsy revealed changes consistent withsevere arterosclerotic cardiovascular disease, a relationship not uncommon in patients withclostridium sepsis. This association as well as the histopathology of the globe are discussed.

Gas gangrene panophthalmitis is a rare conditionusually following penetrating injury to the globe. Inmost of the reported cases the infecting organism hasbeen Clostridiumn perfringens.'

Characteristic findings are brawny swelling of thelids, coffee coloured discharge, hypopyon, ringabscess of the cornea, gas bubbles in the anteriorchamber, and early loss of vision. Systemic manifes-tations include fever and leucocytosis, malaise,nausea, and vomiting. Treatment generally consistsof evisceration or enucleation of the globe andsystemic antibiotics. Extraocular extension of infec-tion is prevented by well timed surgical intervention.To the best of our knowledge, this paper is the first

report of gas gangrene panophthalmitis due toClostridium septiclunm.

Case report

A 78-year-old Caucasian woman was admitted tohospital on 15 October 1981 with a 24-hour history ofnausea, vomiting, and mild abdominal pain. Thediagnosis on admission was dehydration and acutegastroenteritis. There was a history of atheroscleroticheart disease and degenerative arthritis. Vital signs atthe time of admission showed a blood pressure of152/80 mmHg, respiration rate of 20/min, a slighttachycardia, and a temperature of 101°F (38-3°C).Examination revealed a slightly obese Caucasianwoman who was vomiting and complaining ofabdominal pain. The heart and lung examination wasnormal. The abdominal examination revealedCorrcspondencc to Michael S Inslcr. MD.

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tenderness but good bowel sounds. The white cellcount was 28 9x 109/1; the haemoglobin was 13 7 g/dl,and the packed cell volume was 40-1%.

Later on that evening the patient became confusedand hypotensive and had a respiratory arrest. Sheresponded to cardiorespiratory resuscitation and wastransferred to the intensive care unit. The differentialdiagnosis at that time included a myocardial infarc-tion and gastrointestinal haemorrhage. A serousdischarge was noted from the right eye, and lid andconjunctival specimens were taken for culture.Erythromycin 500 mg intravenously six hourly wasadded to the cefamandole begun on admission.Two days after admission while the patient was on

a ventilator her temperature spiked to 104-60F(40 3°C) and blood cultures were obtained. A heartand a perfusion lung scan were performed, and bothwere within normal limits. An ophthalmology con-sultation was obtained, at which time a gas bubblewas noted in the anterior chamber.

Ophthalmic examination on 18 October 1981revealed an opaque cornea and a very tense globe.An anterior chamber paracentesis was performedand approximately 0 1() ml of chocolate colouredfluid was obtained. This material was plated on bloodand chocolate agars and was submitted for anaerobicculture.On 19 October 1981 the patient died. A general

necropsy, performed 21/2 hours after death, revealedsevere atherosclerotic cardiovascular disease,dissecting aortic aneurysm, severe brochopeneu-monia, and changes consistent with sepsis. The aorticaneurysm was not ruptured and did not appear to be

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Clostridium septicum panophthalmitis with systemic complications

the cause of death. No recent myocardial infarctionwas found. Culture of the anterior chamber aspirategrew a pure colony of Clostridium septicum.

PATHOLOGICAL EXAMINATION OF THE EYE

The globe was examined under the dissecting micro-scope in the pathology laboratory. No penetratinginjury could be identified. The corneal surface wasopaque, extremely irregular, and thin in the centre.On transverse sectioning the globe was observed tobe diffusely necrotic. A small amount of purulent,coffee coloured fluid was found in the anteriorchamber and vitreous cavity. The inner surface of theeye was pale and extensively necrotic. The retina wasnot identified. Instead the inner surface of the globewas irregular, elevated, and bullous in appearance.

Histological examination of the eye showed that allocular tissues were involved in an acute necrotisinginflammatory process (Fig. 1). The cornea and sclera(Fig. 2) were diffusely infiltrated with acute inflam-matory cells and had undergone severe collagendegeneration and necrosis. Scleral and episcleralblood vessels were surrounded by acute inflamma-tion and their walls were partially necrotic. Thecentral cornea was extremely thin, with total absenceof the epithelium and more than half of the stroma.The ciliary body and iris were extensively inflamedand necrotic. The choroid was detached in somesegments and was also involved in the diffuse necro-sis; in some areas only the framework of the vascula-

ture was left intact. The choroidal blood vessels werefound to contain many thromboemboli (Fig. 3). Onlyfragments of retinal structures showing severenecrosis could be identified in certain segments of theglobe. In addition to its necrotic appearance thetissue contained empty spaces possibly secondary togas-producing bacteria. The overall bullous appear-ance of the retina and choroid was also consistentwith extensive oedema and gas production. A fewclusters of Gram-positive bacteria were identified,but these did not have the spindle, drumstick appear-ance of Clostridium septicum and did not containspores.

Discussion

Clostridial infections of the eye are devastating.Since Leavelle's' extensive review of 53 previouslyreported cases as well as three of his own nineadditional cases have been reviewed by Frantz et al.5All previously reported cases of gas gangrenepanophthalmitis followed pentrating injuries to theeye and the offending organism was Clostridiumperfringens. Frantz and colleagues' report included a68-year-old white male who presented with fever,pain in the right upper quadrant of the abdomen, andpanophthalmitis of the left eye. Unlike the previouslydescribed cases their case resulted from endogenousinfection of the eye complicating perforation of agangrenous gallbladder.

Fig. I Extensive oedema andnecrosis ofretina and choroid.Retina is totally necrotic. Only ashort segment ofdetached retinalpigment epithelium (RPE) is seen inthefigure. VC: vitreous chamber;C: choroid; S: sclera;EOM: extraocular muscle.(Haematoxylin and eosin, x40).

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Michael S Insler, ZeynelA Karcioglu, and Thomas Naugle Jr

Fig. 2 Diffuse infiltration ofacuteinflammatory cells and necrosis inretina (R), choroid (C), and sclera(S). (HandE, xlOO).

The clinical picture of clostridial panophthalmitisdescribed by Leavelle is one of severe pain and rapidloss of vision within 12 hours of injury. An explosivepanophthalmitis with chemosis and swelling of the lidis usually apparent by 18 hours. Hypopyon, ringabscess of the cornea, coffee coloured discharge, gasbubbles in the anterior chamber, immobilisation ofthe globe, and a total loss of fundus reflex with loss ofvision were signs usually evident by 24 hours. Con-ventional antibiotic therapy has been entirelyimpotent against this disastrous disease, even thoughsome cases were seen very early.

For practical purposes the clostridia may. bedivided into three groups: C. botulinum causingbotulism, C. tetani causing tetanus, and several typesof clostridia causing gas gangrene, commonly C.perfringens, C. novyi, C. septicum, C. histolyticum,and C. fallax. All the clostridia are large Gram-positive rod-like anaerobic bacteria with a largerspore-forming end, giving them a drumstick appear-ance. The clostridia which may be considered aspotential causes of gas gangrene panophthalmitisproduce powerful exotoxins. The most commonmember of this group of organisms is C. perfringens(C. welchii); next are C. novyi and C. septicumin degree of frequency of isolation from warwounds.

C. septicum, an obligate anaerobe, is B-haemolyticon blood agar and highly motile. Spreading growth

can be overlooked, as isolates may form only a thinfilm on the culture plate without the definition ofdistinct colonies. Smears from cultures show Gram-positive sporulating rods with oval terminal andsubterminal spores. C. septicum is differentiatedfrom other clostridia by its carbohydrate fermenta-tion reactions and its lack of lecithinase or lipaseproduction.An association of clostridial infections with malig-

nancy, especially cancer of the colon, has beendemonstrated by several case reports."9 In 1969Alpern and Dowell' reported that 23 of 27 patients(85%) with C. septicum infections whose cultureswere referred to the Center for Disease Control(CDC) for identification had malignant disease. Ofthe four patients who did not have malignant diseasethree developed intestinal tumours one to twomonths after the C. septicum was cultured.Koransky et al.7 reported on the clinical signific-

ance of C. septicum bacteraemia. The medicalrecords of 59 patients were reviewed; 42 (71%) ofthese patients had malignant disease. Half hadhaematological malignant disease and one half hadsolid tumours. Of the 21 patients with solid tumours14 (67%) had cancer of the colon. The caecum anddistal ilieum were thought to be the most probableportals of entry for C. septicum bacteraemia amongthe 28 patients examined at necropsies. Theyreported one patient with distant metastatic infection

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Clostridium septicum panophthalmitis with systemic complications

Fig. 3 Uedema, necrosis, and diffuse acute inflammatorycell infiltration ofthe retina, choroid, and sclera with multiplethromboemboli (T) in choroidal and scleral blood vessels. R:necrotic retina; C: choroid; S: sclera. (H and E, x85).Insert: Organisms, identified in culture as Clostridiumsepticum, within necrotic areas ofthe sclera. (Gram stain,x850, oil immersion).

of the eye who had an enucleation and then was laterfound to have adenocarcinoma of the colon.

Further results of their study showed that of the 17patients with no detectable malignancy six had severeatherosclerotic cardiovascular disease with agangrenous extremity or gangrenous bowel. Infec-tion with C. septicum was the apparent cause of deathin 40 patients (68%). All surviving patients weregiven penicillin, cephalothin, chloramphenicol, orcarbenicillin (antibiotics to which clostridia havebeen found to be sensitive"') soon after they wereadmitted to the hospital.

Post-mortem examination of our patient, whoapparently developed spontaneous gas gangrenepanophthalmitis due to Clostridium septicum, failedto disclose an occult malignant tumour, which must

be ruled out when C. septicum is cultured from a'metastatic' infection outside the bowel.' However,she did have severe atherosclerotic cardiovasculardisease, as did six of 17 patients without malignantdisease in Koransky and colleague's series.7 It hasbeen suggested that arteriosclerosis may have a rolein the development of ischaemia and tissue necrosis,which are important predisposing factors for clostri-dial growth and gangrene formation.7

Although a positive (ante-mortem) blood culturewas not obtained in our case, we attribute this toantimicrobial therapy instituted prior to the sam-pling. Fever, especially when accompanied by gasgangrene, tissue necrosis, and/or the signs of shockwhich characterised our patient's hospital course,should suggest possible septicaemia caused by toxicbacteria such as clostridium.The importance of early recognition and prompt

therapy in patients with Clostridium septicum infec-tion cannot be overemphasised. When these patientsare admitted to hospital they are acutely ill and toxic.Their clinical course is usually fast downhill, andunless the appropriate antibiotics are administeredsoon after admission the outcome is fatal. Bloodcultures, both aerobic and anaerobic, should beperformed rapidly, and therapy should be institutedbefore the results of the cultures are received.Penicillin remains the drug of choice, but somepatients may be treated successfully with chloram-phenicol, carbenicillin, or cephalothin.

References

I Lcavellc RB. Gas gangrcnc panophthalmitis. Arch Ophihalmol1955; 53: 634-42.

2 Walsh TJ. Clostridial ocular infcctions. Casc report of gasgangrcnc panophthalmitis. BrJ Ophthalinol 1965; 49: 472-7.

3 Kurz GH, Wciss JF. Gas gangrcne panophthalmitis. Br JOphthalmol 1969; 53: 323-6.

4 Lcvitt JM, Stam J. Clostridium perfringens panophthalmitis.Arch Ophthalmol 1970; 84: 227-88.

5 Frantz JF, Lcmp MA, Font RL, Stonc R, Eisner E. Acutecndogenous panophthalmitis causcd by Clostridium perfringens.Am J Ophthalmol 1974; 78: 295-3t)3.

6 Alpern RJ, Dowell VR. Clostridium septicum infections andmalignancy. JA MA 1969; 209: 385-8.

7 Koransky JR, Stargel MD, Dowcll VR. Clostridiuin septicumbacteremia. Am J Med 1979; 66: 63-6.

8 Katlic MR, Derkac WM, Coleman WS. Clostridium septicuminfcction and malignancy. Ann Surg 1981: 193: 361-4.

9 Schaaf RE, Jacobs N, Kcivin FM, et al. Clostridium septicuminfcction associated with colonic carcinoma and hcmatologicabnormality. Radiology 198t); 137: 625-7.

1) Gabay EL, Rolfc RD, Fincgold SM. Susccptibility ofClostridium septicum to 23 antimicrobial agents. AntimicrobAgents Chemother 1981; 20: 852-3.

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