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Endogenous Endophthalmitis and Disseminated Intravascular Coagulation Complicating a Klebsiella pneumoniae Perirenal Abscess in a Patient with Type 2 Diabetes
Endogenous Endophthalmitis and Disseminated Intravascular Coagulation Complicating a Klebsiella pneumoniae Perirenal Abscess in a Patient with Type 2 Diabetes KOHZO TAKEBAYASHI, MD, PHD; SACHIKO MATSUMOTO, MD; YAYOI NAKAGAWA, MD; SADAO WAKABAYASHI, MD; YOSHIMASA ASO, MD, PHD; TOSHIHIKO INUKAI, MD, PHD
ABSTRACT: We describe a 56-year-old woman with type 2 diabetes complicated by a Klebsiella pneumoniae perirenal abscess. The patient further developed incipient diabetic ketoacidosis, disseminated intravascular coagulation, and endogenous endophthalmitis. Occurrence of the latter as a metastatic infection from perirenal abscess caused by this organism is very rare, and we know of no previously reported patient with the additional occurrence of disseminated intravascular co-
agulation. Since prompt intravitreal antibiotic administration is needed, physicians should be aware of these rare but severe complications of K pneumoniae infection, especially in patients with poorly controlled diabetes. KEY INDEXING TERMS: Klebsiella pneumoniae; Perirenal abscess; Diabetes mellitus; Disseminated intravascular coagulation; Endogenous endophthalmitis. [Am J Med Sci 2005;329(3):157–160.]
P
previous report in which the K pneumoniae abscess complicated by endophthalmitis was perirenal.14 Further, such a case complicated by DIC has not yet been described. We report a 56-year-old patient with type 2 diabetes complicated by a massive K pneumoniae perirenal abscess. She developed some early features of diabetic ketoacidosis (DKA) and had the additional complications of DIC and finally metastatic endogenous bacterial endophthalmitis.
erirenal abscess, emphysematous cholecystitis, emphysematous pyelonephritis, and necrotizing fasciitis represent severe infectious complications of diabetes.1– 4 Perirenal abscess is caused mainly by Staphylococcus aureus, Staphylococcus epidermidis, and Gram-negative organisms such as Escherichia coli or Klebsiella pneumoniae.5 The abscess usually is accompanied by fever, continuous low back pain, and clinical and laboratory evidence of inflammation, although patients with a chronically progressive abscess often have no symptoms. A case of a diabetic patient with perirenal abscess who developed disseminated intravascular coagulation (DIC) represents a rarity.6,7 Also relatively rare but serious, endogenous bacterial endophthalmitis as a metastatic infection from liver abscess caused by K pneumoniae has been reported recently, especially in Asian patients with diabetes, and carries a poor prognosis for visual acuity7–13; endogenous endophthalmitis arising from a K pneumoniae perirenal abscess is very rare. We know of only one similar From the Department of Medicine, Koshigaya Hospital, Dokkyo University School of Medicine, Koshigaya, Japan. Submitted July 23, 2004; accepted October 26, 2004. Correspondence: Kohzo Takebayashi, MD, Department of Medicine, Koshigaya Hospital, Dokkyo University School of Medicine, 2-1-50, Minami-Koshigaya, Koshigaya, 343-8555, Japan. (E-mail: [email protected]) THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Case Report A 56-year-old woman was transferred to our hospital because of suspected DKA. She had been in good health until mid-October 2003, when she occasionally noted dry mouth and fatigue. She had not been diagnosed with diabetes mellitus. On November 7, 2003, she began to note fatigue, abdominal pain, and low back pain accompanied by moderate diarrhea. On the next day, her temperature rose to 38°C, and she was admitted to a nearby hospital for diagnosis and treatment. On the night of November 9, she developed dyspnea and worsening fatigue, low back pain, and dry mouth. Her mind was clear. Plasma glucose level was extremely high (564 mg/dL), and a dipstick urine test for ketone bodies yielded a positive result. With a diagnosis of suspected DKA, the patient was transferred to our hospital by ambulance at midnight on the next day, November 10. On admission, she showed confusion. Her height and body weight were 149 cm and 49 kg; temperature, blood pressure, and pulse rate were 38.0°C, 152/70 mm Hg, and 128/min. The respiratory rate was 40/min. The skin was only moderately dry. Routine hematologic and serologic tests on admission showed striking elevation of white blood cell (WBC) count and C-reactive protein (CRP) level
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(16400/L and 25.28 mg/dL), suggesting severe inflammation. The lactate dehydrogenase level also was elevated (1625 U/L). Plasma glucose and hemoglobin A1C were 498 mg/dL and 12.6%. The total serum concentration of ketone bodies was elevated (1265 mol/L; normal value, 0 –130), and fasting plasma C peptide immunoreactivity and anti-GAD antibody, respectively, were 2.66 ng/mL (normal value, 0.6 –2.8) and 0.3 U/mL (normal value, 0 –1.5). In addition, the platelet count was markedly decreased, while fibrin/fibrinogen degradation products were increased (0.7⫻104/L and 25.7 g/mL), suggesting DIC. Gas analysis of arterial blood sampled with the patient breathing room air showed a pH of 7.337, a PCO2 of 45.7 Torr, a PO2 of 56.2 Torr, HCO3 level of 23.9 mmol/L, and SaO2 of 84.7%. Admission blood cultures for bacteria yielded no growth. Chest radiography on admission demonstrated slight left pleural effusion and moderate cardiomegaly, and abdominal radiography showed marked dilatation of the colon by gas. Based on clinical and laboratory findings on admission, the patient was diagnosed with DIC, acute respiratory failure, and incipient DKA. Oxygen was given immediately by mask, and intravenous antibiotic therapy (2.0 g/day of imipenem/cilastatin) was initiated for suspected infection. For DIC, continuous intravenous infusion of a protease inhibitor, gabexate mesilate, was initiated at 1000 mg/day. For impending DKA, continuous intravenous insulin was given together with infusion of moderate amounts of normal saline. With this treatment, her mind began to clear on November 14, and findings of inflammation in blood tests lessened (WBC count, 13500/L; CRP, 3.69 mg/dL). On the same day, the platelet count also had increased (13.6⫻104/L). Fasting plasma glucose level was decreased to remain near 100 mg/dL after initiation of insulin therapy. Temperature fell to approximate 37°C. Results of blood gas analysis on November 14 also improved. On the other hand, colonic dilatation in abdominal radiographs did not change. Although abdominal pain, diarrhea, and oral dryness had improved, moderate low back pain and fatigue continued. On November 17, the WBC count and CRP level again rose to 14400/L and 15.5 mg/dL, respectively, as did the temperature (38°C), while bacterial cultures in blood, sputum, and urine on the same day were all negative for growth. In consideration of these findings and the persistent abdominal radiographic abnormalities, abdominal computed tomography was performed on November 21. The computed tomography scan demonstrated a massive left perirenal abscess with involvement of the left iliopsoas muscle (Figure 1). Percutaneous drainage of the abscess was performed on the next day, and abundant pus was obtained. Bacterial culture of the drainage demonstrated growth of K pneumoniae, and this isolate had a sensitivity for most antibiotics, including imipenem/cilastatin, ciprofloxacin, meropenem, and
ofloxacin. Since percutaneous drainage together with a change of intravenous antibiotic (from imipenem/cilastatin to ciprofloxacin, 600 mg/day) on November 21 failed to reduce the patient’s fever or low back pain and since additional change of antibiotics was also noneffective (to meropenem, 2.0 g/day on December 7), the abscess was drained surgically on December 17. Although transient postoperative pain was noted, low back pain gradually abated. Abdominal radiographic findings were also improved. Beginning on December 26, high-grade fever ceased and the WBC count and CRP level had improved (8200/L and 1.12 mg/dL). The lactate dehydrogenase level, platelet count, and fasting plasma glucose level at that time were 479 U/L, 30.5⫻104/L, and 108 mg/dL. HbA1C on January 5, 2004 was 5.3%. Blood, sputum, and urine cultures repeated several times since November 17 showed negative findings for growth. Concurrently with clinical progress concerning the abscess, on November 28, 2003, the patient began to report right orbital pain and impaired vision in the right eye; visual acuity worsened rapidly to light perception alone. An urgent consultation with an ophthalmologist at the hospital on December 1 resulted in a diagnosis of endogenous bacterial endophthalmitis, based on findings of hypopyon associated with severe cellular reaction in the anterior chamber of the right eye (57.4 cells/L; normal values, 0 –5), obscuring the fundus (December 1, Figure 2A). The left eye showed only evidence of simple diabetic retinopathy. Vitreous fluid culture was not performed. Direct intravitreal administration of 2 mg of ceftazidime and 1 mg of vancomycin into the right eye was carried out on the same day; in addition to continuous intravenous ciprofloxacin and instillation of levofloxacin and betamethasone. By December 4, the cellular reaction in the right anterior chamber had decreased somewhat, and the fundus could be visualized to some extent. By late December, visual acuity was improved to permit counting of fingers, and the fundus became more visible (December 27, Figure 2B). Intravenous antibiotics were followed by oral antibiotics (levofloxacin, 300 mg/day) beginning on December 27, 2003. The patient’s general condition and laboratory data have remained favorable since early January 2004. Levofloxacin was discontinued on January 13, and oral nateglinide (270 mg/day) was substituted for insulin injection. The patient was discharged home on January 28, with treatment of diabetes continuing in the outpatient department to successfully maintain good general condition and good diabetic control (HbA1C ⬍6.0%).
Discussion Although our patient was diagnosed with diabetes only immediately before transfer to our hospital,
Figure 1. Findings of abdominal computed tomography: massive perirenal abscess (A), and involvement of the right iliopsoas muscle (B).
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Figure 2. Findings of retina fundus on December 1, onset day (A), and on December 27, when the fundus became more visible (B).
based on the finding of diabetic retinopathy, she most likely had poorly controlled diabetes for a relatively long time. In addition, since GAD antibody was not detected while plasma C peptide immunoreactivity level was relatively high, the patient presumably had type 2 rather than type 1 diabetes. Perirenal abscess is known to occur, particularly in cases of poorly controlled diabetes,1,2 whereas Gramnegative perirenal abscesses, including those caused by K pneumoniae, usually develop from urinary tract infection.5 Other sources of infection were not evident, supporting suspicion of gradual development of an undetected abscess arising from a urinary tract infection. K pneumoniae is associated not only with perirenal abscess, as in our case, but also with liver abscess. In East Asian countries, liver abscess caused by this organism has been reported to be complicated by devastating metastatic endophthalmitis.8 –13 However, a case with endophthalmitis developing from a K pneumoniae perirenal abscess is very rare. We know of only one previous report of such an occurrence.14 Further, no previous report has described a case in which DIC developed in addition to endophthalmitis complicating perirenal abscess. Importantly, our patient initially showed evidence of DIC (low platelet count, elevated fibrin/fibrinogen degradation products level) accompanied by findings indicating severe inflammation. Although DKA, which was present in our case, occasionally can cause DIC,15 our patient’s pH was normal and total ketone bodies in serum showed a relatively modest elevation. Furthermore, dehydration was not evident in terms of reduced skin turgor or plasma osmolality. Therefore, our case appeared to have only incipient DKA, which might not be sufficient to cause DIC. On the other hand, some reports suggest that perirenal abscess caused by various pathogens can induce DIC, presumably via sepsis.6,7 Considering that our patient developed metastatic endophTHE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
thalmitis later, DIC most likely was caused by K pneumoniae sepsis from the perirenal abscess. Notably, the patient developed endophthalmitis despite the use of full-dose broad-spectrum antibiotics showing sensitivity for K pneumoniae and despite the fact that blood cultures were negative for growth. Accordingly, intravenous administration of antibiotics might not be able to completely prevent metastatic endogenous endophthalmitis owing to a possible release of an abundant amount of organism from the infectious sources, even if those have a good sensitivity for the organism. In a report of endogenous endophthalmitis that developed from pneumonia, similar phenomena have been observed.12 As for the reason for the negative results in blood cultures in our case, we consider a possible intermittent, discontinuous release of pathogen from the abscess. Regrettably, we could not directly prove K pneumoniae endophthalmitis, since we did not perform the bacterial culture in our patient’s anterior chamber fluid, although even when this is done, culture does not always yield growth of the responsible organism.16 Thus, we also must note the possibility of metastasis by other antibiotics-resistant organisms from various sources due to a nosocomial infection during the patient’s hospitalization. However, the patient did not show clinical symptoms of other infections, such as pneumonia. In addition, the cultures in sputum and urine as well as in blood did not yield growth of any organism. Therefore, we believe that metastatic endophthalmitis in our case was caused by K pneumoniae from perirenal abscess. K pneumoniae is especially virulent toward the retina, with lost of light perception or requirement for enucleation being frequent outcomes.13,17 The blood-retinal barrier can interfere with attainment of an effective intraophthalmic concentration of an intravenously administrated antibiotic, requiring direct intravitreal administration for treatment of endophthalmitis.13 Fortunately, in our patient, 159
Abscess and Endophthalmitis in Diabetes
timely intravitreal administration may have prevented further deterioration of visual acuity. Early diagnosis and administration of immediate intravitreal antibiotics are indispensable for arresting progression of K pneumoniae endophthalmitis, although even this treatment does not always succeed in restoring vision because of the high retinal virulence of this organism.12–14 Conclusion We consider this report to be the first of a patient with diabetes complicated by K pneumoniae perirenal abscess, complicated in turn by both DIC and endophthalmitis. To permit early diagnosis, physicians need to be aware of the possibility of perirenal abscess, particularly in patients with poorly controlled diabetes who have persistent fever of unknown origin or low back pain. References 1. Kawamura T. Infection and diabetes mellitus [in Japanese]. Diabetes J 1999;28:115–26. 2. Thorley JD, Jones SR, Stanford JP. Perinephrotic abscess. Medicine 1974;53:441–51. 3. Sentochnik DE, Eliopoulos GM. Infection and diabetes. In Kahn CR, Weir GC, editors. Joslins’ diabetes mellitus. 13th ed. Philadelphia: Lea & Febiger; 1994. p. 867– 88. 4. Joshi N, Caputo GM, Weitekamp MR, et al. Infections in patients with diabetes mellitus. N Engl J Med 1999;341: 1906 –11. 5. Mendez G Jr, Isikoff MB, Morillo G. The role of computed tomography in the diagnosis of renal and perirenal abscess. J Urol 1979;122:582– 6.
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6. Takao A, Nakayama Y, Ichkawa T, et al. Septic shock due to pyelonephritis-calculosa: a case report [in Japanese]. Nippon Hinyokika Gakkai Zasshi 2001;92:530 –3. 7. Plaut M, Gardner P. Listeria monocytogenes sepsis with disseminated intravascular coagulation. South Med J 1972; 65:490 –2. 8. Saccente M. Klebsiella pneumoniae liver abscess, endophthalmitis, meningitis in a man with newly recognized diabetes mellitus Clin Infect Dis 1999;29:1570 –1. 9. Wang JS, Liu YC, Lee SSJ, et al. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis 1998;26: 1434 – 8. 10. Harris EW, D’Amico DJ, Bhisitkul R, et al. Bacterial subretinal abscess: a case report and review of the literature. Am J Ophthalmol 2000;129:778 – 85. 11. Naito T, Kawakami T, Tsuda M, et al. A case of endophthalmitis and abscesses in the liver and the lung caused by Klebsiella pneumoniae [in Japanese]. Kansenshogaku Zasshi 1999;73:935– 8. 12. Ang LPK, Lee HM, Au Eong KG, et al. Endogenous Klebsiella endophthalmitis. Eye 2000;14:855– 60. 13. Liao HR, Lee HW, Leu HS, et al. Endogenous Klebsiella pneumoniae endophthalmitis in diabetic patients. Can J Ophthalmol 1992;27:143–7. 14. Stotka JL, Rupp ME. Klebsiella pneumoniae urinary tract infection complicated by endophthalmitis, perinephric abscess, and ecthyma gangrenosum. South Med J 1991;84: 790 –3. 15. Barnett AH, Harrison JH. Disseminated intravascular coagulation in diabetic ketoacidosis. Lancet 1979;14:103. 16. Cheng DL, Liu YC, Yen MY, et al. Septic metastatic lesions of pyogenic liver abscess: their association with Klebsiella pneumoniae bacteria in diabetic patients. Arch Intern Med 1991;151:1557–9. 17. Margo CE, Mames RN, Guy JR. Endogenous Klebsiella endophthalmitis. Ophthalmology 1994;101:1298 –1301.
March 2005 Volume 329 Number 3
ABSTRACT: We describe a 56-year-old woman with type 2 diabetes complicated by a Klebsiella pneumoniae perirenal abscess. The patient further developed incipient diabetic ketoacidosis, disseminated intravascular coagulation, and endogenous endophthalmitis. Occurrence of the latter as a metastatic infection from perirenal abscess caused by this organism is very rare, and we know of no previously reported patient with the additional occurrence of disseminated intravascular co-
agulation. Since prompt intravitreal antibiotic administration is needed, physicians should be aware of these rare but severe complications of K pneumoniae infection, especially in patients with poorly controlled diabetes. KEY INDEXING TERMS: Klebsiella pneumoniae; Perirenal abscess; Diabetes mellitus; Disseminated intravascular coagulation; Endogenous endophthalmitis. [Am J Med Sci 2005;329(3):157–160.]
P
previous report in which the K pneumoniae abscess complicated by endophthalmitis was perirenal.14 Further, such a case complicated by DIC has not yet been described. We report a 56-year-old patient with type 2 diabetes complicated by a massive K pneumoniae perirenal abscess. She developed some early features of diabetic ketoacidosis (DKA) and had the additional complications of DIC and finally metastatic endogenous bacterial endophthalmitis.
erirenal abscess, emphysematous cholecystitis, emphysematous pyelonephritis, and necrotizing fasciitis represent severe infectious complications of diabetes.1– 4 Perirenal abscess is caused mainly by Staphylococcus aureus, Staphylococcus epidermidis, and Gram-negative organisms such as Escherichia coli or Klebsiella pneumoniae.5 The abscess usually is accompanied by fever, continuous low back pain, and clinical and laboratory evidence of inflammation, although patients with a chronically progressive abscess often have no symptoms. A case of a diabetic patient with perirenal abscess who developed disseminated intravascular coagulation (DIC) represents a rarity.6,7 Also relatively rare but serious, endogenous bacterial endophthalmitis as a metastatic infection from liver abscess caused by K pneumoniae has been reported recently, especially in Asian patients with diabetes, and carries a poor prognosis for visual acuity7–13; endogenous endophthalmitis arising from a K pneumoniae perirenal abscess is very rare. We know of only one similar From the Department of Medicine, Koshigaya Hospital, Dokkyo University School of Medicine, Koshigaya, Japan. Submitted July 23, 2004; accepted October 26, 2004. Correspondence: Kohzo Takebayashi, MD, Department of Medicine, Koshigaya Hospital, Dokkyo University School of Medicine, 2-1-50, Minami-Koshigaya, Koshigaya, 343-8555, Japan. (E-mail: [email protected]) THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Case Report A 56-year-old woman was transferred to our hospital because of suspected DKA. She had been in good health until mid-October 2003, when she occasionally noted dry mouth and fatigue. She had not been diagnosed with diabetes mellitus. On November 7, 2003, she began to note fatigue, abdominal pain, and low back pain accompanied by moderate diarrhea. On the next day, her temperature rose to 38°C, and she was admitted to a nearby hospital for diagnosis and treatment. On the night of November 9, she developed dyspnea and worsening fatigue, low back pain, and dry mouth. Her mind was clear. Plasma glucose level was extremely high (564 mg/dL), and a dipstick urine test for ketone bodies yielded a positive result. With a diagnosis of suspected DKA, the patient was transferred to our hospital by ambulance at midnight on the next day, November 10. On admission, she showed confusion. Her height and body weight were 149 cm and 49 kg; temperature, blood pressure, and pulse rate were 38.0°C, 152/70 mm Hg, and 128/min. The respiratory rate was 40/min. The skin was only moderately dry. Routine hematologic and serologic tests on admission showed striking elevation of white blood cell (WBC) count and C-reactive protein (CRP) level
157
Abscess and Endophthalmitis in Diabetes
(16400/L and 25.28 mg/dL), suggesting severe inflammation. The lactate dehydrogenase level also was elevated (1625 U/L). Plasma glucose and hemoglobin A1C were 498 mg/dL and 12.6%. The total serum concentration of ketone bodies was elevated (1265 mol/L; normal value, 0 –130), and fasting plasma C peptide immunoreactivity and anti-GAD antibody, respectively, were 2.66 ng/mL (normal value, 0.6 –2.8) and 0.3 U/mL (normal value, 0 –1.5). In addition, the platelet count was markedly decreased, while fibrin/fibrinogen degradation products were increased (0.7⫻104/L and 25.7 g/mL), suggesting DIC. Gas analysis of arterial blood sampled with the patient breathing room air showed a pH of 7.337, a PCO2 of 45.7 Torr, a PO2 of 56.2 Torr, HCO3 level of 23.9 mmol/L, and SaO2 of 84.7%. Admission blood cultures for bacteria yielded no growth. Chest radiography on admission demonstrated slight left pleural effusion and moderate cardiomegaly, and abdominal radiography showed marked dilatation of the colon by gas. Based on clinical and laboratory findings on admission, the patient was diagnosed with DIC, acute respiratory failure, and incipient DKA. Oxygen was given immediately by mask, and intravenous antibiotic therapy (2.0 g/day of imipenem/cilastatin) was initiated for suspected infection. For DIC, continuous intravenous infusion of a protease inhibitor, gabexate mesilate, was initiated at 1000 mg/day. For impending DKA, continuous intravenous insulin was given together with infusion of moderate amounts of normal saline. With this treatment, her mind began to clear on November 14, and findings of inflammation in blood tests lessened (WBC count, 13500/L; CRP, 3.69 mg/dL). On the same day, the platelet count also had increased (13.6⫻104/L). Fasting plasma glucose level was decreased to remain near 100 mg/dL after initiation of insulin therapy. Temperature fell to approximate 37°C. Results of blood gas analysis on November 14 also improved. On the other hand, colonic dilatation in abdominal radiographs did not change. Although abdominal pain, diarrhea, and oral dryness had improved, moderate low back pain and fatigue continued. On November 17, the WBC count and CRP level again rose to 14400/L and 15.5 mg/dL, respectively, as did the temperature (38°C), while bacterial cultures in blood, sputum, and urine on the same day were all negative for growth. In consideration of these findings and the persistent abdominal radiographic abnormalities, abdominal computed tomography was performed on November 21. The computed tomography scan demonstrated a massive left perirenal abscess with involvement of the left iliopsoas muscle (Figure 1). Percutaneous drainage of the abscess was performed on the next day, and abundant pus was obtained. Bacterial culture of the drainage demonstrated growth of K pneumoniae, and this isolate had a sensitivity for most antibiotics, including imipenem/cilastatin, ciprofloxacin, meropenem, and
ofloxacin. Since percutaneous drainage together with a change of intravenous antibiotic (from imipenem/cilastatin to ciprofloxacin, 600 mg/day) on November 21 failed to reduce the patient’s fever or low back pain and since additional change of antibiotics was also noneffective (to meropenem, 2.0 g/day on December 7), the abscess was drained surgically on December 17. Although transient postoperative pain was noted, low back pain gradually abated. Abdominal radiographic findings were also improved. Beginning on December 26, high-grade fever ceased and the WBC count and CRP level had improved (8200/L and 1.12 mg/dL). The lactate dehydrogenase level, platelet count, and fasting plasma glucose level at that time were 479 U/L, 30.5⫻104/L, and 108 mg/dL. HbA1C on January 5, 2004 was 5.3%. Blood, sputum, and urine cultures repeated several times since November 17 showed negative findings for growth. Concurrently with clinical progress concerning the abscess, on November 28, 2003, the patient began to report right orbital pain and impaired vision in the right eye; visual acuity worsened rapidly to light perception alone. An urgent consultation with an ophthalmologist at the hospital on December 1 resulted in a diagnosis of endogenous bacterial endophthalmitis, based on findings of hypopyon associated with severe cellular reaction in the anterior chamber of the right eye (57.4 cells/L; normal values, 0 –5), obscuring the fundus (December 1, Figure 2A). The left eye showed only evidence of simple diabetic retinopathy. Vitreous fluid culture was not performed. Direct intravitreal administration of 2 mg of ceftazidime and 1 mg of vancomycin into the right eye was carried out on the same day; in addition to continuous intravenous ciprofloxacin and instillation of levofloxacin and betamethasone. By December 4, the cellular reaction in the right anterior chamber had decreased somewhat, and the fundus could be visualized to some extent. By late December, visual acuity was improved to permit counting of fingers, and the fundus became more visible (December 27, Figure 2B). Intravenous antibiotics were followed by oral antibiotics (levofloxacin, 300 mg/day) beginning on December 27, 2003. The patient’s general condition and laboratory data have remained favorable since early January 2004. Levofloxacin was discontinued on January 13, and oral nateglinide (270 mg/day) was substituted for insulin injection. The patient was discharged home on January 28, with treatment of diabetes continuing in the outpatient department to successfully maintain good general condition and good diabetic control (HbA1C ⬍6.0%).
Discussion Although our patient was diagnosed with diabetes only immediately before transfer to our hospital,
Figure 1. Findings of abdominal computed tomography: massive perirenal abscess (A), and involvement of the right iliopsoas muscle (B).
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Figure 2. Findings of retina fundus on December 1, onset day (A), and on December 27, when the fundus became more visible (B).
based on the finding of diabetic retinopathy, she most likely had poorly controlled diabetes for a relatively long time. In addition, since GAD antibody was not detected while plasma C peptide immunoreactivity level was relatively high, the patient presumably had type 2 rather than type 1 diabetes. Perirenal abscess is known to occur, particularly in cases of poorly controlled diabetes,1,2 whereas Gramnegative perirenal abscesses, including those caused by K pneumoniae, usually develop from urinary tract infection.5 Other sources of infection were not evident, supporting suspicion of gradual development of an undetected abscess arising from a urinary tract infection. K pneumoniae is associated not only with perirenal abscess, as in our case, but also with liver abscess. In East Asian countries, liver abscess caused by this organism has been reported to be complicated by devastating metastatic endophthalmitis.8 –13 However, a case with endophthalmitis developing from a K pneumoniae perirenal abscess is very rare. We know of only one previous report of such an occurrence.14 Further, no previous report has described a case in which DIC developed in addition to endophthalmitis complicating perirenal abscess. Importantly, our patient initially showed evidence of DIC (low platelet count, elevated fibrin/fibrinogen degradation products level) accompanied by findings indicating severe inflammation. Although DKA, which was present in our case, occasionally can cause DIC,15 our patient’s pH was normal and total ketone bodies in serum showed a relatively modest elevation. Furthermore, dehydration was not evident in terms of reduced skin turgor or plasma osmolality. Therefore, our case appeared to have only incipient DKA, which might not be sufficient to cause DIC. On the other hand, some reports suggest that perirenal abscess caused by various pathogens can induce DIC, presumably via sepsis.6,7 Considering that our patient developed metastatic endophTHE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
thalmitis later, DIC most likely was caused by K pneumoniae sepsis from the perirenal abscess. Notably, the patient developed endophthalmitis despite the use of full-dose broad-spectrum antibiotics showing sensitivity for K pneumoniae and despite the fact that blood cultures were negative for growth. Accordingly, intravenous administration of antibiotics might not be able to completely prevent metastatic endogenous endophthalmitis owing to a possible release of an abundant amount of organism from the infectious sources, even if those have a good sensitivity for the organism. In a report of endogenous endophthalmitis that developed from pneumonia, similar phenomena have been observed.12 As for the reason for the negative results in blood cultures in our case, we consider a possible intermittent, discontinuous release of pathogen from the abscess. Regrettably, we could not directly prove K pneumoniae endophthalmitis, since we did not perform the bacterial culture in our patient’s anterior chamber fluid, although even when this is done, culture does not always yield growth of the responsible organism.16 Thus, we also must note the possibility of metastasis by other antibiotics-resistant organisms from various sources due to a nosocomial infection during the patient’s hospitalization. However, the patient did not show clinical symptoms of other infections, such as pneumonia. In addition, the cultures in sputum and urine as well as in blood did not yield growth of any organism. Therefore, we believe that metastatic endophthalmitis in our case was caused by K pneumoniae from perirenal abscess. K pneumoniae is especially virulent toward the retina, with lost of light perception or requirement for enucleation being frequent outcomes.13,17 The blood-retinal barrier can interfere with attainment of an effective intraophthalmic concentration of an intravenously administrated antibiotic, requiring direct intravitreal administration for treatment of endophthalmitis.13 Fortunately, in our patient, 159
Abscess and Endophthalmitis in Diabetes
timely intravitreal administration may have prevented further deterioration of visual acuity. Early diagnosis and administration of immediate intravitreal antibiotics are indispensable for arresting progression of K pneumoniae endophthalmitis, although even this treatment does not always succeed in restoring vision because of the high retinal virulence of this organism.12–14 Conclusion We consider this report to be the first of a patient with diabetes complicated by K pneumoniae perirenal abscess, complicated in turn by both DIC and endophthalmitis. To permit early diagnosis, physicians need to be aware of the possibility of perirenal abscess, particularly in patients with poorly controlled diabetes who have persistent fever of unknown origin or low back pain. References 1. Kawamura T. Infection and diabetes mellitus [in Japanese]. Diabetes J 1999;28:115–26. 2. Thorley JD, Jones SR, Stanford JP. Perinephrotic abscess. Medicine 1974;53:441–51. 3. Sentochnik DE, Eliopoulos GM. Infection and diabetes. In Kahn CR, Weir GC, editors. Joslins’ diabetes mellitus. 13th ed. Philadelphia: Lea & Febiger; 1994. p. 867– 88. 4. Joshi N, Caputo GM, Weitekamp MR, et al. Infections in patients with diabetes mellitus. N Engl J Med 1999;341: 1906 –11. 5. Mendez G Jr, Isikoff MB, Morillo G. The role of computed tomography in the diagnosis of renal and perirenal abscess. J Urol 1979;122:582– 6.
160
6. Takao A, Nakayama Y, Ichkawa T, et al. Septic shock due to pyelonephritis-calculosa: a case report [in Japanese]. Nippon Hinyokika Gakkai Zasshi 2001;92:530 –3. 7. Plaut M, Gardner P. Listeria monocytogenes sepsis with disseminated intravascular coagulation. South Med J 1972; 65:490 –2. 8. Saccente M. Klebsiella pneumoniae liver abscess, endophthalmitis, meningitis in a man with newly recognized diabetes mellitus Clin Infect Dis 1999;29:1570 –1. 9. Wang JS, Liu YC, Lee SSJ, et al. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis 1998;26: 1434 – 8. 10. Harris EW, D’Amico DJ, Bhisitkul R, et al. Bacterial subretinal abscess: a case report and review of the literature. Am J Ophthalmol 2000;129:778 – 85. 11. Naito T, Kawakami T, Tsuda M, et al. A case of endophthalmitis and abscesses in the liver and the lung caused by Klebsiella pneumoniae [in Japanese]. Kansenshogaku Zasshi 1999;73:935– 8. 12. Ang LPK, Lee HM, Au Eong KG, et al. Endogenous Klebsiella endophthalmitis. Eye 2000;14:855– 60. 13. Liao HR, Lee HW, Leu HS, et al. Endogenous Klebsiella pneumoniae endophthalmitis in diabetic patients. Can J Ophthalmol 1992;27:143–7. 14. Stotka JL, Rupp ME. Klebsiella pneumoniae urinary tract infection complicated by endophthalmitis, perinephric abscess, and ecthyma gangrenosum. South Med J 1991;84: 790 –3. 15. Barnett AH, Harrison JH. Disseminated intravascular coagulation in diabetic ketoacidosis. Lancet 1979;14:103. 16. Cheng DL, Liu YC, Yen MY, et al. Septic metastatic lesions of pyogenic liver abscess: their association with Klebsiella pneumoniae bacteria in diabetic patients. Arch Intern Med 1991;151:1557–9. 17. Margo CE, Mames RN, Guy JR. Endogenous Klebsiella endophthalmitis. Ophthalmology 1994;101:1298 –1301.
March 2005 Volume 329 Number 3