Two cases of spontaneous epidural abscess in patients with cirrhosis. (Case Report).

Abstract: Medical conditions predisposing to epidural abscess include diabetes, intravenous drug use, alcoholism, and other immuno-compromised states. Although cirrhosis is associated with an increased risk of infection in general it has not previously been identified as a condition predisposing to epidural abscess. We describe two cirrhotic patients with spinal epidural abscesses. We speculate that the underlying immune defects associated with cirrhosis increase the risk of spontaneous epidural abscess and should raise concern for this infection when cirrhotic patients present with fever and back pain.

Spinal epidural abscess is an uncommon condition, with an incidence between 0.2 and 2.8 per 10,000 hospital admissions. Infection of the epidural space may develop by direct extension of infection from an adjacent vertebra or intervertebral disc, from overlying skin, pharynx, and kidney or by hematogenous spread from remote infections. Patients undergoing invasive spinal procedures and patients who suffer blunt trauma to the spine are also at risk for epidural abscess. Medical conditions predisposing to epidural abscesses include diabetes mellitus, intravenous drug abuse, chronic renal failure, alcoholism, and cancer. To our knowledge, chronic liver disease has not previously been identified as a condition predisposing to epidural abscesses. We describe two cases of spontaneous epidural abscess in women with underlying cirrhosis.

Discussion

Infection is an important cause of both morbidity and mortality in patients with cirrhosis. Thirty to fifty percent of hospitalized patients with cirrhosis are infected at the time of presentation or become infected during their hospitalization. The most common sites of infection include the urinary tract, peritoneum, lower respiratory tract, and the skin and soft tissues. (4) Escherichia coli and other aerobic Gram negative bacteria are the most common etiologic agents identified, although Staphylococci and Streptococci are responsible for one fourth of all infections. (5)

Several factors predispose cirrhotic patients to infection (Table 1). Patients with cirrhosis are prone to small bowel bacterial overgrowth, which has been shown to correlate with increased rates of infection, particularly spontaneous bacterial peritonitis (SBP). (6,7) Moreover, portal hypertension induces alterations in the bowel wall and mesenteric lymphatics, which promote translocation of intestinal bacterial from the bowel lumen into regional lymphatics. (8) Indeed, translocation of enteric bacteria has been proposed as an early step in bacteremia in multiple settings including cancer chemotherapy, sepsis, hypovolemic shock, and multiorgan failure and is thought to be a critical element in the pathogenesis of SBP. (9-11) Cirrhosis has also been shown to be associated with depressed phagocytic activity within the liver, spleen and macrophages, decreased neutrophil function, and decreased levels of serum complement and fibronectin, all of which might predispose patients to a variety of infections, includi ng epidural abscesses. (2,12-14)

Conclusion

To our knowledge, this article describes the first series in which a link was found between epidural abscess and cirrhosis. It is not surprising that severe infections such as these exist in patients with cirrhosis; indeed multiple abnormalities of the immune system exist in patients with chronic liver disease. Epidural abscess should be considered as a potential source of infection in cirrhotic patients, especially those with fever and back pain.

Table 1

Mechanisms of immune dysfunction in patients with cirrhosis

Study (ref. no.)                   Subjects

Rimola et al, 1984 (12)            Humans-cirrhosis

Mellencamp and Preheim, 1991 (14)  Rats-cirrhosis model
Sorell et al, 1993 (10)            Rats-cirrhosis model
Gomez et al, 1994 (13)             Humans-alcoholic cirrhosis
Llovet et al, 1994 (9)             Rats-cirrhosis model
Runyon et al, 1994 (8)             Rats-cirrhosis model
Garcia-Tsao Ct al, 1995 (11)       Rats-cirrhosis model
Morencos ct al, 1995 (6)           Humans-alcoholic cirrhosis
Yang et al, 1998 (7)               Humans

Study (ref. no.)                   Mechanism of immune dysfunction

Rimola et al, 1984 (12)            Decreased phagocytic activity
                                   of liver and spleen
Mellencamp and Preheim, 1991 (14)  Decreased neutrophil function
Sorell et al, 1993 (10)            Bacterial translocation
Gomez et al, 1994 (13)             Impaired macrophage function
Llovet et al, 1994 (9)             Bacterial translocation
Runyon et al, 1994 (8)             Bacterial translocation
Garcia-Tsao Ct al, 1995 (11)       Bacterial translocation
Morencos ct al, 1995 (6)           Small bowel bacterial overgrowth
Yang et al, 1998 (7)               Small bowel bacterial overgrowth

Acknowledgments

We acknowledge Philip A. Mackowiak, MD, professor and vice chair, Department of Medicine, University of Maryland School of Medicine, and director, Medical Care Clinical Center, Baltimore Veterans Affairs Medical Center, Baltimore, MD.

Accepted October 30, 2001.

References

(1.) Mackenzie AR, Laing RB, Smith CC, Kaar GF, Smith FW. Spinal epidural abscess: Thc importance of early diagnosis and treatment, J Neural Neurosurg Psychiatry l998;65:209-2 12.

(2.) Hoppe B. Spinal cpidural abscess: Thc nurse's role in early detection and intervention. Heart Lung 1996;25:463-466.

(3.) Hlavin ML, Kaminski HJ, Ross JS, Ganz E. Spinal epidural abscess: A ten-year perspective. Neurosurgery 1990;27:177-184.

(4.) Navasa M, Rimola A, Rodes J. Bacterial infections in liver disease. Semin Liver Dis 1997;l7:323-333.

(5.) Kuo CH, Changchien CS, Yang CY, Sheen IS, Liaw YF. Bacteremia in patients with cirrhosis of the liver. Liver 1991;11:334-339.

(6.) Morencos FC, de las Hems Castano G, Martin Ramos L, Lopez Arias MJ, Ledesma F, Pons Romero F. Small bowel bacterial overgrowth in patients with alcoholic cirrhosis. Dig Dis Sci 1995;40:1252-1256.

(7.) Yang CY, Chang CS, Chen GH. Small-intestinal bacterial overgrowth in patients with liver cirrhosis, diagnosed with glucose H2 or CH4 breath tests. Scand J Gastroenterol l998;33:867-871.

(8.) Runyon BA, Squier S, Borzio M. Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis. J Hepatol 1994;21:792-796.

(9.) Llovet JM, Bartoli R, Planas R, Cabre E, Jimenez M, Urban A, et al. Bacterial translocation in cirrhotic rats: Its role in the development of spontaneous bacterial peritonitis. Gut 1994;35: 1648-1652.

(10.) Sorell WT, Quigley EM, Jin G, Johnson TJ, Rikkers LF. Bacterial translocation in the portal-hypertensive rat: Studies in basal conditions and on exposure to hemorrhagic shock. Gastroenterology 1993;104:1722-1726.

(11.) Garcia-Tsao G, Lee FY, Barden GE, Cartun R, West AB. Bacterial translocation to mesenteric lymph nodes is increased in cirrhotic rats with ascites. Gastroeaterology 1995; 108:1835-1841.

(12.) Rimola A, Soto R, Bory F, Arroyo V, Piera C, Rodes J. Reticuloendo-thelial system phagocytic activity in cirrhosis and its relation to bacterial infections and prognosis. Hepatology 1984;4:53-58.

(13.) Gomez F, Ruiz P, Sehreiber AD. Impaired function of macrophage Fe [gamma] receptors and bacterial infection in alcoholic cirrhosis. N Engl J Med 1994;331:l122-1128.

(14.) Mellencamp MA, Preheim LC. Pneumococcal pneumonia in a rat model of cirrhosis: Effects of cirrhosis on pulmonary defense mechanisms against Streptococcus pneumoniae. J Infect Dis 1991;163:102-108.

RELATED ARTICLE: Case Reports

Patient 1

A 47-year-old woman presented with acute onset of fever, jaundice, flank tenderness, and confusion. Her blood cultures yielded Staphylococcus aureus. She was treated with intravenous vancomycin but continued to have elevated temperatures and bacteremia. A lumbar puncture revealed a white blood cell count of greater than 1,200/[mm.sup.3]. Cerebrospinal fluid Gram's stain and cultures were negative. She had no history of HIV, diabetes, liver or renal disease, cancer, or recent trauma. She had drunk two glasses of Wild Irish Rose per day for years but denied illicit drug use. Physical examination revealed a temperature of 39.4[degrees]C, blood pressure 90/50 mm Hg, and a heart rate of 120 beats/min. The sclerae were icteric. Bibasilar rales were present. A II/VI systolic murmur at the base and lower left sternal border was present. Ascites and anasarca was present. She was not oriented to time or location and asterixis was present. The remainder of the neurologic examination was normal. Laboratory tests reveale d blood urea nitrogen (BUN) of 33 mg/dl, creatinine of 3.3 mg/dl, glucose of 50 mg/dl, aspartate (AST) 78 IU/dl, alkaline phosphatase 135 IU/dl, bilirubin 15.6 mg/dl, and International Normalized Ratio (INR) 1.6. Hepatitis A, B, and C serologies were non reactive. Antinuclear (ANA), antimitochondrial (AMA), and anti-smooth muscle (ASMA) antibodies were also nonreactive. Levels of [[alpha].sub.1]-antitrypsin and ceruloplasmin were normal. Because of her history of alcohol use and abnormal liver synthetic function, she was presumed to have alcoholic cirrhosis. She was given ceftriaxone, vancomycin, furosemide, and lactulose. She was then transferred to our hospital. A contrast computed tomographic scan of the head was unremarkable. Bibasilar atelectasis and small pleural effusions were present on computed tomographic scans of the chest. An echocardiogram revealed no vegetations. A lumbar MRI showed an epidural abscess at L4--L5. During the third week of antibiotic therapy, she developed recurrent fever and lowe r extremity weakness and numbness; because of emerging neurologic deficits, she underwent uneventful L4--L5 laminectomy and drainage of the abscess. Culture of the abscess yielded coagulase negative Staphylococcus.

Patient 2

A 54-year-old woman with cirrhosis due to. chronic hepatitis C infection presented with left sided flank and buttock pain, difficulty ambulating, anorexia, worsening ascites, and confusion. She was given "pain medication" and "antispasmodics" without relief. She was transferred to our hospital for further evaluation. She denied a history of HIV, diabetes, renal failure, cancer, or recent trauma. The patient drank two bottles of beer per week but denied illicit drug use. Physical examination revealed a temperature of 36.7[degrees]C, blood pressure 134/66 mm Hg, and a heart rate of 107 beats/mm. The sclerae were icteric. The pharynx was erythematous and thrush was present. She had decreased breath sounds in the lung bases. A Grade III/VI systolic murmur was present at the left sternal border. The abdomen was tender in the right lower quadrant and ascites was present. The stool examination was Hemoccult positive. She was lethargic but was oriented to person, place, and time. The remainder of the neurologic exam ination was normal. The white blood cell count was 11,400/[mm.sup.3], hematocrit was 23.1%, and platelet count was 100,000/[mm.sup.3]. Total bilirubin was 15.3 mg/dl, AST 271 IU/dl, alanine (ALT) 96 IU/dl, alkaline phosphatase 364 TU/dl, albumin 1.4 g/dl, and total protein 7.3 g/dl. The patient developed nightly fevers and was administered intravenous nafcillin. Blood cultures yielded Staphylococcus aureus; cefazolin was started and nafcillin was discontinued after the sensitivities became available. An echocardiogram did not reveal vegetations. The patient continued to report bilateral buttock pain. A MRI of the lumbar spine revealed an epidural abscess at L5--S 1. Neurosurgery recommended antibiotic treatment without surgical drainage. Intravenous antibiotics were continued for two months, followed by oral dicloxacillin for two months. She remained well off antibiotics.

Key Points

* Cirrhosis is associated with multiple immune defects.

* Infection is a common cause of morbidity and mortality in patients with cirrhosis.

* Spontaneous epidural abscess can occur in patients with cirrhosis.

* Epidural abscess should be considered in patients with cirrhosis who present with fever and back pain.

From the Division of Gastroenterology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD.

Reprint requests to Raymond Cross, MD, University of Maryland Medical System, 22 5. Greene Street, N3W62, Baltimore, MD 21201. Email: [e-mail]

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