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Skeletal infections in cirrhotics   Message List  
Reply | Forward Message #741 of 1769 |
INDIAN JOURNAL OF GASTROENTEROLOGY
Year : 2005 | Volume : 24 | Issue : 4 | Page : 174-175


Skeletal infections in cirrhotics

Rajesh G, Mehta Rajiv, Nandakumar R, Sadasivan Shine, John Anil,
Balakrishnan V
Department of Gastroenterology, Amrita Institute of Medical Sciences, Amrita
Lane, Elamakkara P O, Cochin 682 026, India

Date of Submission 03-Nov-2004
Date of Acceptance 22-Dec-2004


Correspondence Address:
Rajesh G
Department of Gastroenterology, Amrita Institute of Medical Sciences, Amrita
Lane, Elamakkara P O, Cochin 682 026
India
gastro@...


» Abstract

There are few reports of skeletal infections in patients with cirrhosis. We
present two such cases, both with alcoholic liver disease, seen over a
period of one year. The first, a 46-year-old man, presented as pyrexia of
unknown origin, and was found to have pyogenic discitis; he responded to
antibiotic and surgery. The second, a 42-year-old man, presented with chest
wall abscess and was diagnosed to have tubercular osteomyelitis; he expired
despite treatment with non-hepatotoxic anti-tubercular drugs.



How to cite this article:
Rajesh G, Mehta R, Nandakumar R, Sadasivan S, John A, Balakrishnan V.
Skeletal infections in cirrhotics. Indian J Gastroenterol 2005;24:174-175

How to cite this URL:
Rajesh G, Mehta R, Nandakumar R, Sadasivan S, John A, Balakrishnan V.
Skeletal infections in cirrhotics. Indian J Gastroenterol [serial online]
2005 [cited 2006 Mar 14];24:174-175. Available from:
http://www.indianjgastro.com/article.asp?issn=0254-8860;year=2005;volume=24;issu\
e=4;spage=174;epage=175;aulast=Rajesh



Patients with liver cirrhosis are well known to be prone to infections.
These are a source of considerable morbidity and often mortality, and hence
need prompt and aggressive treatment. Skeletal infections are an
often-unrecognized group of infections in patients with liver cirrhosis. We
present two such cases seen over a period of one year.

Case 1: A 46-year-old man with alcohol-related liver cirrhosis with portal
hypertension and diabetes mellitus, presented with fever off and on for 4
months. There was no history of cough, dysuria, headache, or joint pains.
Evaluation done outside was inconclusive. On admission he was pale, febrile,
hemodynamically stable; physical examination was otherwise unremarkable.

Investigations : hemoglobin 7.6 g/dL, white cell count 3,800/cm3, platelets
91,000/cm3, ESR 70 mm in 1st hour, serum bilirubin 1.2 mg/dL (direct 0.6),
AST 27 U/L, ALT 16 U/L, serum protein 6.4 g/dL (albumin 2.4), INR 1.7. Renal
function tests and electrolytes were normal. Routine examination of urine
was normal and culture was sterile. Chest X-ray was normal. Blood culture
showed E. coli bacteremia. ELISA for HIV was negative. Echocardiography did
not reveal any vegetations. He was treated with culture-sensitive
antibiotics and discharged after the fever subsided.

He was readmitted with fever after one month. This time he gave history of
severe low backache increased on prolonged sitting or walking. He had
numbness of both lower limbs. He was found to have weakness of extensor
hallucis longus and dorsiflexors of right lower limb. MRI spine revealed
disk extrusion at L4 - 5 with narrowing of neural foramen and lateral recess
[Figure - 1]. He underwent diskectomy. Intra-operatively the disk space was
found to be infected. Culture of disk material showed E. coli . He was
managed with culture-sensitive antibiotics and analgesics. However, as there
was no relief in pain, re-exploration was done after 2 weeks and posterior
lumbar intrabody fusion was done. He was discharged after one month and was
doing well on follow up at 3 months.

Case 2: A 42-year-old man, previously diagnosed to have alcohol-related
liver cirrhosis with portal hypertension, presented with upper GI bleed and
right-sided chest wall abscess. On examination he was found to be pale and
febrile, with a large parietal swelling on the right side of chest.

Investigations : hemoglobin 6 g/dL, white cell count 32,000/cm3, serum
bilirubin 8.6 mg/dL (direct 3.8), AST 84 U/L, ALT 49 U/L, alkaline
phosphatase 64 U/L, serum protein 7 g/dL (albumin 1.6). ELISA for HIV was
negative. Ultrasonography (USG) showed shrunken liver with coarse
echotexture, splenomegaly and gross ascites. Diagnostic paracentesis of
ascitic fluid did not suggest spontaneous bacterial peritonitis. USG chest
showed a 19 cm x 8 cm heterogeneous cystic lesion with internal echoes
abutting the right chest wall muscles and ribs, almost reaching up to the
axilla, and right-sided pleural effusion. Pleural fluid aspirate showed 788
cells (64% polymorphonuclear), glucose 79 mg/dL, LDH 1430 U/L, and no AFB.
Aspirate from the abscess was thick and hemorrhagic, and sterile on routine
culture.

He was treated with parenteral broad-spectrum antibiotics, vitamin K, packed
RBC, platelet, and plasma transfusions. As his coagulopathy worsened despite
attempts at correction, incision and drainage of abscess was deferred on
surgeon's advice. However he continued to be febrile. CT chest showed a 15.6
cm x 13 cm x 6 cm multi-loculated chest wall abscess on the right side and
right-sided pleural effusion; in addition there were osteomyelitic changes
in the manubrium, axillary lymphadenopathy, and a small apical lung lesion.
Considering the possibility of tubercular osteomyelitis and cold abscess he
was started on non-hepatotoxic anti-tubercular drugs. However he developed
progressive desaturation and hypotension needing mechanical ventilation and
inotropic supports, and eventually expired.

Bacteremia in liver cirrhosis is well known, the risk appearing to increase
with more advanced Child class.[1] Escherichia More Details coli is the
most frequently isolated organism.[1] Susceptibility to infection in
cirrhosis is related to impaired defense mechanisms due to impaired
reticuloendothelial function, portosystemic shunting, increased intestinal
permeability. Recurrent bacteremia may also be due to bacterial factors that
confer a survival advantage (e.g., adhesins that facilitate mucosal
colonization).

Infections in atypical sites, often secondary to previous episodes of
bacteremia, can often pose a diagnostic dilemma. Bacterial arthritis
complicating cirrhosis has been described.[2] Dental infections may also be
a source of recurrent sepsis.[3] However there are very few reports of
skeletal infections in liver cirrhosis described in literature.[4],[5] They
are often detected after repeated failed searches for source of infection.
Co-morbidities like diabetes, alcohol abuse, and immunosuppression are
factors likely to be correlated with mortality with such infections in
cirrhotics.

A high index of suspicion can help in early recognition of skeletal
infections as possible source of infection in cirrhotics that need
appropriate and prolonged courses of antibiotics and other therapeutic
interventions.







» References

1. Levy V, Reed C, Abbott SL, Israelski D. Escherichia coli myonecrosis in
alcoholic cirrhosis. J Clin Gastroenterol 2003; 36:443-5. [PUBMED]
[FULLTEXT]
2. Malnick SD, Attali M, Israeli E, Gratz R, Geltner D. Spontaneous
bacterial arthritis in a cirrhotic patient. J Clin Gastroenterol
1998;27:364-6. [PUBMED] [FULLTEXT]
3. Borowsky SA, Hasse A, Wiedlin R, Lott E. Dental infection in a cirrhotic
patient. Source of recurrent sepsis. Gastroenterology 1979;76:836-9.
[PUBMED]
4. Lee CH, Liu MS, Hsieh SH. Aeromonas hydrophila bacteremia presenting as
non-traumatic acute osteomyelitis in a cirrhotic patient. Chang Gung Med J
2003;26:520-4. [PUBMED]
5. Hung CC, Hsueh PR, Chen YK, Fang CT, Chang SC, Luh KT, et al. Haemophilus
aphrophilus bacteraemia complicated with vertebral osteomyelitis and spinal
epidural abscess in a patient with liver cirrhosis. J Infect 1997;35:304-8.



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