Year : 2009 | Volume
: 20 | Issue : 5 | Page : 822--825
Spontaneous rupture of tuberculous spleen in a HIV seropositive patient on maintenance hemodialysis
Shubhra Rathore1, Pratish George2, Michael Deodhar3, Nalini Calton4, Uttam George1, Basant Pawar3, Pankaj Sircar5,
1 Department of Radiology, Christian Medical College and Hospital, Ludhiana, Punjab, India
2 Department of Internal Medicine, Christian Medical College and Hospital, Ludhiana, Punjab, India
3 Department of Nephrology, Christian Medical College and Hospital, Ludhiana, Punjab, India
4 Department of Pathology, Christian Medical College and Hospital, Ludhiana, Punjab, India
5 Department of Surgery, Christian Medical College and Hospital, Ludhiana, Punjab, India
Department of Internal Medicine, Christian Medical College and Hospital, Brown Road, Ludhiana 141008, Punjab
Spontaneous rupture of the spleen usually occurs secondary to infection, hematological disorders or infiltrative lesions of the spleen. In patients with positive human immunodeficiency virus (HIV) antibodies and the acquired immunodeficiency syndrome (AIDS) who present with acute abdomen, splenic rupture should be considered as a possible cause and should additionally be investigated for co-infection with tuberculosis. Spontaneous rupture of spleen in asymptomatic patients requires a high index of suspicion for diagnosis. We herein report on a HIV-positive patient on maintenance hemodialysis, who presented with spontaneous rupture of a tuberculous spleen.
|How to cite this article:|
Rathore S, George P, Deodhar M, Calton N, George U, Pawar B, Sircar P. Spontaneous rupture of tuberculous spleen in a HIV seropositive patient on maintenance hemodialysis.Saudi J Kidney Dis Transpl 2009;20:822-825
|How to cite this URL:|
Rathore S, George P, Deodhar M, Calton N, George U, Pawar B, Sircar P. Spontaneous rupture of tuberculous spleen in a HIV seropositive patient on maintenance hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2020 Dec 3 ];20:822-825
Available from: https://www.sjkdt.org/text.asp?2009/20/5/822/55369
India has about 5.2 million human immunodeficiency virus (HIV) positive patients with a higher sero-prevalence in patients with tuberculosis (TB) (8%) as compared to the general population (0.9%).  Tuberculosis is the commonest opportunistic disease in patients with the acquired immunodeficiency syndrome (AIDS) in India, which is not unusual considering the country's burden of nearly two million new TB patients each year.  Extra pulmonary infection constitutes up to 50% of TB in HIV positive patients as compared to 10-15% in non-HIV positive patients.  Splenic TB, which is extremely rare in immunocompetent individuals, may not be as rare in patients with HIV/AIDS, especially in areas of high prevalence of coinfection of these diseases.
A 22-year-old male patient with end stage renal disease on maintenance hemodialysis (HD) for three years was detected to be seropositive for HIV one year after being on HD. He presented with abdominal pain, low grade fever and vomiting of two days duration. He was noncompliant with his bi-weekly dialysis schedule and had undergone HD four days earlier, with 5000 units of systemic heparinization during the procedure and no post procedural complications.
Two years prior to this, he was detected to have pleural effusion of tuberculous etiology for which he completed anti-tuberculous treatment (ATT) for six months, with good clinical response and resolution of the effusion. He was put on highly active retroviral treatment (HAART) following which the CD4 count reached 195/cu mm, a year earlier.
On examination, he was pale, tachypneic and hypotensive. The blood urea was 210 mg/dL, serum creatinine was 10.4 mg/dL, hemoglobin was 3 gm/dL, packed cell volume was 12.4%, platelet count was 1.53 lakhs/cu mm, prothrombin time test was 16.6 secs and control was 12 secs, the partial thromboplastin time test was 33 secs and control was 28 secs and total leukocyte count was 7000/cu mm.
Ultrasonography of the abdomen showed hepatosplenomegaly with a heterogeneously echotextured spleen, ascites, left pleural effusion and bilateral small echogenic kidneys. Detailed evaluation with CT imaging of the abdomen showed hepatosplenomegaly and bilateral small nonenhancing kidneys. Cystic areas showing hemorrhage within them were noted in the spleen with extension into the peri-splenic region. A large peri-splenic hematoma and ascites with fluid levels suggestive of hemoperitoneum were present [Figure 1]. Spontaneous rupture of the spleen was diagnosed and he was taken up for emergency splenectomy after resuscitation with blood transfusion, dialysis and fluid replacement.
Intra operative findings showed a large spleen ruptured along the medial surface with 750 mL of peri-splenic clots and 1500 mL of blood in the peritoneal cavity. The splenic vessels were normal. Splenectomy was uneventful and an enlarged spleen 18 × 10 × 8 cm with congestion and focal capsular rupture was seen.
Blood culture was sterile. Post operative evaluation of the ascitic fluid showed lymphocytic predominant ascitic fluid with low serum ascitic albumin gradient (SAAG) (serum albumin 3.8 gm/dL and ascitic albumin 3.1 gm/dL) suggestive of intra-abdominal infection, possibly TB. The CD4 count was 254/cu mm.
Histopathological examination of the spleen showed large areas of hemorrhage and extensive necrosis with occasional poorly formed granulomas comprised of epithelioid cells [Figure 2]. Acid fast bacilli (AFB) were seen on ZiehlNielsen staining. Tissue examination for other bacteria and fungus was negative. A diagnosis of spontaneous rupture of spleen with splenic TB was concluded. He had an uneventful recovery after splenectomy and is currently asymptomatic on maintenance dialysis with ATT and HAART about one year after the event.
Extra-pulmonary TB is seen in patients with advanced immunosupression as a result of HIV and is the commonest cause of pyrexia of unknown origin in such patients.  Splenic TB is found in severe disseminated disease, usually hematogenous in onset, and can present insidiously often with just fever, weight loss, anorexia and hepatosplenomegaly.  It may go unrecognized in patients unless a high index of clinical suspicion is exercised. Imaging with ultrasonography and CT scan has been useful in diagnosis,  and less commonly histopathological confirmation is required.
Few cases have been reported where splenic involvement with TB is noted in a patient seropositive for HIV patient; this might be in conjunction with infection at other intra-abdominal sites or rarely, in isolation. At times, splenic tubercular abscess may be the first presentation of AIDS.  Spontaneous rupture of the spleen is reported rarely. In patients with AIDS, it is a rare cause of emergency surgery, with only one patient reported in a series of 34 emergency laparotomies, over a five-year study period.  Splenic TB has also been discovered incidentally during laparotomy,  as in our patient who presented with a life threatening complication at diagnosis. As his coagulation profile was mildly deranged and the last heparin administration was four days earlier, splenic rupture secondary to coagulopathy or heparin was considered unlikely.
In a study involving HIV positive patients with no detectable TB, on being subjected to splenic biopsy, six out of ten patients showed evidence of TB. All these patients had multiple small hypoechoeic lesions in the spleen on ultrasound examination,  suggesting that splenic TB might be commoner than it is thought to be. Multiple small hypoechoic lesions in the spleen in HIVpositive patients strongly suggest TB.  Involvement of the spleen in TB is suggestive of greater immunosuppression than in those patients with intra-abdominal TB, whose spleen is spared.  Abdominal TB may be dry or wet and ascitic fluid is often helpful in diagnosis although staining for AFB and culture from fluid have low yields (3 and 20% respectively). Lymphocytic predominant, low SAAG ascitic fluid is suggestive of abdominal TB, as in this patient. 
Spontaneous splenic rupture is uncommon and predisposing conditions include hematological diseases with splenic infiltration, splenic infarcts, male sex, massive splenomegaly, rubella and angiosarcoma of the spleen.  Rarely splenic tubercular abscess in an HIV-positive patient may present initially with spontaneous rupture. Occasional cases of spontaneous splenic rupture have been reported in HIV positive asymptomatic and non-thrombocytopenic patients.  This patient presented with an acute abdomen, and CT imaging was suggestive of splenic rupture with ascitis and hemoperitoneum. Intra-operatively, no gross abscesses were seen but histopathological examination revealed granulomas with positive Ziehl Nielsen stain for TB.
It is noteworthy that splenic TB in an otherwise asymptomatic HIV positive patient can present as an acute abdomen. Thus, tubercular splenic rupture should be considered as a differential diagnosis in such situations. This rare and cryptic presentation may be seen more frequently in clinical practice in future years with increase in co-infection with HIV and TB, and requires prompt and proper clinical and pathological evaluation.
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