SPONTANEOUS BLADDER RUPTUR DUE TO TUBERCULOSIS AND
CONCURRENT BACTERIURIA
Yueh-Ting Lee*, Nai-Wen Hsu**, Moan-Shane Tsai*, Lung-Chih Lee*, Chen-Hsiang
Lee *, Wen-Chin Lee*, Wen-Chou Yang***, Chien-Te Lee*
Department of Internal Medicine*, Department of Diagnostic Radiology**,
Department of Urology**, Chang Gung Memorial Hospital-Kaohsiung Medical
Center, Chang Gung University College of Medicine, Taiwan
Correspondence and Reprints:
Dr. Chien-Te Lee
Division of Nephrology, Department of Internal Medicine
Chang-Gung Memorial Hospital, Kaohsiung
123, Ta-Pei Road, Niao-Sung Shang, Kaohsiung Hsien 833, Taiwan
TEL: 886-7-7317123 EXT 8306
FAX: 886-7-7322402
E-MAIL: ctlee33@adm.cgmh.org.tw
Abstract
Spontaneous bladder rupture (SBR) is an uncommon disease and associated with
significant morbidity and mortality. Urinary tract tuberculosis complicated with SBR
has rarely been reported. How to identify this unusual etiology and initiate
appropriate treatment is a clinical challenge. Herein, we present a patient of SBR due
to urinary tract tuberculosis and concurrent Escherichia coli bacteriuria. Conservative
treatment with bladder catheterization accompanied by anti-tuberculosis therapy was
successful in bladder rupture healing as well as tuberculosis treatment. Clinicians
must be aware that urinary tract tuberculosis can be an underlying cause of SBR even
in the presence of bacteriuria
Keywords:
Spontaneous bladder rupture, urinary tract tuberculosis, urinary tract infection
INTRODUCTION
Spontaneous bladder rupture (SBR) is a medical emergency with non-specific
clinical manifestations. It occurs more frequently in patients with predisposing
pathological bladder, such as malignancy, post pelvic irradiation, urolithiasis, or
prolonged cystitis which could weaken bladder wall, and those with obstructive
uropathy, like neurogenic bladder and substance abuse.
1-4
Treatment modalities of
SBR included conservative treatment with indwelling bladder catheter and surgical
intervention with cystostomy repair. 3 SBR secondary to infection is rare and difficult
to make a timely and correct diagnosis. Herein, we report a patient of extraperitoneal
SBR due to urinary tract tuberculosis and concurrent bacterial infection that were not
diagnosed at the first glance but subsequently was treated uneventfully with
conservative treatment in association with anti-tuberculosis therapy.
CASE REPORT
A 78-year-old man was presented to medical emergency with acute low
abdominal pain. The pain was dull in nature with radiation to back and was
exaggerated by micturition. There was neither recent trauma nor history of tobacco,
alcohol, illegal drug use in the past days. His renal function was normal three months
ago prior to presentation.
Upon arrival, he was alert but looked ill. His body temperature was 37.5。C,
heart rate 110 beats per minute, respiratory rate 20 breaths per minute, and blood
pressure was 150/80mmHg. Physical examination showed soft abdomen but
tenderness was found in the lower abdominal area with rebounding pain. Laboratory
tests revealed leukocytosis with left shift (white blood cell count: 27,800 cells/uL,
neutrophil: 91%) and mild anemia (hemoglobin: 11.5 g/dL). Biochemical data
showed blood urea nitrogen 38 mg/dL, serum creatinine 1.4mg/dL, sodium 136
meq/L, potassium 3.8 meq/L, and C-reactive protein 215.1 mg/L. Urinalysis showed
marked pyuria (80-100 pus cells/HPF) and bacteriuria. Abdominal plain X-ray film
did not reveal pneumoperitoneum. Abdominal computed tomography (CT) disclosed
bilateral moderate hydronephrosis, thickened bladder, and presence of perivesical
fluid (figure 1). A clinical diagnosis of peritonitis secondary to extraperitoneal SBR
was thus made. Conservation therapy with indwelling bladder drainage and empiric
antibiotic was given. Urine culture yielded extended-sepctrum beta-lactamase
producing Escherichia coli later and sensitive antibiotics (Meropenam 1.0g Q8H)
were administered. His abdominal pain subsided gradually in the following days.
Cystoscopy on hospital day 7 was performed which revealed multiple patches of raw
surface with blood clots at the base and anterior wall of urinary bladder. No
remarkable perforated lesion was noted. He was discharged with indwelling bladder
drainage for prevention of bladder over-distension after 3 weeks’ hospitalization.
One week later, he was re-hospitalized because of recurrent low abdominal pain.
Follow-up CT scan revealed resolution of perivesicular fluid but there was
progression of inflammatory stranding in upper pelvis (figure 2). Gallium scan
disclosed active inflammatory process over lower abdomen. Chest X-ray showed
consolidation patch over right upper lung filed. Clinical condition got rapid recovery
within 2 days after adequate fluid resuscitation, empiric antibiotics and continuous
bladder catheterization. Because tuberculosis was suspected, sputum and urine were
collected to confirm tuberculosis infection. Subsequently, both cultures grew
Mycobacterium tuberculosis. Accordingly, quadruple anti-tuberculosis regimen
(Isoniazid 400mg QD, Rifampicin 600mg QD, Pyrazinamide 1250mg QD, and
Ethambutol 800mg QD) was initiated thereafter. The following hospitalization course
was uneventful under bladder catheterization in along with anti-tuberculosis therapy.
Half year later, follow-up studies including CT scan and gallium scan revealed
resolution of previous inflammatory process and urine culture did not yield any
microorganism. During a follow-up period of 9 months, anti-tuberculosis therapy was
discontinued and he remained to be symptom-free with normal renal function.
DISCUSSION
The majority of the patients of SBR present with acute suprapubic pain with
decreased urine passage. Urinary analysis usually reveals pyuria and acute oliguric
azotemia secondary to reabsorption of urinary constitutes from peritoneum also may
be found. 4 Because initial presentations are nonspecific, patients with SBR are often
misdiagnosed as urinary tract infection, pelvic inflammatory disease, or intestinal
obstruction. 3 Previous study has shown that overall mortality of SBR is as high as
25-50% which can be contributed to delayed diagnosis and septic complications. 1 A
variety of image studies is reliable to make earlier diagnosis and thus can reduce
complications. The diagnosis tests of choice include retrograde cystogram,
ultrasonography, and CT with or without cystography. 3 In our patient, CT scan was
performed immediately at the initial presentation and extraperitoneal bladder rupture
was suspected promptly with the presence of perivesical fluid accumulation although
there was no apparent bladder lesion. We speculate that as the perforated lesion might
not be large, and cystoscopy was performed days later after CT scan examination, the
bladder lesion had the opportunity to be healed and thereby stigma of rupture was not
observed during cystoscopy. In general, SBR is divided into either intraperitoneal or
extraperitoneal according to the location of bladder leak and fluid accumulation. Most
SBR is intraperitoneal because the dome and posterior wall are the least supported
portions of the bladder. Urgent laparotomy repair or laparoscopic repair is usually
mandatory in these patients. 4 On the contrary, conservative management by drainage
of extravasated collection and indwelling bladder catheter can be tried first for
extraperitoneal SBR. Surgical intervention is indicated if clinical course got worse.
5
For our patient, the clinical condition improved rapidly after accurate diagnosis of
extraperitoneal SBR was made and immediate antibiotic therapy and bladder catheter
drainage were initiated thereafter. However, appropriate and complete treatment was
not achieved until the obscure tuberculosis was confirmed.
Urinary tract tuberculosis is usually caused by haematogenous dissemination of
M. tuberculosis from the lungs and often involves the lower urinary system rather
than the kidney. But only 20% to 30% of patients with urinary tract tuberculosis
documented previous history of pulmonary infection. 6 Bladder tuberculosis usually starts
at the ureteral orifice and stricture formation with hydronephrosis can develop within
one year.
7
Clinically, symptoms of urinary tract tuberculosis are often fickle and
vague. It is difficult to distinguish between urinary tract tuberculosis and bacterial
cystitis because both conditions manifest with urine frequency, dysuria, and hematuria.
6
Thereby the diagnosis and treatment of urinary tract infection are usually ignored
and delayed, even contributes to unnecessary morbidity. In the case presented here,
significant documented bacterial microorganism misled us and falsely excluded the
possibility of urinary tract tuberculosis initially. The coexistence of bacterial cystitis
and urinary tract tuberculosis is not uncommon in clinical practice.8 Pathologic
change of bladder tuberculosis is usually chronic in nature and characterized by
diffuse thickening and contracture of the bladder wall. SBR secondary to tuberculosis
has rarely been described. We assume that in our patient, bladder ruptured as a
consequence of pre-existing tuberculosis and concurrent urinary tract infection which
could aggravate the bladder lesion.
To our knowledge, only two urinary tract tuberculosis complicated with SBR had
been reported previously.9, 10 Including our patient, all three patients presented with
acute abdominal pain. None of them had documented previous pulmonary
tuberculosis infection. The first reported patient was diagnosed as intraperitoneal SBR
by laparotomy with histological proof of tuberculosis. This patient died 3 weeks later
due to development of disseminated tuberculosis despite anti-tuberculosis therapy.
The second patient had intraperitoneal SBR which was diagnosed by cystogram and
ultrasound. This patient survived with the combination treatment of bilateral
percutaneous
nephrostomies,
bladder
catheter
indwelling,
and
continuing
anti-tuberculosis therapy for 9 months. In particular, our patient had extraperitoneal
SBR and tuberculosis was masked by concurrent bacterial infection at the initial
presentation.
In conclusion, SBR should be considered as a cause of acute abdominal pain
even in the presence of urinary tract infection. Furthermore, urinary tract tuberculosis
can be a major pathological etiology of SBR accompanied by bacteriuria.
Conservative treatment with bladder catheter drainage in the initial stage and
anti-tuberculosis therapy has been successful in the treatment of urinary tract
tuberculosis with complication of SBR.
REFERENCES
1. Atalay AC, Karaman MI. Spontaneous rupture of a bladder with invasive
bladder carcinoma. Int Urol Nephrol 1998 ;30:723-4.
2. McAninch JW, Marshall JA, Dixon CM. Substance abuse-related spontaneous
bladder rupture. J Urol 1991; 145: 135-6.
3. Agarwal MM, Singh SK, Naja V, Mavuduru R, Mandal AK . Spontaneous bladder
rupture: a diagnostic and treatment dilemma (case studies and literature review).
UroToday Int J DOI:10.3834/uij.1944-5784.2009.04.04
4. Basavaraj DR, Zachariah KK, Feggetter JG. Acute abdomen - remember spontaneous
perforation of the urinary bladder. J R Coll Surg Edin 2001; 46: 316-7.
5. Kotkin L, Koch MO. Morbidity associated with nonoperative management of
extraperitoneal bladder injuries. J Trauma 1995; 3: 895-8.
6. Wise GJ, Shteynshlyuger A. An update on lower urinary tract tuberculosis. Curr Urol
Rep 2008; 9: 305-13.
7. Eastwood JB, CorbishleyCM, Grange JM. Tuberculosis and the kidney. J Am Soc
Nephrol 2001; 12: 1307–14.
8. Wise GJ, Marella VK.Genitourinary manifestations of tuberculosis. Urol Clin
North Am 2003; 30:111-21.
9. Doig CM. Perforation of a tuberculous bladder. Lancet 1969; 2: 271-2.
10. Kumar RV, Banerjee GK, Bhadauria RP, Ahlawat R. Spontaneous bladder perforation:
an unusual management problem of tuberculous cystitis. Aust N Z J Surg 1997; 67:
69-70.
Table 1 Summary of literature reported spontaneous bladder rupture secondary to urinary
tract tuberculosis
Patients
Age (year) Diagnostic Concurrent
/gender
method
pulmonary
tuberculosis
Ref. 9
34/M
Ref. 10
22/F
Histology
of bladder
Urine
Yes
No
culture
Our patient
78/M
Urine
culture
Yes
Treatment
Outcome
Laparotomy and
repair
Percutaneous
Expired
nephrostomy,
Bladder
catheterization,
Anti-tuberculosis
therapy
Bladder
catheterization,
Anti-tuberculosis
therapy
Survived
Survived
Legends
Figure 1. Moderate bilateral hydronephrosis, thickened bladder, and presence of perivesical
fluid accumulation
Figure 2. Progression of inflammatory strandings in lower abdominal and upper pelvis
泌尿道結核合併尿路感染導致自發性膀胱破裂
李岳庭* 許乃文** 蔡孟憲* 李隆志* 李禎祥* 李文欽* 楊文洲*** 李建德*
高雄長庚紀念醫院
內科部* 放射診斷科** 泌尿科***
長庚大學醫學院
自發性膀胱破裂雖然是不常見的疾病，但一旦發生卻常引起併發症與死亡，
而尿路結核合併自發性膀胱破裂更是罕見。如何識別此種不常見的病因，並採取
適當的治療是臨床工作一大挑戰。在此，我們提出一名 78 歲男性，因泌尿道結
核合併大腸桿菌尿道感染導致自發性膀胱破裂的病例，使用了膀胱導尿及抗結核
病素治療等保守療法，成功地同時讓膀胱破裂癒合及治療結核。我們報告這位病
例，提示臨床醫師針對在自發性膀胱破裂的病人，即使存在有細菌泌尿道感染
時，仍須留意潛在尿路結核之可能。
關鍵詞：自發性膀胱破裂、泌尿生殖結核病、泌尿道感染
抽印本索取：
李建德醫師
833 高雄縣鳥松鄉大埤路 123 號 高雄長庚紀念醫院
電話 :
(07) 7317123-8306
傳真 ： (07) 7322402
電子信箱: ctlee33@adm.cgmh.org.tw
內科部 腎臟科