< Presentation of Case >
A 72-year-old woman presented to the emergency department at this hospital because of nausea, vomiting and a high fever for one day. A deep purple discoloration of the urinary bag was noted for recent 2 weeks (Figure 1). Her past medical history included obesity, type 2 diabetes mellitus, hypertension, and cerebrovascular accident. The patient also had chronic constipation. She had been bedridden after a stroke 3 years earlier prior to this admission, when she began to have an indwelling urinary catheter in the nursing home.
On physical examination, her consciousness was clear. The temperature was 38.4°C, pulse rate 88 beats per minute, respirations 22 per minute and the blood pressure 118/56 mmHg. The conjunctivae were pale, sclerae were anicteric and the pupils were isocoric with prompt reaction to light. The neck was supple without stiffness and no lymphadenopathy was noted. Chest and heart examinations were normal. The abdomen was soft with mild suprapubic tenderness. Neurological examinations showed left hemiparesis. Chest radiography was reportedly normal. Laboratory investigations revealed leucocytosis with shift to the left, normocytic anemia, and an elevated C-reactive protein level. Analysis of a urine specimen showed pyuria with WBC > 100/HPF. The remaining renal function and other general laboratory survey were normal. Under the impression of urinary tract infection, she was admitted.
On admission, cefazolin was begun. However, low-grade fever persisted. Urine culture yielded Escherichia coli with a colony count of more than 100,000 CFU per ml, which was resistant to cephalosporins. The urine catheter was changed and cefazolin was changed to oral ciprofloxacin, after which no purple discoloration or pyuria was observed. Fever gradually resolved and she was discharged later.
< Laboratory data >
1. Hemogram
WBC |
Hb |
HCT |
MCV |
PLT |
Seg |
Lym. |
K/μL |
g/dL |
% |
fL |
K/μL |
% |
% |
19.4 |
10.2 |
31.4 |
93.6 |
194 |
86.4 |
12 |
2. Biochemistries and electrolytes
ALB |
TP |
T-Bil |
AST |
ALT |
ALP |
γ-GT |
Glucose |
g/dL |
g/dL |
mg/dL |
U/L |
U/L |
U/L |
U/L |
mg/dL |
3.4 |
5.2 |
0.8 |
34 |
37 |
118 |
21 |
169 |
BUN |
CRE |
Na |
K |
Ca |
CRP |
mg/dL |
mg/dL |
mmol/L |
mmol/L |
mg/dL |
mg/dL |
18.6 |
1.3 |
141 |
3.6 |
8.9 |
18.2 |
3. Urinalysis
Sp. Gr |
pH |
Protein. |
Glucose |
Ketone |
OB |
Bilirubin |
1.017 |
7.5 |
1+ |
+ |
1+ |
1+ |
- |
Urobilirubin |
RBC |
WBC |
Epi |
Cast |
Crystal |
Nitrite |
- |
5-8 |
>100 |
0-2 |
- |
- |
+ |
< 病例解析 >
紫色尿袋症候群(purple urine bag syndrome)最早在1978年由Barlow及Dickson提出,是一種發生在導尿管路的有菌尿液的生化反應。這類外觀現象下的病患,大多都沒有臨床 症狀。發生率在2005年台灣Su等的研究統計可到8.3%,在國外也有高達9.8%的數據提出。好發因子,包括:老年女性、臥床、鹼性的尿液、便秘、安養機構、塑膠製尿管(plastic foley)等;然而男性、使用silicon foley、酸性的尿液環境等也可能會發生。至於會不會發生紫色尿袋症候群與尿管置留的時間長短、餵食的路徑無關,但若發生了,尿管留置歷史愈久的病人(儘管更換尿管過)尿袋顏色會愈深。常見致病菌為 Providencia var. Spp.,Escherichia coli,Proteus mirabilis,Klebsiella pneumoniae,Pseudomonas aeruginosa ,Morganella morganii,Enterococcus spp.等。
造成紫色尿袋症候群的病理機轉可能是含tryptophanase的腸道菌群,把食物中的tryptophan分解成indole,indole最後經由portal circulation進入肝臟被氧化成indican (indoxyl potassium sulfate)而排泄至尿液,在鹼性的尿液中較容易被具有sulphatase/phosphatase的細菌進一步氧化成medium indigo(藍色素) 及indirubin(紅色素)。Indigo與indirubin沈澱物再與尿袋及尿管物質交互反應就會呈現紫色的變化。
治療方面,因大多沒有症候,多半不須要積極去處理,一般只需要定期勤更換尿管、維持尿路清潔、預防便秘、避免使用bisacodyl等栓劑(因易造成直腸粘膜的傷害)等降低其危險因素的措施即可。若臨床懷疑有泌尿道感染的症狀出現,則可給予經驗性抗生素,首選ciprofloxacin等quinolone類,因此類泌尿道感染對一般一線抗生素多半已有抗藥性。而跟一般泌尿道感染一樣,若在治療前更換導尿管,可加速復原及減少復發的可能。
< 參考文獻 >
- Lin CH, Huang HT, Chien CC, Tzeng DS, Lung FW. Purple urine bag syndrome in nursing homes: ten elderly case reports and a literature review. Clin Interv Aging 2008;3:729-34. Review.
- Harun NS, Nainar SK, Chong VH. Purple urine bag syndrome: a rare and interesting phenomenon. South Med J 2007;100:1048-50.
- Su FH, Chung SY, Chen MH, Sheng ML, Chen CH, Chen YJ, Chang WC, Wang LY, Sung KY. Case analysis of purple urine-bag syndrome at a long-term care service in a community hospital. Chang Gung Med J 2005;28:636-42.
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