泌尿道感染患者- 何時須做尿液培養

uncomplicated UTI in women. 
如果沒有抗藥性細菌的危險, 不需要做尿液細菌培養, 抗藥性細菌風險包括過去三個月內
1. 尿曾分離出抗藥菌
2. 住養護中心/住院病患/住長照中心 (但肺炎抗藥性細菌與此無關, 與宿主本身因素有關)
3. 曾使用廣效抗生素(FQ/TMP-SMX/ 3rd cefa)
4. 曾在高抗藥細菌盛行區旅行(印度,以色列,西班牙,墨西哥)


泌尿道感染患者. 何時須做尿液培養
尿培養仍然是診斷UTI的標準。收集的尿液應立即送培養；如果沒有，應冷藏在 4°C。兩種培養技術（浸玻片、瓊脂）被廣泛使用且準確。

2010 年美國傳染病學會 (IDSA) 對女性膀胱炎和腎盂腎炎的共識限制是，對於乾淨捕獲的中流尿液樣本，菌落形成單位 (CFU)/mL 和 10,000 CFU/mL 以上。歷史上，UTI 的定義是基於單個微生物培養物濃度為 100,000 CFU/mL 時的發現。然而，這會漏掉高達 50% 的有症狀感染，因此現在可接受大於 1000 CFU/mL 的較低菌落率。 [ 22 ]

無症狀菌尿的定義仍沿用歷史閾值。女性無症狀菌尿被定義為無症狀個體的尿液培養物（乾淨捕獲或導管插入的標本）生長超過 100,000 CFU/mL。
請注意，恥骨上抽吸培養物中培養的任何數量的尿路病原體均應被視為尿路感染的證據。大約 40% 的腎週膿腫患者進行了無菌尿培養。
單純性尿路感染（膀胱炎）不需要進行尿培養，除非女性經歷過經驗性治療失敗。對懷疑患有上尿路感染或複雜性尿路感染的患者以及初始治療失敗的患者進行尿培養。
如果患者在過去一個月內曾患過尿路感染，那麼復發可能是由同一種微生物引起的。復發代表治療失敗。再感染髮生在 1-6 個月內，通常是由不同的微生物（或同一微生物的血清型）引起的。對再次感染的患者進行尿培養。

如果對未離心的干淨捕獲的中流尿液樣本進行革蘭氏染色顯示每個油浸區域存在 1 個細菌，則代表每毫升尿液中有 10,000 個細菌。革蘭氏染色後以 2000 rpm 離心 5 分鐘並在高倍鏡下檢查的樣本 (5 mL) 將識別出較低的數字。一般來說，革蘭氏染色的敏感性為 90%，特異性為 88%。

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875701/

尿液培養

從單純性膀胱炎到並發膿毒症的複雜性腎盂腎炎，只有通過尿液培養才能絕對準確地診斷尿路感染。尿培養的主要適應症是：
有尿路感染症狀或體徵的患者；
最近治療的尿路感染的隨訪；
拔除留置導尿管；
妊娠期間篩查無症狀菌尿；患有梗阻性尿路病變和瘀血的患者，在使用儀器之前。
尿液標本必須在2小時內立即培養，或者可以通過冷藏或合適的化學添加劑（硼酸鈉）保存。可接受的收集方法有：
仔細清洗後的中流尿液；
通過單次導尿獲得的尿液；
通過恥骨上針抽吸獲得尿液；從封閉式導管引流系統的管子中無菌針吸出尿液。

培養結果取決於發生菌尿的臨床環境。例如，80-90%的急性單純性膀胱炎和急性單純性腎盂腎炎患者的尿液中發現了大腸桿菌。許多鹿角結石患者的尿液中含有分解尿素的變形桿菌。醫院內常見克雷伯氏菌、假單胞菌和腸桿菌感染。除非存在潛在的危險因素，否則金黃色葡萄球菌的存在通常是並發葡萄球菌菌血症的線索。

年輕男性體內的微生物與導致女性單純感染的微生物相似。腸球菌和凝固酶陰性葡萄球菌在老年男性中更為常見；最有可能代表最近的儀器或導管插入術。除了留置導尿管、院內尿路感染或多個抗生素療程後復發感染的患者外，白色念珠菌很少見。儘管可能的微生物和通常的易感模式足以指導單純性尿路感染的初始經驗性治療，但急性細菌性腎盂腎炎和復雜性尿路感染的充分治療需要基於致病細菌及其抗菌敏感性的分離的精確治療。 [13]


Urine Culture


Urine culture remains the criterion standard for the diagnosis of UTI. Collected urine should be sent for culture immediately; if not, it should be refrigerated at 4°C. Two culture techniques (dip slide, agar) are widely used and accurate.
The 2010 Infectious Disease Society of America (IDSA) consensus limits for cystitis and pyelonephritis in women are more than 1000 colony-forming units (CFU)/mL and more than 10,000 CFU/mL, respectively, for clean-catch midstream urine specimens. Historically, the definition of UTI was based on the finding at culture of 100,000 CFU/mL of a single organism. However, this misses up to 50% of symptomatic infections, so the lower colony rate of greater than 1000 CFU/mL is now accepted. [22]
The definition of asymptomatic bacteriuria still uses the historical threshold. Asymptomatic bacteruria in a female is defined as a urine culture (clean-catch or catheterized specimen) growing greater than 100,000 CFU/mL in an asymptomatic individual.
Note that any amount of uropathogen grown in culture from a suprapubic aspirate should be considered evidence of a UTI. Approximately 40% of patients with perinephric abscesses have sterile urine cultures.
An uncomplicated UTI (cystitis) does not require a urine culture unless the woman has experienced a failure of empiric therapy. Obtain a urine culture in patients suspected of having an upper UTI or a complicated UTI, as well in those in whom initial treatment fails.
If the patient has had a UTI within the last month, relapse is probably caused by the same organism. Relapse represents treatment failure. Reinfection occurs in 1-6 months and usually is due to a different organism (or serotype of the same organism). Obtain a urine culture for patients who are reinfected.
If a Gram stain of an uncentrifuged, clean-catch, midstream urine specimen reveals the presence of 1 bacterium per oil-immersion field, it represents 10,000 bacteria/mL of urine. A specimen (5 mL) that has been centrifuged for 5 minutes at 2000 rpm and examined under high power after Gram staining will identify lower numbers. In general, a Gram stain has a sensitivity of 90% and a specificity of 88%.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875701/
Urine culture
The diagnosis of UTI from simple cystitis to complicated pyelonephritis with sepsis can be established with absolute certainty only by cultures of urine. The major indications for urine cultures are:
Patients with symptoms or signs of UTIs;
Follow-up of recently treated UTI;
Removal of indwelling urinary catheter;
Screening for asymptomatic bacteriuria during pregnancy; and
Patients with obstructive uropathy and stasis, before instrumentation.
Urine specimens must be cultured promptly within 2h or can be preserved by refrigeration or a suitable chemical additive (boric acid sodium formate). Acceptable methods of collection are:
Midstream urine after careful washing;
Urine obtained by single catheterization;
Urine obtained by supra pubic needle aspiration; and
Sterile needle aspiration of urine from the tube of a closed catheter drainage system.
Results of cultures depend on the clinical setting in which bacteriuria occurs. For example, E. coli are found in the urine of 80-90% of patients with acute uncomplicated cystitis and acute uncomplicated pyelonephritis. Many patients with staghorn calculi harbour urea-splitting proteus organisms in their urine. Klebsiella, Pseudomonas and Enterobacter infections are commonly acquired in the hospital. The presence of Staphylococcus aureus often is a clue to concomitant Staphylococcal bacteremia, unless an underlying risk factor exists.
Micro-organisms in young men are similar to the organisms that cause uncomplicated infections in women. Enterococci and coagulase-negative staphylococci are more common in elderly men; most likely representing recent instrumentation or catheterization. C. albicans is rarely encountered except in patients with indwelling catheters, nosocomial UTIs or relapsing infections after multiple courses of antibiotics. Although the likely organism and usual susceptible patterns are sufficient to guide initial empiric therapy of uncomplicated UTI, adequate treatment of acute bacterial pyelonephritis and complicated UTIs necessitates precise therapy based on isolation of the causative bacterium and its antimicrobial susceptibility.[13]

急性憩室炎 acute diverticulitis - StatPearls - NCBI Bookshelf

資料來源. Acute Diverticulitis - StatPearls - NCBI Bookshelf

下面中文部分是直接用 google 翻譯的. 所以有些慣用的字詞與台灣醫界使用的不同. 
例如腸梗阻

介紹

急性憩室炎是由憩室微穿孔引起的炎症。憩室是結腸壁的囊狀突起。約 10% 至 25% 的憩室病患者可出現憩室炎。憩室炎可以是簡單的，也可以是簡單的和復雜的。無並發症併發症的憩室炎沒有任何相關的並發症併發症。複雜性憩室炎與膿腫、瘻管、腸梗阻或直接穿孔的形成有關。憩室炎傳統上被認為是一種主要的外科疾病並被治療，但即使在最急性的階段，它也已轉變為一種醫療管理的實體內科治療的疾病。[1] [2] [3]

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病因學

增加患憩室炎機會的危險因素與憩室病相關的危險因素相同。飲食似乎發揮著重要作用。低纖維、高脂肪和紅肉飲食可能會增加患憩室病和可能的憩室炎的風險。已知肥胖和吸煙會增加憩室炎和憩室出血的可能性。最後，接觸一些藥物，包括非甾體抗炎藥 (NSAID)、類固醇和阿片類藥物，與憩室炎有關。相反，接觸他汀類藥物可能會降低症狀性憩室炎的發生率。儘管人們普遍認為堅果、種子和爆米花與憩室病、憩室炎或憩室出血的風險增加無關。[4] [5]

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流行病學

大約 60% 的 60 歲以上人群患有憩室病。約 10% 至 25% 的憩室病患者會發生憩室炎。根據美國最大的全付費住院護理數據庫全國住院患者樣本 (NIS) 的數據顯示，從 1998 年到 2005 年，急性憩室炎住院人數增加了 26%，擇期手術增加了 38%。顯示年輕患者（18 至 44 歲）比老年患者（45 至 74 歲）更有可能入院。這一趨勢可能是由於診斷測試方式的及時診斷和改進。西方國家絕大多數人可能患有左側憩室病，而亞洲人後裔則可能患有右側憩室病。世界各地的，急性憩室炎入院的平均年齡為 63 歲。儘管最初發現這種疾病在男性中更為普遍，但最近的數據顯示，憩室炎在男性和女性中的分佈是相等的。憩室炎更常見於50歲以下的男性和50至70歲的女性。70歲以上患者發生憩室炎的女性較多。[6]

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病理生理學

憩室炎是憩室壁微觀和宏觀穿孔的結果。此前，醫生認為糞便堵塞結腸憩室會導致憩室內壓力增加，進而導致穿孔。他們現在推測，腔內壓力增加是由於食物顆粒導致憩室壁侵蝕。這會導致該區域的局灶性炎症和壞死，從而導致穿孔。周圍的腸系膜脂肪很容易含有微穿孔。這可能導致局部膿腫形成、鄰近器官瘻管或腸梗阻。最終，如果不進行快速診斷和治療，直接的腸壁穿孔可能會導致腹膜炎和死亡。[7]

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歷史和身體

急性憩室炎的臨床表現根據疾病的嚴重程度而有所不同。患有單純性憩室炎的患者通常會出現左下腹疼痛，這反映了西方國家左側疾病的傾向。然而，亞裔患者主要表現為右側腹痛。疼痛可以是持續性的，也可以是間歇性的。排便習慣的改變，無論是腹瀉（35%）還是便秘（50%），都可能與腹痛有關。患者還可能出現噁心和嘔吐，可能繼發於腸梗阻。膿腫和穿孔患者發燒並不少見。當腸道發炎部分直接接觸膀胱壁時，患者可能會出現排尿困難、尿頻和尿急，這被稱為交感性膀胱炎。

在體檢時，由於腹膜刺激，炎症區域幾乎總是存在觸診壓痛。如果存在膿腫，大約 20% 的患者可能會感覺到腫塊。腸鳴音通常不活躍，但也可以正常。患者可出現腹膜體徵（僵硬、衛衛、反跳痛）並伴有腸壁穿孔。另一方面，發燒幾乎總是存在，但低血壓和休克並不常見。 

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評估

僅根據病史和體格檢查即可在臨床上診斷急性憩室炎。然而，24% 至 68% 的病例臨床診斷可能不准確。因此，實驗室和放射學檢查在急性憩室炎的準確診斷中起著重要作用。實驗室檢查可能顯示白細胞增多和急性期反應物升高，例如紅細胞沉降率 (ESR) 和 C 反應蛋白 (CRP)。急性憩室炎的首選放射學檢查是腹部和骨盆 CT，最好使用水溶性口服或直腸（如果有明顯噁心和嘔吐）造影劑和靜脈注射造影劑，前提是沒有禁忌症。據報導，CT 掃描的敏感性、特異性和陰性預測值大於 97%。[8]

腹部超聲可準確診斷急性憩室炎，與 CT 相比具有相對敏感性（84% 至 94%）和特異性（80% 至 93%）。然而，超聲（US）結果高度依賴於操作者，儘管數據令人鼓舞、成本較低且易於獲得，但其使用仍受到限制。MRI 是另一種可能的診斷方式。由於成本以及無法直接比較敏感性或特異性，通常首選 CT。腹部 X 光片可能只會顯示非特異性異常，例如腸脹氣；然而，如果患者患有腸梗阻，則可能會出現氣液平面。

由於穿孔風險增加，疑似急性憩室炎應避免進行內窺鏡檢查。建議在症狀消失後大約六到八週進行結腸鏡檢查，以排除惡性腫瘤、炎症性腸病或可能的結腸炎（如果患者最近沒有接受過結腸鏡檢查）。

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治療/管理

根據臨床表現，急性憩室炎可以通過門診或住院治療進行治療。根據美國結腸和直腸外科醫生協會的說法，不能耐受口服攝入、過度嘔吐、出現腹膜炎跡象、免疫功能低下或高齡的患者應住院治療。如果不存在這些情況，並且如果可以進行適當的及時隨訪，則可以在門診治療急性憩室炎。據悉，門診管理成功率約為94%至97%。門診護理的標準包括腸道休息、增加液體攝入量和口服抗生素治療（單一或多種藥物療法），涵蓋革蘭氏陰性桿菌和厭氧菌。[8] [3] [9]

憩室炎的住院治療需要靜脈注射抗生素、靜脈輸液和疼痛治療。同樣，抗生素應覆蓋革蘭氏陰性桿菌和厭氧菌，並服用 3 至 5 天，然後改用口服抗生素，療程為 10 至 14 天。對於需要住院的患者，優先選擇腸道休息。通常，應在住院兩到四天內觀察退熱和白細胞增多的改善，否則應懷疑其他診斷或併發症。應考慮立即進行手術評估。

大約 15% 的急性憩室炎患者會出現膿腫，特別是結腸周圍和腸系膜內膿腫。臨床上，如果儘管靜脈注射足夠的抗生素，發燒和白細胞增多仍未消退，則應懷疑膿腫形成。體檢時，腹部壓痛和腫塊壓痛提示可能形成膿腫。小於2厘米至3厘米的膿腫可以用靜脈注射抗生素保守治療。大膿腫應在CT引導下經皮引流。

瘻管形成是急性憩室炎的另一個並發症。據報導，只有不到5%的人會出現瘻管；然而，大約 20% 接受憩室炎手術的患者中發現了這種情況。最常見的瘻管是膀胱瘻管，約佔 65% 的病例。糞尿是結腸膀胱瘺的特有症狀。手術修復瘻管並進行一期吻合術是首選治療方法。結腸陰道瘺、結腸腸瘺、結腸瘺、結腸瘺和結腸皮膚瘺是急性複雜性憩室炎中其他可能出現的瘻管。

結腸腸梗阻引起的部分腸梗阻或假性梗阻也可能發生，可以保守治療。急性憩室炎中完全性腸梗阻很少見。如果發生游離穿孔，應進行手術治療。

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鑑別診斷

• 膽管炎

• 膽囊炎

• 慢性腸系膜缺血

• 便秘

• 腸膀胱瘺

• 婦科疼痛

• 炎症性腸病

• 腸穿孔

• 腸易激綜合症（IBS）

• 大腸梗阻

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預後

憩室炎患者的預後取決於就診年齡、合併症的存在和疾病的嚴重程度。一般來說，年輕人的發病率往往較高，因為他們從不懷疑自己患有這種疾病，而且往往較晚就診。此外，免疫功能低下的患者往往具有較高的發病率和死亡率。[10]

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並發症

• 盆腔膿腫
• 腸穿孔
• 腸瘺
• 腹膜炎
• 腸梗阻
• 敗血症
• 直腸出血

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術後及康復護理

從憩室炎中恢復後，必須對患者進行檢查以排除惡性腫瘤。結腸檢查的選擇包括結腸鏡檢查、CT 掃描或鋇劑灌腸。

患者應開始高纖維飲食、喝充足的水、保持健康的體重和鍛煉。

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威懾和患者教育

高纖維飲食可以預防憩室病。

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現行療法及其他議題

如前所述，大約 15% 的急性憩室炎患者會出現並發症。百分之二十到百分之五十的患者會出現憩室炎反復發作。多次發作似乎不會直接增加並發症的風險。它可能會增加纖維化的風險，導致狹窄形成和隨後的阻塞。一些患者（約 20%）會因腸易激綜合徵或慢性低度憩室炎而出現慢性腹痛。這些患者可能會被轉診進行選擇性結腸切除術以控制症狀。自 1998 年以來，憩室炎的選擇性手術增加了約 30%。

通過適當的保守治療，無並發症的憩室炎的死亡率可以忽略不計。需要手術的複雜性憩室炎可能導致大約 5% 的患者死亡。腸穿孔引起的腹膜炎會使死亡風險增加至 20%。

Continuing Education Activity

Acute diverticulitis is inflammation of a diverticulum, a sac-like protrusion from the colon wall, due to micro-perforation. Diverticulitis presents in 10% to 25% of patients with diverticulosis. In the past, diverticulitis was treated surgically, however it is now a medically-managed entity, even in its most acute phase. This activity reviews the evaluation and management of diverticulitis and highlights the importance of a well-coordinated interprofessional team in caring for patients with this condition

Objectives:

• Identify risk factors for diverticulitis.
• Explain the clinical evaluation of a patient with diverticulitis.
• Explain how to manage a patient with diverticulitis.
• Outline the role of a collaborative interprofessional team in caring for patients with diverticulitis.

Access free multiple choice questions on this topic.

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Introduction

Acute diverticulitis is inflammation due to micro-perforation of a diverticulum. The diverticulum is a sac-like protrusion of the colon wall. Diverticulitis can present in about 10% to 25% of patients with diverticulosis. Diverticulitis can be simple or uncomplicated and complicated. Uncomplicated diverticulitis is without any associated complications. Complicated diverticulitis is associated with the formation of abscess, fistula, bowel obstruction, or frank perforation. Diverticulitis has conventionally been known and treated as a primarily surgical illness, but this has transitioned to be a medically managed entity even in its most acute phase.[1][2][3]

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Etiology

Risk factors that increase the chances of developing diverticulitis are the same as those related to diverticulosis. Diet appears to play a significant role. Low fiber, high fat, and red meat diets may increase the risk for development of diverticulosis and possible diverticulitis. Obesity and smoking are known to increase the potential for both diverticulitis and diverticular bleeding. Finally, exposure to some drugs including nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and opiates are associated with diverticulitis. Conversely, exposure to statin drugs may decrease the incidence of symptomatic diverticulitis.  Despite a common popular belief, nuts, seeds, and popcorn are not associated with increased risk of diverticulosis, diverticulitis, or diverticular bleeding.[4][5]

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Epidemiology

Diverticulosis is present in approximately 60% of people older than 60 years. Diverticulitis occurs in about 10% to 25% of patients with diverticulosis. According to the Nationwide Inpatient Sample (NIS), the largest, all-payer inpatient care database in the United States revealed that there was 26% increase in hospitalizations for acute diverticulitis and a 38% increase in elective operations from 1998 through 2005. It further shows that young patients (18 to 44 years) are more likely to be admitted to the hospital than older patients (45 to 74 years). This trend is likely due to prompt diagnosis and improvement in diagnostic testing modalities. Western nations are overwhelmingly likely to have left-sided diverticulosis, whereas those of Asian descent are likely to have the right-sided disease. Across the world, the mean age for admission for acute diverticulitis is 63 years old. Though the disease was initially noted to be more prevalent in males, more recent data shows that the distribution of diverticulitis is equal in both males and females. Diverticulitis more commonly occurs in men younger than the age of 50 and women 50 to 70 years old. Diverticulitis occurring in patients over the age of 70 are more likely to be female.[6]

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Pathophysiology

Diverticulitis is the result of microscopic and macroscopic perforations of the diverticular wall. Previously, practitioners thought that obstruction of colonic diverticulum with fecaliths led to increased pressure within the diverticulum and subsequent perforation. They now theorized that increased luminal pressure is due to food particles that lead to erosion of the diverticular wall. This causes focal inflammation and necrosis of the region, causing perforation. Surrounding mesenteric fat may easily contain micro-perforations. This can result in local abscess formation, fistulization of adjacent organs, or intestinal obstruction. Ultimately, frank bowel wall perforations can lead to peritonitis and death without rapid diagnosis and treatment.[7]

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History and Physical

Clinical manifestation of acute diverticulitis varies depending on the severity of the disease. Patients with uncomplicated diverticulitis typically present with left lower quadrant abdominal pain, reflecting that propensity of left-sided disease in Western nations. However, patients of Asian descent present with predominantly right-sided abdominal pain. The pain can be constant or intermittent. Change in bowel habits, either diarrhea (35%) or constipation (50%), can be associated with abdominal pain. Patients may also experience nausea and vomiting, possibly secondary to bowel obstruction. Fever is not uncommon in patients with abscesses and perforation. Dysuria, frequency, and urgency can occur in patients when the inflamed portion of the bowel comes into direct contact with the bladder wall, which is called as sympathetic cystitis.

On physical examination, tenderness to palpation over the area of inflammation is almost always present due to irritation of the peritoneum. A mass may be felt in approximately 20% of patients if an abscess is present. Bowel sounds are usually hypoactive but can be normoactive. Patients can present with peritoneal signs (rigidity, guarding, rebound tenderness) with bowel wall perforation. On the other hand, fever is almost always present, but hypotension and shock are uncommon. 

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Evaluation

Diagnosis of acute diverticulitis can be made clinically based on history and physical examination alone. However, clinical diagnosis can be inaccurate in 24% to 68% of cases. Hence, laboratory and radiological tests play an important role in the accurate diagnosis of acute diverticulitis. Laboratory tests may show leukocytosis and elevation of acute phase reactants such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The radiological test of choice for acute diverticulitis is CT of the abdomen and pelvis, preferably with water-soluble oral or rectal (if significant nausea and vomiting) contrast and intravenous contrast provided there be no contraindications. The sensitivity, specificity, and negative predictive value of a CT scan have been reported as greater than 97%. Typical findings of acute diverticulitis in CT scans include bowel wall thickening, pericolic fat stranding, pericolic fluid, and small abscesses confined to the colonic wall as well as contrast extravasation, indicating intramural sinus and fistula formation.[8]

Abdominal ultrasound can accurately diagnose acute diverticulitis, with comparative sensitivity (84% to 94%) and specificity (80% to 93%) as of CT. However, ultrasound (US) results are highly operator dependent, and use is limited despite encouraging data, lower cost, and easy availability. MRI is another possible diagnostic modality. Due to cost and no direct comparison of sensitivity or specificity, CT is usually preferred. Radiographs of the abdomen will probably only show nonspecific abnormalities such as bowel gas; however, if the patient has an intestinal obstruction, air-fluid levels can be present.

Endoscopy should be avoided in suspected acute diverticulitis due to an increased risk of perforation. It is recommended that a colonoscopy is performed approximately six to eight weeks after symptoms have resolved to rule out malignancy, inflammatory bowel disease, or possibly colitis if the patient has not had a recent colonoscopy.

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Treatment / Management

Upon clinical presentation, acute diverticulitis can be managed with either outpatient or inpatient care. According to American Society of Colon and Rectal Surgeons, a patient who cannot tolerate oral intake, is excessively vomiting, shows signs of peritonitis, is immunocompromised, or at an advanced age should be hospitalized. In the absence of these conditions, and if appropriate prompt follow-up can be established, acute diverticulitis can be managed on an outpatient basis. It is reported that success rate of outpatient management is about 94% to 97%. The standard of outpatient care includes bowel rest, increase fluid intake, and oral antibiotic therapy (single or multiple drug regimen) that covers gram-negative rods and anaerobic bacteria. The most common regimen used in the United States consists of quinolones (ciprofloxacin) or sulfa drugs (trimethoprim/sulfamethoxazole) in combination with metronidazole  (or clindamycin, if the patient is intolerant to metronidazole) or single agent amoxicillin-clavulanate for 7 to 10 days.[8][3][9]

Inpatient management of diverticulitis requires intravenous antibiotics, intravenous fluids, and pain management. Again, antibiotics should cover gram-negative rods and anaerobes and be given for three to 5 days before switching to oral antibiotics for a ten to 14-day course. Bowel rest is preferred in patients requiring inpatient admission. Typically, defervescence and improvement in leukocytosis should be observed for two to four days of hospitalization, if not an alternative diagnosis or complications should be suspected. Prompt surgical evaluation should be considered.

About 15% patients with acute diverticulitis develop an abscess, specifically pericolonic and intra-mesenteric. Clinically, abscess formation should be suspected if fever and leukocytosis do not subside despite adequate intravenous (IV) antibiotics. On physical exam, a tender abdomen and tender mass suggest possible abscess formation. Abscesses that are less than 2 cm to 3 cm can be treated conservatively with IV antibiotics. Large abscesses should be drained percutaneously with CT guidance.

Fistula formation is another complication of acute diverticulitis. It is reported that less than 5% develops fistula; however, it has been found in about 20% of patients who undergo surgery for diverticulitis. The most common fistula is colovesicular fistula which occurs in about 65% of cases. Fecaluria is pathognomonic for colovesicular fistula. Surgical repair of the fistula with primary anastomosis is the treatment of choice. Colovaginal, coloenteric, colouterine, colourethral, and colocutaneous are other possible fistulae seen in acute complicated diverticulitis.

Partial bowel obstruction or pseudo-obstruction due to colonic ileus can occur as well, which can be managed conservatively. Complete bowel obstruction is rare in acute diverticulitis. Free perforation, if it occurs, should be managed surgically.

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Differential Diagnosis

• Cholangitis

• Cholecystitis

• Chronic mesenteric ischemia

• Constipation

• Enterovesical fistula

• Gynecological pain

• Inflammatory bowel disease

• Intestinal perforation

• Irritable bowel syndrome (IBS)

• Large-bowel obstruction

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Prognosis

The prognosis of patients with diverticulitis depends on age at presentation, the presence of comorbidity and severity of the disease. In general, younger people tend to have a higher morbidity as they never suspect they have the disorder and often present late. In addition, patients who are immunocompromised tend to have high morbidity and mortality.[10]

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Complications

• Pelvic abscess
• Intestinal perforation
• Bowel fistula
• Peritonitis
• Bowel obstruction
• Sepsis
• Bleeding per rectum

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Postoperative and Rehabilitation Care

After recovering from diverticulitis, the patient must be examined to rule out a malignancy. Options for investigation of the colon include colonoscopy, CT scan or a barium enema.

The patient should start a high-fiber diet, drink ample water, maintain a healthy weight and exercise.

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Deterrence and Patient Education

A high-fiber diet can prevent diverticulosis.

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Pearls and Other Issues

As previously stated, approximately 15% of patients with acute diverticulitis develop complications. Twenty percent to 50% of patients develop recurrent episodes of diverticulitis. Having multiple episodes does not appear to increase the risk for complications directly. It may increase the risk of fibrosis, leading to stricture formation and subsequent obstruction. Some patients, approximately 20%, will experience chronic abdominal pain due to either irritable bowel syndrome or chronic low-grade diverticulitis. These patients may be referred for elective colectomy for symptom control. Elective operations for diverticulitis have increased by approximately 30% since 1998.

The mortality rate in uncomplicated diverticulitis is negligible with appropriate conservative therapy. Complicated diverticulitis requiring surgery may lead to death in approximately 5% of patients. Perforation of the bowel with resulting peritonitis increases the risk of death to 20%.

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Enhancing Healthcare Team Outcomes

Acute diverticulitis has enormous morbidity and while there are no universal guidelines, expert opinion recommends an interprofessional approach for diagnosis and management. The disorder needs to be staged radiologically. In addition, the patient needs a dietary consult regarding a high-fiber diet. Nurses need to assist in educating the patient on following dietary restrictions. An infectious disease consultant and a gastroenterologist need to determine the duration of antibiotic therapy and a general surgeon is necessary to develop a protocol for management of any pelvic abscess. Finally, a general or colorectal surgery should determine the proximal levels of colon resection but the amount of clear proximal margin needed remains unknown. Because the risk of colon cancer in patients with acute diverticulitis is slightly increased, a screening program has to be established.[11][12] [13] (Level III)

Outcomes

Many cases studies reveal that the majority of patients treated for acute diverticulitis do not have a recurrence after initial medical treatment. However, in patients with recurrence, surgical excision of the diseased bowel is recommended, especially in patients over the age of 50. (Level V) Finally, the decision to perform laparoscopic or open surgery for managing acute diverticulitis remains debatable. One study showed no difference in postoperative morbidity between the two. [2][14](Level III) Randomized clinical studies are needed to determine which surgery and what type of surgery is ideal for patients with acute diverticulitis.

B肝治療手冊-台灣-財團法人肝病防治學術基金會-醫療法人好心肝基金會 2022-06

2024-03-22 中午 12:01

B肝抗病毒藥物停藥條件
體內已經測不到B肝病毒，且GPT值持續正常已超過一年半以上，可以考慮先停藥，

e抗原陽性轉陰性之後可再用一年藥物. 之後停藥

HBeAg 陽性. 且血清HBV DNA連續3次，每次間隔6個月，均檢驗不出HBV DNA時可停藥
移植手術後. 肝移植患者可長期使用. 非肝臟的其他器官移植. 當B肝發作時可長期使用
B肝帶原, 癌症化療期間B肝發作, 可長期使用
化療之前若擔心造成B肝發作. 可會診GI之後作為預防性使用. 化療前一周至化療結束六個月內可給藥

B肝復發定義: 病毒量 >2000（IU/mL），肝功能超過正常值2倍

B肝帶原者使用抗病毒藥物治療需檢測項目
1. 超音波. 評估是否肝硬化或有肝腫瘤
2. e抗原(HBeAg) 評估病毒是否大量繁殖
3. GOT/GPT
4. HBV DNA
5. HBsAg 
6. Bilirubin/ PT 評估是否發生肝功能不全

肝功能不全. 詳細說明放最下面. 
黃疸指數膽紅素（bilirubin）上升及凝血酶原時間（prothrombin time）延長或出現併發症如腹水，即稱為「肝功能代償不全」

好心肝會刊: 2017-07-15 B肝抗病毒藥物健保給付放寬，我符合規定嗎？諮詢∕林姿伶（好心肝門診中心主治醫師）撰稿∕黃靜宜

e抗原陰性或陽性 健保規定不同

上述案例中的陳先生為e抗原陰性之B肝病人，健保用藥治療3年後改為自費用藥至今，依規定無法直接由自費再轉為健保。如果體內已經測不到B肝病毒，且肝發炎指數GPT值持續正常已超過一年半以上，可以考慮先停藥，保持密切追蹤。停藥後若仍不幸復發，則可接續使用健保療程。

但如果治療前為e抗原陽性、也符合健保給付條件的病患，健保治療到期後未停藥又接續自費治療，且e抗原至今仍為陽性者，可以由自費直接轉健保，直到e抗原轉陰再鞏固治療一年。

簡而言之，e抗原陰性且服藥達三年而仍持續自費用藥者，無法直接轉為健保用藥。但若停藥後不幸又復發，就能再由健保給付。

健保B肝抗病毒藥物給付條件中，除肝硬化患者外，慢性B型肝炎患者服藥期間仍有限制，但若停藥後復發，則可再接受治療，且不限次數。主要理由還是健保經費有限，且目前仍無理想指標確保停藥後不會復發。

Q 我有B型肝炎帶原，我需要服藥治療嗎？有健保給付嗎？

A 有B型肝炎帶原，該不該用藥？健保給付之藥物有哪些限制？可分為以下幾種情況：

◎如果你是「慢性Ｂ型肝炎帶原者，且已發生肝代償不全」：

(1)以Lamivudine 100mg、Entecavir 1.0mg、 Telbivudine 600mg、或Tenofovir 300mg治療。

(2) HBeAg陽性病患治療至e抗原轉陰並再給付最多12個月治療。

(3) HBeAg陰性病患治療至少2年，治療期間需檢驗血清HBV DNA，並於檢驗血清HBV DNA連續3次，每次間隔6個月，均檢驗不出HBV DNA時可停藥，每次療程至多給付36個月。停藥後復發時得再接受治療，不限次數。

◎如果你是慢性Ｂ型肝炎帶原者：

(1)接受非肝臟之器官移植後，Ｂ型肝炎發作者，可長期使用。

(2)接受肝臟移植者可預防性長期使用。

(3)接受癌症化學療法期間Ｂ肝發作者，經照會消化系專科醫師同意，可長期使用。

(4)接受癌症化學療法，經照會消化系專科醫師同意後，可於化學療法前1週開始給付使用，直至化學療法結束後6個月，以預防Ｂ型肝炎發作。

◎如果你是ｅ抗原陽性的慢性Ｂ型肝炎患者：

(1)HBsAg(+)超過6個月及HBeAg(+)超過3個月，且ALT值大於（或等於）正常值上限5倍以上（ALT≧5X），符合前述條件者，其給付療程為治療至e抗原轉陰並再給付最多12個月。

(2)HBsAg(+)超過6個月及HBeAg(+)超過3個月，其ALT值介於正常值上限2至5倍之間（2X≦ALT <5X），且血清HBV DNA≧20,000 IU/ mL，或經由肝組織切片證實肝細胞內HBcAg陽性之患者，其給付療程為治療至e抗原轉陰並再給付最多12個月。 

◎如果你是ｅ抗原陰性的慢性Ｂ型肝炎患者：

HBsAg(+)超過6個月及HBeAg(-)超過3個月，且ALT值半年內有兩次以上（每次間隔3個月）大於或等於正常值上限2倍以上（ALT≧2X），且血清HBV DNA≧2,000 IU/mL，或經由肝組織切片證實肝細胞內HBcAg陽性之患者，至少治療2年。治療期間需檢驗血清HBV DNA連續3次，每次間隔6個月，均檢驗不出HBV DNA時可停藥，每次療程至多給付36個月。停藥後復發時，得再接受治療，不限次數。

◎如果你是肝硬化病患，可長期使用：

需同時符合下列二項條件：

(1)HBsAg(+)且血清HBV DNA≧2,000IU/mL者。

(2)診斷標準：

a.肝組織切片（Metavir分期F4或Ishak分期5分以上）；

b.超音波或電腦斷層診斷有肝硬化且胃鏡檢查發現食道或胃靜脈曲張，或超音波或電腦斷層診斷有肝硬化併脾腫大。

註：上述條文為「全民健康保險藥物給付項目及支付標準共同擬訂會議」對於慢性Ｂ型肝炎治療的修正藥品給付規定，自106年1月1日開始實施。

[Q&A]

Q.停藥後，如何知道B型肝炎是否復發？

A.復發與否要靠抽血檢查，通常是病毒量先高起來，肝功能才會接著變高。如果病毒量超過兩千國際單位（IU/mL），肝功能也超過正常值2倍，就要考慮復發了。停藥後的一年內最容易復發，所以要密集追蹤。建議前一年每1至2個月追蹤一次。每次追蹤都要檢測肝功能、且在肝功能指數達到兩倍以上時檢測病毒量。

Q.B肝帶原者若醫療上建議需用口服抗病毒藥物，是否還有健保不給付的狀況？

A.肝帶原者若患有風濕免疫疾病，需使用生物製劑，或因各種疾病（如風濕免疫疾病或腎臟病）等需要用到或長或短的類固醇，也可能會有B型肝炎發作的風險，但目前健保尚未給付這部分，所以建議這類病患應與醫師討論是否要使用口服B肝抗病毒藥物預防B肝發作。

B肝治療手冊2022-06
台灣以前成人的B肝帶原率高達 15%, 經大規模疫苗接種, 目前降到 1% 以下.
B肝疫苗適應症:
1. 非B型肝炎帶原者
2. 血液中沒有表面抗體(Anti-HBs)及核心抗體者(Anti-HBc)

但施打B肝疫苗後, 約 5%~15% 的人不會產生表面抗體.

B肝病毒感染後變成B肝帶原機率
1. 母子垂直傳染, 若母體 e抗原陽性, 小孩 90% 成為帶原. 若母體 e抗原陰性, 小孩 5-10% 成為B肝帶原
2. 兒童期感染, 25% 成為帶原者
3. 成人感染, 70% 會痊癒, 30% 會出現黃疸, 不到 5% 會成為帶原者, 0.1%~0.5%會出現猛爆性肝炎

B肝帶原, 90% 沒有症狀.
有些人抽血和超音波正常(病毒DNA小於 2000iu/mL)
有些肝指數輕微上升. 有些人肝指數上升超過五倍以上.
有些經過慢性發炎進展成肝硬化,
少部分患者不經過肝硬化直接變成肝癌.

e抗原臨床意義是評估病毒是否正在大量繁殖.
當血液檢查 e 抗原為陽性時，代表 B 型肝炎病毒正在大量增殖，
參考資料. 國泰醫院- e抗原是什麼

許多 B 型肝炎帶原者，習慣定期追蹤檢查表面抗原（HBsAg）及肝功能。但是不少帶原者卻忽略了 e 抗原（HBeAg）的重要性。
e 抗原是由 B 型肝炎病毒基因之核心前區及核心區，於製造肝炎病毒過程中，產生而分泌入血液之多胜鍵。當血液檢查 e 抗原為陽性時，代表 B 型肝炎病毒正在大量增殖，這個時候血液中之 B 型肝炎病毒核醣核酸（HBV-DNA）通常為陽性，它代表血液體液中含有大量的病毒，且具有高度傳染性。患者本身可能因為發生免疫反應，而造成肝細胞壞死、肝功能異常等肝炎現象。
如果 e 抗原為陰性，而 e 抗原之抗體（anti-HBe）為陽性時，通常表示 B 型肝炎病毒已經不再大量增殖，患者之肝功能通常是正常的，血液中之 HBV-DNA通常是陰性，也就是患者之血液體液較不具有傳染性。

B 型肝炎帶原者之表面抗原通常不易消失，要掌握肝炎之活動性，除了定期檢查肝功能外，也應定期檢查 e 抗原及 e 抗體，充分掌握病毒之活動性，才能於適當時機使用藥物治療病毒之活動性。


B肝帶原者的檢查頻率. 若抽血跟超音波正常, 之後六個月抽血一次, 一年至少做一次腹部超音波追蹤
肝硬化患者, 至少先做一次胃鏡.




B肝的藥物治療
目前抗病毒藥物僅能阻止B肝病毒複製, 無法根除病毒, 因此吃藥的時間通常要很長(幾個月至幾年). 服藥的目標是將肝指數降到正常, 血中測不到病毒的量. 停藥之後 90% 的病毒數量會再次增加, 約 50% 需要再次服藥.

另. 2023年B肝抗病毒藥物條件有放寬
e抗原陰性者 B肝藥物健保給付規範10月起放寬！

新修訂給付規範與原給付規範，主要差別在於病毒量大於2000 IU/mL者，ALT值超過正常值上限兩倍以上只要有一次就可以給付；肝纖維化F3條款改成只要F2即可，對照表如下。
半年內有兩次肝指數上升沒有達兩倍. 之間間隔需 3 個月. 可開立抗病毒藥物




事實上，世界三大肝病醫學會早就建議，e抗原陰性且血清B肝病毒量大於2000 IU/mL的病人，血中ALT值超過正常值上限兩倍，不用等3個月後再看ALT值就直接用藥，因為臨床觀察發現e抗原陰性病人會自行好轉的機會其實很低，而反覆發炎對肝臟會造成傷害，肝纖維化也會不斷累積。

依據健保規範，e抗原陰性的慢性B型肝炎病人每次用藥2～3年後需停藥，停藥以後若復發可再用藥，亦沿用同樣的新條款，病人用藥的機會將大幅上升。

不過，由於各家藥廠考量不同，上述放寬條件適用的臨床常用B肝藥物為貝樂克和韋立得，惠立妥及其相關學名藥之使用，仍沿用舊的給付規範。

抽血檢驗B肝病毒表面抗原（HBsAg）持續陽性超過6個月，就是慢性B肝帶原者。並非每位B肝帶原者都需要使用抗病毒藥物治療，台灣健保署參酌醫界的專業建議，訂定給付抗病毒藥物的規範，這些規範較國際通用之規範嚴格。為了照顧更多的病人，健保署近期已開會通過2023年10月1日起放寬給付規範，這次放寬給付的對象主要是血清B肝病毒e抗原（HBeAg）陰性的病人。

2012-07-15 好心肝會刊 肝功能代償不全 定義

肝臟是人體最重、也最重要的器官，重量約為一個標準體重成人的2.2%。它在人體運作中扮演多重的關鍵角色，包括合成功能，可合成蛋白質、凝血因子；代謝功能，可代謝體內的毒素；分泌功能，協助分泌膽汁；還具有免疫功能。 

正常人只要剩下30%到40%的健康肝臟，即可能維持正常運作之所需求。可是，一旦肝臟嚴重受損，抽血檢查黃疸指數膽紅素（bilirubin）上升及凝血酶原時間（prothrombin time）延長或出現併發症如腹水，即稱為「肝功能代償不全」。若肝功能持續無法恢復，甚至需要考慮換肝一途。  

◎肝臟移植VS心、腎移植 

肝臟移植以後有極高的感染風險，因為肝臟移植後的「接頭」較多，例如肝動脈、門靜脈、肝靜脈、膽管等，細菌和病毒可能入侵的「管道」多。任何一條血管的阻塞，都可能造成肝組織壞死併發感染；膽管接合處的阻塞或者滲漏，也很容易造成細菌的感染。 

以肝臟和心臟來比較，一般心臟移植只要接合左右心房和兩條大動脈（主動脈和肺動脈）；肝臟移植最基本要接合肝靜脈、門靜脈、肝動脈、膽管4條脈管，臨床上還有不少人血管構造複雜，同時有2、3條肝靜脈，接合的血管就要多至6、7條。此外，成人心血管直徑約有30到40毫米，但小兒肝臟血管只有2毫米，細如髮絲，因此在肝臟移植手術中，血管接合部分，需進行顯微手術。 

肝臟同時也還是凝血因子合成的重要器官，當肝不好的患者（如肝硬化），其凝血因子產生不足，再加上血液回流至肝臟受阻導致脾臟腫大，破壞血小板而造成血小板數過低，使得手術時容易出血。另外，此時還易生成側枝血管，脆弱易破，提高手術中血管接合的困難度，所以肝臟移植手術「步步驚心」，平均要10到20個小時，遠比心臟和腎臟移植平均約3、4個小時，來得費時。

 

◎肝臟移植如何進行？配對的原則？ 

一名肝病患者一旦被評估需要換肝，醫療院所就會將個案登錄在衛生署器官捐贈移植中心的名單中，醫院通常會同時進行屍肝捐贈的等待和親屬間活肝捐贈的評估，以利加速病患重生的機會。

 

屍肝由腦死患者大愛捐出，必須依病情評分後按排名先後等候；活肝捐贈則需是患者5等親內血親或姻親，年齡在20歲以上、或18歲到20歲間經家長或監護人同意，經健康檢查後，身心狀況及肝臟大小符合捐贈標準，才得捐贈。

 

肝臟移植配對原則包括：

器捐者和受贈者血型要相同或相容：相同血型，即是O型血捐給O型、A型血捐給A型…；相容血型則是兩者血型可以相容，如O型可捐給任何血型的人、AB型血者可接受任何血型者的捐贈，A型和B型血除了可接受自己同血型者也可接受O型血的捐贈。

兒童的屍肝，只能捐給兒童的肝病患者。因為兒童肝臟小、器捐來源也少，故做此限制。

病情最危急的第一等級患者，是優先受贈的對象。

同一個「器官捐贈勸募中心（OPO）」組織體系下的醫院勸募的器官，優先給結盟的移植醫院使用。

 

至於活體肝臟移植，除了血型相同和相容的比對外，為確保捐贈者的健康，捐肝者的肝臟容積保留也有嚴謹的規範：

受贈者依病情的狀況，一般患者需要的肝臟大小，約為自己原本肝容積的35%；但若已肝昏迷的患者，則需要40%左右。

 

捐贈者捐給受贈者所需的肝臟後，留下的肝臟需足夠自己身體的運作。

 

體型小捐給體型大者，若捐出的是較大的右肝，剩餘的肝臟容積需保留35%以上才達到安全標準；若為30%到35%之間，則需經由個案評估。