眼科前房的六大迷思：在眼科中的誤解與批判性思考
中文摘要
我們一直在努力尋求真理，以改善患者的護理。然而多年來，某些基於神話而非事實的觀念滲透到我們的專業中。本文旨在重點闡明6個例子，告知我們的社群，解釋這些神話為何持續存在，並考慮如何著手解決這個問題。
神話1：Hutchinson的徵象是疱疹性眼部炎的獨特預測指標 Hutchinson的徵象是指在第五腦神經（V1）的第一皮膚神經節疱疹的情況下，鼻尖的受牽連預示著眼睛受牽連的風險較高。然而，根據大規模研究，V1疱疹在鼻膜皮膚範圍（不僅僅是鼻尖）有一定的預測價值，但偽陰性和偽陽性發現普遍存在，對Hutchinson的徵象的診斷用途產生質疑。然而，皮膚節徵象的真正價值在於幫助非眼科醫生確定哪些患者需要轉介進行眼科評估。一項對急診部門的V1疱疹患者的前瞻性研究得出結論，Hutchinson的徵象（鼻膜疹）不能預測眼睛受累，但額上神經的皮疹卻可以。因此，對於所有患有V1疱疹的患者，都應全面評估是否涉及眼部。
神話2：嬰兒洗髮精眼瞼清潔是眼瞼炎的一線治療 每位眼科醫生可能都被教導使用嬰兒洗髮精來治療眼瞼炎。然而，2012年的Cochrane回顧研究得出結論，對於慢性眼瞼炎的任何治療都缺乏堅實的證據。而嬰兒洗髮精除了色素和香料外（這兩者都可能導致過敏），還含有可能破壞淚液膜並傷害眼表面的肥皂成分。事實上，嬰兒洗髮精公司明確表示不建議在眼周使用該產品。因此，嬰兒洗髮精不應作為首選治療推薦。
神話3：Thygeson superficial punctate keratitis僅限於角膜上皮 Thygeson superficial punctate keratitis（TSPK）是一種角膜表層點狀炎症。然而，自Thygeson首次描述TSPK以來，一些作者發表了病例系列報告，描述了具有前部間質炎(anterior stromal keratitis)、角膜疤痕的患者（其中一些患者甚至是由Thygeson本人診斷為TSPK），但這些報告大多被忽視，因為它們與Thygeson的最初描述相矛盾。Thygeson可能未能發現前部間質炎和疤痕的原因是由於當時裂隙燈的品質（他更喜歡使用放大鏡）以及他對這些患者的相對短暫的follow-up。儘管如此，教科書上仍然教授TSPK僅涉及角膜上皮且不會形成疤痕，但有時我們需要質疑這一觀點。
神話4：上部輪狀角膜結膜炎(superior limbic keratoconjunctivitis) 是由上眼瞼緊繃造成的 這種疾病與甲狀腺眼病和移植物對宿主病（GVHD）有關，並且透過局部輸注類固醇而改善。然而，問問任何角膜科醫學住院醫師SLK的原因，他們會告訴你這是一種上眼瞼緊繃的假設性理論，幾乎沒有支持性數據。只有少數甲狀腺眼病患者表現出SLK，並且這些患者的上眼瞼緊繃程度並不比對照組參與者更嚴重。眼部GVHD患者SLK的發生率遠高於甲狀腺眼病患者，而患有GVHD的患者的眼瞼鬆弛程度比同齡對照組參與者更大。儘管有數據顯示SLK是與較鬆的眼瞼相關的炎症性疾病（至少對於GVHD患者而言），但緊繃眼瞼仍被視為SLK的原因。
神話5：如果患者經常使用人工淚液，應開立無防腐劑人工淚液 人工淚液的使用非常普遍，儘管幾乎沒有數據支持其對任何病症的治療價值。人們通常認為使用人工淚液不會對眼睛造成傷害，並可能會有些好處。確實，一些患者報告使用人工淚液會短暫緩解眼部不適。然而，人工淚液對患者來說是一種成本，通常不受保險公司賠償，可能導致傷害（多達75％的經驗豎滴劑的用戶會將瓶蓋觸摸到球瞳或眼周組織），可能導致感染，增加藥物使用阻力（越多藥物，越低的依從性），並且可能引起眼睛毒性。此外，我們未能找到證據支持常見教導的觀點，即如果患者每天使用人工淚液超過4次，應開立無防腐劑人工淚液，這將大大增加患者的負擔。也許更好的做法是，如果使用保存劑產品引起眼部刺激，則轉換到無防腐劑的產品。
神話6：局部類固醇需要進行逐漸減量 作為眼科醫生，我們經常聽到同行教導的觀點，即逐漸減少局部類固醇的用量以避免反彈炎症(rebound inflammation)。然而，這種教導有兩個問題，也許更多地與用詞選擇有關，但詞語很重要，會影響我們的學員如何思考。首先，我們未能找到支持這樣一個觀念的數據，即一旦開始使用眼睛類固醇，眼睛就變得依賴類固醇，必須進行類固醇逐漸減量來使眼睛戒斷藥物依賴。其次，在這個上下文中使用“反彈”這個詞，暗示在減少類固醇時會發生一個特殊的病理過程，即當抗炎治療停止時，將發生未解決的炎症進一步復發。眼科醫生減少局部類固醇的頻率和劑量，以找到控制疾病並最小化副作用所需的最低治療劑量。遵循這種邏輯有兩種類固醇減量模式，兩者都與反彈性炎症無關。第一種模式是預定的類固醇減量，用於已知未來的眼部炎症模式。例如，白內障手術後定期減少局部類固醇的方法就是一個很好的例子，這通常是在沒有臨床監督的情況下進行的。在手術後，外科醫生對不同時間點的手術後可能需要多少類固醇有很好的了解，並以此為依據，給患者制定了一個預定的類固醇減量計劃。相反，當眼科專家治療眼部炎症時，通常進行受監督的類固醇減量，因為他們通常不事先知道所治療的疾病的預期時間。了解這一點後，他們會給患者制定一個監督的類固醇減量計劃。患有GVHD的患者。然而，在減少慢性全身類固醇時，他們還會考慮已造成腎上腺抑制的可能性，因此慢慢逐漸減少全身類固醇的低劑量，以避免增加阿迪生氏症(Addison’s syndrome)的發生率。眼科醫生在減少類固醇眼藥水時無需擔心這個問題，但這可能導致慢慢逐漸減少類固醇眼藥水來預防眼部反彈性炎症的概念。
English Abstract
We have been continuously striving to seek the truth in order to improve patient care. However, over the years, certain myths based on folklore rather than facts have infiltrated our profession. This article aims to highlight six examples to inform our community, explain why these myths persist, and consider how to address this issue.
Myth 1: Hutchinson’s sign is a unique predictor for herpes zoster ophthalmicus (HZO). Hutchinson’s sign refers to involvement of the tip of the nose, indicating a higher risk of ocular involvement when the first branch of the trigeminal nerve (V1) is affected by herpes zoster. However, large-scale studies have shown that V1 herpes zoster has some predictive value beyond just the tip of the nose. False negatives and false positives are commonly found, raising doubts about the diagnostic utility of Hutchinson’s sign. Nevertheless, the true value of this dermatomal sign lies in helping non-ophthalmologists identify patients who require ophthalmic evaluation. A prospective study of V1 herpes zoster patients in the emergency department concluded that Hutchinson’s sign (nasal rash) does not predict ocular involvement, but rashes on the forehead nerve can. Therefore, all patients with V1 herpes zoster should undergo a comprehensive evaluation for ocular involvement.
Myth 2: Baby shampoo eyelid scrubs are a first-line treatment for blepharitis. Every ophthalmologist might have been taught to use baby shampoo for treating blepharitis. However, a Cochrane review in 2012 concluded that there is a lack of robust evidence for any treatment of chronic blepharitis. Baby shampoo contains surfactants, which, apart from pigments and fragrances (both of which can cause allergies), can disrupt the tear film and damage the ocular surface. In fact, baby shampoo companies explicitly advise against using the product around the eyes. Therefore, baby shampoo should not be recommended as the first-line treatment.
Myth 3: Thygeson’s superficial punctate keratitis (TSPK) is limited to the corneal epithelium. TSPK is a form of superficial punctate inflammation on the corneal surface. However, since Thygeson first described TSPK, some authors have reported case series describing patients with anterior stromal keratitis and corneal scars (some of whom were even diagnosed with TSPK by Thygeson himself). Nevertheless, these reports have been mostly ignored because they contradict Thygeson’s initial description. Thygeson might have missed the anterior stromal keratitis and scars due to the quality of slit lamps (he preferred magnifying glasses) and his relatively short follow-up of these patients. Despite this, textbooks still teach that TSPK is limited to the corneal epithelium and does not form scars, but sometimes, we need to question this perspective.
Myth 4: Superior limbic keratoconjunctivitis (SLK) is caused by tight upper eyelid. This disease is associated with thyroid eye disease and graft-versus-host disease (GVHD) and improves with local steroid injections. However, ask any cornea fellow the reason for SLK, and they will tell you that it is a hypothetical theory of tight upper eyelid tension with almost no supporting data. Only a few patients with thyroid eye disease show SLK, and their superior eyelid tension is not significantly more severe than that of control participants. The occurrence of SLK in patients with eye GVHD is much higher than in patients with thyroid eye disease, and those with GVHD have greater eyelid laxity than age-matched controls. Although data suggest that SLK is an inflammatory disease associated with looser eyelids (at least for GVHD patients), tight eyelids are still considered the cause of SLK.
Myth 5: Preservative-free artificial tears should be prescribed if patients use artificial tears frequently. The use of artificial tears is widespread, despite scarce data supporting their therapeutic value for any condition. People generally believe that using artificial tears will not harm the eyes and may have some benefits. However, artificial tears are a cost for patients, usually not covered by insurance, which may lead to in-hospital harm (up to 75% of users of multidose vials touch the bottle cap to the conjunctiva or periocular tissue), potential infections, increased medication usage resistance (more medications lead to lower adherence), and possible ocular toxicity. Additionally, we found no evidence supporting the common teaching that if patients use artificial tears more than four times a day, preservative-free artificial tears should be prescribed, which would significantly increase the burden on patients. Perhaps a better approach is to switch to preservative-free products if preserved products cause ocular irritation.
Myth 6: Topical steroids need to be tapered gradually. As ophthalmologists, we often hear the view taught by peers that topical steroids should be tapered gradually to avoid rebound inflammation. However, this teaching has two problems, perhaps more related to word choice, but words matter and influence how our learners think. Firstly, we found no data supporting the notion that once topical steroids are started, the eyes become dependent on steroids, necessitating a gradual taper to wean off the drug. Secondly, the use of the word “rebound” in this context suggests a specific pathological process where unresolved inflammation flares up further when anti-inflammatory treatment is discontinued. Ophthalmologists reduce the frequency and dose of topical steroids to find the minimum therapeutic dose required to control the disease and minimize side effects. Following this logic, there are two patterns of steroid tapering, both of which have nothing to do with rebound inflammation. The first pattern is scheduled steroid tapering, used for diseases with a known future pattern of ocular inflammation. For example, the method of gradually reducing topical steroids after cataract surgery is a good example of this, and it is often done without clinical supervision. After surgery, the surgeon has a good idea of how much steroids will be needed at different time points after surgery and uses this to create a scheduled steroid tapering plan for the patient. In contrast, when ophthalmologists treat ocular inflammation, it is usually under supervised steroid tapering since they typically do not know the expected duration of the disease they are treating. Understanding this, they develop a supervised steroid tapering plan for the patient. This is also a strategy in patients with GVHD, where the corticosteroids have likely caused adrenal suppression, and they gradually taper systemic corticosteroids to avoid increasing the occurrence of Addison’s disease. Ophthalmologists do not need to worry about this when tapering topical steroids, but it may lead to the concept of slowly tapering topical steroids to prevent ocular rebound inflammation.
