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Introduction: Trochlear nerve palsy (TNP) is a common cause of vertical diplopia resulting from superior oblique muscle weakness. While herpes zoster is a well-documented cause of cranial neuropathies, reports of TNP associated with herpes zoster infection remain limited. Case Presentation: We report a case of a 65-year-old patient with typical herpes zoster ophthalmicus on the left side of his face with subsequent corneal endotheliitis and isolated TNP. The MRI revealed a faint enhancement at the cavernous sinus on the same side as the TNP. Cerebrospinal fluid detected human herpesvirus 3, confirming the diagnosis. An intravenous antiviral was administered for 14 days with prolonged maintenance to prevent recurrence. Oral corticosteroids were also used as an adjuvant to reduce inflammation. After treatment, the uveitis subsided, and the vertical diplopia recovered partially. TNP from herpes zoster is a rare presentation. The underlying pathogenic mechanisms, including potential direct viral invasion, inflammatory responses, and possible vasculopathy affecting the trochlear nerve, are explored. Conclusion: TNP can be a rare neuro-ophthalmic complication of herpes zoster infection. Clinicians should maintain a high index of suspicion when assessing patients with cranial neuropathies in the context of herpes zoster. Prompt antiviral therapy and supportive measures can aid in the resolution of symptoms and alleviate potential long-term sequelae.

Abstract Purpose To describe unusual clinical features and therapeutic management of a case of cytomegalovirus (CMV) ocular disease in a patient on immunomodulatory therapy. Setting/venue Moorfields Eye Hospital NHS Foundation Trust, London, UK. Methods Medical history, clinical findings, investigation results, and multimodal imaging were retrospectively collected. Results A 61-year-old, South-East Asian man, developed CMV-related endotheliitis and occlusive retinal vasculitis, diagnosed by wide-angle fluorescein angiography. No retinitis was present on the fundus examination. Suspicion of CMV etiology was based on anterior segment findings, especially the presence of coin-shaped endothelial lesions. The diagnosis was confirmed by aqueous polymerase chain reaction (PCR) analysis which was positive for CMV DNA. The combined use of topical and systemic valganciclovir resulted in significant improvement of the picture. Conclusions CMV can manifest in the eye as occlusive retinal vasculitis without the presence of typical retinitis.

Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID.

Severe acute respiratory syndrome coronavirus-2 causes hyperinflammation and activation of coagulation cascade and, as a result, aggravates endothelial cell dysfunction. N-acetylcysteine and Sulodexide have been found to mitigate endothelial damage. The influence on coronary artery endothelial cells of serum collected after 4 ± 1 months from coronavirus infection was studied. The concentrations of serum samples of interleukin 6, von Willebrand Factor, tissue Plasminogen Activator, and Plasminogen Activator Inhibitor-1 were studied. The cultures with serum of patients after coronavirus infection were incubated with N-acetylcysteine and Sulodexide to estimate their potential protective role. The blood inflammatory parameters were increased in the group of cultures incubated with serum from patients after coronavirus infection. Supplementation of the serum from patients after coronavirus infection with N-acetylcysteine or Sulodexide reduced the synthesis of interleukin 6 and von Willebrand Factor. No changes in the synthesis of tissue Plasminogen Activator were observed. N-acetylcysteine reduced the synthesis of Plasminogen Activator Inhibitor-1. N-acetylcysteine and Sulodexide increased the tPA/PAI-1 ratio. N-acetylcysteine may have a role in reducing the myocardial injury occurring in the post-COVID-19 syndrome. Sulodexide can also play a protective role in post-COVID-19 patients.

In the early months of the outbreak (2020–2022), COVID-19 was responsible for acute respiratory distress syndrome (ARDS) and an exceptional number of intensive care unit (ICU) admissions. Weaning difficulties from invasive mechanical ventilation (IMV) and many deaths related to COVID-19 were associated with persistent pulmonary hyperinflammation leading to pulmonary fibrosis and sometimes, in the first wave of the pandemic and before the use of dexamethasone was introduced, pulmonary cystic necrosis. A 72-year-old man hospitalized with severe COVID-19 required IMV and died on day 31 of refractory ARDS. Postmortem examination of the lungs found obliterative endotheliitis proximal to pulmonary cystic necrosis. The presence of SARS-CoV-2 envelope and complement/lectin (MASP-2) deposits near the endotheliitis lesions suggested that the virus acted directly on vascular involvement by a complement-mediated mechanism. Together with classic features of ARDS (epithelial lesions and diffuse alveolar damage), endothelial involvement with endotheliitis was the hallmark of severe COVID-19. Corticosteroids and complement blockade were sometimes beneficial for treating severe COVID-19, perhaps by preventing microvascular damage.

Here, we report the case of a patient with multiple parallel-line endotheliitis with myopic shift, which has not been previously reported. A 36-year-old man visited our clinic with blurred vision in his left eye. A slit lamp examination revealed an interesting pattern of multiple parallel lines of keratic precipitates, along with subtle corneal edema. The spherical equivalents measured in the right and left eyes were −9.25 and −11.875 diopter, respectively, with the left eye showing more myopic progression. On specular microscopy, endothelial cell loss was found in the left eye. After administration of a weak topical steroid, keratic precipitates and corneal edema resolved completely within 2 days. The myopic shift in his left eye recovered to −10.0 diopters. Multiple parallel-line endotheliitis can be easily treated with a weak topical steroid in a short period. A temporary myopic shift may occur, which in this case resolved upon disease recovery. However, corneal endothelial cell loss is inevitable; therefore, careful monitoring is needed.

Purpose: To examine the clinical outcomes in chronic or recurrent anterior uveitis in the presence or absence of cytomegalovirus (CMV) and investigate the predictive factors for uveitic activity and recurrence. Methods: Polymerase chain reaction (PCR) was performed in a prospective cohort of immunocompetent adults with recurrent or chronic anterior uveitis to detect CMV in aqueous humor. The clinical outcomes were compared between eyes with and without CMV DNA. Logistic regression was performed to evaluate associations between iris depigmentation, CMV-PCR status, uveitic activity, and recurrence. Results: Thirty-eight eyes of 38 subjects with a mean age of 61.1 ± 11.2 years old were analyzed. Fifteen eyes were positive for CMV. More eyes with CMV developed recurrences and remained actively inflamed at 6, 12, and 24 weeks though the differences were insignificant. The presence of iris depigmentation was predictive of a greater odd of uveitic recurrences by 12 and 24 weeks (Odds ratio (OR) = 9.17 and 5.72, P = 0.007 and 0.034 respectively), whereas positive CMV-PCR predicts a greater odd of uveitic activity at postoperative 12 and 24 weeks (OR = 13.08, 34.30; P = 0.027, 0.007). Conclusion: Eye with and without detectable CMV behaved similarly in their clinical course. Our findings suggested that iris depigmentation was predictive of more frequent uveitic recurrence, regardless of the PCR status, whereas the presence of CMV in aqueous humor was associated with persistent uveitic activity. Iris changes may be present during the earlier phase of the disease and precede the detection of virus from the aqueous humor at a later stage of CMV infection.

Po-Jui Chen,1 I-Huang Lin,1 Yi-Chun Chi,2 Chun-Chieh Lai,1 Jia-Horung Hung,1 Sung-Huei Tseng,1 Yi-Hsun Huang1 1Department of Ophthalmology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan; 2Department of Ophthalmology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, TaiwanCorrespondence: Yi-Hsun Huang, Department of Ophthalmology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Email jackhyh@gmail.comAbstract: Purpose: This study aimed to evaluate the therapeutic efficacy and long-term outcomes of treatment with topical 2% ganciclovir solution in immunocompetent patients with aqueous humor polymerase chain reaction (PCR)-proven cytomegalovirus (CMV) anterior uveitis and corneal endotheliitis.Methods: We retrospectively reviewed the findings for immunocompetent patients diagnosed with CMV uveitis or endotheliitis based on clinical manifestations and polymerase chain reaction (PCR) examination results and treated with topical 2% ganciclovir solution at National Cheng Kung University Hospital. Clinical outcome measurements included evaluations of the response rate, relapses, resolution of anterior chamber inflammation, visual acuity, and intraocular pressure.Results: The study included 38 eyes of 32 patients. Long-term administration of topical 2% ganciclovir significantly decreased keratic precipitates (p = 0.001), anterior chamber cells (p = 0.001), and reduced intraocular pressure (p < 0.001). Only one eye was unresponsive to topical ganciclovir treatment, and the recurrence decreased to 0.13 relapses per year. The presence of keratic precipitates and higher intraocular pressure at the initial presentation were significantly associated with recurrence (p = 0.036 and p = 0.001, respectively).Conclusions:: Long-term use of topical 2% ganciclovir solution is effective, safe, and applicable when commercialized ganciclovir gel is not available.Keywords: cytomegalovirus, endotheliitis, ganciclovir, uveitis

We describe 3 patients in California, USA, with trichodysplasia spinulosa polyomavirus (TSPyV) infection of endothelium after steroid administration. We detected TSPyV RNA in tissue specimens by in situ hybridization, which revealed localization to endothelial cells. These cases suggest that diseases associated with endothelial inflammation could be associated with TSPyV infection.

Abstract Background The current case report presents acute hemorrhagic necrotizing encephalopathy (AHNE) as an example of a fatal complication, the etiology of which could be coronavirus disease 2019 (COVID-19) with multiple organ damage along with the existing respiratory tuberculosis. Case presentation A male in his 20s had severe symptoms of central nervous system lesion, which developed against the background of COVID-19 and respiratory tuberculosis, for which he was treated in the intensive care unit. Autopsy confirmed that he died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated AHNE in adults with severe fatal endothelial dysfunction and respiratory tuberculosis. The main morphological signs of brain damage were desquamative endotheliitis, thrombosis, parenchymal hemorrhagic necrosis, encephalitis, severe necrobiotic neuronal damage. Conclusion The defeat of endothelial cells with the development of generalized endotheliitis in COVID-19, especially in conjunction with comorbid pathology, in particular tuberculosis, can lead to a fatal complication that affects the nervous system—AHNE. Therefore, it is worth paying close attention to the appearance of neurological symptoms in patients with a similar combination of diseases.

Abstract Given the scarcity of data regarding ocular complications following COVID‐19 vaccination, the approach toward patients with suggestive symptoms and established clinical practice is lacking. Herein, we report the first case of herpetic endotheliithis and secondary stromal keratitis following inactivated COVID‐19 vaccination who experienced a relapse due to poor adherence.

Abstract Background Cytomegalovirus (CMV) can manifest as corneal endotheliitis in immunocompetent individuals. Early diagnosis is prudent to prevent endothelial cell loss, which could ultimately lead to corneal decompensation. CMV DNA was first detected in an eye with corneal endotheliitis in 2006; since then, clinical evidence from numerous case reports and case series have accumulated. Main text In this narrative review, we identified several drugs, including ganciclovir, valganciclovir, and their combination in oral, intravenous, intravitreal, and topical forms in different concentrations, together with the judicious use of topical steroids, have reported variable success. There has yet to be any prospective comparative study evaluating the efficacy and safety of these assorted forms of treatment; clinical evidence is based on case reports and case series. CMV endotheliitis presenting with corneal edema can masquerade as other corneal diseases and thus poses a great challenge especially in post-keratoplasty eyes. Heightened awareness is needed before and after keratoplasty to start prompt prophylaxis and treatment. Conclusion There is no consensus on the management of CMV endotheliitis. Further studies are much needed to elucidate the optimal treatment modality, regime, and duration in the treatment and prophylaxis of CMV endotheliitis.

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

Extrapulmonary manifestations of COVID-19 (Coronavirus disease 2019) are increasingly recognized. Secondary spinal infections are dangerous complications reported in a few cases in the literature. However, to our knowledge, there is no reported case of a severe spondylodiscitis (SD) complicated with a large psoas abscess in a COVID-19 patient. We would like to report a 43-year-old male patient living in central Anatolia and dealing with farming who presented to the hospital with a complaint of severe back pain. The patient who was given oral treatment with analgesic, anti-inflammatory, and myorelaxant agents was readmitted with increased complaints. His nasopharyngeal swab was positive for COVID-19 without pneumonia on chest computed tomography (CT). He spent the quarantine and treatment period at home but was admitted to our outpatient clinic with a wheelchair with increased complaints and right leg pain preventing daily activities. The control nasopharyngeal swab was negative for COVID-19 but further increase in C-reactive protein (CRP) (152,8 mg/L) and creatine kinase (CK) level (549 IU/L) were revealed. Lumbar magnetic resonance imaging (MRI) showed SD in the L3-L4 level along with right-sided prevertebral inflammatory soft tissue and a large right psoas muscle abscess. Pyogenic lumbar SD complicated with the right psoas abscess in the setting of COVID-19 was considered and antibacterial treatment was started following hospitalization. On the same day, percutaneous aspiration from the psoas abscess under CT guidance was performed and revealed no growth in the culture. After 3 weeks, follow-up MRI showed worsening of all the bone, soft tissue and disc findings. Myalgia is a common manifestation in viral infections, which was also demonstrated in COVID-19 patients, with possible increase in muscle enzymes. Secondary spinal infections and its soft-tissue complications should be considered in the management of COVID-19 patients with neuromuscular symptoms, and detailed neurological and neurosurgical evaluation should be performed in order to avoid progression and permanent damage.

Abstract The corneal endothelium plays an integral role in regulating corneal hydration and clarity. Endotheliitis, defined as inflammation of the corneal endothelium, may disrupt endothelial function and cause subsequent visual changes. Corneal endotheliitis is characterized by corneal edema, the presence of keratic precipitates, anterior chamber inflammation, and occasionally limbal injection, neovascularization, and co-existing or superimposed uveitis. The disorder is classified into four subgroups: linear, sectoral, disciform, and diffuse. Its etiology is extensive and, although commonly viral, may be medication-related, procedural, fungal, zoological, environmental, or systemic. Not all cases of endothelial dysfunction leading to corneal edema are inflammatory in nature. Therefore, it is imperative that practitioners consider a broad differential for patients presenting with possible endotheliitis, as well as familiarize themselves with appropriate diagnostic and therapeutic modalities.

COVID-19 receives a lot of attention due to its threat to global public health. Research is ongoing to find universal methods to assess the baseline health status of a patient to determine prognosis and management strategies. This study aims to assess the predictive potential of the EASIX (Endothelial Activation and Stress Index) and two of its modifications (mEASIX and sEASIX) in terms of the need for admission to the ICU (intensive care unit), the use of IMV (invasive mechanical ventilation) and death due to COVID-19. The medical data of 370 severely ill patients hospitalised in the COVID-19 departments of the Regional Specialist Hospital in Wroclaw (Poland), including the ICU, were analysed retrospectively. The mortality rate in the group studied was 65.7% (243 cases). In the case of all three indices, EASIX, mEASIX and sEASIX, there was a statistically significant correlation between the need for admission to the ICU (p = 0.026, p = 0.019, p = 0.001, respectively) and the risk of death (p < 0.001). In terms of the risk of death, the high values of the assessed indices (EASIX ≥ 2.36, mEASIX ≥ 704.03, sEASIX ≥ 3.81) were characterised by low sensitivity (≤40%), high specificity (approximately 90%) and low NPV (negative predictive value) (approximately 40%) with high PPV (positive predictive value) (approximately 80%). Due to the ease of implementation and the low cost of performing basic laboratory tests, the above-mentioned indices can be used as an additional, but not universal tool for the initial assessment of the health condition of patients admitted to the hospital.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications.

ABSTRACT SARS-CoV-2 causes COVID-19, an acute respiratory distress syndrome (ARDS) characterized by pulmonary edema, viral pneumonia, multiorgan dysfunction, coagulopathy, and inflammation. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) receptors to infect and damage ciliated epithelial cells in the upper respiratory tract. In alveoli, gas exchange occurs across an epithelial-endothelial barrier that ties respiration to endothelial cell (EC) regulation of edema, coagulation, and inflammation. How SARS-CoV-2 dysregulates vascular functions to cause ARDS in COVID-19 patients remains an enigma focused on dysregulated EC responses. Whether SARS-CoV-2 directly or indirectly affects functions of the endothelium remains to be resolved and is critical to understanding SARS-CoV-2 pathogenesis and therapeutic targets. We demonstrate that primary human ECs lack ACE2 receptors at protein and RNA levels and that SARS-CoV-2 is incapable of directly infecting ECs derived from pulmonary, cardiac, brain, umbilical vein, or kidney tissues. In contrast, pulmonary ECs transduced with recombinant ACE2 receptors are infected by SARS-CoV-2 and result in high viral titers (∼1 × 107/ml), multinucleate syncytia, and EC lysis. SARS-CoV-2 infection of ACE2-expressing ECs elicits procoagulative and inflammatory responses observed in COVID-19 patients. The inability of SARS-CoV-2 to directly infect and lyse ECs without ACE2 expression explains the lack of vascular hemorrhage in COVID-19 patients and indicates that the endothelium is not a primary target of SARS-CoV-2 infection. These findings are consistent with SARS-CoV-2 indirectly activating EC programs that regulate thrombosis and endotheliitis in COVID-19 patients and focus strategies on therapeutically targeting epithelial and inflammatory responses that activate the endothelium or initiate limited ACE2-independent EC infection. IMPORTANCE SARS-CoV-2 infects pulmonary epithelial cells through ACE2 receptors and causes ARDS. COVID-19 causes progressive respiratory failure resulting from diffuse alveolar damage and systemic coagulopathy, thrombosis, and capillary inflammation that tie alveolar responses to EC dysfunction. This has prompted theories that SARS-CoV-2 directly infects ECs through ACE2 receptors, yet SARS-CoV-2 antigen has not been colocalized with ECs and prior studies indicate that ACE2 colocalizes with alveolar epithelial cells and vascular smooth muscle cells, not ECs. Here, we demonstrate that primary human ECs derived from lung, kidney, heart, brain, and umbilical veins require expression of recombinant ACE2 receptors in order to be infected by SARS-CoV-2. However, SARS-CoV-2 lytically infects ACE2-ECs and elicits procoagulative and inflammatory responses observed in COVID-19 patients. These findings suggest a novel mechanism of COVID-19 pathogenesis resulting from indirect EC activation, or infection of a small subset of ECs by an ACE2-independent mechanism, that transforms rationales and targets for therapeutic intervention.

We present the case of a young adult with stroke and very mild coronavirus disease 2019 (COVID-19). Results of hematologic work-up suggest SARS-CoV-2-induced endotheliitis. No concurrent etiology for stroke was detected. This case illustrates the possibility of stroke in healthy SARS-CoV-2-infected patients without hyperinflammatory state or excessive systemic coagulation activation.

Clinical course, presentation profile, response to treatment of two patients who developed a toxic anterior segment syndrome (TASS) following uneventful phacoemulsification. Both the patients underwent slit-lamp examination and dilated fundus examination, in each follow-up and aggressive treatment with topical and systemic steroids. The white to white corneal edema and anterior chamber reaction subsided on follow-up at 1st and 2nd month, respectively, with improvement in vision. The report highlights key features such as relatively quiet eye on the first postoperative day with classical TASS picture seen on the fifth postoperative day and moderate recovery within a month necessitating a thorough examination of patients till the first week of surgery.

Objective: To highlight the clinical presentation of CMV endotheliitis and the challenge in diagnosing this condition in recurrent failed penetrating keratoplasty (PK). Methods: Case seriesResults: There are 3 cases of recurrent failure in PK secondary to CMV endotheliitis presented. Case 1 and 2 were pseudophakic patients, while in case 3, the patient had a previous history of recurrent anterior uveitis. Case 1 and 3 had four and one previous failed PK respectively, while case 2 had endothelial keratoplasty twice before the diagnosis of CMV endotheliitis was made, following positive culture of aqueous humour. The visual acuity ranged from 1/60 to hand movement. All patients had pigmented KP, and two of them had typical coin-shaped KP. Oral valganciclovir was instituted for all patients consisting of bidaily for two weeks, followed by 900 mg once daily for six months. Additionally, topical ganciclovir eyedrop 0.5% was given every four hours with topical dexaminim four times a day. Repeated anterior chamber (AC) tap after six months of treatment was negative for CMV in case 3 while cases 1 and 2 are still on treatment. CMV endotheliitis is an increasingly important cause of failed corneal transplant. We recommend anterior chamber tap in suspicious cases of repeatedly failed corneal transplant, regardless of the presence of coin-shaped KP or not. Minim treatment with oral valganciclovir is important to eradicate the problem, before proceeding with another corneal transplant.Conclusion: It is important to make an accurate early diagnosis by good clinical judgement in preventing loss of corneal endothelial cells. High index of suspicion for CMV endotheliitis as a cause of graft failure must be made especially when the patient presents with coin-shaped KP. Therefore unnecessary treatment resulting from misdiagnosis in these patients can be prevented. Early recognition and treatment of this condition is important to prevent permanent endothelial cell loss and corneal decompensation.

Purpose: To report a case of herpes simplex virus (HSV) endotheliitis following simultaneous phacoemulsification, intraocular lens (IOL) implantation and descemet‘s membrane endothelial keratoplasty (DMEK). Case Report: A;45 year-old female with corneal endothelial decompensation and a mature cataract, and history of anterior uveitis underwent simultaneous phacoemulsification, IOL implantation and DMEK. Increased corneal edema and descemet‘s membrane (DM) detachment occurred on postoperative day 3 and 5, respectively. One week after surgery, active keratic precipitates (KPs) appeared. Polymerase chain reaction (PCR) analysis was performed on an aqueous sample which was positive for herpes simplex virus (HSV). After initiating oral acyclovir and frequent topical corticosteroids, the corneal edema resolved and the donor tissue became spontaneously reattached to the recipient corneal stroma. Conclusion:HSV endotheliitis may occur in the early postoperative period after DMEK and manifest as endothelial dysfunction leading to donor detachment. Anti-viral medication may help treat the acute phase and reduce the risk of recurrence.