*3.2.2 Tubular reactor setup (type 1)*

The tubular flow reactor was fabricated using perfluroalcoxy alkane (PFA) tubes with internal diameter 1.58 and 3.175 mm (supplied by Swagelok) coiled with the definite volume rolled into a disc form, connected with a T- joint and a static mixer (supplied by ColeParmer) and immersed into a bath circulator. Two pumps A and B (QG50, supplied by FMI, Inc) were used to pump the reaction mixture at a definite flow rate. The open bath circulator (supplied by Huber, Germany) was used to control the temperature of the flow reactor. The schematic and actual image of the experimental setup is shown in **Figure 2**.

**Figure 1.** *Schematic and actual image of the batch reactor.*

**Figure 2.** *Schematic and actual image of the tubular reactor.*

### *3.2.3 Packed bed reactor (type 2)*

The packed bed reactor (fabricated through ComBiotech, Bengaluru) was made up of glass, filled with glass beads of 2 mm thickness with a sintered disc at the bottom. The diameter and the length of the reactor are 24 and 240 mm respectively. The volume of the column is 105 mL, with packing is around 56 mL. The PFA tubes were used for all fluid connections. The reactor jacket inlet and outlet (12 mm threaded ends) were connected to a bath circulator (supplied by Huber, Germany), to maintain the required temperature of the reactor. The reactor inlet was connected to two pumps (QG50, Fluid metering, Inc) to pump the reaction mixture along with a static mixer in-line to the reactor and a k-type thermocouple was placed in the packed bed to monitor the internal bed temperature. The schematic and actual image of the experimental setup is shown in **Figure 3**. The output of the reactor was connected to a collection vessel. The samples were drawn from the collection tube and analyzed through a conductivity meter. The reactions were performed both in an upward and downward flow to study the process variations in detail.


**1. Introduction**

Judo is a highly technical sport based on the principle of "maximum efficiency with minimum effort" [1]. A judo fight starts with the opponents both standing, attempting to throw each other off balance. After a throw, judokas transition to ground-fighting, the so-called "ne-waza" [2].

The fighting environment consists of constant changes of actions with applications of different movement structures [3]. The more athletes train and compete, the greater the range of powerful throwing techniques they are exposed to, and the chance of injury [4–8]. The frequency and number of injuries, as well as the severity of the injury, influences further training and competitions [9].

**Citation:** Błach, W.; Smolders, P.; Rydzik, Ł.; Bikos, G.; Maffulli, N.; Malliaropoulos, N.; Jagiełło, W.; Ma´ckała, K.; Ambrozy, T. Judo ˙ Injuries Frequency in Europe's Top-Level Competitions in the Period 2005–2020. *J. Clin. Med.* **2021**, *10*, 852. https://doi.org/10.3390/ jcm10040852

Academic Editor: David Rodríguez-Sanz

Received: 17 January 2021 Accepted: 16 February 2021 Published: 19 February 2021

**Publisher's Note:** MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

**Copyright:** © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

Recent studies analysing the frequency and type of injury in judo are available [10–15]. The rate of injury ranges between 12.3% and 30% [16,17]. Data on a large population (all ages and levels of performance) of French judokas during contests showed an injury incidence slightly above 1.1% [18].

The aim of the present investigation was to assess the frequency of injury in Europe's top-level judokas during high-level contests.

#### **2. Materials and Methods**

#### *2.1. Subjects*

Data were collected from a group of 26,862 high-performance judokas (15,571 men and 11,291 women) aged between 19 and 35 years in all judo weight categories competing in 128 international tournaments under the auspices of the European Judo Union (EJU), including European Judo Championships, in the period between 2005 and 2020. The participants were informed of the protocol and procedure of the EJU Injury registration form. Athletes signed the informed consent form. The EJU Injury registration form was approved by the Medical Commission of EJU. The study was approved by the Bioethics Committee at the Regional Medical Chamber (No. 287/KBL/OIL/2020).

#### *2.2. Study Design*

All relevant information was obtained using the questionnaire controlled and supervised by the European Judo Union (EJU) Medical Commissioner present at each competition. When judokas were injured, they were asked to complete this questionnaire and provide relevant information, with the help of the local medical staff and the EJU medical commissioner present. "Minor" injuries, such small nose bleeds or skin abrasions, which do not influence the athlete's performance in any way, were not counted. "Serious" injuries were defined as injuries so severe they needed transportation of the athlete to hospital. The Cronbach's alpha (=0.71, which is considered an acceptable value) was used to assess the validation of the EJU Injury registration form.

#### *2.3. Data Acquisition*

In the present study, an injury was defined as the physical condition which necessitated an intervention or medical advice by the medical team present at the judo tournament or a visit to the hospital. After each medical intervention, the injured athlete or the medical staff was asked to complete the medical form. The first part of the form asked the judokas to give general information, including their gender and weight category. In the second part, the medical staff was able to collect data on the anatomical location of the injury, type of injury, structure involved, side of the lesion, and whether the judoka was allowed to continue the fight. The diagnosis of the injury was always filled in on the medical form by the treating physician, either the team doctor or the physician of the local medical team. To ensure the privacy of the injured athlete, individual names were never mentioned. When the judoka had to be transferred to hospital, the injury was defined as "serious".


**4. Corneal infections**

transmitted disease and both mates should be treated. Gonorrhea conjunctivitis is character‐ ized by copious purulent discharge while other agents cause mucopurulent, mucoid or serous discharge. A form of viral conjunctivitis is hemorrhagic conjunctivitis in which conjunctival

**Figure 2.** Viral conjunctivitis. Note the conjunctival congestion without corneal or intraocular involvement.

migrate into the lacrimal drainage system and cause obstruction.

qid for 3 weeks is effective for prevention and treatment.

*Haemophilus aegyptius* and Listeria.

Conjunctival myiasis is conjunctival infestation by larvae of different types of flies depending on the habitat [9]. The larvae are tiny white and move quickly. They cause conjunctival hyperemia and the patient complains of unilateral ocular irritation. Rarely, the larva may

Infectious agents include bacteria, virus and chlamydia. Most microorganisms cannot invade intact epithelium.  In neonates occurring in the first month of life, ophthalmia neonatorum is an entity that may be caused by various microorganisms such as chlamydia and less commonly by *Neisseria gonorrhoeae*. Tetracycline 1% or erythromycin 0.5% ointment

Most of the acute viral conjunctivitis forms are self‐limited and treatment is aimed to decrease discomfort and prevent secondary infection. Topical antibiotic such as sulfacetamide 10% (Sulfacid®) qid may be applied. In G6PD and sulfa‐sensitive patients, other antibiotics such as Gatifloxacin (Zymar®) bid, a quinolon, may be prescribed. It is best to defer topical corticoste‐ roid for a week to ascertain that the conjunctivitis is not herpetic or adenoviral. If no improve‐ ment is observed after a week, topical corticosteroid such as fluorometholone (FML®) 0.1% qid may be used for 1–2 weeks in tapered dosage. Patients should be instructed to prevent eye‐ finger‐eye contact (and other contact means) especially with adenoconjunctivitis. The disease

hyperemia is accompanied by subconjunctival hemorrhages.

6 Advances in Common Eye Infections

The general name for corneal infection or inflammation is keratitis. The conjunctiva is usually secondarily involved as conjunctival hyperemia. The clinical manifestations vary and include corneal ulcer, abscess and/or infiltrate [10]. Corneal ulcer is distinguished from abscess and infiltrate by its staining with fluorescein. Abscess and infiltrate do not stain. The clinical findings may overlap between different etiologies.

The diagnosis of all corneal infections is based on scrapping for direct staining with hema‐ toxylin and eosin or Giemsa, and cultures, which should be taken routinely before com‐ mencing with empiric broad‐spectrum topical antibiotics. The only exceptions for obtaining corneal scarps and cultures are a marginal (near the limbus) smaller than 3 mm width flat ulcer(s) and certain typical findings such as dendrite suggesting herpetic keratitis or bilater‐ al multiple epithelial minute defects (epitheliopathy) suggesting adenoviral (epidemic) keratoconjunctivitis.

**Figure 3.** *Pseudomonas aeruginosa* corneal ulcer at the acute stage.

Bacterial keratitis or bacterial ulcer is usually a single solid ulcer with distinctive borders (**Figure 3**). Its size and depth may vary. It may be accompanied by an infiltrate in its base or by localized corneal edema. Infiltrate is white, more dense and distinct and is well localized in contrast to the grayish appearance and less distinctive borders of edema. A grayish, glistening appearance with secretions is a common manifestation of Pseudomonas ulcer. Flare and cells or hypopyon may accompany bacterial ulcer and they may be sterile or infected. If they appear under treatment, they indicate worsening of the infectious process. Any flare or

cells in the vitreous in phakic or pseudophakic eyes indicates the development of endoph‐ thalmitis. Predisposing factors for corneal ulcer include contact lens wear, ocular trauma, dry eyes and long use of topical antibiotics and/or corticosteroids.

Herpetic keratitis a characterized by dendrites in the secondary infection. In Herpes simplex, dendrites vary in number (usually 1–3). They are coarse with widening of their ends (terminal bulbs) (**Figure 4**). Thus, they differ from Herpes zoster dendrites, which are usually numerous, small, thin and without terminal bulbs (**Figures 5**, **6**). Involvement of the tip of the nose (Hutchison's sign) indicates an involvement of the eye on the same side of herpes zoster (**Figure 7**). In repeated Herpes simplex infections, the epithelial defects may form a geographic pattern and may accompanied by corneal vascularization. An important clinical test is corneal sensitivity, which is reduced in recurrent infections. Another finding is patchy sectorial atrophy of the iris that occurs mainly in the midperiphery after herpetic keratouveitis or uveitis.

**Figure 4.** Corneal scar as a result of the ulcer seen in **Figure 3**.

**Figure 5.** Recurrent herpetic keratitis with dendrite in corneal graft. The dendrite is large and has terminal bulbs.

**Figure 6.** Corneal dendrites in herpes zoster. The dendrites are multiple and very fine. They represent immunologic reaction rather than true infection.

Fungal keratitis appears usually as multiple foci of feathery opacification of the cornea with satellites (**Figures 8** and **9**). Hyphae and yeast may be identified by confocal microscopy in the affected cornea.

**Figure 7.** Herpes zoster ophthalmicus. The vesicular rash involves the dermatome innervated by the ophthalmic branch of the trigeminal nerve. Involvement of the tip of the nose indicates involvement of the eye (Hutchison's sign).

**Figure 8.** Fungal keratitis. Note the multiple foci.

cells in the vitreous in phakic or pseudophakic eyes indicates the development of endoph‐ thalmitis. Predisposing factors for corneal ulcer include contact lens wear, ocular trauma, dry

Herpetic keratitis a characterized by dendrites in the secondary infection. In Herpes simplex, dendrites vary in number (usually 1–3). They are coarse with widening of their ends (terminal bulbs) (**Figure 4**). Thus, they differ from Herpes zoster dendrites, which are usually numerous, small, thin and without terminal bulbs (**Figures 5**, **6**). Involvement of the tip of the nose (Hutchison's sign) indicates an involvement of the eye on the same side of herpes zoster (**Figure 7**). In repeated Herpes simplex infections, the epithelial defects may form a geographic pattern and may accompanied by corneal vascularization. An important clinical test is corneal sensitivity, which is reduced in recurrent infections. Another finding is patchy sectorial atrophy of the iris that occurs mainly in the midperiphery after herpetic keratouveitis or uveitis.

**Figure 5.** Recurrent herpetic keratitis with dendrite in corneal graft. The dendrite is large and has terminal bulbs.

eyes and long use of topical antibiotics and/or corticosteroids.

8 Advances in Common Eye Infections

**Figure 4.** Corneal scar as a result of the ulcer seen in **Figure 3**.

Acanthamoeba infection may vary in presentation. The earliest clinical signs include multiple corneal epithelial cell swellings (as seen in adenoviral keratoconjunctivitis but here they are unilateral) and/or corneal edema. Late signs include perineural sheathing and stromal ring(s) (**Figure 10**). Acanthamoeba cysts may be identified by confocal microscopy. A history of contact lens wear and/or bathing in pools or sea is common and symptoms of pain are more striking than the clinical appearance. When diagnosis by cultures is impossible especially in recurrent disease, polymerase chain reaction of the involved tissue may establish the diagnosis.

**Figure 9.** Fungal keratitis with multiple foci and indistinct borders.

**Figure 10.** Immune ring in Acanthamoeba keratitis.

Corneal co‐infections as other co‐infections or mixed infections should be suspected when the course of the disease is atypical or when the condition deteriorates despite of treatment according to cultures and sensitivities. In such cases, repeated cultures should be obtained and broaden accordingly.

All corneal infections may result in either scarring (**Figure 10**) or melting and perforation.

The treatment approach differs between central and peripheral ulcers. Central ulcers are treated with topical antibiotics and are followed frequently to monitor their size and depth. Peripheral ulcers are treated with topical antibiotics and corticosteroids may be cautiously added. Treatment includes broad‐spectrum topical antibiotics such as fortified cefazolin and gentamicin or moxifloxacin (Vigamox®) 0.5% every 30 min–1 h until sensitivity is obtained. Then antibiotic treatment is dictated by the sensitivity of the microorganism. In cases of pain and/or flare and cells in the anterior chamber, topical cycloplegic agent (e.g. cyclopentolate hydrochloride 1% tid) is added to decrease the pain originating from the ciliary body and/or prevention of posterior synechiae. Suspicion of infection other than bacteria should be made when no response is achieved or when the condition worsens under treatment. Additional treatment modalities include topical autologous serum, antipolymorphonuclear migration agents such as tetracycline 1% and/ or citrate 10%, which cause decrease of collagenase activity by chelating free calcium ions that are required for collagenase activity. Vitamin A (ascorbic acid) either topically 10% and/or PO (Vitamin A 500 mg bid). Liberal use of partial tarsorrhaphy is useful especially in recurrences of ulcers, exposure, dryness, corneal anesthesia or trophic ulcers and deep ones. All these means should be used in severe ulcer. Topical corticosteroids should be avoided at the acute phase of the keratitis and when the epithelium is not intact because they cause potentiation of collagenase that may lead to perforation and may also promote secondary infection. They may be used in later stage only after the epithelium healed (no corneal staining) to decrease stromal scarring. If descemetocele occurs, several surgical options exist and include anterior corneal grafts such as deep anterior lamellar keratoplasty (DALK) or non‐Descemet's membrane endothelial keratoplasty (DMEK). A relatively historic treatment is placement of histoacryl for corneal perforation or descematocele. This promotes healing but also corneal vascularization, which impairs vision. Conjunctival flap (Gunderson operation) is indicated for perforation only for eyes with no potential for vision.


**Abbreviations**

SNP: single nucleotide polymorphism, CHD: coronary heart disease, TWB: Taiwan Biobank, NHIRD: National Health Insurance Research Database, OR: odds ratio, CI: confidence interval, BMI: body mass index, *ICD*-*9*-*CM:* International Classification of Diseases, Ninth Revision, Clinical Modification.