Surgical numbers
\r\n\tAnimal food additives are products used in animal nutrition for purposes of improving the quality of feed or to improve the animal’s performance and health. Other additives can be used to enhance digestibility or even flavour of feed materials. In addition, feed additives are known which improve the quality of compound feed production; consequently e.g. they improve the quality of the granulated mixed diet.
\r\n\r\n\tGenerally feed additives could be divided into five groups:
\r\n\t1.Technological additives which influence the technological aspects of the diet to improve its handling or hygiene characteristics.
\r\n\t2. Sensory additives which improve the palatability of a diet by stimulating appetite, usually through the effect these products have on the flavour or colour.
\r\n\t3. Nutritional additives, such additives are specific nutrient(s) required by the animal for optimal production.
\r\n\t4.Zootechnical additives which improve the nutrient status of the animal, not by providing specific nutrients, but by enabling more efficient use of the nutrients present in the diet, in other words, it increases the efficiency of production.
\r\n\t5. In poultry nutrition: Coccidiostats and Histomonostats which widely used to control intestinal health of poultry through direct effects on the parasitic organism concerned.
\r\n\tThe aim of the book is to present the impact of the most important feed additives on the animal production, to demonstrate their mode of action, to show their effect on intermediate metabolism and heath status of livestock and to suggest how to use the different feed additives in animal nutrition to produce high quality and safety animal origin foodstuffs for human consumer.
",isbn:"978-1-83969-404-2",printIsbn:"978-1-83969-403-5",pdfIsbn:"978-1-83969-405-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"8ffe43a82ac48b309abc3632bbf3efd0",bookSignature:"Prof. László Babinszky",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10496.jpg",keywords:"Technological Feed Additives, Feed Industry, Quality of Compound Feed, Non-Antibiotic Growth Promoter, Product Quality, Additive Enzymes, Digestibility of Nutrients, NSP Enzymes, Farm Animals, Livestock, Immunity, Microbiome",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 24th 2020",dateEndSecondStepPublish:"December 22nd 2020",dateEndThirdStepPublish:"February 20th 2021",dateEndFourthStepPublish:"May 11th 2021",dateEndFifthStepPublish:"July 10th 2021",remainingDaysToSecondStep:"2 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"Professor Emeritus from the University of Debrecen, Hungary who authored 297 publications (papers, book chapters) and edited 3 books. Member of various committees and chairman of the World Conference of Innovative Animal Nutrition and Feeding (WIANF).",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"53998",title:"Prof.",name:"László",middleName:null,surname:"Babinszky",slug:"laszlo-babinszky",fullName:"László Babinszky",profilePictureURL:"https://mts.intechopen.com/storage/users/53998/images/system/53998.jpg",biography:"László Babinszky is Professor Emeritus of animal nutrition at the University of Debrecen, Hungary. From 1984 to 1985 he worked at the Agricultural University in Wageningen and in the Institute for Livestock Feeding and Nutrition in Lelystad (the Netherlands). He also worked at the Agricultural University of Vienna in the Institute for Animal Breeding and Nutrition (Austria) and in the Oscar Kellner Research Institute in Rostock (Germany). From 1988 to 1992, he worked in the Department of Animal Nutrition (Agricultural University in Wageningen). In 1992 he obtained a PhD degree in animal nutrition from the University of Wageningen.He has authored 297 publications (papers, book chapters). He edited 3 books and 14 international conference proceedings. His total number of citation is 407. \r\nHe is member of various committees e.g.: American Society of Animal Science (ASAS, USA); the editorial board of the Acta Agriculturae Scandinavica, Section A- Animal Science (Norway); KRMIVA, Journal of Animal Nutrition (Croatia), Austin Food Sciences (NJ, USA), E-Cronicon Nutrition (UK), SciTz Nutrition and Food Science (DE, USA), Journal of Medical Chemistry and Toxicology (NJ, USA), Current Research in Food Technology and Nutritional Sciences (USA). From 2015 he has been appointed chairman of World Conference of Innovative Animal Nutrition and Feeding (WIANF).\r\nHis main research areas are related to pig and poultry nutrition: elimination of harmful effects of heat stress by nutrition tools, energy- amino acid metabolism in livestock, relationship between animal nutrition and quality of animal food products (meat).",institutionString:"University of Debrecen",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Debrecen",institutionURL:null,country:{name:"Hungary"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"25",title:"Veterinary Medicine and Science",slug:"veterinary-medicine-and-science"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"185543",firstName:"Maja",lastName:"Bozicevic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/185543/images/4748_n.jpeg",email:"maja.b@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"49707",title:"Principles of Strabismus Surgery for Common Horizontal and Vertical Strabismus Types",doi:"10.5772/61849",slug:"principles-of-strabismus-surgery-for-common-horizontal-and-vertical-strabismus-types",body:'Teaching strabismus surgical technique in the most common strabismus types is the goal of this chapter. However, it is almost impossible to do on only one book chapter. Thus, this chapter is simply an appetizer for further reading in well-known textbooks written by experienced great strabismus surgeons who are mentioned here. This chapter aims to describe indications for strabismus surgery, planning for a successful surgery result, and do\'s and don’ts for effective surgical procedures for horizontal and vertical strabismus, including incision techniques, muscle tightening, weakening procedures, and transposition surgery. In addition, complications are concerns of the chapter. Our hope is that this book chapter will help surgeons of diverse experience and improve the care of strabismus patients.
The actions of the extraocular muscles and the relative contributions of each muscle to the various ocular positions are important to understand for planning surgery. The muscles act together in order to produce smooth eye movements.
The horizontal recti have only one primary action, while the vertical and obliques each have three actions, which vary depending on the horizontal position of the eye. The relative strengths of these actions depend upon the direction of gaze. In abduction, the vertical muscles have a vertical action only, but in adduction, they become tortors of the eye.
The superior rectus acts as an intortor in extreme adduction, but in abduction, intorsion is lost and exchanged by its elevating primary function. The inferior rectus acts as an extorter when the eye is in adduction; when the eye is abducted, it acts as a pure depressor.
The superior oblique acts as an intortor, depressor, and abductor. It is the principal intortor of the eye produced by the anterior fibers of the tendon. The posterior fibers mediate depression. In adduction, it becomes a pure depressor; in abduction, it is a pure intortor. The inferior oblique acts as extorter, elevator, and abductor. It is the principal extorter of the eye. In extreme adduction, it becomes a pure elevator; in abduction, it is a pure extortor.
These muscles act in concert with cooperation between ipsilateral and contralateral groups of muscles, abiding Sherrington’s and Hering’s laws. Sherrington’s law of reciprocal innervation describes that contraction of a muscle is accompanied by relaxation of its ipsilateral antagonist muscle ensuring smooth movements of the eye. Hering’s law of equal innervation regards binocular movements and explains that equal contractions occur in the muscles that are contralateral synergists and ensures that equal movements of the two eyes occur, if both muscles are normal.
The indications for strabismus surgery fall into two categories: binocular function and cosmetic appearance with psychosocial impact. The indication and surgical goal should be based on the patients need prior to surgery and direct the surgical plan in order to achieve a successful result. Therefore, prior to surgery, the strabismus surgeon needs to establish the treatment goals by asking “Why are we operating”? Is it to establish binocular fusion, eliminate diplopia, expand the field of binocular vision, correct a compensatory head position, or improve cosmetic appearance?
Signs of binocular fusion potential include intermittent strabismus, acquired strabismus, binocular fusion after neutralizing the deviation with prisms, child <2 years old, equal vision, and incomitant strabismus with compensatory face turn. Patients with fusion potential generally require large amounts of surgery, larger than standard surgical numbers to avoid undercorrection. However, in patients without binocular fusion, it is better to do less surgery, as a small residual esotropia is more stable and cosmetic acceptable than a consecutive exotropia.
Furthermore, defining the whished function outcome influences the selection of type of surgery. Monocular recession–resection surgery results in incomitance, which is not preferable in a fusing patient, as incomitance can cause diplopia in eccentric positions of gaze. Monocular surgery, however, is the procedure of choice for sensory strabismus to protect the seeing eye.
A specific strabismus diagnosis should be established preoperatively, and the exact etiology of the strabismus should be determined, if impossible, by an MRI of the head and orbit may be indicated. If the cause is unknown after a complete work up, then it is appropriate to operate for the strabismus taking into account the ductions, versions, and presence of incomitance.
Each patient requires an individual surgical approach to the management of their strabismus, but the following information and measurements may be of assistance as a guide for how much muscle surgery is required for concomitant deviations without previous surgery or underlying muscle or neurological pathology, particularly for those beginning strabismus surgery.
Concomitant eso- and exodeviations are deviations with full ductions and the same deviation in all fields of gaze. Many horizontal deviations have an accommodative element.
Different horizontal concomitant strabismus types require different considerations when planning for successful strabismus surgery outcome and are therefore important to diagnose exactly. A table guide in planning strabismus surgery is given in Table 1. The numbers have been derived from Parks, with professor Dr. Kenneth Wright’s personal modifications according to the professors own surgical experience [11, 13]. The measurement recommended is only for concomitant deviations and should be altered based on the surgeon’s personal results.
\n\t\t\t\t\tBinocular surgery\n\t\t\t\t | \n\t\t\t|||
\n\t\t\t\t\t\n\t\t\t\t\t\tEsotropia\n\t\t\t\t\t\n\t\t\t\t | \n\t\t\t\t\n\t\t\t | ||
\n\t\t\t\t | \n\t\t\t\t\tMR OU Recession\n\t\t\t\t | \n\t\t\t\t\n\t\t\t\t\tLR OU resectiona\n\t\t\t\t\t\n\t\t\t\t | \n\t\t\t|
15Δ\n\t\t\t | \n\t\t\t3.0 mm | \n\t\t\t3.5 mm | \n\t\t|
20Δ\n\t\t\t | \n\t\t\t3.5 mm | \n\t\t\t4.5 mm | \n\t\t|
25Δ\n\t\t\t | \n\t\t\t4.0 mm | \n\t\t\t4.0 mm | \n\t\t|
30Δ\n\t\t\t | \n\t\t\t4.5 mm | \n\t\t\t6.0 mm | \n\t\t|
35Δ\n\t\t\t | \n\t\t\t5.0 mm | \n\t\t\t6.5 mm | \n\t\t|
40Δ\n\t\t\t | \n\t\t\t5.5 mm | \n\t\t\t7.0 mm | \n\t\t|
50Δ\n\t\t\t | \n\t\t\t6.0 mm | \n\t\t\t8.0 mm | \n\t\t|
\n\t\t\t\tExotropia\n\t\t\t | \n\t\t\t\n\t\t\t | \n\t\t | |
\n\t\t\t | \n\t\t\t\tLR OU recessionb\n\t\t\t\t\n\t\t\t | \n\t\t\t\n\t\t\t\tMR OU resection\n\t\t\t | \n\t\t|
15Δ\n\t\t\t | \n\t\t\t4.0 mm | \n\t\t\t3.0 mm | \n\t\t|
20Δ\n\t\t\t | \n\t\t\t5.0 mm | \n\t\t\t4.0 mm | \n\t\t|
25Δ\n\t\t\t | \n\t\t\t6.0 mm | \n\t\t\t5.0 mm | \n\t\t|
30Δ\n\t\t\t | \n\t\t\t7.0 mm | \n\t\t\t5.5 mm | \n\t\t|
35Δ\n\t\t\t | \n\t\t\t7.5 mm | \n\t\t\t6.0 mm | \n\t\t|
40Δ\n\t\t\t | \n\t\t\t8.0 mm | \n\t\t\t6.5 mm | \n\t\t|
50Δ\n\t\t\t | \n\t\t\t9.0 mm | \n\t\t\t7.0 mm | \n\t\t|
\n\t\t\t\t\tMonocular surgery\n\t\t\t\t | \n\t\t|||
\n\t\t\t\tEsotropia\n\t\t\t | \n\t\t\t\n\t\t\t | \n\t\t | |
\n\t\t\t | \n\t\t\t\tMR recession\n\t\t\t | \n\t\t\t\n\t\t\t\tLR resectionb\n\t\t\t\t\n\t\t\t | \n\t\t|
15Δ\n\t\t\t | \n\t\t\t3.0 mm | \n\t\t\t3.5 mm | \n\t\t|
20Δ\n\t\t\t | \n\t\t\t3.5 mm | \n\t\t\t4.0 mm | \n\t\t|
25Δ\n\t\t\t | \n\t\t\t4.0 mm | \n\t\t\t5.0 mm | \n\t\t|
30Δ\n\t\t\t | \n\t\t\t4.5 mm | \n\t\t\t5.5 mm | \n\t\t|
35Δ\n\t\t\t | \n\t\t\t5.0 mm | \n\t\t\t6.0 mm | \n\t\t|
40Δ\n\t\t\t | \n\t\t\t5.5 mm | \n\t\t\t6.5 mm | \n\t\t|
50Δ\n\t\t\t | \n\t\t\t6.0 mm | \n\t\t\t7.0 mm | \n\t\t|
\n\t\t\t\tExotropia\n\t\t\t | \n\t\t\t\n\t\t\t | \n\t\t | |
\n\t\t\t | \n\t\t\t\tLR recessionb\n\t\t\t\t\n\t\t\t | \n\t\t\t\n\t\t\t\tMR resection\n\t\t\t | \n\t\t|
15Δ\n\t\t\t | \n\t\t\t4.0 mm | \n\t\t\t3.0 mm | \n\t\t|
20Δ\n\t\t\t | \n\t\t\t5.0 mm | \n\t\t\t4.0 mm | \n\t\t|
25Δ\n\t\t\t | \n\t\t\t6.0 mm | \n\t\t\t4.5 mm | \n\t\t|
30Δ\n\t\t\t | \n\t\t\t6.5 mm | \n\t\t\t5.0 mm | \n\t\t|
35Δ | \n\t\t\t7.0 mm | \n\t\t\t5.5 mm | \n\t\t|
40Δ\n\t\t\t | \n\t\t\t7.5 mm | \n\t\t\t6.0 mm | \n\t\t|
50Δ\n\t\t\t | \n\t\t\t8.5 mm | \n\t\t\t6.5 mm | \n\t\t
Surgical numbers
aWhen a lateral rectus resection is done for residual esotropia after a large medial rectus recession (6 mm or larger), these numbers should be lowered.
bAvoid large LR recessions if lateral incomitance is present.
cIf the horizontal angle is greater for near deviation than distance deviation, relatively more should be done to the medial rectus than the lateral rectus and vice versa.
For angles >50, diopters perform bilateral surgery to more than 2 horizontal recti. This three muscle surgeries may be planned for the primary operation. The amount of surgery may be judged from the above tables. In adults, adjustable suture technique is recommended, placed on the eye where two muscles are being operated.
Strabismus can be congenital or develop later in life giving rise to different consideration for correct surgical strategy to choose. In the following, we will describe how to handle the most common strabismus types of early and later onset strabismus.
Infantile esotropia is an esotropia present during the first 6 months of life. This includes several types, with the most common being: small angle neonatal esotropia, accommodative infantile esotropia, Ciancia’s syndrome, and congenital esotropia. The latter is described below.
The etiology of congenital esotropia is unknown, but genetic aspects are suspected. Congenital esotropia (CE) is characterized by a large angel constant esotropia of 40 PD or more (Figure 1) and later developing motor dysfunctions, including inferior oblique overaction (IOOA) (60%), dissociated vertical deviation (DVD) (40%), and latent nystagmus (40%). Low hypermetropia is often present in an extent not giving indication for glasses. Amblyopia is present in 50% of patients with CE, however vision screening in childhood may lower this occurrence as described by Høeg et al. [17]. Smooth pursuit asymmetry is also often present as described by Wright [14]. Spontaneous resolution is rare (<4%), as shown by the Congenital Esotropia Observational Study (CEOS) if the angle is stable or increasing [6], which makes congenital esotropia a surgical disease requiring strabismus surgery.
Infantile esotropia
Ciancia’s syndrome
The management and preoperative evaluation includes examination of the following:
Ductions, which often has a mild limitation of abduction (-1), with intact abduction saccades shown by doll head maneuver or vestibular stimulation. If limited abduction and abduction saccadic movement, consider following differential diagnosis listed by decreasing incidence: Ciancia’s syndrome with abduction deficiency and compensatory head turn (Figure 2), Duane’s syndrome, congenital fibrosis syndrome, congenital VI nerve palsy, and infantile myasthenia gravis.
Versions, to evaluate the presence of IOOA and V patterns
Amblyopia, which is revealed by strong fixation preference for one eye. Treat amblyopia before surgery by patching the dominant eye 4 h per day and follow-up every 1 to 2 weeks for small kids under 1 year (longer interval for older kids typically in Europe), until the patient holds fixation with the nondominant eye. The patients’ cross-fixates usually indicate the absence of amblyopia, unless strong fixation preference is present.
Deviation size by prism alternate cover test at near and distance deviations if possible, verified by Krimsky testing. The near deviation measure is most reliable and therefore used as the surgical measure.
Cycloplegic refraction using cyclopentolate 1% one or two doses, 5 min apart, followed by refraction 30 min after last dose. If the cycloplegic refraction shows >+3.00 sphere, then prescribe the full hypermetropic correction. Repeat the cycloplegia if fluctuating readings is found on retinoscopy. After wearing the full correction constantly for 1 month, evaluate the patient for fixation preference. If an esodeviation of >10 PD persists after prescribing the full hypermetropic correction, surgery is indicated.
The timing of surgery for congenital esotropia is controversial, as no randomized clinical controlled trials have never been conducted due to ethical aspects and low incidence. Therefore, different approaches are used in different continents. In the United States, early surgery (before 2 years of age) is performed routinely when the CEOS [6,7] parameters are present (i.e., angle
The surgical procedure of choice depends on age, fusion potential, and visual acuity. Bilateral medial rectus (MR) muscle recession using the near deviation as the target angle is the preferred strategy in infants without amblyopia. Patients with irreversible dense amblyopia should have monocular surgery on the amblyopic eye (recession-tightening procedure) to avoid surgical risk to the sound eye.
The goal of surgery is to align the eyes early to within 8 to 10 PD to stimulate the development of binocular fusion, as described by Dr. Marshall Parks. Larger esotropia will not allow binocular fusion. Therefore, a residual esotropia of 10 PD or larger should be considered for further treatment. The standard surgical chart (Appendix I) numbers are designed to give infants with possible fusion potential a slight immediate overcorrection (5–10 PD exotropia). This is desired as fusional convergence will pull the eyes together to become straight, fusing the small exotropia. However, patients with poor prognosis for binocular fusion (e.g., older patients >2 years old, and patients with dense irreversible amblyopia 20/50 or worse) due to long-standing congenital esotropia should be considered for surgery based on cosmetic indications. In these older patients with poor fusion potential, the surgeon should aim to slightly undercorrect and leave an esotropia of 6 to 8 PD. Using the chart numbers will correctly result in a desired slight undercorrection in older patients with poor fusion potential that predisposes to drift outward to exotropia with time. Therefore, the surgical chart numbers can be used for all patients as they self-adjust for age and fusion potential. In general, patients older than 2 years with uncorrected infantile esotropia have a poorer prognosis for binocular fusion. Even older patients, however, will occasionally show an outcome of good binocular function and some degree of stereo acuity; this could be caused by an inaccurate anamnesis.
Residual esotropia of at least 10 PD first repeat the cycloplegic refraction and prescribe the full hypermetropic correction if 1.5 sphere or more to correct ET to within 10 PD. If there persists a residual ET of 15 PD or more after prescribing glasses, then consider further surgery. If the primary surgery was bilateral MR recession of 5 mm or less, both medial rectus muscles can be further recessed. However, if the primary bilateral MR recessions were >5 mm, both lateral recti would be resect with reduced standard numbers of 1.5 mm to avoid consecutive exotropia, which is a common occurrence after LR resections for residual esotropia.
Consecutive exotropia of
Inferior oblique overaction (IOOA) is often bilateral and associated with IE, developing after 1.5 years of age. If significant IOOA (
Prognosis for motor alignment and binocularity is good for surgical cases in hands of trained surgeons. Alignment to within 10 PD of orthotropia can be achieved in 80%. If this is achieved before 2 years of age, about 70% achieve some degree of peripheral fusion and gross stereopsis (monofixation syndrome). Very early surgery (3–4 months of age) increases the chance of binocular fusion and high-grade stereo acuity. Late surgery (after 2 years of age) minimizes the chance of obtaining binocular fusion.
Acquired esotropia is a subacute emergency that requires urgent consult for two reasons: (1) fusion potential diminishes in proportion to the duration of ET while early intervention is important to restore high-grade binocular fusion. Prompt dispensing of hypermetropic spectacle correction is therefore important to correct the esotropia totally or partially and reduce the occurrence of amblyopia. (2) Acquired esotropia can be the presenting sign of intracranial (brain tumor, Arnold–Chiari malformation) or neurological disease (myasthenia gravis or chronic progressive external ophthalmoplegia) causing a sixth nerve paresis, which can be concomitant in the beginning as described by Buch Hesgaard and Vinding [1].
The most common types of acquired esotropia are the accommodative, the nonaccommodative, the cyclic, and the sensory esotropia. These often have an intermittent beginning. More seldom acute acquired concomitant esotropia develops [1]. Only the most frequent type, i.e., accommodative esotropia, will be described. Accommodative esotropia can have an infantile onset at 2 months to 1 year of age but typically develop between 1 and 3 years of age. It is characterized by initially intermittent with progression to constant moderate to large angle of deviation (20–50 PD) associated with hypermetropia (+2.00 to +6.00 sphere). The deviation is often initially intermittent and becomes constant.
The etiology is related to hypermetropia that necessitates increased accommodation for the child to achieve a clear image. This overaccommodation results in overconvergence and esotropia, depending on the AC/A ratio and divergence amplitudes.
The goal is to establish straight eyes within 8 to 10 PD of orthotropia to stimulate binocular fusion. This can be achieved in some patients with optical correction alone, and surgery is not indicated then. The patients that do not get straight eyes wearing full hypermetropic correction, as the child in Figure 3, needs urgent surgery. Therefore, these patients should be aggressively treated with early optical correction and surgery if indicated to avoid or treat amblyopia and stimulate binocular function in the small kids (2 months to 2 years), restore binocularity in older children (2 years to 6 years), and eliminate diplopia and regain stereo acuity in the children over 6 years of age. The younger the children the more vulnerable is the binocularity, and visibility could be lost if treatment is delayed. These authors agree with the late Dr. Marshall Parks that recent onset accommodative esotropia is an ophthalmic emergency, and the patient should be seen at an urgent appointment.
Partially accommodative esotropia
The management and preoperative evaluation includes the same examination procedures as patients with infantile esotropia, including the examination of ductions, versions, and evaluation for and treatment of amblyopia after full hypermetropic correcting spectacles is prescribed, following the same method as described previously. Then if residual esotropia persists (>10 PD), surgery is indicated. However, important additional preoperative orthoptic considerations and examinations are necessary:
Urgent performance of cycloplegic refraction and prescription of the full hypermetropic correction, even at babies only 2 months of age, is necessary in order to avoid development of amblyopia and loss of binocularity that is lost proportionally with the time after onset. There are 3 common responses to prescribing full hypermetropic spectacles for acquired accommodative esotropia: (a) correction results in ortotropia (<8 PD) for distance and near deviations. Single vision glasses are to be continued, and surgery is not indicated. This is termed accommodative esotropia. (b) Correction results in correction for distance, but there is a residual esotropia >10 PD for near deviation. Measure the AC/A ratio, and if the AC/A ratio is high in accommodative esotropia, prescribe bifocal spectacles and surgery can be indicated if the angle is only partially corrected with bifocal spectacles as described below. (c) Correction results in a residual esotropia >10 PD for both distance and near deviations, i.e., partially accommodative esotropia, and requires single vision glasses to be continued and surgery is indicated as described below.
Measure the AC/A ratio. It is vital to know the AC/A ratio in those with convergence excess esotropia and those with distance exotropia in making the definitive diagnosis and management plan. The gradient method of measuring AC/A ratio is the most accurate method to use, measuring the angle at near deviation with full hypermetropic correction, without (-L) and with (+L) +3 diopter (D) sphere lens: -L - (+L) / 3D. Specifically for esodeviations, if the AC/A ratio is high (
Lens gradient formula:
Dev w lens = deviation in prism diopters measured with the inducing lenses
Dev org = original deviation in prism diopters without the lens
Lens power (denominator) = inducing lens power in diopters
For AC/A formulas, exodeviations are minus and esodeviations are plus:
Example: The patient, in Figure 4, has a deviation of ET 20 with full hypermetropic correction but without extra lenses. When +3.00 lenses are placed over both eyes, as illustrated in Figure 5, the patient does not have to accommodate 3 diopter-inducing divergence so the deviation now measures ET 5. The AC/A ratio is calculated below and is 5 PD/D:
ET without extra lenses.
Less ET with +3.00 lenses placed over the eyes.
Test for binocularity and stereo acuity using Bagolini-striated test, Titmus, Lang, or TNO test with correcting prism bar, depending on the age of the child and level of stereo acuity present. The surgeon should aim to slightly overcorrect those patients with binocular potential but undercorrect those patients with no binocular function, e.g., long-standing acquired esotropia, which is often seen in Europe. Since accommodative esotropia is acquired, and the eyes are aligned during the early period of visual development, most patients have good binocular potential at the onset of the esotropia.
The goal is to achieve orthotropia within 10 PD of esotropia to establish high-grade stereo acuity. The surgical goal for partially accommodative esotropia is not to operate patients out of glasses but to achieve alignment and fusion with full hypermetropic correction. Patients having cycloplegic refraction of +2.5 sphere or more will require their hypermetropic spectacles after surgery to maintain a stable angle. Surgery is indicated if residual esotropia of >10 PD persists with full hypermetropic correction worn for 2 months. Surgery is urgent as the longer the esotropia persists, the worse the prognosis for establishing binocular fusion. For infants, distance measurements are difficult to obtain; try to get this measurement but base the surgery on the near deviation. Therefore, surgery for infantile partially accommodative esotropia requires bilateral medial rectus recessions augmented surgery (Wright and Bruce-Lyle 1998) using the augmented formula, i.e., for a target angle between the deviation with and without hypermetropic correction. Average the near deviation with correction and the near deviation without correction or bilateral MR recessions 5.5 mm (see Appendix I on surgical numbers). Bilateral medial rectus recessions are also the treatment of choice for partially accommodative esotropia in older children. It is recommended to use the “augmented surgery formula” developed by Professor Wright to achieve alignment. This formula have improved outcome by increasing the alignment success rate from 70% to 90% by increasing the amount of surgery [16].
Surgery is indicated in high AC/A ratio accommodative esotropia if there is a significant esotropia in the distance that disrupts fusion, even if a bifocal add results in fusion at near deviation. A relatively small distance deviation and large near measurement is more difficult to manage as the near distance discrepancy tends to persists postoperatively. It is recommended to perform bilateral medial recessions using a target angle based on the augmented formula with slight reduction in the numbers to prevent consecutive exotropia at distance. The patients should be informed that bifocal spectacles may be required after surgery.
There are 3 methods for determining the target angle for partially accommodative ET. These are described in the following examples:
Standard surgery formula uses the residual distance deviation with full hypermetropic correction as the target angle. It gives the highest rate of undercorrection (25%–30%), for example, Dcc ET 30 PD; target angle: 30 PD; surgery: BMR recessions 4.50 mm.
Augmented surgery formula uses the target angle, which is the average between near deviation without correction (largest) and distance deviation with correction (smallest). This improves successful results to >90% [16], for example, average Nsc ET 60 PD and Dcc ET 30 PD; target angle: 45 PD; surgery: BMR recessions 5.75 mm.
Prism adaptation determines the target angle by placing a base out press-on prism for the full deviation on the patient’s glasses. Then have the patient wear the glasses for 1 week. The deviation is then remeasured, and if it increases, additional base out prism is applied. This process is repeated until the deviation is stabilized. Prescribe 30 PD base out press-on prisms over full hypermetropic correction and return in 1 week. At follow-up visit, there is no change in the deviation, after placing the 30 PD base put prism; target angle: 30 PD; surgery: BMR recessions 4.50 mm.
A residual esotropia larger than 10 PD will not allow binocular fusion and should be considered for further treatment as described above, by repeating cycloplegic refraction, prescribe full hypermetropic correction, and if there persists a residual esotropia at distance and near deviations of >10 PD, then consider further surgery if the patient has fusion potential.
Patients with preoperative high AC/A ratio will often have a residual esotropia at near deviation after surgery. To establish fusion at near deviation, bifocal add (+2.00 to +3.00 sphere) is required if the residual esotropia at near deviation is >10 PD, but the eyes are aligned at distance.
On the other hand, if a small consecutive exotropia of >10 PD results from surgery, try reducing the hypermetropic correction but not more than +2D as this leads to alignment instability. If the exotropic angle persists more than 3 months, reoperation should be considered. If the exotropia is large and associated with even mild adduction deficit, stretched scar or slipped muscle should be suspected, and the medial muscle should be explored and advanced if there is an insertion dehiscence. Surgery plan is the same as for consecutive exotropia as described above in congenital esotropia.
The normal eye position of rest is divergent due to the divergent positioning of the orbits. Therefore, small exophorias <10 PD are considered normal and the innate fusional convergence is strong (25 PD), facilitating fusion of small exodeviations.
Intermittent exotropia is a large exophoria (usually between 20 and 40 PD) that is difficult to fuse and intermittently breaks down and manifests especially when fatigued, daydreaming, or takes sedatives or drinking alcohol. Patients with intermittent exotropia have perfect stereoacuity when aligned (phoria phase), but no stereoacuity when tropic because the patient suppress the image from the deviated eye (tropia phase). Rarely patients will see double or have ARC when tropic. This is the case in patients with late onset exotropia during late childhood or adulthood. Patients with intermittent exotropia do not get strabismuc amblyopia because they have intermittent binocular fusion with high-grade stereoacuity that provides binocular visual stimulation. Patients with intermittent exotropia can have anisometropic amblyopia with the same incidence as the general population. Approximately 80% of intermittent exotropia patients will show progressive loss of fusion control and increase in the exotropia with time.
Intermittent exotropia, tropia phase.
Intermittent exotropia, phoria phase.
Figures 6 and 7 show a child with intermittent exotropia and straight eyes when the deviation is fused (phoria phase), and moments later, where the patient lost concentration, fusion broke and exodeviation became manifest (tropia phase).
For the most part, the treatment of intermittent exotropia is surgical. The indication for surgery is poor fusion control. Large deviations over 20 PD will eventually need surgery as they are difficult to fuse and will increase over time.
Small to moderate exodeviations (<20 PD) are usually well controlled and do not need treatment but can temporally be treated nonsurgically, but this is rarely effective in the long term. Nonsurgical options is not effective except for convergence exercises for convergence insufficiency, which is the preferred management in that disorder. Convergence exercises consist of pencil push-ups, which improve fusional convergence for near deviation, useful for convergence insufficiency, but will not reduce the distance exodeviation. Other nonsurgical treatment options is over minus glasses and monocular occlusion. Over minus glasses reduce the exotropia by stimulating accommodative convergence, which is not well tolerated because it requires the patient to constantly overaccommodate. It can be used for small angle exotropia (<15 PD) associated with concurrent myopia. Increase myopic correction by -2.5 sphere over existing correction. Monocular occlusion by patching the dominant eye for 2 to 4 h a day has been described, but recent prospective study shows no significant effect [8].
A surgical indication is poor fusion control. If the deviation is difficult to control and becomes manifest more than 50% of waking hours, then surgery is indicated. In general, it is preferable to operate after 4 years of age. This is because a small consecutive esotropia can occur after surgery, and as young children have the ability to suppress and develop amblyopia, they can loose stereoacuity after surgery. Older children with deviations greater than 20 PD are difficult to fuse and can causes eye strain, so these patients should be considered for surgery.
The procedure of choice for intermittent exotropia is bilateral rectus recessions. Monocular recess/resect procedures induce incomitance and cause diplopia in side gaze. A small consecutive esotropia (4–8 PD) immediately after surgery is desirable as the late recurrence of the exotropia is common. This consecutive exotropia will cause diplopia but usually resolve in a few days. The standard surgical number chart (Appendix I) have this small overcorrection built in.
The pattern of the deviation is important for determining the surgical plan. Exopatterns are classified based on difference of deviation, distance deviation versus near deviation: (1) basic, (2) convergence insufficiency, and (3) divergence excess divided into pseudo and true divergence excess.
The basic type of intermittent exotropia is responsible for 60% and have a similar deviation distance and near deviations, e.g., Dsc X (T) 30 and Nsc X(T): 35; target angle = XT 35 bilateral LR recessions.
Convergence insufficiency intermittent exotropia type includes patients with weak convergence with a greater esotropia for near deviation. If the eyes are straight for distance, it is best to avoid surgery and treat with convergence exercises. Convergence insufficiency is the one strabismus that can be helped by exercises, e.g., Dsc Ortho. Nsc X(T) 30; plan: convergence exercises—no surgery.
Note: If there is a significant X(T) >15 PD in the distance, then consider bilateral lateral rectus recessions for 5 PD more than the distance angle. Patients will require convergence exercises after surgery for an X(T) at near deviation.
Divergence excess X(T) intermittent is when the exotropia is larger for distance than near, by at least 10 PD, e.g., N X(T) 15. D X(T) 30. There are 2 types of divergence excess:
Pseudo (90%) – tenacious fusional convergence
True (10%) – high AC/A ratio
Tenacious fusional convergence is near convergence that persists for several minutes after monocular occlusion. Patients with pseudo divergence pattern intermittent exotropia have strong tenacious fusional convergence that “falsely” diminishes the near deviation. Patching one eye for 45 min breaks tenacious fusional convergence. If the near exodeviation increases to be similar to the distance angle, e.g., 30 PD X(T) after the patch test, this indicates pseudo divergence excess, and bilateral LR recessions with a target angle of 30 PD is indicated. If the near exodeviation does not increase with the patch test, this indicates true divergence excess and is associated with a high AC/A ratio. Bilateral LR recessions with target angle somewhere between distance and near deviations; see example below:
Dsc X(T) 30, Nsc X(T) 15
Patients with true divergence excess have a high AC/A ratio, and there is a high incidence of persistent esotropia and diplopia at near after surgery. Therefore, bifocals and more than one surgery are likely, and patients should be told this preoperatively.
The immediate postoperative goal of surgery for intermittent exotropia is to achieve a small consecutive esodeviation of about 5 PD esotropia; in the long term, it is common for exotropia to recur. Larger consecutive esodeviations will often require further surgery. Children under 4 years of age with a small consecutive esotropia can rapidly develop amblyopia. That is why Dr. Wright suggests to postpone surgery to after 4 years of age if possible. However, if absolutely indicated because of loss of stereoacuity, part-time (2–3 h a day) alternate eye occlusion therapy may prevent amblyopia until the esotropia resolves. In older patients, the initial consecutive esotropia causes diplopia, and therefore it is important to inform the patients that diplopia may be present for some weeks to achieve a better long-term result. Hardesty et al. [2] has suggested prescribing prism glasses in the early postoperative period to neutralize the esodeviation and leave a small esophoria to stimulate divergence. For a persistent esotropia, after a week in a patient of any age, consider prescribing base out prism glasses to eliminate the diplopia and preserve binocular fusion. Give just enough prism to allow fusion while leaving a small esophoria to build divergence. If after 4 to 6 weeks the esotropia persists, then additional strabismus surgery should be considered. Either advance the lateral rectus muscle or recess the medial rectus muscles. Consider the possibility of a slipped lateral rectus muscle if abduction is limited and the esotropia is greater for distance. If the lateral has slipped, resect the stretched scar and replace at the intended recession point.
Vertical deviations can be caused in 3 different ways, which will be described as follows: (1) overaction of the rectus muscles, i.e., superior rectus muscles, ipsilateral dissociated vertical deviations (DVD); (2) dysfunction of the horizontal rectus muscles, i.e., pattern deviations (A and V patterns); and (3) overaction of the superior and inferior oblique muscles, i.e., primary or secondary to ipsilateral IV nerve palsy or contralateral superior rectus palsy.
All the preoperative examinations and considerations previously mentioned should be performed, but additionally two important orthoptic tests are necessary to find the correct diagnosis and plan the surgery for successful results. These tests that assist the surgeon in the diagnosis of vertical muscle weakness in patients with vertical strabismus are (1) the three-step test and (2) the Bielchowsky head tilt test.
Dr. Parks described the classical three-step test for diagnosing a cyclovertical muscle palsy. It helps to differentiate SOP from contralateral superior rectus palsy and to detect bilateral SOP and includes the following:
Step 1.cover test identifies which eye is hypertropic. The elevators of the low eye (IO or SR) or the depressors of the high eye (SO or IR) are affected.
Step 2.Side gaze to the right and left changes the degree of height. If the height increases when the eyes move away from the high eye, the possible weak muscle is either SO of the adducted eye or the contralateral SR (elevates the eye in abduction). Conversely, if the height increases when the eye move in the direction of the higher eye, it suggests either weak IR of the abducted eye (depresses the eye in abduction) or weak IO of the contralateral adducted eye.
Step 3.determine the hypertropia in up- and downgaze by cover test. This identifies which of the contralateral muscles is responsible for the vertical deviation. A modification to make this easier is “Wright’s rule” described by Dr. Wright, which is a 2-step process: (1) Do the head tilt test first. If the hypertropia increases on head tilt to the side if the hypertropia, this indicates an oblique muscle palsy, and if the hypertropia increases opposite to the hypertropia, it is a rectus muscle palsy. (2) Test horizontal gaze to see where the hypertropia is greatest and match to the field of action of the cyclovertical muscle in question from step 1.
The Bielchowsky head tilt test helps to further identify a superior oblique weakness. When the head is tilted to the right, the right eye intorts by action of the intorters (SO and SR) of the eye, and their vertical pulls cancel each other if both are healthy. However, if the SO is weak, the moderately unopposed SR causes a hypertropia to develop in the intorting eye, as illustrated in Figure 8.
Explanation of the Bielchowsky head tilt test.
When the correct diagnosis and the weak muscle have been found, a plan for successful strabismus surgery outcome can be made by using the following five-step guideline:
Choose the right muscle to work on. In concomitant deviations, the balance between the vertical rectus muscles (which elevate and depress the eye in abduction) and the obliques (which elevate and depress in adduction) must be maintained. Therefore, always work on ipsilateral antagonists and contralateral synergists.
Choose the right amount of muscle surgery. However, it is more difficult to provide guidance tables for vertical deviations as they are less likely than horizontal deviations to be concomitant. A rule of thumb for vertical surgery is 3 prism diopters of vertical correction for every millimeter of recession of height in the primary position.
Aim to correct a vertical deviation in primary position and downgaze principally; upgaze is much less important.
Inferior rectus recessions can result in late overcorrection [3]. Therefore, great care must be taken with this muscle and aim to be conservative, and do not recess the inferior rectus muscle more than 5 mm to 6 mm. Superior rectus recessions for dissociated vertical deviation (DVD) must be large, on the other hand.
Long-standing vertical deviations, especially due to thyroid eye disease and congenital IV nerve palsies, should be slightly undercorrected due to large vertical fusional reserves.
Dissociated vertical deviation (DVD) occurs in patients with infantile esotropia and can occur with any disorder that disrupts normal binocular visual development. DVD is commonly associated with CE in Europe, where late surgery is the timing of choice. However, the incidence of surgery demanding severe DVD has dropped in the United States, probably due to early surgery with better sensory outcome. DVD is typically latent. However, when one eye is occluded (Figure 9), or when the patient is fatigued or daydreaming, it manifests, having three components: elevation, abduction, and extorsion. The vertical component is predominant. DVD is characterized by slow drift of one eye up and out with extorsion. It is usually bilateral and asymmetric and can be distinguished from a true hypertropia by the lack of a corresponding hypotropia in the contralateral eye, when the hypertropic eye returns to primary position. The indication for surgery for DVD is primarily based on the patients psychosocial requirements.
Bilateral DVD with a right hypertropia with the right eye covered and left hypertropia with the left eye covered.
Surgery is indicated if the deviation is larger than 10 PD, increases in frequency, and becomes obvious or symptomatic. Surgery for DVD is ipsilateral large superior rectus recession often between 5 mm to a maximum of 9 mm (fixed suture technique) as suggested by professor Dr. K. Wright.
Most cases require bilateral surgery. If the DVD is asymmetric, perform asymmetric superior rectus recessions. Unilateral surgery is indicated in patients with amblyopia >2 lines, which will not fixate with the amblyopic eye, where ipsilateral superior rectus recession is indicated. If DVD and inferior oblique overaction coexist, an inferior oblique anteriorization procedure is indicated and sufficient in most cases. Only in severe cases combined surgery of inferior oblique anteriorization and superior rectus recession is necessary. In this case, the superior rectus recession should be minimized to avoid limitation of up gaze.
These are patterns of strabismus in which the horizontal deviation alters on upgaze and downgaze so that the pattern resembles the letter A or V and is considered significant if the horizontal angle varies by more than 10 PD (A pattern) or 15 PD (V pattern) diopters between up- and downgaze. An example of a V pattern esotropia is shown in Figure 10. The underlying cause may be as follows: (1) horizontal muscle dysfunction caused by abnormal insertion or action of the medial/lateral recti (spontaneously or secondary to surgery); (2) vertical rectus dysfunction (tight superior rectus/inferior rectus muscle weakness for A pattern and vice versa for V pattern), or (3) oblique muscles dysfunction (inferior oblique under action/superior oblique overaction for A patterns and vice versa for V patterns).
An example of a V pattern esotropia with arrow pattern.
If the pattern is small, not affecting fusion and not causing a compensatory head position, then it can be observed. If the pattern is significant and symptom producing, the treatment of choice is either by inducing an abnormal head posture to maintain binocular vision or by interfering with maintenance of binocular function binocular surgery. The surgical procedure depends on underlying muscle dysfunction. If the pattern is due to horizontal rectus muscle dysfunction without oblique and vertical rectus muscle dysfunction, surgery should be carried out to the horizontal rectus muscles and should be combined with recession ± resection of these muscles to treat any associated eso- or exotropia in primary position. In bilateral surgery, the surgeon needs to elevate or depress the positions of medial or lateral rectus insertions. This is done by symmetrical full tendon vertical transposition surgery to contralateral MRs or LRs. The surgeon needs to move MRs toward the apex of the pattern (upward in A pattern and downward for V pattern, i.e., in the direction of the greatest esodeviation) or LRs away from the apex of the pattern (downward for A pattern and upward for V pattern, in the direction of the greatest exodeviation), as illustrated in Figure 11. The pattern breaking effect can be increased by recessing the upper or lower margin of the appropriate transposed horizontal muscle insertion 2 mm more in the direction where more weakening is required.
Move MRs toward the apex of the pattern or LRs away from the apex of the pattern.
When unilateral recess/resect surgery is indicated, i.e., cases with unilateral amblyopia, or strabismus with equal near and distance angles, the horizontal rectus muscles are transposed elevating RL and depressing MR in V pattern and vice versa for A pattern. To increase the effect, the rectus muscles can be resutured to the globe with the upper and lower parts of the insertion placed at different distances from the limbus, e.g., place the lower margin of the medial rectus in a preferentially weaker position than upper margin, and vice versa for lateral rectus muscles in V patterns. Some authors [5] even prefer this repositioning to elevating or depressing the insertions as it reduces the risk of inducing unwanted torsion effects.
Each horizontal muscle is resected or recessed as specified by the magnitude of the horizontal deviation. Half width elevation or depression collapses pattern by 10 to 15 PD diopters. Full-width elevation or depression collapses pattern by up to 25 diopters. The latter is used for patterns exceeding 25 PD. Expect relatively more effect for the surgical amounts for larger pattern deviations.
If oblique overaction is present, appropriate oblique muscle surgery should be performed.
Inferior oblique overaction (IOOA) is a common form of strabismus. It can be primary (idiopathic) or secondary caused by a superior oblique palsy (SOP). The clinician can give the right diagnose by performing the head tilt test. With primary IOOA, head tilt test is negative, and with SOP, head tilt is positive.
Figure 12 shows a +3 left IOOA with left upshoot on right gaze. Right eye is fixing, allowing the left adducting eye to elevate. Bilateral IOOA is associated with a V pattern because the inferior oblique muscles are abductors in the field of action in upgaze.
IOOA left eye.
Primary IOOA is usually bilateral and asymmetrical. It is often associated with horizontal strabismus, typically infantile esotropia (60%), but it can occur isolated. Signs of IOOA are upshoot in adduction, V pattern, and extorsion on fundus examination. The V pattern associated with primary IOOA is a Y with little or no change in the horizontal deviation from primary to downgaze. This patient had an upgaze preference and adopted chin down posturing to obtain binocular fusion (Figure 13).
V pattern esotropia with compensatory chin down head posture.
Secondary IOOA is most commonly due to a unilateral congenital SOP and less commonly bilateral acquired SOP. Differences and characteristics of unilateral and bilateral SOP are summarized in Table 2. Since the SO muscle is a depressor, a weak SO muscle can cause an ipsilateral IOOP and hypertropia in primary. A bilateral SOP will have cancelling hypertropia, so typically there is a small or no hypertropia in primary position. The key sign of SOP is hypertropia with the hypertropia increasing on tilt to the same side as the hypertropia and hypertropia increasing on horizontal gaze opposite to the hypertropia, as shown on photos below. In addition, patients with unilateral SOP will adopt a compensatory head tilt opposite to the side of the SOP to facilitate binocular fusion (R-SOP compensates with tilt left). In primary IOOA, the head tilt is negative, but the extorsion can be seen on fundus exam. Patients with congenital SOP do not have subjective extorsion. However, patients with acquired SOP will experience torsional diplopia that can be measured on Maddox rod testing.
\n\t\t\t\t\tClinical sign\n\t\t\t\t | \n\t\t\t\t\n\t\t\t\t\tUnilateral\n\t\t\t\t | \n\t\t\t\t\n\t\t\t\t\tBilateral\n\t\t\t\t | \n\t\t\t
Hyper in primary | \n\t\t\tLarge >5 PD | \n\t\t\tSmall <5 PD | \n\t\t
“V” pattern | \n\t\t\tSmall <10 PD | \n\t\t\tLarge >10 PD | \n\t\t
Maddox rod | \n\t\t\tExtorsion <10° | \n\t\t\tExtorsion >10° | \n\t\t
Head tilt test | \n\t\t\tHyper increases on tilt to the side of the palsy | \n\t\t\tRH tilt R and LH tilt L | \n\t\t
Unilateral versus bilateral superior oblique paresis
Congenital SO palsy is usually unilateral with a relatively large hypertropia (10–30 PD), which is intermittently binocular fused so the eyes appear well aligned, facilitated by a compensatory head tilt and face turn away from the hypertropia. Therefore, facial asymmetry is common with the smaller side opposite to the SO palsy, as shown in Figure 14.
Congenital SOP, compensatory head tilt, and face turn away from the hypertropia.
Patients with congenital SO palsy usually have excellent stereoacuity and have exaggerated vertical fusion amplitudes, and they can fuse large hyperdeviations up to 25 to 30 PD, whereas normal vertical fusion amplitudes are at 2–3 PD. The hypertropia will manifest when the patient is fatigued, much like patients with intermittent exotropia. When tropic, patients usually suppress diplopia, but some will note double vision. There is usually a significant IOOA with minimal under action of the SO. The etiology of congenital SO palsy is unknown, but some cases have been associated with a lax or absent SO tendon (rare).
Patients typically have control over the deviation in younger age, but as fusional control weakens over time, they may present late even as senior adults with intermittent vertical strabismus and manifest the hyperdeviation when they are fatigued. Typically, patients with decompensated congenital SO palsy present with large HT in primary with the HT increasing on head tilt to the affected side and in gaze to the contralateral side (Figures 15–19). Patients with intermittent vertical strabismus, facial asymmetry, and long-standing head tilt, which can be documented on early childhood family photos, have congenital SOP until proven otherwise. Unfortunately, patients with congenital SO palsy are misdiagnosed and receive multiple consultations, CT, MRI scans, and even surgery for the torticollis. Avoid this by knowing the 7 key findings of congenital SOP, which are as follows: (1) large vertical fusion amplitudes, (2) ipsilateral IO overaction, (3) positive head tilt (>hyper on tilt to the hyper), (4) torticollis (compensatory head tilt opposite to SOP), (5) minimal or no vertical diplopia before it decompensates, (6) no torsion on Maddox rod, and (7) facial asymmetry.
Congenital SO palsy with large RHT in primary with the RHT increasing on head tilt right and in left gaze (R-IOOA).
Congenital SO palsy with large RHT in primary with the RHT increasing on head tilt right and in left gaze (R-IOOA).
Congenital SO palsy with large RHT in primary with the RHT increasing on head tilt right and in left gaze (R-IOOA).
Congenital SO palsy with large RHT in primary with the RHT increasing on head tilt right and in left gaze (R-IOOA).
Congenital SO palsy with large RHT in primary with the RHT increasing on head tilt right and in left gaze (R-IOOA).
Masked bilateral SOP can look like a unilateral SOP as only one eye will show significant IOOA. The presence of a V-pattern and bilateral extorsion on fundus examination also suggests bilateral involvement in patients with a presumed unilateral SOP. In these cases of masked bilateral SOP, if surgery is performed on one eye, the contralateral SOP will become evident postoperatively
Traumatic SO palsy is caused by closed head trauma. It is almost always bilateral as the 4th nerves exit the brain close together, so both nerves get traumatized with a traumatic shift of the tentorium. Since the strabismus is acquired, patients complain of torsional, vertical, and horizontal diplopia, worse in downgaze (SO field of action). Because both SO muscles are weak, the verticals cancel each other so there is minimal to no hypertropia in primary position. These patients have significant torsional diplopia because there is bilateral extorsion, which can be seen on fundus exam and on double Maddox rod testing. The fundus photos will show bilateral extorsion with the foveae below the lower pole of the optic disc. The pattern of strabismus for bilateral SO palsy is reversing hypertropia: (1) RHT on tilt right and LHT on tilt left and (2) RHT in left gaze and LHT on right gaze and a V pattern with esotropia in downgaze (Table 3).
\n\t\t\t\t\tTilt R–RH 12\n\t\t\t\t | \n\t\t\t\t\n\t\t\t\t | \n\t\t\t\t\tTilt L–LH 10\n\t\t\t\t | \n\t\t\t
\n\t\t\t\tR-gaze\n\t\t\t | \n\t\t\tOrtho | \n\t\t\t\n\t\t\t\tL-gaze\n\t\t\t | \n\t\t
LH 8 | \n\t\t\tRH 4 | \n\t\t\tRH 10 | \n\t\t
\n\t\t\t | ET 10 | \n\t\t\t\n\t\t |
Example of measurements of bilateral SOP.
Bilateral SOP has a characteristic V pattern that is an arrow subtype. Since the SO muscles are abductors in downgaze, bilateral SOP causes lack of abduction in down gaze, thus causing an esotropia in downgaze. This causes a V-arrow pattern because most of the eso-shift occurs from primary position to downgaze. The big eso-shift from primary position to downgaze typical of an arrow pattern, which is virtually pathognomonic for bilateral SOP, as shown in Figure 10.
Selection of the appropriate surgical procedure is based on the amount of inferior oblique dysfunction. Inferior oblique overaction is clinically estimated on a scale of +1 through +4. Quantify the upshoot by bringing the fixing eye straight across to the lateral canthus and observe the adducting eye for upshoot (Figure 20).
Quantifying the IOOA on a scale of +1 through +4.
Quantification of upshot in inferior oblique overaction: the abducting eye is fixating. The adducting eye is free to manifest the overaction. (A) Minimal upshoot (+1). (B) Upshoot (+2) of the adducting eye is obvious when the abducting eye looks straight across the lateral canthus. (C) Severe upshoot (+3) of adducting eye. (D) Very severe upshoot (+4) of adducting eye.
The basic rule of thumb is that patients with +2 or more IOOA are candidates for an inferior oblique surgery, and those with +1 or less can be followed except those with significant V pattern (>15 PD). These should be considered for IO weakening procedure even with only +1 IOOA. In cases of asymmetric overaction, bilateral surgery should be done, even when one eye only displays +1 overaction, to avoid unmasking the minimal overaction. If amblyopia is present (greater than 2 Snellen lines), it is safer to restrict surgery to the amblyopic eye. Monocular surgery is sufficient in these amblyopic cases as the sound eye is always fixing and will not manifest an upshoot.
Weakening procedure of the IO muscle is the treatment for IO overaction, that is, IO recession (Figure 21), myectomy (Figure 22), or anteriorization (Figure 23). Inferior oblique overaction can be reduced by surgically moving the insertion anterior toward the equator and nasally so it is closer to the inferior rectus muscle (see the red arrow in the drawing below). Moving IO insertion nasally toward the inferior rectus slackens the IO, thus weakening its function and is called an IO recession. Myectomy weakens the inferior oblique, as removing a portion of muscle reduces the chance of local reattachment. Moving the IO insertion anterior to the equator changes the IO from an elevator to more of a depressor, and this is called IO anterior transposition. The graded anteriorization procedure is the authors’ procedure of choice for mild to severe inferior oblique overaction. The basis of the graded anteriorization procedure is that the more anterior the inferior oblique insertion, the greater the weakening effect, tailoring the amount of IOOA to the amount of anteriorization. The IO muscle is placed 4 mm posterior to the inferior rectus insertion for +1 IOOA, and 3 to 4 mm to IR for +2 IOOA, 1 to 2 mm to IR for +3 IOOA, and at IR insertion for +4 IOOA. Severe bilateral DVD and IOOA needs the “J” deformity full anteriorization of the entire IO insertion, including the posterior fibers. The “J” deformity limits elevation of the eye.
Recession.
Myectomy.
Anteriorization.
In general, avoid antielevation by keeping the IO muscle 2 mm posterior to the IR insertion and avoid “J” deformity by keeping the IO posterior fibers posterior, as described in detail at the end of this chapter.
The final surgical decision must be based on a combination of factors, including the amount of V pattern and the presence of a vertical deviation in primary position. If no vertical deviation is present in primary position, then consider symmetrical surgery. Asymmetric-graded anteriorization is indicated if a hypertropia is present, and more anteriorization of the IO should be done on the side of the hypertropia. A full anteriorization (at the IR insertion, without “J” deformity) corrects about 6 PD hypertropia. An anteriorization with “J” deformity can correct up to 18 PD of hypertropia.
Surgery is indicated for a significant head tilt, a hypertropia causing asthenopia, and symptomatic diplopia. The surgery timing is controversial. In the United States, early surgery is suggested to prevent secondary facial asymmetry, while otters advocate waiting until 2 to 3 years of age. Late surgery is advocated in Europe as strabismus measures are more reliable and binocular function more mature and stable. There is no evidence to clearly choose, as no controlled clinical randomized trials have ever been conducted. The authors’ advice is to wait until 2 years of age as long as the head tilt is mild, or if binocular fusion is compromised, early surgery is indicated.
Prisms are usually of limited value because of the incomitance, but in some older adults, prisms can be used to help control the deviation. If prisms are used, undercorrect the deviation to stimulate vertical fusion amplitudes.
The surgical plan depends on the pattern of the strabismus, depending on unilateral or bilateral location. In general, the treatment strategy is based on where the deviation is greatest and designing a surgical plan to correct the deviation in the primary position while reducing the incomitance.
Unilateral SOP with hypertropia <18 PD can be treated with graded anteriorization ipsilateral IO muscle. Unilateral hypertropia >18 PD can be treated by graded anteriorization, ipsilateral IO muscle, and contralateral IR recession (if there is significant hyper in down gaze). Bilateral SOP with hypertropia <8 PD can be treated by bilateral IO-graded anteriorization with greater anteriorization on the hypertropic side. A masked bilateral can be treated by ipsilateral IO anteriorization and contralateral IR recession plus contralateral IO recession. If there is residual head tilt after IO weakening procedure, perform the Harada–Ito procedure on the opposite side to the head tilt. SO tendon tuck is reserved for extreme lax SO tendon.
Observe conservatively for at least 6 months, taking serial measurements of the deviation. If, after 6 months of observation, the SOP persists with diplopia, surgery should be considered. Prism glasses are usually not useful because of the torsion and incomitance of the deviation.
Surgical plan for most traumatic bilateral SOP with extorsion, esotropia
Muscle surgery to the horizontal rectus muscles, in the form of recessing and resecting, is commonly performed for esotropia and exotropia. These muscles can also be moved away from their original line of action to treat vertical deviations, pattern strabismus (A and V), and nerve palsies. Surgery to the vertical rectus muscles is fundamentally similar to horizontal rectus muscles surgery but is less commonly performed. Each patient requires an individual surgical approach to the management of their strabismus, but the tables provided in Appendix I may be of assistance as a guide in deciding on measurements.
Before surgery, make sure that the patient’s head position is optimal avoiding flex of the neck. Have the patients neck extended so that the patient is looking at the surgeon sitting at the head of the surgical table. A towel roll placed under the patient’s shoulders may be helpful to get the chin up (Figure 24).
Correct head position.
It is important to choose a proper conjunctival incision, as this can have an impact on your strabismus surgery as emphasized as one of the 10 commandments for strabismus surgery by Dr. Wright [12]. The limbal incision is made at the limbus (Figure 25) and is suitable for older patients over 40 years, as the conjunctiva is friable. For patients under 40 years, both limbal and fornix incisions are usable for rectus surgery. The fornix incision is 8 mm posterior to the limbus in the inferior fornix (Figure 26) and should therefore always be preferred for inferior and superior oblique surgery. Fornix incision is preferred to a Swan incision, which is over the muscle insertion, as Swan can leave a conjunctival scar making future surgery difficult, and careful closure is therefore required.
The limbal incision.
The fornix incision.
Posterior Tenon’s capsule separates orbital fat from the extraocular muscles and sclera (Figure 27). If during periocular surgery one ruptures posterior Tenon’s capsule, fat will prolapse and scar attaches to the extraocular muscle and/or the sclera (Figure 28). The scar is an adhesion that contracts causing restriction of ocular rotations (restrictive strabismus), called fat adherence, first described by Marshall M. Parks MD.
Anatomy of the posterior Tenon’s capsule.
Anatomy of the posterior Tenon’s capsule.
The scleral thickness behind the rectus muscle insertion is extremely thin, measuring only 0.3 mm. Because of the thin sclera, perforation into the globe is a significant risk during the scleral needle pass when suturing the muscle to sclera. Therefore, proper needle selection is important to reduce the risk of perforation. The preferred side cutting or spatulated needle has a flat top and bottom (Figure 29). The flat bottom reduces the chance of inadvertent perforation deep into the globe and the flat top prevents cutting into the roof of the scleral tunnel above. Furthermore, to avoid inadvertent perforation of the globe, it is critical that the scleral needle pass is shallow and controlled keeping the tip up and passing the needle horizontally during the scleral needle pass in a flat and straight manner.
Side cutting or spatulated needle is preferred.
To hook a rectus muscle successfully, keep a small hook perpendicularly and firmly to the sclera. Then pass the hook under the rectus insertion, keeping the perpendicular orientation until the hook is under the muscle (Figure 30). This will prevent splitting of the rectus muscle as the tip of the hook stays on the sclera. After hooking the muscle, replace the small hook with the large hook as a Jameson or Helveston hook.
When hooking the muscle, remember perpendicular orientation of the hook.
The pole test, disclose a split muscle.
The pole test should then be performed to ensure the entire rectus muscle is hooked. A small hook is placed at the tip of the larger hook holding the muscle. The small hook is then pulled supero anteriorly with the tip perpendicular to the sclera (Figure 30). If the muscle is split (Figure 31), the residual fibers will restrict the small hook from moving anteriorly.
After hooking the entire rectus muscle, avoiding rupture of the posterior Tenon’s capsule as previously described, it is important to secure the muscle by full-thickness locking bites, centrally and then at each edge of the muscle for three point fixation (Figure 32). Full-thickness pass at the edges is very important, as a partial thickness pass will result in a partially slipped muscle occurring at the edge that was not secured with full-thickness bite (Figure 33).
Secure the muscle by full-thickness locking bites.
Partial thickness pass will result in a partially slipped muscle.
Rectus muscle recession is a weakening procedure, where the rectus muscle is detached from the globe and replaced further from the limbus. The muscle is detached from its insertion and recessed some specific mm and sutured to sclera. This shortens the distance between the origin and the insertion of the muscle and therefore has a weakening effect (Figure 34).
Recession.
If a rectus muscle is not widely splayed, there will be redundant muscle and central sag causing a larger recession than intended. Prevent central sag by adequately separating the muscle poles and by securing the center of the muscle with a central security knot. Central sag can be corrected with the same suture that holds the muscle (Figure 35)
The center of the muscle is secured with a central security knot.
Rectus muscle resection tightens the muscle by removing a segment of the muscle then advancing the muscle to the original insertion (Figure 36). Tightening effect increases when the eye rotates away from the resected muscle because the muscle gets tighter.
Rectus muscle plication has the same effect as resection as it tightens the muscle. Sutures are attached to the muscle posterior to the insertion then passes thorough sclera anterior to the insertion (Figure 37, top). The sutures are pulled up to fold the muscle (Figure 37, bottom). Plication tightens the muscle without the need for muscle disinsertion; thus, it is safer than resection. Plication spares the anterior ciliary vessels, thus reducing the risk of anterior segment ischemia. The rectus plication was invented by professor and coauthor Dr. Kenneth Wright during his fellowship and published in 1991 (Figure 37).
Resection.
Plication.
To perform rectus muscle recessions, resections, and plications, replace the standard hook (Jameson or Helveston hook) with the titanium Wright grooved hook (Figure 38). This hook allows for suturing the muscle insertion over the groove (Figure 39), thus preventing inadvertent scleral perforation and making it easy to get full-thickness locking bites and keep suture placement precise and consistent: not too posterior—not too anterior. Especially when suturing tight muscles, the Wright hook helps pulling the muscle to the surgical field and provides space to suture the muscle (Figure 40). Dr. Wright holds a U.S. patent on the hook design.
Wright groove hook.
Suturing rectus muscle insertion over groove hook.
Suturing rectus muscle insertion over groove hook.
The two long posterior ciliary arteries and the anterior ciliary arteries supply circulation to the anterior segment. Each group contributes about 50% of the anterior segment blood flow. The anterior ciliary arteries course with the rectus muscles (Figure 41). The MR, SR, and IR muscles having 2 arteries and are major suppliers, while the RL has one artery and contributes little to anterior segment circulation. Removing a rectus muscle will permanently disrupt the blood flow from the corresponding anterior ciliary arteries, and the arteries do not recanalize. In children, the long posterior ciliary arteries can maintain enough flow, so even if all the rectus muscles were removed, the child will not get anterior segment ischemia. In senior adults, however, the posterior ciliary supply can be compromised from small vessel disease, and removing the 3 major supplier rectus muscles (i.e., MR, SR, and IR) can result in anterior segment ischemia. Anterior segment ischemia can cause uveitis, hypotonia, and corneal edema. Anterior ischemia is usually transient, lasting a few weeks to a couple of months; however, severe cases can result in vision loss. Treatment is low dose topical corticosteroid drops. Anterior segment ischemia has been reported to occur 10 to 20 years after strabismus surgery. The iris angiogram (Figure 42) shows hypoperfusion of the superior iris, indicating the superior rectus muscle has been removed and its ciliary vessels gone. Once a rectus muscle is removed, its ciliary vessels are permanently destroyed. Over 3 months, the collateral circulation improves especially in young persons, and the iris angiogram can revert to normal. There is no formula for the number of rectus muscles that can be safely detached. As a general rule, do not detach more than two rectus muscles at one time, unless absolutely necessary. As the two vertical and the medial rectus muscles provide the major anterior ciliary blood supply to the anterior segment, try to preserve at least one of these muscles.
The anterior ciliary arteries course with the rectus muscles.
The iris angiogram shows hypoperfusion localized to the superior iris due to resection of the superior rectus muscle.
Inferior oblique overaction, both primary and secondary, can be treated by weakening the IO muscle. The three most frequently performed procedures to weaken the inferior oblique muscle is illustrated in Figure 43 and include inferior oblique (A) myectomy—remove a segment of muscle, (B) recession—move insertion toward the origin to slacken the muscle, and (C) anteriorization—move insertion anterior to equator to change the vector of forces so the IO is no longer an elevator; it is more or less vertically neutral. If the IO is placed anterior to the inferior rectus, then the IO will pull the front of the eye down and cause limited elevation, e.g., “antielevation.” It is a complication of placing the inferior oblique too anterior but can be used to treat DVD. Avoid IO myotomy, as it is not effective, because the cut ends of the muscle inevitably reunite or scar to sclera, causing residual IOOA.
The three most frequently performed procedures to weaken the inferior oblique muscle: (A) myectomy, (B) recession, and (C) anteriorization.
The ciliary nerve courses with the IO nerve, so trauma during IO surgery to the nerve can rarely cause the complication of pupil dilatation and reduced accommodation. Avoid this by using direct visualization of the posterior border of the IO muscle during hooking off the muscle. Avoid “deep blind” posterior passes to hook the muscle and use the Wright grooved hook for suturing the inferior oblique muscle insertion while protecting the sclera in the area of the macular (Figure 44).
The Wright grooved hook used in IO recession protects the sclera in the area of the macular.
A neurovascular bundle attaches to the posterior aspect of the IO muscle. If the posterior fibers of the IO muscle are anteriorized to the level of the inferior rectus insertion, this will stretch the neurovascular bundle and cause a “J” deformity of the IO muscle (Figure 45). The tight neurovascular bindle attached to the IO muscle will pull the eye down and limit elevation (antielevation). A better surgical technique is to keep the posterior muscle fibers posterior to avoid antielevation, unless some limitation of elevation is desired such as the case of treating DVD.
The posterior fibers of the IO muscle are anteriorized to the level of the inferior rectus insertion, stretching the neurovascular bundle and causing a “J” deformity of the IO muscle.
Two procedures that tighten the SO tendon include the full tendon tuck and the Harada–Ito procedure, which is a tightening of the anterior tendon fibers by a partial tuck or advancement of the anterior tendon fibers.
Extorsion associated with acquired SO palsy can be treated by tightening the anterior SO tendon fibers. The anterior SO tendon fibers are responsible for intorsion, while the posterior fibers cause depression and abduction. The SO full tendon tuck (Figure 46) tightens the tendon by pinching and folding the entire tendon. This results in intorsion, depression, and abduction. It can be used in cases of lax SO tendon causing an SOP and is therefore useful for correcting extorsion, hyperdeviation, and convergence in down gaze. If the full tendon tuck is made too tight, it will cause limited elevation worse in adduction due to tightening of the posterior tendon fibers, termed iatrogenic Brown’s syndrome. Care must be taken to balance the superior oblique tightening against an induced Brown’s syndrome by performing intraoperative forced ductions of the superior oblique tendon after tucking.
The SO full tendon tuck.
There are clinical situations that require selective correction of extorsion without a significant change in vertical or horizontal alignment. A full tendon tuck in this situation is not appropriate as it would induce a hypotropia and iatrogenic Brown’s syndrome. The Harada–Ito procedure is designed to selectively correct extorsion, as it tightens the anterior tendon thus intorting the eye. Specifically, the procedure corrects extorsion, usually caused by an SOP, as only the anterior tendon fibers of the SO are tightened so there is little depressor or abduction effect. Iatrogenic Brown’s syndrome is uncommon. Harada–Ito is the procedure of choice to correct extorsion without significant vertical strabismus. Figure 47 shows the Harada–Ito as the anterior fibers in red are pulled temporally toward the lateral rectus muscle to intort the eye as shown by the red arrow.
Harada–Ito procedure includes anterior fibers of SO pulled temporally toward the LR.
There are two ways to perform the Harada–Ito as illustrated in Figure 48: (A) remove the anterior 1/3 of the fiber and advance temporally toward the lateral rectus; (B) the classic Harada–Ito procedure—leave the tendon insertion intact but split the anterior fibers and pull them temporally toward the lateral rectus muscle (plication).
Two ways to perform the Harada–Ito procedure.
The anterior SO tendon fibers are looped with a suture and displaced laterally without disinsertion (Figure 49, left drawing). The anterior fibers are sutured to sclera 8 mm posterior to the superior border of the lateral rectus muscle (Figure 33, right photo). This procedure has the advantage of being easy reversible. To undo the classic Harada–Ito, simply cut the suture and the tendon will be back to normal. This must be done within 24 to 48 h after surgery, or the tendon will scar in place.
The classic Harada–Ito (plication) method where the anterior fibers are looped with a suture and sutured to sclera laterally.
General anesthesia is used most frequently in strabismus surgery. All strabismus surgery on children requires general anesthesia. Patient anxiety, reoperations, and SO surgery are also indications for general anesthesia. An experienced anesthesiologist, familiar with pediatric anesthesia and potential life-threatening complications like malignant hyperthermia, is an essential member of the surgical team.
Local anesthesia can be used in cooperative adults for unilateral surgery. A retrobulbar injection of 4 ml of lidocaine is given. If the patient experiences intraoperative pain, it can be treated with an additional local injection of lidocaine near the muscle being careful not to inject directly into the muscle. Topical anesthesia and sub-Tenon anesthesia is a good option for adult patients requiring a unilateral or bilateral recession or even resection procedures. With gentle manipulation, avoiding pulling on the muscle, topical anesthesia strabismus surgery can be done with minimal pain, without bearing the risk of general anesthesia.
A 5-0 vicryl suture with S-24 double-arm spatula needles, or a 6-0 vicryl suture with S-29 spatula needles, are the usual sutures of choice for strabismus surgery. A 5-0 mersilene suture (nonabsorbable) is indicated for muscles that may develop a postoperative stretched scar, advancement of a slipped muscle, the Harada–Ito procedure, and Wright’s silicone tendon expander procedure.
Magnification of 2 times is helpful or use the lowest magnification of a surgery microscope. High magnification should be avoided as it significantly limits depth of focus and field size. A head lamp is advised if a surgery microscope is not used.
Immediate recovery: NPO is necessary for 2 h after surgery, depending on the age of the patient. Restricting all oral intake helps reduce nausea and vomiting postoperatively. Do not use eye patches unless an adjustable suture was used or it was a multiple reoperation.
Prescribe antibiotic-steroid ointment, b.i.d. × 10 days. No swimming for 2 weeks, and schedule a follow-up postoperative visit in the first week, then a second postoperative visit usually in 6 weeks, depending on the patient’s condition and age. Young patients with intended overcorrection of intermittent exotropia need to be followed more frequent. Patients should be warned of the possibility of periocular infection and to return immediately if redness or swelling persists.
If you want to dig even deeper into strabismus surgery, we suggest you to read the books and papers mentioned below.
The most important rule for the strabismus surgeon is to continue learning from experience. Surgery should be done carefully and should preoperatively be planned and thought out logically. Unexpected results should be questioned. Procedures that do not measure up to the surgeon’s expectations should be altered. The surgeon should work on improving his or hers skills and develop his or hers own set of guidelines. However, it is apparent that not all surgeons will have the opportunity to operate on a sufficient number of patients to be innovative. In that case, the surgeon should select his or her authority carefully and remain appropriately skeptical and positively critical. It is not about “how many” but rather “how” you perform. Our patients deserve no less than this.
The pandemic Covid-19 outbreak has severely disrupted the economic systems across European countries during the 2020 first semester. Widespread lockdowns have brought to a halt for a few months the firms’ production and services delivering in many countries and major concerns have arisen on the capacity of many firms to survive the real and financial shocks induced by the current pandemic. Despite all governments and public authorities vast subsidizing programs deployed to help economy recovery, still small and medium sized enterprises (SMEs) remain particularly exposed to the negative consequences of the current Covid-19 outbreak due to their higher perceived financial vulnerability.
Among European countries, Italy has been the first country to be harshly hit by the coronavirus outbreak and one of the more exposed to negative economic consequences of the pandemic. Moreover, its economic system is very much reliant on SMEs on the economy supply side. Anecdotal evidence points out that many small businesses are struggling to re-open and resume their activities after the slow easing up of the government lockdown measures.
Under these circumstances, the present study aims to test the financial policies that Italian SMEs have developed across the years starting from the aftermath of the 2008 financial crisis and the ensuing 2011 Greek sovereign debt crisis, up to recent years. There are many ways to deal with this issue and its many specifics. We opt to focus on how SMEs in Italy have chosen to diversify their debt funding away from bank lending through corporate bonds funding, since SME access to the debt capital market is largely considered a valuable source of debt funding diversification, especially for growth firms with a prominent exposure on bank debt [1, 2, 3, 4, 5]. Beyond that, one of the main goals of a firm’s sound financial policy, particularly in the case of SMEs, should be to devise financial choices that may help reducing the financial vulnerability to potential unexpected financial shocks [6, 7].
There are several reasons for our research focus. First, it is well documented that SMEs tend to be over-reliant on bank debt, especially short-term lending [8]. Second, the last global financial crisis heightened in southern European countries by the spillover of Greek sovereign debt crisis in 2011 has produced a lasting credit crunch propelled by risk aversion from banks and their concerns on borrowers default risk, which it has been particularly severe for SMEs [9, 10]. Third, in order to counter the negative effect of this credit crunch on SMEs, the Italian government has promoted in June 2012 a raft of reforms in order to facilitate the SMEs and unlisted firms’ access to bond financing1 [3]. A new junior bond market for mini-bonds, named ExtraMot-Pro, within the domestic Borsa Italiana stock exchange, has been launched in February 2013, with a set of soft requisites for SMEs issuers. In brief, the new junior bond market is characterized by minimal regulations and simplified admission requirements in comparison with those set up for the senior corporate bond market.
More in particular, we analyze in this chapter whether mini-bond issuers have improved their financial resilience thanks to this market-based financial choice across the years between the two major recent crises (i.e., the 2011 Greek sovereign crisis and the 2020 pandemic-induced crisis). By focusing on this topic, our study may contribute to shed new light on the emerging debate on how small businesses can recover from the current crisis triggered by the Covid-19 pandemic.
Our empirical analysis is performed using regression models based on a proprietary hand-collected dataset of 127 mini-bonds issued by nonfinancial firms across 2013–2017 years jointly with a sample of nearly 5200 Italian private firms that have not issued corporate bonds across the same years. The dataset combines evidence on mini-bonds issuers, collected from Borsa Italiana website and admission prospectuses, with detailed financial statements data from Bureau Van Dijk’ Amadeus/Aida dataset.
The chapter is organized as follows. Section 2 discusses our research question and the testable hypothesis. Section 3 describes our dataset and provides sample description. Section 4 illustrates the research design and the empirical methodology. Section 5 sets out the empirical results and discusses the main implications of the study. Section 5 concludes the paper.
In our research setting, we are interested in testing one of the key ingredients that normally shapes the firms’ financial policy [11, 12]: how firms’ external funding choices could make them less financial fragile when facing potential unforeseen real or financial shocks like those induced by the current coronavirus pandemic. The basic idea, here, is the more the firm is less dependent from a unique or very few sources of external funding (for instance, bank lending), the better for the firm from a financial vulnerability point of view. We reckon that this topic is nowadays extremely important in particular for SMEs, which are the firm size-class clearly more at risk of survival in the current economic climate at least in those countries most affected by the pandemic.
In order to tackle this issue we ask ourselves whether the choice of debt diversification away from bank lending can improve or not the firms’ financial fragility and, thus makes them, at least on paper, more resilient to potential external financial shocks or crises.
Prior literature on SME access to debt capital market have focused on the benefits that corporate bonds offers in terms of: positive management culture change linked to the firm financial life-cycle when approaching market-based finance [13]; enhanced market visibility on prospective investors [14, 15, 16, 17]; acclimatization function and progressive step toward other more complex forms (even equity) of capital market funding [18]; and, even, reduced financial costs on subsequent bank lending thanks to heightened bargaining power in the firm-bank relationships [19]. On the contrary, there is still less evidence on the role that corporate bond financing may play on addressing the SMEs financial fragility issue. It is true that, at least on paper, any opportunity of debt diversification may help small businesses achieve a better and more balanced financial policy, but it is important also to verify whether this goal is somehow supported by the empirical data as we cannot take for granted that smaller firms are in practice able to improve their financial resilience through this channel of funding since there can be the suspicion that firms are replacing one form of debt (bank lending) with another one (debt securities). This is a quite relevant question in the current economic climate dominated by the pandemic crisis.
Ideally, to develop a comprehensive study on this research topic we should need a large dataset across years of firms’ financial data around the crisis (in this case the pandemic) both before and after the event. Since we can only source data before the coronavirus outbreak, we are obliged to use firm-level data in the years before the 2020 pandemic crisis. We, thus, consider the firm’s choice of corporate bond funding as the major external debt diversification solution molding the firm financial policy.
Under these circumstances, we formulate the following main research question. Does corporate bond financing make SMEs more resilient to potential crisis? To answer this research question we opt to create a firm-level financial fragility indicator using core financial reports data both before and after the time of mini-bonds funding for issuer firms and compute the variation reported by this indicator across the years. The basic idea is that the difference between ex-post (after the bond issuance) score and the ex-ante score (before the mini-bond funding) of our financial fragility indicator should give us a good proxy of the impact of the treatment (the corporate bond funding) on the firm financial fragility and, thus, on the ability of the firms’ financial policy to reach its desired outcome in terms of improved (less) financial fragility.
Even if financial vulnerability can be measured along many dimensions, and there is not always a wide consensus on how measure it, we are confident that our metric that include five different financial ratios commonly used by scholars and practitioners in assessing firms’ financial health is reasonable robust. We then use this indicator as our dependent variable in our regressions as depicted later in our Section 4. Among the explanatory variables, together with other control variables, we employ a mini-bond financing dummy which is equal to one in case of SME funding through this channel and zero otherwise.
In this way, we can empirically test our main hypothesis on whether Italian SMEs mini-bond issuers are able to reduce ex-post their financial vulnerability as a consequence of this debt diversification choice in comparison with similar and comparable nonissuer firms. In sum our hypothesis is the following:
H.: Italian SME mini-bond issuers that diversify their debt funding through the access to the debt capital-market become ex-post less financial fragile.
If the above hypothesis is positively confirmed by our tests, we can claim that corporate bond funding may prove to be a key ingredient of a firm’s sound financial policy aiming to improve its financial resilience to potential unexpected financial shocks, particularly in the case of SMEs.
Since we cannot test the counterfactual assumption of our hypothesis, i.e. what could happen to the financial vulnerability of those issuers firms if they have not chosen to access the debt capital market, we have to rely on a matched control group of private firms that have not issued corporate bonds across the same years under investigation. This control group is created from a large sample of around 6000 Italian firms extracted from Bureau Van Dijk’ Amadeus/Aida dataset (hereafter Amadeus).
Therefore, in order to analyze the role of corporate bond funding in changing SMEs financial fragility, we have sourced data for two different samples. First, the listed mini-bonds sample (i.e. issuers firms) and, second, the matched control group sample formed by comparable private firms that have not issued mini-bonds (nonissuers firms).
For the first sample, we source data on mini-bonds listed on the junior bond market ExtraMot Pro, from its starting date in 2013 up to the end of December 2017. We obtained from the Borsa Italiana website the raw information on listed bonds and its issuers on the 15th January 2020. The total number of bonds net of delisting is 241, from 160 different firms. We consider only first time issuers, so we eliminate subsequent bond offerings from the same firm, since the decision to access the capital market could be persistent across time, following the standard approach used in the going public literature, dating back to the seminal work of Pagano et al. [20]. Then, we match the obtained dataset with accounting information about the issuers, collected from the Amadeus database. Due to a lack of complete accounting information for some issuers, the dataset comprises 127 mini-bonds issued by nonfinancial companies. We consider only nonfinancial firm issuers because financial statements information for financial and nonfinancial companies are not easily comparable.
As regards our control group, we source from the same Amadeus database a subset of nearly 40,000 private Italian nonfinancial firms with a number of employees between 1 and 2000 units, total asset between 0.3 and 1500 €/million, and with at least 5 years of available accounting data across the years where we have corporate bonds offerings. From this large dataset, we randomly draw 1200 nonissuing firms’ observation, with a comparable size of the issuers’ firms, for each year of mini-bond issuance (from 2013 up to 2017). In this way, we are able to match issuers in a given year with a control group randomly drawn for the same year. Hence, the final raw control group is composed by 6000 firms. However, due to lack of some relevant accounting information, our final sample consists of 5319 firms (127 issuers and 5192 from the control group).
For what concerns firm-level accounting data for constructing our dependent and independent variables, we collect for the two firms’ samples not only ex-ante data, (i.e. before the time of bond funding for issuers and the same year for the matched control group) but also data of 2 years after. For example, for mini-bond issuers that first-time entered the debt capital market during the 2017, we have collected financial statements data for the years 2016 and 2019. For a firm in the control group, the procedure is the same: if the firm is drawn in the 2017 sub-sample, we collected data for the years 2016 and 2019. In this way, we have homogeneous data between the issuers sample and the control group.
Our corporate bond issuers sample, which is composed by 127 offerings, is depicted in Table 1 which illustrates the distribution of issuers by size (in terms of sales) using the firms’ financial reports from the most recent year prior to the issuance date. In accordance with the standard EU Commission definition, we define a SME as a firm with fewer than 250 employees, total assets lower than €43 million, or sales lower than €50 million. A small firm is defined as a firm with fewer than 50 employees, total assets lower than €10 million, or sales lower than €10 million.
Size class | # of observation | frequency |
---|---|---|
<10 million | 12 | 9.45% |
Between 10 and 50 million | 50 | 39.37% |
Between 50 and 100 million | 18 | 14.17% |
>100 million | 47 | 37.01% |
Total | 127 | 100.00% |
Issuers distribution by size class.
The sample is split accordingly to four different size classes based on sales in €/million. The table shows the number of the observations and the percentage with respect to the total for each category. Our elaboration on proprietary dataset.
Table 1 distribution highlights that SMEs cover around 49% of our sample (i.e. first two size classes). Table 2 shows the distributions of issuer firms by industry. The majority of these bonds were issued by manufacturing firms, followed by the retail sector. The positive correlation between issuers’ size and mini-bond capital raised is confirmed in Table 3. As a matter of fact, larger bonds are issued by unlisted firms with more than 50 €/million sales. For SMEs with sales under the 50 €/million threshold, the average capital raised remains quite low. Table 4 displays the issuance motivations as declared in the bonds prospectuses, and highlights that the main use of proceeds of the mini-bond funding is to exploit growth opportunities but still debt restructuring and diversification of funding are acknowledged by a high percentage (around 23%) of issuers, behind supporting firms’ growth target. Table 5 divides our sample into four groups according to the issuer-size in order to provide a more detailed examination of the issuers’ characteristics through selected financial ratios. It is useful to highlight that smaller issuers are more leveraged, but, interestingly, have a higher interest coverage ratio (the ratio between EBITDA and interest expenses) and EBITDA over sales with respect to larger firms, while asset tangibility (as measured as tangible fixed asset over total assets) is, as expected, lower. Lastly, Table 6 exhibits the differences in key financial ratios between the control group and minibond-issuers. The two samples present strong similarities in terms of size and profitability (i.e. ROI), which can guarantee us a good fit of our control group. On the other hand, issuers are overall more indebted, and in particular to banks. This evidence confirms that the use of mini-bond funding is aimed to exploit growth opportunities when bank lending is particularly costly and/or rationed, or to diversify the funding sources.
Sector | # of observation | Frequency |
---|---|---|
Accommodation and catering | 2 | 1.57% |
Agriculture, silviculture and fishing | 2 | 1.57% |
Arts, sports and entertainment | 2 | 1.57% |
Buildings and constructions | 7 | 5.51% |
Energy | 5 | 3.94% |
Health and social care | 2 | 1.57% |
ICT | 7 | 5.51% |
Manufacturing | 54 | 42.52% |
Professional and scientific activities | 8 | 6.30% |
Real estate | 2 | 1.57% |
Rental and travels | 6 | 4.72% |
Retail activities | 16 | 12.60% |
Transports and storing | 3 | 2.36% |
Water, sewer and waste | 11 | 8.66% |
Total | 127 | 100.00% |
Issuer distribution across sectors, using the ATECO 2007 classifications.
The number of firms and the frequencies are displayed. Our elaboration on proprietary dataset.
Size class | Average issue | Total volume | Total volume (%) |
---|---|---|---|
<10 million | 11.80 | 141.58 | 3.17% |
Between 10 and 50 million | 6.17 | 308.33 | 6.90% |
Between 50 and 100 million | 14.89 | 267.45 | 5.98% |
>100 million | 79.88 | 3754.16 | 83.96% |
Total | 35.21 | 4471.52 | 100% |
Issues’ volume (€/millions), by issuers’ size classes.
Principal capital raised, by issuers size class. The table depicts the average capital raised and the total volume of principal capital for the four issuers size classes. Values are displayed in €/million. Our elaboration on proprietary dataset.
Motivation | # of observation | Frequency |
---|---|---|
Support working capital | 20 | 10.10% |
Growth | 84 | 42.42% |
Exploit merge/acquisition opportunity | 13 | 6.57% |
Internationalization | 22 | 11.11% |
Debt restructuring/diversification of funding | 45 | 22.73% |
Not declared/unavailable | 14 | 7.07% |
Total | 198 | 100% |
Use of proceeds.
Motivations declared by issuers in the bond prospectuses. This table shows the motivations reported in the bond prospectus, divided into 5 main categories: Supporting the working capital, growth, exploit M&A opportunity, internationalization, debt restructuring or diversification of funding. The number of declared use of proceeds exceeds the number of issuers due to the fact that some issuers have declared more than one use of proceeds.
Category | D/E Ratio | Bank debt exposure | Interest coverage | Short-term bank debt ratio | Current ratio | ROI | EBITDA/Sales | Tangible ratio |
---|---|---|---|---|---|---|---|---|
<10 million | 2.61 | 34.82% | 17.85 | 16.85% | 1.15 | 6.6 | 23.03% | 21.00% |
4.73 | 29.28% | 37.07 | 17.53% | 0.42 | 10.16 | 34.92% | 27.51% | |
Between 10 and 50 million | 2.53 | 50.39% | 7.91 | 26.78% | 1.22 | 8.13 | 14.56% | 27.28% |
2.52 | 18.30% | 13.20 | 13.50% | 0.51 | 6.78 | 10.13% | 24.53% | |
Between 50 and 100 million | 2.18 | 45.16% | 6.06 | 26.58% | 1.06 | 10.19 | 12.79% | 20.33% |
1.4 | 15.06% | 9.14 | 14.77% | 0.17 | 8.81 | 9.40% | 19.75% | |
>100 million | 1.58 | 43.49% | 5.96 | 25.04% | 1.17 | 8.77 | 12.36% | 25.45% |
2.21 | 18.25% | 4.70 | 15.86% | 0.44 | 7.53 | 8.45% | 18.81% | |
Total | 2.14 | 45.62% | 7.71 | 25.16% | 1.17 | 8.55 | 14.30% | 25.02% |
2.58 | 19.47% | 14.08 | 15.06% | 0.44 | 7.64 | 13.90% | 22.11% |
Selected financial ratios by issuers’ size class.
Issuers’ descriptive statistics. The table reports selected financial ratios for issuers, divided into four size classes (in terms of sales). Means and standard deviations (in italics) are reported. D/E Ratio is the issuer’s debt to equity ratio; Bank debt exposure is the ratio between the bank debt to total debt. The interest coverage ratio is the ratio between the issuer’s EBITDA and its interest expenses. The short-term bank debt ratio is the ratio between bank short term debt and total debt. The current ratio is the ratio between issuer’s current assets and current liabilities. Tangible asset ratio is the ratio between tangible fixed assets and total assets. Our elaboration on proprietary dataset.
Variable | Issuers | Control sample | |
---|---|---|---|
Sales (Natural logarithm) | 17.69 | 18.05 | |
1.68 | 1.06 | ||
D/E Ratio | 2.14 | 1.46 | |
2.58 | 3.53 | ||
Bank debt exposure | 45.62% | 29.72% | |
19.47% | 23.81% | ||
Interest coverage | 7.71 | 24.77 | |
14.08 | 46.68 | ||
Short-term bank debt ratio | 25,17% | 20.31% | |
15.06% | 19.42% | ||
Current ratio | 1.17 | 1.42 | |
0.44 | 0.75 | ||
ROI | 8.55 | 8.65 | |
7.64 | 7.81 | ||
EBITDA/Sales | 14.30% | 7.37% | |
13.90% | 8.45% | ||
Tangible ratio | 25.02% | 19.22% | |
22.11% | 17.79% | ||
# of observation | 127 | 5192 |
Differences between the two samples (issuers and nonissuers).
Difference between the issuers’ sample and the control group. Standard deviations are reported in italics. Size is measured by the natural logarithm of sales. D/E Ratio is the issuer’s debt to equity ratio; Bank debt exposure is the ratio between the bank debt to total debt. The interest coverage ratio is the ratio between the issuer’s EBITDA and its interest expenses. The short-term bank debt ratio is the ratio between bank short term debt and total debt. The current ratio is the ratio between issuer’s current assets and current liabilities. Tangible ratio is the ratio between tangible fixed assets and total assets.
In order to study whether the access to the mini-bond market reduces firms’ financial fragility, we perform a set of OLS regression models using the pooled sample of issuers and nonissuers of mini-bonds across the years analyzed (2013–2017). This methodology has often been employed in the prior going public literature, starting from the Pagano et al. study [20], on IPOs equity markets.
We choose as the dependent variable a measure of financial fragility (or vulnerability) using an equally weighted basket of financial ratios that aims to capture the exposure of the firm to the negative consequences of potential real and financial shocks.
In the OLS regressions, we estimate beta coefficients using a proxy of financial fragility as the dependent variable and combinations of the explanatory variables for different specifications, as depicted in the next section. More in detail, we compute the variation in the score of our financial fragility indicator for each firm between 2 years after the event (the corporate bond issuance) and the year before the same event. When the difference is positive, it means that our proposed financial fragility metric has worsened (becoming higher), the opposite if the difference is negative.
The basic structure of our regressions is as follows:
where Minibondi,t is a dummy variable equal to 1 in case of mini-bond funding of firm i at time t and zero otherwise, and FirmControlsi,t−1 is a vector of firm-specific control variables about the issuers and nonissuers characteristics using the last available accounting information at the date of the bond offering. We control for sector and time fixed effects.
As indicated previously, our dependent variable is the change in firms’ financial fragility, and it portrays the exposure of the firms to the negative consequences to potential financial shocks. We build a measure of financial fragility (or vulnerability) using an equally weighted scoring indicator of five financial ratios that capture the most significant dimensions of firms’ financial health. They are the following: interest coverage financial ratio; current ratio; short-term bank debt over total debt; financial leverage (i.e. debt to equity ratio), bank debt exposure (bank debt over total debt). The procedure is the ensuing: for each year and for each five financial ratio we create a ranking system starting from a score of 1 (lowest financial fragility) up to 5 (highest financial fragility) based on a quintile classification of the financial ratio (we used also different ranking criteria, but our empirical results remain robust and are not affected significantly). For example, for year 2016 we have a starting sample of 28 mini-bond issuers and 1200 firms in the control group. Then, for each financial ratio we compute the score for all firms. Then, we compute the financial fragility indicator for all firms by computing the average of all 5 scores (with equal weights).
Next, we calculate the difference of the score of the financial fragility indicator between t + 2 and t − 1, relative to the reference year. We think that a two-year time span after the event is a good compromise in order to assess the effect of the firms’ financial policy choices on the desired outcomes in terms of better financial resilience. Longer event windows (up to 3 year after the event or more) have undesired features such as: the loss of a significant number of observations in our issuers sample since for mini-bond issued during 2017 we do not have a 3 year ex-post track record of financial reports; and the longer the time horizon the more the effects on our financial fragility indicator can be influenced by other factors than merely the financial policy choice under scrutiny. Table 7 shows the differences in the average financial fragility indicator score for the two sub-samples. As a matter of fact, mini-bond issuers have a higher average score because they are more leveraged, more indebted to banks and have a lower interest coverage with respect to the control group.
Variable | Issuers | Control sample | Total |
---|---|---|---|
Before t0 | 3.91 | 3.2 | 3.21 |
0.64 | 0.98 | 0.98 | |
After t0 | 3.73 | 3.12 | 3.14 |
0.62 | 0.93 | 0.93 | |
Difference | −0.18*** | −0.07*** | −0.07*** |
0.63 | 0.58 | 0.58 | |
# of observation | 127 | 5192 | 5319 |
Differences in the financial fragility average score.
Financial fragility scores for the two samples before and after the bond issuance date. Standard deviations are reported in italics. T0 is the event year of bond issuance for both samples. Values are average scores of the financial fragility indicator that spans from a score of 1 (lowest financial fragility) to a score of 5 (highest financial fragility). Stars denote the standard level of p-value significance: *=10%, **=5%, ***=1%. Our elaboration on proprietary dataset.
As far as concerned the explanatory variables, we introduce a mini-bond financial dummy variable (MiniBond) which is equal to one in case of mini-bond funding of firm i at time t and zero otherwise. Beyond that, we consider a selection of firm-specific control variables: firm size (as log of total asset), profitability (measured as the EBITDA on sales), tangibility (measured as tangible fixed assets over total assets), and book value of equity over fixed assets ratio as a measure of firms’ asset-liability mismatch. We introduce also two size dummies, a SME and a Small dummy variable, that controls for the issuers’ classification according to EU Commission standard definition as a SME (Small) or not. SMEs are naturally opaque firms and obtain funds almost exclusively through private equity and bank debt [13]. In general, the informational asymmetry issue may cause shortage of finance and credit rationing and may lead to a disparity in access to bond financing between SMEs and large firms [21, 22]. The dummy size variables aim to test whether is actually more difficult for private SMEs or smaller firm to improve their financial resilience. Appendix A summarizes and describes our firm-specific variables that we have used in the regressions, while Tables 8 and 9, report the descriptive statistics and correlation coefficients for the empirical variables, respectively.
Mean | Std. Dev. | Min | Max | obs | |
---|---|---|---|---|---|
ΔFinFragility | −0.075 | 0.583 | −3.4 | 2.6 | 5319 |
Minibond | 0.024 | 0.152 | 0 | 1 | 5319 |
Tangible ratio | 0.194 | 0.179 | 0.001 | 0.983 | 5319 |
EBITDA/Sales | 7.55% | 8.69% | −19.36% | 99% | 5319 |
Asset-liability mismatch | 8.713 | 18.201 | 0.017 | 76 | 5319 |
Size | 19.691 | 1.232 | 12.638 | 22.777 | 5319 |
SME | 30.28% | 49.86% | 0 | 1 | 5319 |
Small | 5.41% | 22.61% | 0 | 1 | 5319 |
Variables’ descriptive statistics.
Descriptive statistics of the pooled sample variables. ΔFinFragility is the difference in the financial fragility indicator between t + 2 and t − 1; Minibond is a dummy variable equal to 1 if the firm issued minibond at t0; Tangible ratio is the ratio between the tangible fixed assets and the total assets. EBITDA/Sales is the ratio between EBITDA and Sales; the asset liability mismatch variable is the book value of equity over fixed assets ratio; size is the natural logarithm of total assets; SME (Small) is a dummy variable equal to 1 if the firm is a SME (Small) as defined in appendix A.
ΔFinFragility | Minibond | Tangible ratio | EBITDA/Sales | Asset-liability mismatch | Size | SME | Small | |
---|---|---|---|---|---|---|---|---|
ΔFinFragility | 1.00 | |||||||
Minibond | −0.0284 | 1.00 | ||||||
Tangible ratio | −0.0871 | 0.0493 | 1.00 | |||||
EBITDA/Sales | 0.0029 | 0.1210 | 0.3055 | 1.00 | ||||
Asset-liability mismatch | 0.0428 | −0.0223 | −0.4125 | −0.0223 | 1.00 | |||
Size | −0.0945 | 0.0622 | 0.3201 | 0.3528 | −0.1249 | 1.00 | ||
SME | 0.0404 | −0.0606 | −0.2672 | −0.2907 | 0.1182 | −0.7613 | 1.00 | |
Small | 0.0555 | −0.0156 | −0.1413 | −0.0990 | 0.0811 | −0.4259 | 0.2583 | 1.00 |
Correlation coefficients.
Correlation coefficients of the variables used in the OLS regressions. ΔFinFragility is the difference in the financial fragility indicator between t + 2 and t − 1; Minibond is a dummy variable equal to 1 if the firm issued minibond at t0; Tangible ratio is the ratio between the tangible fixed assets and the total assets. EBITDA/Sales is the ratio between EBITDA and Sales; the asset liability mismatch variable is the book value of equity over fixed assets ratio; size is the natural logarithm of total assets; SME (Small) is a dummy variable equal to 1 if the firm is a SME (Small) as defined in appendix A.
Table 10 shows the outcomes of our regressions, in which the beta coefficients and standard errors (in italics) are displayed. The effect of the mini-bond financing dummy on the change reported in the score of the financial fragility indicator 2 years after the event is negative and highly statistically significant (at the 5 percent level). Thus, the access to the debt capital market is conducive for the Italian companies to a decrease in the financial fragility after the event relative to the same indicator value displayed before this relevant change in their financial policy previously adopted. Consequently, our research hypothesis is confirmed.
Dependent variabile: ΔFinFragility | |||||
---|---|---|---|---|---|
Specification: | 1 | 2 | 3 | 4 | |
Minibond | −0.115** | −0.117** | −0.118** | −0.118** | |
0.056 | 0.056 | 0.056 | 0.056 | ||
Tangible ratio | −0.273*** | −0.274*** | −0.290*** | −0.282*** | |
0.054 | 0.054 | 0.054 | 0.054 | ||
EBITDA/Sales | 0.238 | 0.219 | 0.188 | 0.190 | |
0.137 | 0.137 | 0.135 | 0.135 | ||
Asset-liability mismatch | 0,0003 | 0.0003 | 0.0003 | 0.0003 | |
0.0004 | 0.0005 | 0.0005 | 0.0005 | ||
Size | −0.028* | −0.017 | |||
0.013 | 0.013 | ||||
SME | −0.074*** | −0.066** | −0.036* | −0.043** | |
0.026 | 0.026 | 0.019 | 0.019 | ||
Small | 0.095* | 0.117** | |||
0.047 | 0.045 | ||||
Constant | 0.554 | 0.335 | 0.029 | 0.030 | |
0.367 | 0.372 | 0.281 | 0.280 | ||
Industry dummies | YES | YES | YES | YES | |
Year dummies | YES | YES | YES | YES | |
R squared | 0.045 | 0.046 | 0.044 | 0.046 | |
#obs | 5319 | 5319 | 5319 | 5319 |
OLS regressions on financial fragility.
=10%.
=5%.
=1%.
Outcome of the OLS Regressions with four different specification. The dependent variable is the difference of the financial fragility indicator between t + 2 and t − 1. Minibond is a dummy variable equal to 1 if the firm issued minibond at t0; Tangible ratio is the ratio between the tangible fixed assets and the total assets. EBITDA/Sales is the ratio between EBITDA and Sales; the asset liability mismatch variable is the book value of equity over fixed assets ratio; size is the natural logarithm of total assets; SME (Small) is a dummy variable equal to 1 if the firm is a SME (Small) as defined in appendix A. In all specifications industries dummies and year dummies are included. Beta coefficients and robust standard errors (in italics) are displayed. Stars denote the standard level of p-value significance.
As regards the other firm-specific control variables, we note that the tangibility variable displays a statistically significant (at 1 percent level) negative beta coefficient implying that the firms that presents higher tangible asset at the event date are more able to reduce their financial vulnerability. Here, our results suggest that SMEs with more intangible assets tends to develop, ceteris paribus, a more fragile financial structure and this it is happened even before the current pandemic crisis. We reckon that this is an interesting result as it shows that the presence of consistent tangible assets not only offers a wider scope for pledging collateral to potential investors playing a mitigating role regarding the borrower default risk [23, 24] but it can also be helpful to reduce the financial fragility.
Size variables presents a mixed picture. On one hand, in the specification 1 in which size is measured as log of total asset, we have a statistically negative coefficient showing that size as expected matters: the larger the firm the better its financial resilience. On the other hand, when we consider more in detail the two size dummies (SME e Small), the former has a negative coefficient implying that, inside the small-medium size class, the larger firms are still less vulnerable from a financial point of view. On the contrary, the Small dummy in all regression specifications changes beta coefficient sign and becomes positive and statistically significant indicating that smaller firms (i.e. firms with sales lower that 10 million euro) tends to worsen across time their financial fragility score. This result is not totally unexpected as smaller firms are fundamentally less financial resilient as showed by substantial prior literature [5, 25] and by the anecdotal evidence. Other control variables such as, for instance, profitability are not statistically significant.
Even if our findings are quite robust, we must be aware that our study is limited to a firm-level dataset which is confined to the years up to the coronavirus outbreak and we cannot include in our tests the actual effects on firm financial data of the current global pandemic. Therefore, our results must be read with great caution as it is highly probable that the current crisis may display asymmetric effects across countries, geographical areas and industries that are not reflected in our dataset. Future researches based on new post-pandemic data can fully address this void.
The goal of our study is to contribute to shed new light on the emerging debate on how small businesses can recover from the current crisis triggered by the Covid-19 pandemic. Since SME access to the debt capital market is widely viewed as a valuable source of firm debt diversification, especially for growth firms with a prominent exposure on bank debt, we test whether SME bond issuers are able to reduce their financial vulnerability thanks to this financial policy. The aim is to assess the extent to which SMEs financial choices regarding nonequity external funding can become a key factor in facing real and financial shocks like those triggered by the current Covid-19 pandemic.
Our empirical analysis has been performed using OLS regression models based on a proprietary hand-collected dataset of 127 first-time mini-bonds issuers across 2013–2017 years jointly with a control sample of around 5200 Italian private firms that have not issued corporate bonds across the same years.
Based on our empirical analysis we find a robust evidence on the role that corporate bond financing can play on addressing the SMEs financial fragility issue. Debt diversification away from bank lending helps smaller firms to achieve a more balanced and sound financial policy and, thus in turn, firms are able to improve their financial resilience through this channel of funding. We think that this circumstance is becoming more and more relevant in the current economic climate dominated by the adverse effects on SMEs of the global pandemic crisis. Corporate bond funding offers benefits for SMEs that are not merely confined to what previous literature has already described such as: (a) hastening a more capital market-oriented management culture linked to the firm life-cycle; (b) enhanced market visibility on prospective investors; (c) providing an acclimatization function and a platform for progressive steps toward other more complex forms (even equity) of capital market funding; and (d) reduced costs on subsequent bank lending thanks to heightened bargaining power in the firm-bank relationships.
As a matter of fact, we offer empirical evidence that corporate bond financing has reduced the financial fragility of Italian SMEs. For these reasons, we can expect that even after the pandemic outbreak the mini-bond funding channel may still play a key, and maybe even enhanced, role in order to overcome the negative consequences of the current financial climate for SMEs where firms will be probably more and more indebted and more reliant on bank lending. Although our study is limited to the Italian unlisted firm context, we reckon that our findings can provides useful insights to other countries particularly considering that the economic effects of the current pandemic have been so pervasive.
Variable name | Definition | Source | Notes |
---|---|---|---|
ΔFinFragility | Difference between the financial fragility indicator at t + 2 and the financial fragility indicator at t − 1 | Self-constructed from financial ratios from Amadeus—Bureau van Dijk database | See section 4.2 |
Minibond | Minibond dummy variable | Borsa Italiana website | Equal to 1 if the firm issued mini-bond, zero otherwise |
Tangible ratio | Tangible ratio is the ratio between the tangible fixed assets and the total assets | Amadeus—Bureau van Dijk database | |
EBITDA/Sales | The ratio between EBITDA and sales | Amadeus—Bureau van Dijk database | |
Asset-liability mismatch | The book value of equity over fixed assets ratio | Amadeus—Bureau van Dijk database | A level below 1 of the ratio indicates a mismatch |
Size | Natural log of Total Assets | Amadeus—Bureau van Dijk database | |
SME | SME dummy variable | Self-constructed | Equal to 1 if the firm employees are less than 250 and total asset less than € 43 million and sales lower than € 50 million, zero otherwise |
Small | Small dummy variable | Self-constructed | Equal to 1 if the firm employees are less than 50 and total asset and sales less than €10 million, zero otherwise |
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