**Hip Fractures and Arthroplasty**

[6] Modig J. The role of lumbar epidural anaesthesia as antithrombotic prophylaxis in total

[7] Davis FM, Laurenson VG, Gillespie WJ, et al. Leg blood flow during total hip replacement under spinal or general anaesthesia. Anaesthesia and Intensive Care. 1989;**17**:136

[8] Djelonah I, Lefevre G, Ozier Y, et al. Fat embolism in orthopedic surgery: Role of bone

[9] Frestein GS: Etiology and pathogenesis of rheumatoid arthritis. In: Kelly WN, Harris ED Jr, Ruddy S, et al. Textbook of Rheumatology. 5th ed. Philadelphia: WB Saunders; 1997.

[10] Carli F, Halliday D. Continuous epidural blockade arrests the postoperative decrease in muscle protein fractional synthetic rate in surgical patients. Anaesthesiology.

[11] Dyson A, Henderson AM, Chamlley D, et al. An assessment of postoperative oxygen therapy in patients with fractured neck of femur. Anaesthesia and Intensive Care

[12] Williams-Russo P, Sharrock NE, Mattis S, et al. Cognitive effects after epidural vs general anaesthesia in older adults: A randomized trial. Journal of the American Medical

[13] Moiniche S et al. A qualitative and quantitative systematic review of pre-emptive analgesia for postoperative pain relief: The role of timing of analgesia. Anesthesiology.

[14] Busoni P. Central or peripheral blocks? Techniques in Regional Anesthesia and Pain

[15] American Society of Anesthesiologist Task Force on Acute Pain Management. Practice guidelines for acute pain management in the perioperative setting: An updated report by the American Society of Anesthesiologist Task Force on acute pain management.

[16] Lunn TH, Husted H, Solgaard S, Kristensen BB, Otte KS, Kjersgaard AG, Gaarn-Lansen L, Kehlet H. Intraoperative local infiltration analgesia for early analgesia after total hip arthroplasty: A randomized, double-blind, placebo controlled trial. Regional Anesthesia

[17] Lunn TH, Kristensen BB, Gaarn-Lansen L, Husted H, Kehlet H. Post-anaesthesia care unit stay after total hip and knee arthroplasty under spinal anaesthesia. Acta Anaes-

hip replacement. Acta Chirurgica Scandinavica. 1991;**151**:1721

marrow fatty acid. Anesthesia and Analgesia. 1997;**85**:441

p. 851

1997;**86**:1033

64 Total Hip Replacement - An Overview

Medicine. 1988;**16**:405

Association. 1995;**274**:44

Management. 2002;**6**:95-98

Anesthesiology. 2012;**116**(2):248-273

and Pain Medicine. 2011;**36**:424-429

thesiologica Scandinavica. 2012;**56**:1139-1145

2002;**96**(3):526-527

**Chapter 5**

**Provisional chapter**

**Hip Fracture: Anatomy, Causes, and Consequences**

**Hip Fracture: Anatomy, Causes, and Consequences**

DOI: 10.5772/intechopen.75946

Fall-induced hip fracture is a major worldwide health problem among the elderly population. Nowadays, hip replacement surgery represents a big part of the orthopedic surgeons' workload and has associated remarkable clinical and social cost implications. Hip fractures have several complications including medical and surgical treatment. A significant number of biomechanical models have been introduced to study hip fracture risk. The purpose of proposing the biomechanical models for predicting the hip fracture risk is to introduce prevention and protection activities that may reduce the number of hip fractures. For accurate prediction of hip fracture risk, the fracture procedure and the parameters that affect the risk of hip fracture should be well studied. The objective of this study is to investigate in-depth the hip fracture anatomy, causes, and consequences.

**Keywords:** hip fracture causes, hip anatomy, fall, hip impact force, hip fracture

Low-trauma hip fracture has become a common health problem among the elderly all over the world [1–21], mainly due to the population aging and the prevalence of osteoporosis. Of all osteoporotic fractures, hip fracture has the highest morbidity and mortality rate [22]. Approximately 50% of patients have permanent functional disability greater than that before fracture [23, 24]. The incidence of hip fracture appears to be increasing in many countries [10], and the total number of hip fractures is estimated to be more than five million by 2050 [25]. Socioeconomic impacts of hip fracture are twofold. On the one hand, hip fracture increases the morbidity and mortality in the elderly [26–28]; on the other hand, it is a substantial source of healthcare expenditure [29, 30]. Therefore, there is an urgent need to accurately assess hip fracture risk and then develop preventive and protective measures. In this chapter, hip

> © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

distribution, and reproduction in any medium, provided the original work is properly cited.

Masoud Nasiri Sarvi

Masoud Nasiri Sarvi

**Abstract**

consequences

**1. Introduction**

Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.75946

#### **Hip Fracture: Anatomy, Causes, and Consequences Hip Fracture: Anatomy, Causes, and Consequences**

DOI: 10.5772/intechopen.75946

#### Masoud Nasiri Sarvi Masoud Nasiri Sarvi

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.75946

**Abstract**

Fall-induced hip fracture is a major worldwide health problem among the elderly population. Nowadays, hip replacement surgery represents a big part of the orthopedic surgeons' workload and has associated remarkable clinical and social cost implications. Hip fractures have several complications including medical and surgical treatment. A significant number of biomechanical models have been introduced to study hip fracture risk. The purpose of proposing the biomechanical models for predicting the hip fracture risk is to introduce prevention and protection activities that may reduce the number of hip fractures. For accurate prediction of hip fracture risk, the fracture procedure and the parameters that affect the risk of hip fracture should be well studied. The objective of this study is to investigate in-depth the hip fracture anatomy, causes, and consequences.

**Keywords:** hip fracture causes, hip anatomy, fall, hip impact force, hip fracture consequences

### **1. Introduction**

Low-trauma hip fracture has become a common health problem among the elderly all over the world [1–21], mainly due to the population aging and the prevalence of osteoporosis. Of all osteoporotic fractures, hip fracture has the highest morbidity and mortality rate [22]. Approximately 50% of patients have permanent functional disability greater than that before fracture [23, 24]. The incidence of hip fracture appears to be increasing in many countries [10], and the total number of hip fractures is estimated to be more than five million by 2050 [25]. Socioeconomic impacts of hip fracture are twofold. On the one hand, hip fracture increases the morbidity and mortality in the elderly [26–28]; on the other hand, it is a substantial source of healthcare expenditure [29, 30]. Therefore, there is an urgent need to accurately assess hip fracture risk and then develop preventive and protective measures. In this chapter, hip

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

anatomy is first reviewed, and hip fractures are classified by anatomic location. Then, prevalence of hip fracture is presented, followed by a description of the significance of accurately assessing hip fracture risk.

More than 90% of all hip fractures occur in falls [36] as the femur is subjected to a high-level impact force. As shown in **Figure 1(b)**, in a sideways fall, the greater trochanter and the femoral head are subjected to the impact and the joint force, respectively, from the ground and the acetabulum. The forces produce a moment at the intersection of the neck-shaft axes. Muscles that are attached to the femur also produce forces during the fall. As it is shown in **Figure 1(b)**, the applied forces in a fall are mainly on the proximal femur, and it may explain why the majority of fall-induced hip fractures occur at the proximal femur [37]. A hip fracture refers to any fracture of the proximal femur down to a level of approximately 5 cm below the lower border of the lesser trochanter [38]. The extent of the break depends on the forces that are involved.

Hip Fracture: Anatomy, Causes, and Consequences http://dx.doi.org/10.5772/intechopen.75946 69

Hip fracture is usually caused by an applied force that exceeds the strength of the femur bone [39]. Therefore, any situation that either induces a high level of force on the femur bone or

The main cause of hip fracture is falling (90–92%) [36, 40–42], in particular falling in sideways direction (63–69% in fall-related fractures) [8, 43], as it induces a high level of force on the femur. Parameters that increase the risk of fall and apply a high level of force on the femur,

• Impaired neuromuscular coordination and neurological diseases (e.g., hemiplegia, Parkin-

In the elderly, most fractures occur after a low-trauma fall, which would not cause any severe injury to a healthy individual. Therefore, low bone strength is another main cause of hip fracture. Osteoporosis as a progressive bone disease, which is characterized by decreases in bone mass and density, has been identified as one of the main contributors of hip fracture [46, 47]. Osteoporosis advances when bone resorption exceeds bone formation, and therefore it is more common among the elderly [48]. Approximately three to four out of ten women over the age of 50, and one in eight men, suffer osteoporotic fracture in their lifetime [49].

Apart from osteoporosis, several other causes may reduce the strength of the bone such as bone cancer and medical side effects [38]. Other factors associated with reduction in bone

decreases the bone strength should be considered as a hip fracture cause.

• Inability to effectively use the arms to reduce the energy of the fall

• Reduced soft tissue padding over the hip [44, 45]

**3. Hip fracture causes**

especially in the elderly, are:

• Impaired muscle reactions

• Slow reflex response

• Impaired vision

son's disease)

strength include [38]:

• Mental impairment and confusion


**7. Implementing accelerated updates for the C(Z) algorithm**

We build on the relationships identified in Section 4 to apply them to the more general C(Z) algorithm. By the implications described earlier, our general updates also apply directly to the C(W) and C(Y) algorithms by respectively replacing Z with W and Y (hence Znext with Wnext and Ynext) and replacing MinCostC(∙) by MinCost(∙) and MinCostB(∙).


[35] Putcha GV, Bejjani BA, Bleoo S, Booker JK, Carey JC, Carson N, et al. A multicenter study of the frequency and distribution of GJB2 and GJB6 mutations in a large North

dromic and Acquired Causes. AJNR Am J Neuroradiol. 2012;33:399-406.

287432, 5 pages, 2012. DOI: 10.1155/2012/287432.

rRNA A1555G mutation. Gene. 2007;393:11-19.

noglycosides. American J Human Genet. 1998;62:27-35.

9th edition. New York. McGraw-Hill; 1996. pp.1103-1221.

Seattle. GeneReviews®; 2014; 1993-2015.

ed. New York: Oxford University Press; 2004.

American cohort. Genet. Med. 2007;9:413-426.

2012. ISBN: 978-953-51-0366-0.

1993;4:289-294.

82 Update On Hearing Loss

2007;71: 379-391.

2003;24:418-426.

[50] Yariz KO, Duman D, Seco CZ, et al. Mutations in OTOGL, encoding the inner ear protein otogelin-like, cause moderate sensorineural hearing loss. Am J Hum Genet.

[51] Zheng J, Miller KK, Yang T, et al. Carcinoembryonic antigen-related cell adhesion molecule 16 interacts with alpha-tectorin and is mutated in autosomal dominant

[52] Yan D, Zhu Y, Walsh T, et al. Mutation of the ATP-gated P2X2 receptor leads to pro‐ gressive hearing loss and increased susceptibility to noise. Proc Natl Acad Sci.

[53] Schraders M, Haas SA, Weegerink NJD, et al. Next-generation sequencing identifies mutations of SMPX, which encodes the small muscle protein, X-linked, as a cause of

[54] Pierce SB, Walsh T, Chisholm KM, et al. Mutations in the DBP-deficiency protein HSD17B4 cause ovarian dysgenesis, hearing loss, and ataxia of Perrault syndrome.

[55] Pierce SB, Chisholm KM, Lynch ED, et al. Mutations in mitochondrial histidyl tRNA synthetase HARS2 cause ovarian dysgenesis and sensorineural hearing loss of Per‐

[56] Sirmaci A, Walsh T, Akay H, et al. MASP1 mutations in patients with facial, umbili‐ cal, coccygeal, and auditory findings of Carnevale, Malpuech, OSA, and Michels syn‐

[57] Klein CJ, Botuyan MV, Wu Y, et al. Mutations in DNMT1 cause hereditary sensory

[58] Levenson D. New testing guidelines for hearing loss support next-generation se‐

[59] Anne B, Skvorak G, Cynthia C, Morton. Cytogenetics and Cochlear Expressed Se‐ quence Tags (ESTs) for Identification of Genes Involved in Hearing and Deafness. In: Keats, Bronya J.B., Fay, Richard R. editors. Genetics of Auditory Disorders. Springer

[60] Helga VT, Shelley S. Hereditary Hearing Loss and Its Syndromes. Chapter 5: Syn‐ drome diagnosis and investigation in the hearing impaired patient. Oxford Universi‐

[61] Ponnuraj KT. Cytogenetic Techniques in Diagnosing Genetic Disorders, Advances in the Study of Genetic Disorders. In: Dr. Kenji Ikehara Editor. InTech. 2011; ISBN:

[62] Wieacker P, Steinhard J. The Prenatal Diagnosis of Genetic Diseases. Deutsches Arz‐

teblatt Inter. 2010;107:857-862. DOI: 10.3238/arztebl.2010.0857.

Handbook of Auditory Research. 2002; pp. 92-120. ISBN: 978-0-387-21853-3

neuropathy with dementia and hearing loss. Nat Genet. 2011;43:595-600.

quencing. Am. J. Med. Genet. 2014;164:7-8. DOI: 10.1002/ajmg.a.36643

progressive hearing impairment. Am J Hum Genet. 2011;88:628-634.

rault syndrome. Proc Natl Acad Sci. 2011;108:6543-6548.

dromes. Am J Hum Genet. 2010;87:679-686.

hearing loss (DFNA4) Proc Natl Acad Sci. 2011;108:4218-4223.

2012;91:872-882.

84 Update On Hearing Loss

2013;110:2228-2233.

ty Press. 2013; p89.

978-953-307-305-7, DOI: 10.5772/17481.

Am J Hum Genet. 2010;87:282-288.

Engineering News. 2014;92. pp. 12-17. http://cen.acs.org/articles/92/i14/Sound-Sci‐ ence.html.

[91] Rivolta MN. Stem cells in the inner ear: Advancing towards a new therapy for hear‐ ing impairment. In: Martini A, Stephens D, Read AP. Genes, Hearing, and Deafness: From Molecular Biology to Clinical Practice. CRC Press; 2007. p. 279.

[77] Raphael Y, Frisancho JC, Roessler BJ. Adenoviral-mediated gene transfer into guinea

[78] Fire A, Xu S, Montgomery MK, Kostas SA, Driver SE, Mello CC. Potent and specific genetic interference by double-stranded RNA in,*Caenorhabditis elegans*. Nature.

[79] Maeda Y, Fukushima K, Nishizaki K Smith RJ. *In vitro* and *in vivo* suppression of GJB2 expression by RNA interference. Hum Mol Genet. 2005;14:1641-1650.

[80] Hildebrand MS, Newton SS, Gubbels SP, Sheffield AM, Kochhar A, De Silva MG, Dahl HH, Rose SD, Behlke MA, Smith RJ. Advances in Molecular and Cellular Thera‐ pies for Hearing Loss. Molecular Therapy. 2007;16:224-236. DOI: 10.1038/sj.mt.

[81] Kanzaki S, Beyer L, Karolyi IJ, Dolan DF, Fang Q, Probst FJ, et al. Transgene correc‐ tion maintains normal cochlear structure and function in 6-month-old Myo15a mu‐

[82] Staecker H, Kopke R, Malgrange B, et al. NT-3 and/or BDNF therapy prevents loss of auditory neurons following loss of hair cells. Neuroreport. 1996;7:889-894.

[83] Pickles JO, Harter C, Rebillard G. Fibroblast growth factor receptor expression in out‐

[84] Stover T, Yagi M, Raphael Y. Transduction of the contralateral ear after adenovirus-

[85] Kawamoto K, Yagi M, Stover T, et al. Hearing and hair cells are protected by adeno‐

[86] Nakaizumi T, Kawamoto K, Minoda R, Raphael Y. Adenovirus-mediated expression of brain-derived neurotrophic factor protects spiral ganglion neurons from ototoxic

[87] Bermingham NA, Hassan BA, Price SD, Vollrath MA, Ben-Arie N, Eatock RA, et al. Math1: An essential gene for the generation of inner ear hair cells. Sci. 1999;284:

[88] Kawamoto K, Ishimoto S, Minoda R, Brough DE Raphael Y. Math1 gene transfer gen‐ erates new cochlear hair cells in mature guinea pigs *in vivo*. J Neurosci. 2003;23:

[89] Izumikawa M, Minoda R, Kawamoto K, Abrashkin KA, Swiderski DL, Dolan DF, et al. Auditory hair cell replacement and hearing improvement by Atoh1 gene therapy

[90] Jarvis LM. Sound Science. Emerging technology and a wide-open market are spur‐ ring more companies to pursue drugs to treat or prevent hearing loss. Chemical &

viral gene therapy with TGF-β1 and GDNF. Mol. Ther. 2003;7:484-492.

er hair cells of rat cochlea. Neuroreport. 1998;9:4093-4095.

mediated cochlear gene transfer. Gene Ther. 2000;7:377-383.

damage. Audiol. Neurootol. 2004;9:135-143.

in deaf mammals. Nat Med. 2005;11:271-276.

pig cochlear cells in vivo. Neurosci Lett. 1996;207:137-141.

1998;391:806-811.

86 Update On Hearing Loss

6300351.

1837-1841.

4395-4400.

tant mice. Hear Res. 2006;214:37-44.

[116] Bauer PW, Geers AE, Brenner C, Moog JS, Smith RJH. The effect of GJB2 allele var‐ iants on performance after cochlear implantation. Laryngoscope. 2003;113:2135-41.

[103] Matsuoka AJ, Kondo T, Miyamoto RT, Hashino E. Enhanced survival of bone-mar‐ row-derived pluripotent stem cells in an animal model of auditory neuropathy. The

[104] Hu Z, Ulfendahl M, Olivius NP. Central migration of neuronal tissue and embryonic stem cells following transplantation along the adult auditory nerve. Brain Res.

[105] Ulfendahl M. Tissue transplantation into the inner ear. In: Martini A, Stephens D, Read A P. Genes, Hearing, and Deafness: From Molecular Biology to Clinical Prac‐

[106] Ito J, Murata M, Kawaguchi S. Regeneration and recovery of the hearing function of the central auditory pathway by transplants of embryonic brain tissue in adult rats.

[107] Lang H, Ebihara Y, Schmiedt RA, Minamiguchi H, Zhou D, Smythe N, et al. Contri‐ bution of bone marrow hematopoietic stem cells to adult mouse inner ear: mesenchy‐

[108] Matsuoka AJ, Kondo T, Miyamoto RT, Hashino E. *In vivo* and *in vitro* characteriza‐ tion of bone marrow-derived stem cells in the cochlea. Laryngoscope.

[109] Chen W, Cacciabue-Rivolta DI, Moore HD, Rivolta MN. The human fetal cochlea can be a source for auditory progenitors/stem cells isolation. Hear Res. 2007;233:23-29.

[110] Nishimura K, Nakagawa T, Ito J. Potential of Pluripotent Stem Cells for the Replace‐ ment of Inner Ears, Embryonic Stem Cells - Recent Advances in Pluripotent Stem Cell-Based Regenerative Medicine, Prof. Craig Atwood editor. InTech. 2011; ISBN:

[111] Revoltella RP, Papini S, Rosellini A, et al. Cochlear repair by transplantation of hu‐ man cord blood CD133+ cells to nod-scid mice made deaf with kanamycin and noise.

[112] Da Costa V, O'Grady G, Jackson L, Kaylie D, Raynor E. Improvements in sensorineu‐ ral hearing loss after cord blood transplant in patients with mucopolysaccharidosis. Arch Otolaryngol Head Neck Surg. 2012;138:1071-6. DOI: 10.1001/jamaoto.2013.597.

[113] Available from: https://clinicaltrials.gov/show/NCT01343394 [Accessed: 2015-02-01].

[114] Forge A, Li L, Corwin JT, Nevill G. Ultrastructural evidence for hair cell regeneration

[115] Warchol ME, Lambert PR, Goldstein BJ, Forge A, Corwin JT. Regenerative prolifera‐ tion in inner ear sensory epithelia from adult guinea pigs and humans. Sci.

mal cells and fibrocytes. J Comp Neurol. 2006;496: 187-201.

Laryngoscope*.* 2007;117:1629-1635.

tice. CRC Press. 2007. p. 294.

Exp Neurol. 2001;169:30-5.

2006;116:1363-1367.

978-953-307-198-5, DOI: 10.5772/10541.

in the mammalian inner ear. Sci. 1993;259:1616-1619.

Cell Transplant. 2008;17:665-78.

1993;259:1619-1622.

2004;1026:68-73.

88 Update On Hearing Loss

### **Hearing Loss in Infectious and Contagious Diseases**

Luiz Alberto Alves Mota, Paula Cristina Alves Leitão, Paulo Marcelo Freitas de Barros and Ana Maria dos Anjos Carneiro Leão

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/61818

#### **Abstract**

Hearing loss can occur for various reasons, whether it is of a genetic, congenital or ac‐ quired character. Infectious diseases stand out among those causing this type of deficien‐ cy and account for approximately 25% of all cases of profound hearing loss. Of these, one-fifth are due to congenital causes. As to classifying hearing loss, this can be done ac‐ cording to where this is in the hearing system, to whether the loss is unilateral or bilater‐ al, and to its intensity or degree. Regarding where the hearing system is affected, hearing loss can be about transmission (or conduction), perception (sensorineural), or mixed. Hearing losses arising from any affection of the outer and middle ear are called transmis‐ sion or conductive losses. Sensorineural losses occur due to lesions on the hair cells of the cochlear organ of Corti (inner ear) and/or of the cochlear nerve. When there is concomi‐ tant conductive and sensorineural affection, the loss is classified as mixed. Hearing loss can interfere in the lives of affected individuals, since besides affecting communication, it can influence the quality of life, when the loss leads to feelings of sadness and anxiety, or even to social isolation. In children, it can moreover represent consequences for develop‐ ment. Thus, appropriate treatment and/or monitoring of infectious diseases is important, the purpose of which is to see to it that hearing loss is prevented or diagnosed early.

**Keywords:** Hearing loss, infectious diseases, etiology

#### **1. Introduction**

The hearing process begins when sound waves enter the outer ear and travel along the ear canal to the eardrum, causing it to vibrate. These vibrations are transmitted to the ossicles of the middle ear, which cause the sound vibration to be amplified before transmission to the inner ear. The inner ear has a part called the cochlea, which is filled with liquid and contains hair cells.[1]

© 2015 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The frequencies and intensities of the sound determine which hair cells will move. This causes electrical impulses to be generated and sent through the auditory pathways to the brain so that it may process the information. These electrical impulses are the codes that the brain can process and, on understanding them, assigns them various specific meanings.[1]

Hearing losses can be classified according to the location of the portion of the hearing system affected, to whether the loss is unilateral or bilateral, and to its intensity or degree. The location of the portion affected of hearing loss has to do with transmission (or conduction), perception (sensorineural), or a mixture of these (mixed). Sensorineural losses arising from some affection of the outer and middle ear are called transmission or conductive losses. Sensorineural losses result from lesions on the hair cells of the cochlear organ of Corti (inner ear) and/or of the cochlear nerve. When there are concomitant conductive and sensorineural affections, the hearing loss is classified as mixed.[2]

Hearing loss can occur due to a genetic, congenital, or acquired cause.[3] Among the acquired causes, many could sometimes be avoided, e.g., infections that occur during pregnancy, meningitis, and even due to using ototoxic medication.[4]

### **2. Epidemiology**

Deafness is a global problem that affects individuals, families, societies, and governments. According to the World Health Organization (WHO), deafness affects between 1 and 4 people per 1,000 individuals, and there has been a considerable increase in poor countries. In 2005, for example, about 278 million people had degrees of hearing loss between moderate and profound, and 80% of them live in poor and developing countries.[5] Prevalence greater than 1 per 1000, however, indicates a serious public health problem that needs urgent attention.[6]

Infectious diseases are the leading cause of hearing loss and produce about 25% of profound losses. Of these, the causes of one-fifth are congenital.[7] The main infections include diseases such as rubella, cytomegalovirus, and measles.[7]

In the newborn, congenital infections are an important cause of hearing loss, which may have implications for the development of the child.[8]

#### **3. Pathogenesis**

The mechanisms that lead to the onset of viral hearing loss may include infections of the upper airways, may progress to subsequent involvement of the middle ear, and may occur with conductive hearing loss.[3]

Moreover, viral invasion of the inner ear can occur.[3] The viruses that can damage the inner ear may do so at different stages of the life cycle: during intrauterine life, childhood, adoles‐ cence, or adulthood. The pathological changes that predominate in the basal cochlea include degeneration of the organ of Corti, atrophy of the stria vascularis, displacement and distortion of the tectorial membrane, and degeneration of the saccule. The utricle and semicircular canals tend to be preserved.[9]

### **4. Main infectious and contagious diseases related to loss of hearing**

#### **4.1. Infections by virus**

The frequencies and intensities of the sound determine which hair cells will move. This causes electrical impulses to be generated and sent through the auditory pathways to the brain so that it may process the information. These electrical impulses are the codes that the brain can

Hearing losses can be classified according to the location of the portion of the hearing system affected, to whether the loss is unilateral or bilateral, and to its intensity or degree. The location of the portion affected of hearing loss has to do with transmission (or conduction), perception (sensorineural), or a mixture of these (mixed). Sensorineural losses arising from some affection of the outer and middle ear are called transmission or conductive losses. Sensorineural losses result from lesions on the hair cells of the cochlear organ of Corti (inner ear) and/or of the cochlear nerve. When there are concomitant conductive and sensorineural affections, the

Hearing loss can occur due to a genetic, congenital, or acquired cause.[3] Among the acquired causes, many could sometimes be avoided, e.g., infections that occur during pregnancy,

Deafness is a global problem that affects individuals, families, societies, and governments. According to the World Health Organization (WHO), deafness affects between 1 and 4 people per 1,000 individuals, and there has been a considerable increase in poor countries. In 2005, for example, about 278 million people had degrees of hearing loss between moderate and profound, and 80% of them live in poor and developing countries.[5] Prevalence greater than 1 per 1000, however, indicates a serious public health problem that needs urgent attention.[6]

Infectious diseases are the leading cause of hearing loss and produce about 25% of profound losses. Of these, the causes of one-fifth are congenital.[7] The main infections include diseases

In the newborn, congenital infections are an important cause of hearing loss, which may have

The mechanisms that lead to the onset of viral hearing loss may include infections of the upper airways, may progress to subsequent involvement of the middle ear, and may occur with

Moreover, viral invasion of the inner ear can occur.[3] The viruses that can damage the inner ear may do so at different stages of the life cycle: during intrauterine life, childhood, adoles‐ cence, or adulthood. The pathological changes that predominate in the basal cochlea include

process and, on understanding them, assigns them various specific meanings.[1]

hearing loss is classified as mixed.[2]

**2. Epidemiology**

92 Update On Hearing Loss

**3. Pathogenesis**

conductive hearing loss.[3]

meningitis, and even due to using ototoxic medication.[4]

such as rubella, cytomegalovirus, and measles.[7]

implications for the development of the child.[8]

#### *4.1.1. Epidemic parotiditis*

Epidemic parotiditis or mumps is an acute systemic and contagious viral infection. A *Paramyxovirus*, with an RNA genome, is involved.[10]

The most typical clinical manifestations are sialadenitis, epididymo-orchitis, pancreatitis, meningitis, and hearing loss. Sensorineural hearing loss occurs in up to 5/10,000 cases and may appear some days or weeks after the parotiditis.[11]

Deafness is usually sudden, profound, associated with or without nausea, vomiting, dizziness, and tinnitus.[9] Hearing loss, which is unilateral in 80% of cases, is more common for high frequencies of sound and may present reduced caloric responses to the vestibular test.[11]

There may be atrophy of the organ of Corti and of the stria vascularis, with minimal effect on the vestibular system. Also observed are endolymphatic hydrops and obliteration of the endolymphatic duct.[11]

#### *4.1.2. Infection by cytomegalovirus*

Cytomegalovirus (CMV), which belongs to the herpesvirus family, is an enveloped virus that has the largest genome among the viruses that infect animal species. In immunocompetent individuals, it is generally responsible for asymptomatic infections.[12]

The highest incidence of the primary infection occurs in two peak periods: the first is in childhood, with early acquisition as a result of perinatal infection, and the second is in adolescence, through sexual transmission or by kissing.[12] It infects up to 70% of children who spend the day in kindergartens, and about 1–2% of infants are infected with CMV.[13]

In the congenital form, clinical manifestations range from the unapparent to the severe and widespread. Cytomegalic inclusion disease develops in about 5% of the infected fetuses. The most common manifestations at presentation are petechiae, hepatosplenomegaly, and jaundice. The occurrence of microcephaly with or without intracranial calcifications delayed intrauterine growth, and prematurity in 30–50% of cases is observed.[12] Deafness occurs in 20–65% of infants with this disease, which is typically bilateral.[13]

In patients with hearing loss, a consistent pattern follows, and this can develop over a period of years. Among asymptomatic patients, the rate of hearing loss of such children ranges from 7% to 13% and should therefore be considered in patients with nonsyndromic and nongenetic hearing loss.[13]

#### *4.1.3. Rubella*

This is a disease with an acute rash caused by an RNA virus of the genus *Rubivírus* and the Togaviridae family, which is highly contagious and mainly affects children.[13]

The clinical state is characterized by a maculopapular and diffuse pinpoint rash, starting on the face, scalp, and neck, later spreading to the trunk and limbs.[13]

The infection acquired after birth usually causes a mild or even subclinical disease. The main symptoms of this form are retroauricular, cervical and suboccipital lymphadenopathy, rash, and fever. Complications are uncommon.[10]

Maternal infection during early pregnancy can lead to infection of the fetus, resulting in congenital rubella.[10] Congenital rubella syndrome (Gregg's syndrome) affects most organ systems, causing cataracts, microphthalmia, heart defects, skin rash, retardation of growth, and hearing loss. In general, hearing loss affects about 50% of individuals with the disease and is normally severe to profound. Auditory manifestations may occur months to years after the initial infection.[11]

#### *4.1.4. Measles*

Measles is an acutely infectious viral disease that is potentially serious, transmittable, and extremely contagious. Its etiologic agent is an RNA virus of the genus *Morbilliviru*s, family Paramyxoviridae.[13]

Among the clinical manifestations, it is characterized by high fever, above 38.5°C, a widespread maculopapular rash, cough, coryza, conjunctivitis, and Koplik spots (small white spots on the oral mucosa, prior to the rash).[13]

It may cause severe degeneration of the organ of Corti, the stria vascularis, cochlear neurons, and vestibular damage. Inflammation, fibrous deposit, and ossification in the basal turn of the cochlea may also be present. Hearing loss tends to be asymmetrical, bilateral, and severe. Vestibular abnormalities are not rare.[11]

#### *4.1.5. Viral meningitis*

Viral meningitis is characterized by a clinical state of neurological changes, which usually develops benignly. Approximately 85% of cases are due to the group of Enteroviruses, among which the poliovirus, echovirus, and coxsackievirus stand out. Other less common groups are arboviruses, herpes simplex virus, and varicella, mumps, and measles viruses.[14]

It occurs most frequently in children over two years old and can lead to sensorineural hearing loss.[3]

#### *4.1.6. Herpes simplex*

Herpes simplex has been considered one of the most common viral contamination agents in humans and is subdivided into two groups: type 1 and type 2.[15]

Infections caused by herpes simplex type 1 usually affect areas such as the lips, mouth, intraoral region, nose, eyes, while infections caused by herpes simplex type 2 are mainly found in the genital and surrounding areas. Trigger factors include fever, exposure to cold temperatures or ultraviolet rays, skin or mucous abrasions, emotional stress, and nerve injury. In the case of occurrence in newborns, the onset of infection can be at different periods: prenatal (congenital infection), perinatal (infection through the birth canal), or postnatal (infection through contact with infected individuals).[15]

The virus of the herpes group is regarded as causing sensorineural loss. In pregnancy, it can also cause spontaneous miscarriages, still births, and congenital defects.[15]

#### *4.1.7. Infectious mononucleosis and other viral agents*

Infectious mononucleosis (IM) is caused by the Epstein–Barr virus (EBV), characterized by fever, pharyngitis, lymphadenopathy, and atypical lymphocytosis. EBV is a member of the Herpesviridae family.

One of the main viral agents associated with sensorineural hearing loss in adulthood is the IM virus. Other agents that can also often affect this age-group and are related to hearing loss are adenovirus, enterovirus, influenza, and parainfluenza.[3]

#### **4.2. Infections by bacteria**

*4.1.3. Rubella*

94 Update On Hearing Loss

initial infection.[11]

Paramyxoviridae.[13]

*4.1.5. Viral meningitis*

*4.1.6. Herpes simplex*

loss.[3]

oral mucosa, prior to the rash).[13]

Vestibular abnormalities are not rare.[11]

*4.1.4. Measles*

This is a disease with an acute rash caused by an RNA virus of the genus *Rubivírus* and the

The clinical state is characterized by a maculopapular and diffuse pinpoint rash, starting on

The infection acquired after birth usually causes a mild or even subclinical disease. The main symptoms of this form are retroauricular, cervical and suboccipital lymphadenopathy, rash,

Maternal infection during early pregnancy can lead to infection of the fetus, resulting in congenital rubella.[10] Congenital rubella syndrome (Gregg's syndrome) affects most organ systems, causing cataracts, microphthalmia, heart defects, skin rash, retardation of growth, and hearing loss. In general, hearing loss affects about 50% of individuals with the disease and is normally severe to profound. Auditory manifestations may occur months to years after the

Measles is an acutely infectious viral disease that is potentially serious, transmittable, and extremely contagious. Its etiologic agent is an RNA virus of the genus *Morbilliviru*s, family

Among the clinical manifestations, it is characterized by high fever, above 38.5°C, a widespread maculopapular rash, cough, coryza, conjunctivitis, and Koplik spots (small white spots on the

It may cause severe degeneration of the organ of Corti, the stria vascularis, cochlear neurons, and vestibular damage. Inflammation, fibrous deposit, and ossification in the basal turn of the cochlea may also be present. Hearing loss tends to be asymmetrical, bilateral, and severe.

Viral meningitis is characterized by a clinical state of neurological changes, which usually develops benignly. Approximately 85% of cases are due to the group of Enteroviruses, among which the poliovirus, echovirus, and coxsackievirus stand out. Other less common groups are

It occurs most frequently in children over two years old and can lead to sensorineural hearing

Herpes simplex has been considered one of the most common viral contamination agents in

arboviruses, herpes simplex virus, and varicella, mumps, and measles viruses.[14]

humans and is subdivided into two groups: type 1 and type 2.[15]

Togaviridae family, which is highly contagious and mainly affects children.[13]

the face, scalp, and neck, later spreading to the trunk and limbs.[13]

and fever. Complications are uncommon.[10]

#### *4.2.1. Bacterial meningitis*

Meningitis is frequently associated with a high mortality rate. A large portion may still present sequelae of the disease, among which is hearing loss. This disease is held to be among the main ones responsible for postnatal acquired hearing impairment.[16]

Among the mechanisms elucidated, as being responsible for hearing damage, is the direct invasion of the bacteria into the cochlea and labyrinth, lesion of cranial nerve VIII, by toxins, and blockage of small vessels and ototoxic action of the antibiotics used. Regarding the degree of loss, a high percentage of profound hearing loss (66.95%) has been evidenced. However, hearing loss of all degrees (mild to anacusis) was observed.[16]

In a study of 124 children recruited from 21 hospitals in England and South Wales, aged between 4 weeks and 16 years old, with a recent diagnosis of bacterial meningitis, 92 (74%) had meningococcal and 18 (15%) had pneumococcal meningitis. All cases showed obvious hearing loss in the first assessment. Three children had permanent sensorineural hearing loss. Thirteen children (10.5%) had reversible loss, nine of which were resolved within 48 hours of diagnosis.[17]

The impact on the development of the child after meningitis can be devastating. In the postmeningitis period, a possibility of rehabilitation for patients with severe and profound sensorineural loss is a cochlear implant.[18]

In cases of postmeningitis hearing loss, it is particularly important to do the implant as early as possible due to the intracochlear ossification that may occur, thus preventing the placement of electrodes in the lumen of the cochlea.[19]

#### *4.2.2. Syphilis*

During the decade of 2003–2012, the diagnosis of primary syphilis increased 61% in men in England, while in contrast, this diagnosis in women decreased by 16%.[20] In the 2004 Sentinela Parturiente (Mother in Labour Sentinel) Study of the Ministry of Health in Brazil, the preva‐ lence of syphilis in pregnant women was 1.6%, about four times higher than HIV infection in the same group, the estimate being that a total of 48,425 pregnant women were infected in that year. Between 2005 and June 2012, 57,700 cases of syphilis in pregnant women were registered in SINAN (the Brazilian statutory body for notifiable diseases), most of which occurred in the Southeast and Northeast regions.[21]

Syphilis is an infectious disease caused by a bacterium, *Treponema pallidum*, which is predom‐ inantly transmitted sexually. If left untreated, the disease can progress to stages that adversely affect the skin and internal organs such as the heart, liver, and nervous system central.[18] Hearing loss can occur because of syphilis, but currently this is rare, and this being most often in the tertiary phase.[3]

Otosyphilis may be present in the form of a sudden and fluctuating sensorineural loss, episodic vertigo, with progressive unilateral or bilateral loss.[11]

Acquired syphilis may also affect the inner ear, simulating Ménière's disease. Hearing loss can progress rapidly progressive, initially with good discrimination; tinnitus and vestibular symptoms disappear to the extent that the destruction of the labyrinth is completed.[9]

Congenital syphilis is due to the hematogenous spread of *Treponema pallidum* of pregnant women who have not been treated or inadequately treated for their unborn child, via the placenta. Transmission can occur at any stage of pregnancy and in any stage of the disease.[22]

Congenital syphilis can cause severe deafness and separately affect both ears. Manifestation occurs when a child is around two years old or between 8 and 20 years old.[9]

#### **4.3. Protozoan infections**

#### *4.3.1. Toxoplasmosis*

Toxoplasmosis is caused by infection with the obligate intracellular parasite *Toxoplasma gondii*. Both in its acute and in its chronic form, it is related to the appearance of a clinically evident disease, including lymphadenopathy, encephalitis, myocarditis, and pneumonitis.[10]

In immunocompetent individuals, acute toxoplasmosis is habitually asymptomatic and goes unnoticed in 80–90% of adults and children with acquired infection. In the congenital form, the infection of the placenta determines the hematogenous infection of the fetus. The propor‐ tion of fetuses that are infected increases as pregnancy progresses, but the severity of the infection declines.[10]

*Toxoplasma gondii* has been associated with lesion of the auditory pathways with a demon‐ stration of calcium deposits (similar to the calcifications found in the brains of children with congenital toxoplasmosis) in the spiral ligament and the cochlea. A hearing deficit has been reported in about 20% of cases of congenital toxoplasmosis.[23]

### **5. Final remarks**

In cases of postmeningitis hearing loss, it is particularly important to do the implant as early as possible due to the intracochlear ossification that may occur, thus preventing the placement

During the decade of 2003–2012, the diagnosis of primary syphilis increased 61% in men in England, while in contrast, this diagnosis in women decreased by 16%.[20] In the 2004 Sentinela Parturiente (Mother in Labour Sentinel) Study of the Ministry of Health in Brazil, the preva‐ lence of syphilis in pregnant women was 1.6%, about four times higher than HIV infection in the same group, the estimate being that a total of 48,425 pregnant women were infected in that year. Between 2005 and June 2012, 57,700 cases of syphilis in pregnant women were registered in SINAN (the Brazilian statutory body for notifiable diseases), most of which occurred in the

Syphilis is an infectious disease caused by a bacterium, *Treponema pallidum*, which is predom‐ inantly transmitted sexually. If left untreated, the disease can progress to stages that adversely affect the skin and internal organs such as the heart, liver, and nervous system central.[18] Hearing loss can occur because of syphilis, but currently this is rare, and this being most often

Otosyphilis may be present in the form of a sudden and fluctuating sensorineural loss, episodic

Acquired syphilis may also affect the inner ear, simulating Ménière's disease. Hearing loss can progress rapidly progressive, initially with good discrimination; tinnitus and vestibular symptoms disappear to the extent that the destruction of the labyrinth is completed.[9]

Congenital syphilis is due to the hematogenous spread of *Treponema pallidum* of pregnant women who have not been treated or inadequately treated for their unborn child, via the placenta. Transmission can occur at any stage of pregnancy and in any stage of the disease.[22] Congenital syphilis can cause severe deafness and separately affect both ears. Manifestation

Toxoplasmosis is caused by infection with the obligate intracellular parasite *Toxoplasma gondii*. Both in its acute and in its chronic form, it is related to the appearance of a clinically evident disease, including lymphadenopathy, encephalitis, myocarditis, and pneumonitis.[10] In immunocompetent individuals, acute toxoplasmosis is habitually asymptomatic and goes unnoticed in 80–90% of adults and children with acquired infection. In the congenital form, the infection of the placenta determines the hematogenous infection of the fetus. The propor‐ tion of fetuses that are infected increases as pregnancy progresses, but the severity of the

occurs when a child is around two years old or between 8 and 20 years old.[9]

of electrodes in the lumen of the cochlea.[19]

Southeast and Northeast regions.[21]

vertigo, with progressive unilateral or bilateral loss.[11]

in the tertiary phase.[3]

**4.3. Protozoan infections**

*4.3.1. Toxoplasmosis*

infection declines.[10]

*4.2.2. Syphilis*

96 Update On Hearing Loss

Hearing loss can interfere with the life of affected individuals because in addition to affecting communication, this can influence the quality of life, on expressing feelings such as sadness and anxiety, or can even lead to social isolation. In infancy, hearing loss can still represent consequences for development.

Thus, proper treatment and/or monitoring of infectious diseases for the purpose of establishing the prevention or early diagnosis of hearing loss is important. With regard to congenital infections, public measures that encourage primary prevention and early identification of these affections in newborns are needed. Therefore, hearing health will depend on epidemiological studies of each location and on a perfect integration between health and education authorities working in an integrated way with all other sectors of society.

### **Author details**

Luiz Alberto Alves Mota1\*, Paula Cristina Alves Leitão2 , Paulo Marcelo Freitas de Barros3 and Ana Maria dos Anjos Carneiro Leão4

\*Address all correspondence to<EMAIL_ADDRESS>
1 Faculty of Medical Sciences, Universidade de Pernambuco, Brazil

2 Faculty of Medical Sciences, Universidade de Pernambuco, Recife/PE, Brazil

3 Universidade Católica de Pernambuco, Brazil

4 Department of Animal Morphology and Physiology, Universidade Federal Rural de Pernambuco, Brazil

### **References**

[1] Instituto Brasileiro do sono. Available at: http://www.institutobrasileirodoso‐ no.com.br/. Accessed on 16 November 2014.

[18] Bevilacqua MC, Moret ALM, Costa Filho OA, Nascimento LT, Banhara MR. Cochlear implant in deaf children due to meningitis. Rev Bras Otorhinolaryngol. 2003; 69(6): 760–4.

[2] Vieira ABC, Macedo LR, Gonçalves DU. O diagnóstico da perda auditiva na infância.

[3] Vieira ABC, Mancini P, Goncalves DU. Infectious diseases and hearing loss. Rev Med

[4] Pereira T, Costa KC, Pomilio MCA, Costa SMS, Rodrigues GRI, Sartorato EL. Investi‐ gação etiológica da deficiência auditiva em neonatos identificados em um programa

[5] World Health Organization. Deafness and hearing impairment. Available at: http:// www.who.int/mediacentre/factsheets/fs300/en/index.html. Accessed on 21 January

[6] Bubbico, LRA.; Spagnolo, A. Prevalence of prelingual deafness in Italy. Acta Otorhi‐

[7] Catlin FI. Prevention of hearing impairment from infection and ototoxic drugs. Arch

[8] Gatto CI, Tochetto TM. Infantile hearing loss: implications and solutions. Rev CE‐

[9] Miniti, Aroldo. Otorrinolaringologia: Clínica e Cirúrgica. 2a edição. São Paulo: Edi‐

[10] Harrison. Medicina interna. 17º edição. Rio de Janeiro: McGraw-Hill Interamericana

[11] K. J. Lee. Princípios de Otorrinolaringologia. Cirurgia cabeça e pescoço. 9º edição.

[12] Mendrone Junior, A. Prevalência da infecção pelo citomegalovírus: a importância de

[13] Brasil. Ministério da Saúde. Secretaria de Vigilância em Saúde. Guia de Vigilância em Saúd. Brasília: Ministério da Saúde, 2014. Available at: <www.saude.gov.br/bvs> Ac‐

[14] Secretaria de Estado da Saúde de São Paulo. Divisão de Doenças de Transmissão

[15] Schuster LC, Buss C. Herpes and its hearing implications: a literature review. Rev.

[16] Romero, JH., Carvalho, MS., Feniman, MR. Achados audiológicos em indivíduos

[17] Richardson MP, Reid A, Tarlow MJ, Rudd PT. Hearing loss during bacterial meningi‐

Respiratória. Meningites virais. Rev Saúde Pública. 2006; 40(4), 748–50.

estudos locais. Rev Bras Hematol Hemoter. 2010; 32(1): 7–8.

pós-meningite. Rev Saúde Pública. 1997; 31(4): 398–401.

de triagem auditiva neonatal universal. Rev. CEFAC. 2014; 16(2): 422–9.

Pediatria (São Paulo). 2007; 29(1):43–49.

Minas Gerais. 2010; 20(1): 102–6.

nolaryngol. 2007; 27: 17–21.

FAC. 2007; 9(1): 110–15.

tora Atheneu, 2000.

do Brasil, 2008.

Otolaryngol. 1985; 111(6):377–84.

São Paulo: McGraw-Hill, 2008.

cessed on 13 February 2015.

CEFAC. 2009; 11(4):695–700.

tis. Arch Dis Child. 1997; 76:134–8.

2010.

98 Update On Hearing Loss


3.2.2. Moisture Content

The moisture content (%) was significantly different within the individual honey type, namely, local and imported honey samples (Tables 3 and 4). The moisture content ranged from 13.1 ± 0.0 to 17.1 ± 0.1%, with a mean value of 14.9 ± 0.2% among local honey, (Table 3), and from 14.7 ± 0.0 to 19.4 ± 0.0%, with a mean value of 17.2 ± 0.3% for imported honey (Table 4).

Table 5 shows the moisture content values after comparison among local and imported honey samples. The imported honey possessed a significantly higher moisture content (17.2 ± 0.3%) than local honey (14.9 ± 0.2%) (Table 5), but these were within the permitted range (>20%) according to the international standards for honey [9,10].