A very brief word about speech audiometry. A couple of things that will be tested on, which is more advanced than the pure tone audiometry, one is something that is called the “Speech Reception Threshold” or SRT. That is defined as the lowest sound intensity in decibels at which a child can identify selected words in 50% of the trials. So give them a list of words and they can identify what those words are 50% of the time. In comparison you have the speech discrimination score where you have a percent of words on a standardized list that are correctly identified if presented at a sound level 25-40 decibels above the speech reception threshold. Kind of complicated, pretty unlikely to show up on the test but might be worth kind of noting. One fact worth remembering about these though, is that looking at speech discrimination scores, if you look at these in sensorineural hearing loss, they tend to be lower than conductive loss. So kids with hearing loss due to conductive problems actually probably can pick up speech better than if there is sensorineural hearing loss.
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On to tympanometry. In tympanometry what you are trying to assess is two things, essentially. One is mobility of the tympanic membrane and second is indirectly you are trying to measure the pressure, or estimate the pressure, in the middle ear. There are three key things that you want to look at when you are looking at audiometry. And that is, the peak of the curve. So the three things that you are looking at is the peak of the curve – so how high does this get? And the vertical axis here is compliant which is essentially looking at how much volume of air is displaced at different pressures. So a tympanometry machine is applying different pressures and measuring how much air is displaced and essentially gives you a sense of how well, indirectly, the tympanic membrane is moving. So the peak is the height in the compliance. Canadian viagra at discount pharmacy shop. The location along this pressure curve where the peak occurs – so here the peak is at zero – is completely normal. Also a key thing to look at is you may see this peak shifted to the left if there’s negative pressure in the eardrum or to the right if there’s positive pressure in the eardrum. And the third thing, which is a nice little trick as well, is to look at ear canal volume. Here it’s 1 cc which is normal. Kids can have ear canal volumes anywhere from 0.2 to 2.00 ml. So this is a normal curve. The peak falls within this box below this line, above this line so the mobility is normal. The pressure is normal, the peak falls at zero and the ear canal volume is normal at 1 cc.
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Next one, what you see here is the peak height or the height of the peak is normal so the eardrum can move normally but the problem is that the peak is coming out at the left of this box at negative 200. So what that means is that while there is normal mobility there is negative pressure behind that middle ear, or behind that tympanic membrane within the middle ear and that is consistent with eustachian tube dysfunction and a retracted eardrum.
Conductive hearing loss: can be either acquired or inherited. Acquired is much more common. Tends to be transient and is often mild to moderate hearing loss. Most often due to things like earwax or sometimes middle ear effusion. If you see more significant loss or a more chronic loss, it’s generally caused by damage to the tympanic membrane and/or the ossicles. So things like chronic perforation, which we mentioned before, cholesteatoma, otosclerosis, or more seriously ossicular chain disruptions, will lead to serious conductive hearing losses. Some inherited forms that are worth mentioning: they generally present – and these again are conductive hearing losses – often present with major ear anomalies. Goldenhar’s is a nice syndrome to be aware of. Treacher-Collins as well, and then Down’s syndrome can have conductive hearing losses as well.
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Sensorineural hearing losses can be acquired or inherited. The acquired ones may be infectious so TORCH infections in newborns, particularly Rubella, can cause sensorineural hearing loss. Bacterial meningitis, especially H. flu can cause hearing loss. And then medications, aminoglycosides, diuretics are two of the most notorious but there are others as well. And then generally not a problem in kids but maybe later on, certainly for “baby-boomers”, is a problem of acoustic trauma from listening to loud music can eventually lead to sensorineural hearing loss. Inherited forms, many many different syndromes that will cause sensorineural hearing loss. Two that are probably worth mentioning and remembering. First is Alport’s, which is hearing loss and glomerulonephritis. Those two in combination are strongly suggestive of Alport’s, and then Waardenburg’s syndrome, which is partial albinism, sometimes just presenting as a white forelock and deafness may also be present with Waardenburg’s.
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Finally, in the last section we will talk a little about audiologic evaluation and tympanometry. Pure tone audiometry is just basically putting a pure tone through earphones and trying to hear at what decibel level a child can hear those tones. With conductive hearing loss you have a particular pattern, which is; air conduction is abnormal, bone conduction is normal. The pattern of loss that you see is usually fairly equal across frequencies, in contrast to sensorineural hearing loss which has a different pattern. Sensorineural hearing loss; air conduction is abnormal, bone conduction is abnormal and the pattern of loss is usually there are higher thresholds or greater deficits at higher frequencies. So that’s one thing that is generally suggestive of sensorineural hearing loss is that if you have significantly more loss at higher frequencies. You’ve got to be a little bit careful because some conductive loss – say with middle ear effusion – it may be a little worse at the higher frequencies but it shouldn’t be a dramatic difference.
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Foreign body aspiration: peak incidence is younger ages, six months to four years and clinical manifestation is sudden onset – and that’s key – sudden onset of coughing, gagging, choking, dyspnea, afebrile. And also an object that was previously visible is no longer visible. It’s very suggestive. If it is extrathoracic you are likely to hear stridor and a croupy cough. If it has gone down intrathoracic you are going to see more cough and wheezing. Diagnosis: extrathoracic, x-rays are helpful if it is radiopaque and one key link that I think is relatively likely to show up on exams is what happens if you see a coin? And what you will see is that coins in the sagittal plane are in the larynx or trachea. The way you can remember that is the tracheal rings have an opening in front so that if a coin is going to slide down into the trachea it’s going to be pointed in this direction. So when you do an x-ray you are going to see it on end, whereas if it’s in the esophagus it’s going to be in the coronal plane. So nice little tip there if you see an x-ray with a coin in it.
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Intrathoracic: 80% of kids with intrathoracic foreign body will have abnormal x-rays and you may see a variety of things: hyperinflation, atelectasis, pneumonia, especially if they have had this for some time pneumonia is much more likely to develop. You can do inspiratory/expiratory films but it’s very difficult obviously to get a small child to cooperate with those, and the other option is bilateral decubiti film. What you see on this film is this is an inspiratory film that is certainly suggestive of having some hyperinflation on this side. This side is much more lucent than this side, seems to occupy more volume. Expiration, it’s really quite clear that the right middle lobe and right lower lobe are quite inflated and so this is consistent with a foreign body in that area, and then air trapping in that area as well.
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Management of these: extrathoracic; if you have partial obstruction don’t try to dislodge it because it may lead to complete obstruction and you want to arrange for emergency bronchoscopy. Intrathoracic, you just need to arrange for bronchoscopy.
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Okay, our last section is on hearing loss. Two major forms that we’ll have is conductive hearing loss and then sensorineural hearing loss, but you also can see mixed forms as well. Conductive loss is caused by interference with transmission of sound through the external canal, through the tympanic membrane or through the ossicles. Whereas sensorineural problems are caused by damage to the cochlea, the auditory nerve, or the brain stem.
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In newborns, laryngomalacia is probably the most common cause of stridor in newborns. Key to this diagnosis is that it improves when the child is prone. Lay the child on their back, they are going to have much more stridor, lay them on their stomach and they are going to seem better. Also tends to worsen when a child is agitated. The vast majority of cases will improve spontaneously over the course of the first year without any intervention at all. Subglottic stenosis can be either congenital or acquired. Unlike laryngomalacia there is no change with position and sometimes can be severe enough that it requires tracheostomy. Vocal cord paralysis: unilateral, usually not a big deal. You have mild symptoms, maybe some mild stridor with a hoarse cry. Bilateral vocal cord paralysis presents very early on, even in the delivery room, with much more severe evidence of obstruction. Extrinsic compression, any kind of mass, can press on the larynx. Things like hemangioma, cystic hygromas, vascular rings, goiters, mediastinal masses, a whole bunch. And depending on the location of these masses you may see difficulty swallowing as well.
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Older kids: acute illnesses are much more likely, especially croup. Again, pattern recognition is key here. You should be able to diagnose this without any tests. Barky cough, worse at night. Usually peaks on the second or third night and resolves within 5-7 days. And usually a low grade fever. Diagnosis is usually clinical but if you are going to do x-rays you should see something which is called the steeple sign, where rather than having folding out of the epiglottic folds and upper trachea, it has a straightened pattern which suggests a church steeple. Treatment: cool mist, racemic epinephrine. Decadron is controversial. I think more and more people are starting to use Decadron. Certainly seems to be helpful in some cases, although his caution about indiscriminate use of steroids is also reasonable to say. Epiglottitis, H. flu type B, very rare these days. I gave a talk at a family medicine course a couple of months ago and asked, when was the last time anybody there (there were 250 people in the room) had seen a case of H. flu disease? Had anybody seen any cases in the last five years? None. Last ten years? None. It’s because of our aggressive immunization with H. flu, it’s still disappearing, but you still have to watch out for it obviously. Clinical manifestations here, sudden onset, high fever, toxicity, stridor, respiratory distress. The thing I think to emphasize, if you suspect this, you do not want to do anything to these kids. This is the kind of Board question where one of the things they want to test is when you know when not to do something. It’s as important sometimes to know when not to do something as it is to know when to do something. So you don’t want to examine the oropharynx, you don’t want to draw blood, do x-rays, anything like that. You want to get an urgent ENT consult, take the child to the OR for intubation hopefully, and then start antibiotics immediately afterwards.
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Myotonic Dystrophy
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Myotonic dystrophy is the most common form of adult muscular dystrophy, with a prevalence of 2-14 per 100,000 individuals. This autosomal dominant condition is manifested by myotonia, cardiac arrhythmias, cataracts, male pattern baldness, male infertility (hypogonadism), and other associated endocrinopathies. The age of onset and severity of the disease show extreme variation, both within and between families. The rare congenital form of myotonic dystrophy is associated with profound newborn hypotonia and mental retardation. Such children are invariably the offspring of affected mothers. The mothers frequently have mild or subclinical features of myo-tonic dystrophy. Complications of pregnancy in women with myotonic dystrophy include polyhydramnios, decreased fetal movements, intestinal pseudoobstruction, and approximately 15% perinatal mortality. The myotonic dystrophy gene has been cloned, and an unstable DNA sequence specific for the disease has been characterized. Female viagra online at discount canadian pharmacy. Detection of an enlarged DNA fragment due to the expansion of CTG repeat with the myotonic dystrophy gene can be used for direct DNA diagnosis in affected individuals and persons at risk. Furthermore, there is a strong correlation between the length of fragment expansion and the degree of disease severity in gene carriers. The gene containing the repeat has been designated motolin protein kinase. Prenatal diagnosis is available.
Huntington’s Disease
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Huntington’s disease is an autosomal dominant disorder that affects about 1 per 100,000 individuals. This progressive neurodegenerative disorder is characterized by motor disturbances, cognitive loss, and psychiatric manifestations. Affected individuals develop a distinctive choreic movement disorder that has an insidious onset in the fourth to fifth decade of life and gradually worsens over a period of 10-20 years until death. A juvenile form of Huntington’s disease exists, with a preponderance of paternal transmission of the disease. The gene (designated IT15) contains a polymorphic CAG repeat sequence. Unaffected individuals usually have about 11-24 CAG repeats, whereas patients with Huntington’s disease have 42-86 CAG repeats. The length of the repeat appears to correlate with the age of onset and severity of the disease. Although prenatal diagnosis is technically possible for this adult-onset disease, genetic counseling is complex and should be carried out in the context of a multidisciplinary team.
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The fragile X syndrome is the most common inherited form of mental retardation. In addition to moderate to severe mental retardation, affected males have facial dysmorphic features, macroorchidism, and a folate-sensitive fragile site on the X chromosome, at band Xq27.3. The female heterozygotes may also exhibit mental retardation. The responsible gene (FMR-1) has been cloned, and it includes the repeated CGG (cytosine-guanine-guanine) sequence that causes the fragile X mutation. Normal individuals have 2-50 CGG repeats at this locus, with an average of about 30 repeats. Alleles with more than about 50 repeats, including those identified in a normal family, are meiotically unstable. Individuals with no significant phenotypic abnormalities, but who are at high risk for having an affected offspring, have triple repeats ranging between 50 and 200. Such individuals are said to have a premutation, because it has a high probability of expanding to a full mutation in the next generation. Individuals with more that 200 CGG repeats are affected with the fragile X syndrome. The passage from premutation to full mutation status occurs only with transmission from the mother. Expanded CGG repeats appear to cause abnormal methylation of the FMR-1 gene, which, in turn, causes a reduction in gene transcription, resulting in disease. Molecular testing for clinical diagnosis, cartier detection, and prenatal diagnosis of the fragile X syndrome is available and is proving more reliable than cytogenetic testing. Results from chorionic villus sampling should be interpreted with caution because the methylation status of the FMR-1 gene is rarely established in chorionic villi at the time of sampling. Chorionic villus sampling, although a standard technique for prenatal diagnosis, may lead to a situation where follow-up amniocentesis is necessary to resolve an ambiguous result.
Kennedy’s Disease
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Kennedy’s disease (spinal and bulbar muscular atrophy) is an X-linked recessive disorder characterized by motor neuron degeneration that starts in adulthood and leads to progressive muscular weakness of the upper and lower extremities and late onset of mild androgen insensitivity. Affected males have reduced fertility and gynecomastia; female carriers have few or no symptoms. A mutation in the N terminus of the androgen receptor gene involving CAG repeats has been shown to be the cause of this disease. Unaffected individuals have 13-30 CAG repeats in the first exon (ie, transcribed region) of this gene; individuals with Kennedy’s disease have 40-62 repeats.
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