Hearing loss

Ok so yeah it has been over 6 months but it is getting harder to get this down since lots of things are still up in the air. This one is on hearing loss since both of my boys have a hearing loss. They are not completely deaf but they cannot hear like any other person out there either. They have a rather unique slope of loss. A slope means that for an hearing test they make sound at a certain level to see if the child can hear the tone. They do the low tones and the high tones. My kids have a rising slope which is not the normal. In other words they can hear the higher tones better. In order to hear the higher tones the hair has to be undamaged in the middle and the lower tones are heard by the hair that is undamaged on the outer side. Maybe this will explain it a little better.

Severity of hearing loss

Hearing loss is also measured in decibels (dB). Conversational speech is around 60dB. The degrees of hearing loss include:

Degree of Hearing Loss

Degree of hearing loss refers to the severity of the loss. The numbers are representative of the patient's thresholds, or the softest intensity at which sound is perceived. The following is one of the more commonly used classification systems:

Degree of hearing loss	Hearing loss range (dB HL)
Normal	-10 to 15
Slight	16 to 25
Mild	26 to 40
Moderate	41 to 55
Moderately severe	56 to 70
Severe	71 to 90
Profound	91+

Source: Clark, J. G. (1981). Uses and abuses of hearing loss classification. Asha, 23, 493-500.

Hearing is graphed on an audiogram, a graph of the softest sounds you can hear. The graph is laid out like a piano keyboard, with low to high frequencies (low to high pitches) going from left to right, ... and the graph is laid out from soft sounds on the top to loud sounds on the bottom.

So once your graph is filled in (x represents the left ear, o the right), ... it shows your hearing sensitivity for different frequencies at different intensities (at different pitches and different volumes).

Hearing is NOT measured in percentages. Instead, it is measured in an arbitrary unit of loudness called the DECIBEL. The decibel (dB, or dB HL) is a logrithmic scale. Physically, every 6 dB increase represents a doubling of sound pressure level. Perceptually, every 10 dB increase sounds twice as loud.

Every increase of 10 decibels (10 dB) sounds twice as loud. 20 dB sounds twice as loud as 10 dB... 40 dB sounds twice as loud as 30 dB and 8 times as loud as 10 dB (10 to 20 to 30 to 40 = 2 x 2 x 2 = 8).

Normal hearing ranges from 0 to 20 dB in all frequencies.

Damaged hair cells and deafness There are a series of hair cells contained in the cochlea (inner ear) that are key to most people's hearing. They are called the "inner hairs" (more on this later). It is damage to, or lack of the inner hair cells that cause most deafness. High decibels i.e. loud music or sounds above 140 db. will cause some of these hairs to die, as will some serious infections. Once an inner hair dies, it cannot be replaced. Because we initially are born with only about 3500 of these hairs, loss of a few can make a big difference in our hearing capacity.

The Cochlea

The cochlea is the second part of the inner ear and is the actual organ of hearing. It is embedded in the skull in what is called the mastoid area, a spongy part of the skull just behind where the jaw hinges. The mastoid bone acts as an amplifier for some sounds, especially those in the lower frequency ranges.

The cochlea is made up of:

The oval window to which the stirrup from the middle ear is attached

The round window which acts as a sound magnifier

Three fluid-filled canals (vestibular labyrinth) that run the length of the cochlea and separated by thin membranes.

1. The vestibular canal (scala vestibuli)
2. The tympanic canal (scala tympani)
3. The cochlear canal (scala media) that contains the Organ of Corti which in turn contains:
   • The hairs that move when pressure waves of a certain frequency move the basilar membrane under them (inner hairs)
   • Stiffer hairs (outer hairs) that run parallel to the inner hairs and act as inner hair and basilar membrane inhibitors
   • The basilar membrane in which the inner hairs are embedded that transmits fluid movement to the inner hairs
   • The tectorial membrane in which the tops of the outer hairs are lightly embedded
   • The auditory nerves that run through the middle of the cochlea from the opening to close proximity to the helicotrema. These nerves from the inner hair roots link to the 8th nerve that transmit information to the brain

How the Various Canals Work

The cochlea begins at the oval window where the middle ear stirrup is attached and curves into a shape that resembles a snail shell, where the chambers get narrower towards the end. The coiled tube inside the snail-like apparatus contains three parallel canals discussed above, that run the length of the cochlear envelope.

The doctors say that my boys have a conductive loss and with surgery they might be able to get it back. The doctors must think I am nuts if they want me to risk my child's life to see IF they could fix their hearing.

Hearing loss

Conductive Hearing Loss

Conductive hearing loss occurs when sound is not conducted efficiently through the outer ear canal to the eardrum and the tiny bones, or ossicles, of the middle ear. Conductive hearing loss usually involves a reduction in sound level, or the ability to hear faint sounds. This type of hearing loss can often be medically or surgically corrected.

Examples of conditions that may cause a conductive hearing loss include:

• Conditions associated with middle ear pathology such as fluid in the middle ear from colds, allergies (serous otitis media), poor eustachian tube function, ear infection (otitis media), perforated eardrum, benign tumors
• Impacted earwax (cerumen)
• Infection in the ear canal (external otitis)
• Presence of a foreign body
• Absence or malformation of the outer ear, ear canal, or middle ear

Degree of hearing loss refers to the severity of the loss. The numbers are representative of the patient's thresholds, or the softest intensity at which sound is perceived.

My boys cannot hear the low tones very good but the high tones they can hear better. The doctors are not sure why they would flow against the majority but in most ways they do just that. They have a Moderately Severe rising to Mild loss. I am going to post and audiogram and put green 'x' on the places that my son's hear at so you know the red part is where normal people hear and the green is where my boys hear at.



This is as good as I could do showing you what my boys hear like with out looking at an audiogram. Since I can't find one at the moment. But it looks almost identical to this. One of my boys do wear hearing aids and the other should be he keeps getting infections in his ears and so it is hard to have him were any at the moment. From the charts at the tops of this post you can see what a normal hearing loss looks like.

Wow this is one crazy post so if it helps you in any way please feel free to let me know. Thanks.

Long Pause

It has been a very long time since I posted but we had a long bout of medical issues and now that they are letting up just a little bit I will hopefully post again soon. Thank you for your patience with me.

Ok jumping once again

Since we are skipping around then we will go ahead and cover my other little boy. He was born with Craniosynostosis. When we first hear of this we were stumped. We didn't have a clue as to what the doctor was talking about. The doctor found out that he had it a week to a month before he turned 2 months, but didn't tell us until he was 2 months old. The day he turned 3 months he had to go in for surgery in order to fix the problem. These are some of the things that I found on this subject.



Craniosynostosis

Craniosynostosis,[1] is a medical condition in which some or all of the sutures in the skull of an infant or child close too early,[2] causing problems with normal brain and skull growth. It can result in craniostenosis, which is the skull deformity caused by the premature closure of the cranial sutures. Also intracranial pressure can be increased.

Normal skull development

In humans, the adult skull is normally made up of 28 bones. The flat bones making up the cranial vault are joined together by sutures: rigid articulations permitting very little movement.

At birth, the human skull is made up of 45 separate bony elements. As growth occurs, many of these bony elements gradually fuse together into solid bone (for example, the frontal bones).

The bones of the roof of the skull are initially separated by regions of dense connective tissue. At birth these regions are fibrous and moveable, necessary for birth and later growth. Larger regions of connective tissue, called fontanelles, occur where certain bony elements meet. As growth and ossification progress, the connective tissue of the fontanelles is invaded and replaced by bone. The posterior fontanelle usually closes by eight weeks, but the anterior fontanelle can remain up to eighteen months.

Pathophysiology

When one or more sutures fuse prematurely, skull growth can be restricted perpendicular to the suture. If multiple sutures fuse while the brain is still increasing in size, intracranial pressure can increase.

Primary craniosynostosis is believed to be a result of primary defect in the mesenchymal layer ossification in the cranial bones. Secondary craniosynostosis is a result of primary failure of brain growth.

Diagnosis

Physicians diagnose craniosynostosis through physical examination, plain x-rays, and CT scans. [3]

Syndromes

Craniosynostosis often occurs alone, however about 20% of cases are associated with syndromes. A syndrome is diagnosed by considering the presence of a variety of features, signs, and symptoms throughout the body. Genetic testing may be available to confirm the diagnosis of a specific syndrome. A family history of abnormal head shape can sometimes be found with genetic syndromes, though many syndromes are caused by new genetic mutations, and there is no family history of the disorder. [3]

The most common causes of syndromic craniosynostosis are Crouzon syndrome and Apert syndrome. However, there are over 150 syndromes associated with craniosynostosis. [3] The following table lists some of the craniosynostosis syndromes, as well as prominent additional symptoms that are found in these syndromes — this is not a comprehensive list of all symptoms that could occur within each syndrome. There is considerable overlap of symptoms between many of these syndromes, and clinical evaluation by a geneticist may be necessary to determine the most appropriate diagnosis.

Differential diagnosis

A separate cause of abnormal head shape is positional plagiocephaly — flattened or misshapen areas on the head that may develop due to sleeping position. While the appearance may look rather similar to craniosynostosis, the distinction is important. Positional plagiocephaly does not require surgery[4] — treatment can be as simple as occasionally repositioning the child's head while sleeping or, in some cases, wearing a cranial band to mold the skull. [3] It has recently been discovered that using certain prescription drugs during pregnancy may lead to this disorder. (sertraline)

Treatment

Surgery is typically used to separate the fused sutures of the skull as well as to reshape the skull. To treat the cosmetic troubles, a combination of orthodontic and orthognathic surgery can be used to relieve some of the midface deficiency.



Typical surgery begins with a zigzag incision from ear to ear across the top of the head. The scar left by this type of incision makes the hair look more natural than that left by a straight incision would. Leroy clips are typically used to curtail bleeding, as cauterization would not result in an aesthetically pleasing result upon healing. Once the scalp is peeled back, pilot holes are drilled through the skull. These pilot holes are then connected, separating the skull into several pieces. Once reshaped, these pieces are placed back on the head (typically in an altered configuration) and held together by a combination of dissolving sutures, plates, and screws. These plates and screws are typically composed of a copolymer comprised of polyglycolic and polylactic acid and will break down into water and carbon dioxide within a year. Demineralized bone matrix or bone morphogenetic proteins are often used to fill gaps left by the expanded skull, encouraging the body to grow new bone in a process called intramembranous ossification. Once the hemostatic scalp clips are removed, sutures are again used to close the incision.

Newer approaches include minimally invasive endoscopic assisted removal of the closed suture followed by treatment with custom made molding helmets. These surgeries are associated with significantly less blood loss, swelling, hospital length of stay and pain. The results have been excellent in the majority of patients treated this way. Endoscopic surgery, however, is indicated only for very young infants(< 6 months of age). Older children require the more extensive surgery described above.

The result of our treatment is a happy little boy who will most likely not ever have to worry about this again.





Best thing we could have done for him and we are very grateful that we did.

Heart

Ok so we will skip to my daughter for a minute and let you know what we found out about her. She was born with a VSD. That is just a heart mummer that is actually quite common. But it was a shock to find out after we left the hospital that she had it. Apparently the smaller the hole in the heart the louder it gets. Hers is really loud. Scared a few doctors because it is so loud. A VSD is a hole in the heart that lets blood pass through it. She is followed by cardiology and thankfully we only have to go in every 3 year now instead of every year! I was so excited to her that from the doctor.

Here is what I found on it. Yes it is a lot but it there is some great information.

VSD Mummer

A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.

The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes. The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children.[1][2]

Congenital VSDs are collectively the most common congenital heart defects.

A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be performed.

VSDs are the most common congenital cardiac anomalies. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 10000 births. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously.[4] Prospective studies give a prevalence of 2-5 per 100 births of trabecular VSDs that closes shortly after birth in 80-90% of the cases.

Treatment is either conservative or surgical. Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively. In cases necessitating surgical intervention, a heart-lung machine is required and a median sternotomy is performed. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms. This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic.

Ventricular septal defect (VSD) is the second most common cardiac malformation, accounting for approximately one fifth of all congenital cardiac anomalies. It is usually diagnosed during childhood. In adults, it is diagnosed less often, owing to the fact that, during the patient's early years, large VSDs are corrected surgically, and smaller VSDs close spontaneously.

A VSD is a defect in the interventricular septum, which is composed of muscular and membranous segments. VSDs are classified into 3 main categories according to their location and the appearance of the margins of defects. The clinical significance of the VSD depends on its size and location, the level of pulmonary pressure, and the left ventricular (LV) outflow resistance associated with the VSD. A restrictive VSD produces a small shunt and does not cause significant hemodynamic derangement. In contrast, a large VSD may progressively lead to higher pulmonary resistance and, finally, to irreversible pulmonary vascular changes, producing the so-called Eisenmenger syndrome (reversal of shunt to right-to-left shunt).

Clinically, VSDs produce a characteristic systolic murmur and are associated with recurrent upper respiratory infections. The anatomic localization of all VSDs is facilitated by using 2-dimensional (2D) echocardiographic images with a Doppler system and by superimposing a color-coded direction and velocity of blood flow on the real-time images. Clinically significant VSDs require surgical correction; clinical outcomes are usually excellent.

Pathophysiology

The functional disturbance caused by a ventricular septal defect depends primarily on its size and the status of the pulmonary vascular bed rather than on the location of the defect.

The physical size of the VSD is a major, but not the only, determinant of the size of the left-to-right shunt. The magnitude of the shunt is also determined by the level of pulmonary vascular resistance relative to the systemic vascular resistance. The magnitude of intracardiac shunts is usually described by the Qp:Qs ratio, where Qp is the pulmonary resistance and Qs is the systemic resistance. If the left-to-right shunt is small (Qp:Qs < 1.75:1), the cardiac chambers are not appreciably enlarged, and the pulmonary vascular bed is likely normal. If the shunt is large (Qp:Qs > 2:1), left atrial and LV volume overload occurs, as does right ventricular and pulmonary arterial hypertension. The main pulmonary artery, left atrium, and LV are enlarged.

When a small communication is present (usually <0.5 cm2), the VSD is called restrictive, and the right ventricular pressure is normal. Such a VSD produces a significant pressure gradient between the LV and the right ventricle. It is accompanied by a small (<1.5/1.0) shunt, and it does not cause significant hemodynamic derangement. A small VSD with high resistance to flow permits only a small left-to-right shunt.

A moderately restrictive VSD is accompanied by a moderate shunt (Qp:Qs = 1.5-2.5:1.0) and poses a hemodynamic burden on the LV. This leads to left atrial and LV dilation and dysfunction, as well as a variable increase in pulmonary vascular resistance. Important atrial arrhythmias and, less often, ventricular arrhythmias may occur.

In large nonrestrictive VSDs (usually >1.0 cm2), right and LV pressures are equalized. In these defects, the direction of shunting and the shunt magnitude are determined by the ratio of pulmonary resistance to systemic vascular resistance. Such a VSD results initially in LV volume overload early in life, with a progressive increase in pulmonary artery pressure. The natural history of VSDs has a wide spectrum of findings, ranging from spontaneous closure to congestive cardiac failure and death in early infancy. Within this spectrum are the possible development of pulmonary vascular obstruction, right ventricular outflow tract obstruction, aortic regurgitation, and infective endocarditis.

After patients with a large VSD are born, pulmonary vascular resistance may remain higher than normal, and thus, the size of the left-to-right shunt may initially be limited. As pulmonary vascular resistance continues to decrease in the first few weeks after birth, owing to the normal involution of the media of small pulmonary arterioles, the size of the left-to-right shunt increases. Eventually, a large left-to-right shunt ensues, and clinical symptoms become apparent.

In most cases during early infancy, pulmonary vascular resistance is only slightly elevated, and the major contribution to pulmonary hypertension is the extremely large pulmonary blood flow. However, in some infants with a large VSD, pulmonary arteriolar medial thickness never decreases. With continued exposure of the pulmonary vascular bed to high systolic pressure and high flow, pulmonary vascular obstructive disease develops. When the ratio of pulmonary to systemic resistance approaches 1:1, the shunt becomes bidirectional, signs of heart failure abate, and the patient becomes cyanotic (Eisenmenger physiology).

Frequency

United States

Ventricular septal defects are the second most common congenital anomalies of the heart, accounting for approximately 20% of all congenital cardiac malformations.1, 2

Mortality/Morbidity

• Small ventricular septal defects pose an ongoing and relatively high risk of endocarditis.
• Perimembranous or outlet VSDs may be associated with progressive aortic valve regurgitation caused by prolapse of the aortic cusp into the defect.
• The late development of subaortic and subpulmonary stenosis has been reported.

Race

No particular racial predilection has been reported for ventricular septal defect.

Sex

No difference in the incidence of ventricular septal defect in male and female patients has been reported.

Age

Ventricular septal defect is usually diagnosed in children.

• Infants: In unusual circumstances, a VSD causes difficulties in the immediate postnatal period, although congestive heart failure during the first 6 months of life is a frequent occurrence. Early diagnosis is helpful in ensuring more careful observation of the affected infant. The examining physician usually suspects the diagnosis because of a harsh systolic murmur at the lower left sternal border. The ECG and chest radiographic findings are within normal limits in the immediate neonatal period because appreciable left-to-right shunting occurs only after pulmonary vascular resistance decreases as the pulmonary vessels lose their fetal characteristics. These infants should be closely monitored.
• Children: After the first year of life, a variable clinical picture emerges in children with VSD. If a small defect is present, the child is usually asymptomatic, the ECG usually appears normal, and the chest radiograph shows normal or mildly increased pulmonary vascular markings. Effort intolerance and fatigue are associated with moderate left-to-right shunts. These children have cardiomegaly with a forceful LV impulse and a prominent systolic thrill along the lower left sternal border. The second heart sound is normally split, with moderate accentuation of the pulmonic component; a third heart sound and rumbling diastolic murmur that reflects increased flow across the mitral valve are audible at the cardiac apex. The characteristic murmur, which results from flow across the defect, is harsh and holosystolic. This murmur is best heard along the third and fourth interspaces to the left of the sternum and is widely transmitted over the precordium. A basal midsystolic ejection murmur caused by an increase in flow across the pulmonic valve also may be heard. The ECG reveals left ventricular hypertrophy or combined ventricular hypertrophy, and the chest radiograph and CT scan show cardiomegaly, left atrial enlargement, and vascular engorgement.

Anatomy

The ventricular septum comprises 4 compartments: the membranous septum; the inlet septum; the trabecular septum; and the outlet, or infundibular, septum.

Defects result from a deficiency of growth or a failure of alignment or fusion of component parts. Defects are most commonly classified as occurring in or adjacent to 1 or more of the septal components.

The most common defects occur in the region of the membranous septum and are referred to as paramembranous or perimembranous defects because they are larger than the membranous septum itself and are associated with a muscular defect at a portion of their perimeter. They also are known as infracristal, subaortic, or conoventricular defects. These perimembranous defects also may be defined by their adjacent areas as an inlet, trabecular, or outlet defect.

A second type of defect is one with an entirely muscular rim. Such muscular defects also may be defined as inlet, trabecular, central, apical, marginal or Swiss cheese, or outlet types. They vary greatly in size, shape, and number.

A third type of defect occurs when the outlet septum is deficient. This is commonly referred to as supracristal, subpulmonary, outlet, infundibular, or conoseptal. Because the aortic and pulmonary valves are in fibrous continuity, this type of defect also may be referred to as a doubly committed subarterial defect.

A septal deficiency of the site of the atrioventricular (AV) septum characterizes defects called AV septal, AV canal, or inlet septal defects.

The other feature of any defect may be a malalignment of the septal components. Either the inlet septum or the outlet septum may be malaligned. Malalignment of the inlet septum produces either mitral or tricuspid valve override and/or straddle. Malalignment of the outlet septum may be to the right or the left of the trabecular septum. When it is to the left of the trabecular septum, the VSD is characteristic of tetralogy of Fallot; double-outlet ventricle; truncus arteriosus; and, in some cases, transposition of the great arteries.

Presentation

The clinical presentation of patients with a ventricular septal defect varies according to the size of the defect and the pulmonary blood flow and pressure.3, 4, 5, 6, 7

Symptoms

Small VSDs with trivial left-to-right shunts and normal pulmonary arterial pressures are the most common. Patients with these VSDs are asymptomatic; the cardiac lesion is usually found during routine physical examination.

Patients with a moderately restrictive VSD often present with dyspnea in adult life. In patients with large nonrestrictive VSDs, the condition frequently progresses to Eisenmenger syndrome.

Signs

Physical examination typically reveals a displaced cardiac apex with a similar holosystolic murmur, as well as an apical diastolic rumble and third heart sound (S3) at the apex, caused by the increased flow through the mitral valve.
Characteristically, a loud, harsh, or blowing holosystolic murmur is best heard over the lower left sternal border in the third or fourth intercostal space. This is frequently accompanied by a thrill. Sometimes, the murmur ends before the second heart sound, presumably because of closure of the defect during late systole.
A short, harsh systolic murmur localized at the apex in a neonate is often a sign of a tiny muscular VSD. In the immediate neonatal period, the left-to-right shunt may be minimal because of higher right-sided pressures; thus, the systolic murmur may not be audible during the first few days of life. In premature infants, the murmur may be heard early because pulmonary vascular resistance decreases more rapidly.
Large VSDs with excessive pulmonary blood flow and pulmonary hypertension are responsible for dyspnea, feeding difficulties, poor growth, profuse perspiration, recurrent pulmonary infections, and cardiac failure in early infancy. Cyanosis is usually absent, but duskiness is sometimes noted during periods of infection or when crying. Prominence of the left precordium is common, as are a palpable parasternal lift, a laterally displaced apical impulse and apical thrust, and a systolic thrill.
The holosystolic murmur of a large VSD is usually less harsh than that of a small VSD and is more blowing in nature because of the absence of a significant pressure gradient across the defect. It is even less likely to be audible in newborns. The pulmonic component of the second heart sound may be increased, indicating pulmonary hypertension. The presence of a mid-diastolic, low-pitched rumble at the apex is caused by increased blood flow across the mitral valve and indicates a Qp:Qs of 2:1 or greater.

Natural history

The natural course of a VSD depends to a large degree on the size of the defect.
A significant number (30-50%) of small defects close spontaneously, most frequently during the first 2 years of life. Small muscular VSDs are more likely to close (as many as 80%) than membranous VSDs (as many as 35%). The vast majority of defects that close do so before the patient is 4 years of age, although spontaneous closure has been reported in adults.

Most children with small defects remain asymptomatic, without evidence of an increase in heart size, pulmonary arterial pressure, or resistance. One of the long-term risks for these patients is infective endocarditis. Some long-term studies of adults with small VSDs that are not treated with surgery indicate an increase in the incidence of arrhythmia, subaortic stenosis, and exercise intolerance. The Council on Cardiovascular Disease in the Young of the American Heart Association states that an isolated, small, hemodynamically insignificant VSD is not an indication for surgery.

More commonly, infants with large defects have repeated episodes of respiratory infection and heart failure despite optimal medical management. Many of these infants experience heart failure, manifested as a failure to thrive. Pulmonary hypertension occurs as a result of high pulmonary blood flow. These patients are at risk for the eventual development of pulmonary vascular disease if the defect is not repaired.

Patients with VSD are also at risk for the development of aortic valve regurgitation; the risk is greatest for patients with supracristal VSD.
A VSD that either decreases in size or closes completely during the first year of life presents no problem to the practicing physician.

Spontaneous closure occurs by 3 years of age in about 45% of patients born with VSD. In some patients, spontaneous closure does not occur until 8-10 years or age, or even later. Spontaneous closure is more common in patients born with a small VSD; nonetheless, about 7% of infants with a large defect who experience congestive heart failure early in life also experience spontaneous closure. Partial, rather than complete, closure is common in patients with both large and small VSDs. Spontaneous closure of a perimembranous VSD (from tricuspid leaflet tissue apposition) or of a small muscular VSD during adulthood is uncommon (<10%).

Preferred Examination

Echocardiography

Two-dimensional and Doppler color-flow mapping may be used to identify the type of defect in the ventricular septum. Perimembranous VSDs are characterized by septal dropout in the area adjacent to the septal leaflet of the tricuspid valve and below the right border of the aortic annulus.

The subaortic or anterior malalignment type of VSD appears just below the posterior semilunar valve cusps, entirely superior to the tricuspid valve. Subpulmonary VSD appears as echo dropout within the outflow septum and extending to the pulmonary annulus. One or two of the aortic cusps may be seen to be protruding through the defect into the right ventricular outflow tract. The inlet AV septal-type of VSD extends from the fibrous annulus of the tricuspid valve into the muscular septum; it is often entirely beneath the septal tricuspid leaflet.

Muscular defects may appear anywhere throughout the ventricular septum. They may be either large and single or small and multiple.

The anatomic localization of all VSDs is facilitated by coupling 2D sonograms with a Doppler system and by superimposing a color-coded direction and velocity of blood flow on the real-time images.

Chest radiography

In patients with small VSDs, the results of chest radiographs are usually normal. With medium-size VSDs, minimal cardiomegaly and a borderline increase in pulmonary vasculature may be observed. In large VSDs, the chest radiograph shows gross cardiomegaly with prominence of both ventricles, the left atrium, and the pulmonary artery. The pulmonary vascular markings are increased, and frank pulmonary edema, including pleural effusions, may be present.

Electrocardiography

The ECG mirrors the size of the shunt and the degree of pulmonary hypertension.
Small restrictive VSDs usually produce a normal tracing. Medium-size VSDs produce a broad, notched P wave characteristic of left atrial overload. Signs of LV volume overload — namely, deep Q and tall R waves with tall T waves in leads V5 and V6 — are present. In addition, signs of atrial fibrillation are often present. Large VSDs produce right ventricular hypertrophy with right-axis deviation. With further progression, the ECG shows biventricular hypertrophy; P waves may be notched or peaked.

Limitations of Techniques

The 2D echocardiogram shows the position and size of the ventricular septal defect. Small defects, especially those of the muscular septum, may be difficult to image; they might be visualized only by means of color Doppler examination.
In defects of the membranous septum, a thin membrane may partially cover the defect and limit the volume of the left-to-right shunt. Although the membrane is called a ventricular septal aneurysm, it consists of tricuspid valve tissue.

I hope this information helped you as much as it helped me understand things better.

Next

Ok so it has been a while. We have had quite a year to say the least. The next thing would be the small long bones. Having said that the ribs are the longest bones in the body, and since we already covered the small chest cavity we will worry about the other bones that are small. Most of the time babies fingers are usually long and dainty right? Well My 2 boys fingers are short and kind of stubby looking. Those are also long bones, same with the toes. Here is some info that I found on long bones.

Long Bones

The long bones are those that are longer than they are wide, and grow primarily by elongation of the diaphysis, with an epiphysis at the ends of the growing bone. The ends of epiphyses are covered with a hyaline cartilage ("articular cartilage"). The longitudinal growth of long bones is a result of endochondral ossification at the epiphyseal plate. Bone growth in length is stimulated by the production of growth hormone (GH), a secretion of the anterior lobe of the pituitary gland.

The long bones include the femurs, tibias, and fibulas of the legs, the humeri, radii, and ulnas of the arms, metacarpals and metatarsals of the hands and feet, and the phalanges of the fingers and toes. The long bones of the human leg comprise nearly half of adult height. The other primary skeletal component of height is the spine and skull.

The outside of the bone consists of a layer of connective tissue called the periosteum. Additionally, the outer shell of the long bone is compact bone, then a deeper layer of cancellous bone (spongy bone) which contains red bone marrow. The interior part of the long bone is the medullary cavity with the inner core of the bone cavity being composed of (in adults) of yellow marrow. They are found more in women.

In the picture you can see that my son is short, well maybe you can't. In this picture he is 9 1/2 years old. He is about a head taller then the chair that is also in the picture. In the other picture is my other son and his cousins. They are all within 3 months of age. The 2 bigger boys are 1 and my son turned 1 less than a month after this picture was taken.

Ok 1st

The first thing we had to go through with our oldest was the small chest cavity.

But since he had a small chest cavity it made it so his lungs were small. He was on oxygen from the time he was born until he was 10 months old. Them he was placed back on oxygen around the age of 3 until he was at least 5 1/2 I think. By the time he was 4 he was on 1 1/2 to 2 liters oxygen and his blood saturation was at 91 or 92 and falling every day. In other words he was dying. We had taken him to a orthopedics doctor for a little tiny scoliosis in the very bottom of his spine. The doctor took x-rays and held them up to x-rays taken when He was 1 and it might have changed maybe like a 1/2 centimeter difference. The doctor looked at us and told us that his spine was not even a medical issue. The needed to expand his chest cavity and they needed to do it soon. There was a new device out there called the titanium rib or veptor. It wasn't even approved by the government when we were trying to get it.

We did everything we needed to get the authorization we needed to get the insurance to pay for the surgery and they were denying us right and left. Right before the surgery we were going to go in and make a presentation to the insurance people to get them to approve it. Right before we were leaving the house like 10 min. the doctor called me and let me know that he had made a case for our son and the insurance approved the surgery. We were so blessed. The doctor who invented the device flew in from TX to train the people up here in UT to be able to do this surgery. There were quite a few different doctors watching from around the world while our son was in surgery. They placed the right side and a month later they placed the left side. Now every 6 months he is in for surgery to expand the veptors or have them replaced when he out grows them. Here is a picture of the x-ray that was last done. You will be able to see just how small the chest cavity really is and how the veptors have helped. when I am able i will have to place an before picture, but for now all I have it a after one.


Here is the definitions that I found on chest cavity.

Small Chest Cavity

The thoracic cavity (or chest cavity) is the chamber of the human body (and other animal bodies) that is protected by the thoracic wall (thoracic cage and associated skin, muscle, and fascia).

Structures within the thoracic cavity include:

• structures of the cardiovascular system, including the heart and great vessels, which include the thoracic aorta, the pulmonary artery and all its branches, the superior and inferior vena cava, the pulmonary veins, and the azygos vein
• structures of the respiratory system, including the trachea, bronchi and lungs
• structures of the digestive system, including the esophagus,
• endocrine glands, including the thymus gland,
• structures of the nervous system including the paired vagus nerves, and the paired sympathetic chains,
• lymphatics including the thoracic duct.

It contains three potential spaces lined with mesothelium: the paired pleural cavities and the pericardial cavity. The mediastinum comprises those organs which lie in the centre of the chest between the lungs.

chest cavity - the cavity in the vertebrate body enclosed by the ribs between the diaphragm and the neck and containing the lungs and heart

thoracic cavity

bodily cavity, cavum, cavity - (anatomy) a natural hollow or sinus within the body

mediastinum - the part of the thoracic cavity between the lungs that contains the heart and aorta and esophagus and trachea and thymus

chest, pectus, thorax - the part of the human torso between the neck and the diaphragm or the corresponding part in other vertebrates

Going to do

Ok so this is what I am going to try to do. I am going to go into a detail everything that I have dealt with with my kids explaining all that medical terminology and hoping to help out others who need to have the same thing done, or have the same thing hoping to connect to others. I will be hoping to start this next month since this month is just slightly over whelming as it is. But I truly hope you have a wonderful New Year no matter what!