Ccam Looking for a support group Did your baby have Congenital Cystic Adenomation Malformation?

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My son first child had a ccam. He was born in March of 2006. He only lived 30 minutes. Saw discovery channel show called This scar saved my life. 10 year old boy had a tumor on his lung. Which I believe was a ccam. Congenital Cystic Adenomatoid Malformation. We would like to do something in his memory.
maybe start an organization commited to devoloping research about ccam. start a donation process. i would contact salvation army they might help.  (+ info)

Has anyone had a baby diagnosed with a CCAM (Congenital Cystic Adenomatoid Malformation)?

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Our daughter was diagnosed at her 23 wk ultrasound scan that she had a CCAM in the right lung. I am now 34 weeks, but have been on strict bedrest since 26 weeks for preterm labor. The CCAM has not gotten any bigger since it was diagnosed and would like to know what the outcomes are for babies born with small Type 3 CCAMs? I am considering having the baby near our home which doesn't offer a Level 3 NICU b/c we live 35 minutes away from the tertiary hospital. Is that a bad idea? Open for suggestions!
These cysts can enlarge rapidly and have a prenatal natural history distinct from the solid tumor which grow more slowly. Serial measurements of CAM volumes and CVRs show that the growth of CCAMS is exponential between 20 and 25 weeks gestation after which the CCAM growth reaches a plateau.

The mean gestational age at which this growth plateau is reached is 25 weeks gestation, but can range from 23 to 30 weeks. After the plateau is reached there is a slow decrease in the size of the CCAM. Subjectively this may appear to be a greater decease in the appearance of the CCAM as the fetus continues to grow around the CCAM.

No fetus that we have followed by serial CVRs had developed hydops once they have reached the growth plateau. This is an important milestone as the fetus is usually assured of a favorable outcome once the growth plateau is reached.

Everywhere suggests giving birth to a CCAM level 3 infant at a tertiary hospital since it is important to ensure the mass is completely removed if neonatal surgery was preformed or if steroids were used instead.

I wish you the very best of luck having a safe and healthy baby!  (+ info)

Baby diagnosed with Cystic Adenomatoid Malfunction of the lung?

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has anyone been through this and have any advise for me?? really scared feel like dying!!!
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seeking any information on babies who have been diagnosed with congenital cystic adnomatoid malformation?

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My 20 wk ultrasound shows that my baby girl has ccam. I have found little info and would like to know how common this is and what others with the same thing have experienced and what the outcome has been. and when do the doctors tell you what type the ccam is.we live 2 hours away from a neo natal unit. and find all this very frightening. any info would be great. email me at [email protected]
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congential cystic adenomatoid malformation?

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has anyone got any information about this ???
A congenital cystic adenomatoid malformation (CCAM) is a cystic piece of abnormal lung tissue that does not work like normal lung tissue. It usually replaces one part (lobe) of the lung. CCAMs occur with equal frequency in both lungs. Cystic tissue involved will never function as normal lung tissue.  (+ info)

cystic adenomatoid malformation?

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Background: Ch'in and Tang first described cystic adenomatoid malformation (CAM) as a distinct entity in 1949. CAM is a developmental hamartomatous abnormality of the lung with adenomatoid proliferation of cysts resembling bronchioles. CAM represents approximately 25% of all congenital lung lesions.


Pathophysiology:


Pathogenesis and pathophysiologic features

CAM is believed to result from focal arrest in fetal lung development before the seventh week of gestation secondary to a variety of pulmonary insults. Depending on the time and type of insult, 4-26% of cases can be associated with other congenital abnormalities. However, arrest of pulmonary development with distortion of architectural differentiation may take place at any stage of embryonic development.

CAM differs from normal lung tissue because of a combination of increased cell proliferation and decreased apoptosis. A well-defined intrapulmonary bronchial system is lacking, and normally formed bronchi supplying the mass are absent.

Types of CAM

CAM is subdivided into 3 major types.

Type I lesions, the most common, are composed of 1 or more cysts measuring 2-10 cm in diameter. Larger cysts are often accompanied by smaller cysts, and their walls contain muscle, elastic, or fibrous tissue. Cysts are frequently lined by pseudostratified columnar epithelial cells, which occasionally produce mucin. Mucinogenic differentiation is unique to this subtype of CAM.

Type II lesions are characterized by small relatively uniform cysts resembling bronchioles. These cysts are lined by cuboid-to-columnar epithelium and have a thin fibromuscular wall. The cysts generally measure 0.5-2 cm in diameter.

Type III lesions consist of microscopic, adenomatoid cysts, and are grossly a solid mass without obvious cyst formation. Microscopic adenomatoid cysts are present.

CAM receives its blood supply from the pulmonary circulation and is not sequestered from the tracheobronchial tree. However, type II and III lesions can occasionally coexist with extralobar sequestration, and in such cases, they may receive systemic arterial supply. CAM may also occur in combination with a polyalveolar lobe. A polyalveolar lobe is a form of congenital emphysema with increased number of alveoli with normal bronchi and pulmonary vasculature. CAM usually occurs early in fetal life, whereas polyalveolar lobe occurs late.

Differential diagnosis

CAM is differentiated from other congenital cystic disease by 5 characteristics including the following: (1) absence of bronchial cartilage (unless it is trapped within the lesion); (2) absence of bronchial tubular glands; (3) presence of tall columnar mucinous epithelium; (4) overproduction of terminal bronchiolar structures without alveolar differentiation, except in the subpleural areas; and (5) massive enlargement of the affected lobe that displaces other thoracic structures.


Frequency:


Internationally: In Canada, the estimated incidence of CAM is 1 case per 25,000-35,000 pregnancies.
Mortality/Morbidity: The prognosis primarily depends on the size of the lesion. In a Canadian series of 48 patients, the incidence of postnatal demise was 10% (10 of 40 patients) with 8 spontaneous and voluntary abortions. Larger lesions have a higher incidence of mediastinal shift, vascular compromise, polyhydramnios, pulmonary hypoplasia, and hydrops, which may lead to intrauterine fetal demise or neonatal death.

Type III CAM tends to be extensive and therefore tends to have a poor prognosis. The prognosis is also poor with bilateral lung involvement, prematurity, and severe associated malformations. The most commonly associated anomalies occur in the type II form. The anomalies affect the renal (cystic disease, agenesis, dysgenesis), intestinal (atresias), cardiac, and osseous systems.

When CAM is identified in utero, as many as 56% of the lesions detected can regress spontaneously, although initially, they may progress. As the lesion decreases in size, mediastinal shift is corrected. Persistent lesions may only be discovered later in life, and some may be asymptomatic. Eventual removal of even asymptomatic masses is recommended because of potential risk of secondary infection, hemorrhage, and reports of carcinomas arising in CAM.
In fetuses with life-threatening lesions such as the development of hydrops, the anticipated mortality rate is nearly 100%.
Race: No clear racial predilection for CAM exists.

Sex: Sex-related incidences are equal for CAM.

Age: Most cases of CAM are diagnosed in the patient's first 6 months of life, with 70% of patients presenting in the first month of life. As many as 90% of cases are reported within the patient's first 2 years of life. Occasionally, CAM is discovered later in life, usually as a result of chronic or recurrent pulmonary infection.

When CAM was diagnosed prenatally in one study, the mean gestational age at diagnosis was 22.6 weeks ± 3.3.

Anatomy: Communication with the tracheobronchial tree usually is retained, and the vascular supply and venous drainage are to the pulmonary circulation, unless CAM is associated with sequestration, as discussed above. Lesions occur with equal frequency in either lung, but the lesions have a slight predilection for the upper lobes. Lobar involvement is seen most often, but multiple lobes, the entire lung, or segments of both lungs may be involved.

Clinical Details: In the newborn, 80% of CAMs present with some degree of respiratory distress secondary to mass effect and pulmonary compression or hypoplasia. Severe symptoms may be related to air trapping within the lesions. The affected region is dull to percussion, and air entry is poor. Older patients may present with persistent or recurrent pneumonia.

Preferred Examination: CAM may be initially detected during prenatal ultrasonography. After birth, chest radiography should be performed first. Although lesions remain filled with fluid, postnatal sonography can be used for a more detailed assessment, particularly in type III lesions. Once lesions are air-filled, CT scanning is necessary for determination of the type and extent of the lesions.

Limitations of Techniques: Prenatal ultrasonography is accurate in diagnosing CAM. Prenatally diagnosed lesions may be asymptomatic at birth (71%), and they have normal radiographic findings (57%). A concurrent sequestration may not be identified. Usually, radiographic findings are apparent in a symptomatic individual, but they may not be as apparent in an asymptomatic child.

Most often, the diagnosis can be made by using plain radiographs. CT scans may be used to diagnose confusing cases. Overlapping CT features exist among cases of CAM, pulmonary sequestration, bronchogenic cyst, and other foregut malformations. CT is more accurate than radiography or ultrasonography in classifying the type of CAM.  (+ info)

Congenital Cystic Adenomation Malformation? ccam?

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Looking for someone who might have been diagnose with a ccam before they were born.
i guess this illness is not that common since nobody has answered yet if they were diagnosed with ccam before they were born..  (+ info)

How much does a lung transplant help with cystic fibrosis?

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A couple of days ago, a guy I knew back in my hometown got a double lung transplant. He has cystic fibrosis. I know removiing the lungs takes away the bacteria but does it get rid of the disease?
nope it gets rid of the lung problem but doesn't cure the person, cystic fibrosis does not only affect the lungs but the pancreas as well...it inhibits the pancreas' abiltiy to secrete enzymes need for digestion which causes poor growth, fatty diarrhea and deficiency in fat-soluble vitamins.

cystic fibrosis is a multi system disease  (+ info)

What is the life expectancy after a double lung transplant if you have Cystic Fibrosis?

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My little sister is a teenager and has Cystic Fibrosis. Her doctor said she will need to have a double lung transplant eventually...her lung function is not good, and she gets frequent infections. She also has a lot of problems with digesting and has to have a feeding tube to provide extra nutrients. I was wondering, does anyone who's knowledgeable know what the life expectancy is after a double lung transplant considering she has Cystic Fibrosis? And the probability of just surviving the lung transplant surgery?
I don't know but I would guess it would double her age, she would have new lungs but they would wear down like her original lungs.  (+ info)

What is life like for a person with Cystic Fibrosis after a lung transplant?

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I want to know if anyone has any experiences/knowledge here, such as how long do you have to be in the hospital after the surgery? What is the quality of life like after a double lung transplant? Will the I develop Cystic Fibrosis problems in the new lungs? I'm 17 and will have to have a douple lung transplant eventually because of my Cystic Fibrosis and poor lung function because of the disease. I'm nervous about it.
http://www.cff.org/treatments/LungTransplantation/  (+ info)

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