Open Botall's soul

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Open duct of Botall
Ductus arteriosus Botalli
File:Botall's persistent spirit.jpg
CT Botall's persistent spirit

Patent ductus arteriosus patens (ductus arteriosus patens, PDA) is acyanotic congenital heart defect in which the ductus arteriosus of Botalli, the ductus arteriosus Botalli, has not closed '. The duct of Botall is a vessel that connects the pulmonary artery to the aorta and is important in fetal circulation where it allows blood to bypass the lungs by shunting from the pulmonary artery to the aorta.

In healthy full-term newborns, a 'functional closure of the duct occurs shortly after birth. Complete closure occurs in almost half of full-term newborns within 24 hours of birth, in 90% within 48 hours, and in all within 96 hours of birth. Failure to close and persistence of this fetal junction is called a patent or persistent ductus arteriosus (PDA).[1]

PDA is more common in premature. A patent ductus can vary in width and length, and there is a wide spectrum of severity of symptoms, from occasional murmurs to severe acute heart failure.[2]

Risk Factors[edit | edit source]

A higher incidence of PDA is associated with the following factors:

Conversely, a lower incidence of PDA' is associated with the following factors:

  • antenatal administration of corticosteroids (induction of lung maturity in immature newborns),
  • IUGR,
  • premature outflow of amniotic fluid (PROM).[3]

Pathophysiology[edit | edit source]

The fetal ductus arteriosus diverts blood flow from the pulmonary artery to the descending aorta, thus bypassing the pulmonary basin in which there is high vascular resistance. The closure or persistence of the ductus after birth is determined by the action of various factors. Oxygen promotes airway closure, and prostaglandins E, on the other hand, open the airway. Susceptibility to these factors varies with gestational age. The younger the fetus, the smaller the contracting effect of oxygen, the more the dilating effect of prostaglandin E2 increases and the sensitivity to indomethacin, which is used for pharmacological closure of the duct, increases.[1]

Clinical picture[edit | edit source]

Small duct is usually asymptomatic. Large airways result in slow growth, failure to thrive, collapsing peripheral pulsations, hypotension (may be the first symptom in ELBW), ventilatory difficulties, heart failure (with pulmonary edema and hepatomegaly). Peripheral pulsations are noticeably lively, the precordium is active. Resting tachycardia and tachypnea are conspicuous.

A wide short wind causes heart failure, pulmonary hypertension, manifestations of cyanosis of the lower half of the body. A moderately significant cough can cause repeated respiratory infections and failure of the child to thrive. Narrow duct is asymptomatic. All patients are at risk of infective endocarditis.

In premature infants with RDS (respiratory distress syndrome) open trachea can lead to dependence on artificial pulmonary ventilation. In infants, it causes circulatory failure, manifested by expiratory dyspnea from pulmonary edema.

Cave!!!.png: continuous systolic-diastolic locomotive murmur (so-called three-beat rhythm) under the left clavicle, the maximum of the murmur during II. sounds[4] (we hear the low-frequency sound of "coke spilling").

Diagnosis[edit | edit source]

We establish the diagnosis based on

Differential diagnosis

Patients with an aortopulmonary window (direct communication ascending aorta and truncus pulmonalis) have a similar clinical picture.

Therapy[edit | edit source]

  • Asymptomatic PDA' - observation, most close spontaneously (mainly in premature infants)[2]
  • symptomatic PDA;
    • limited fluid intake,
    • ensuring sufficient blood oxygenation,
    • treatment of heart failure: furosemide,
    • consider pharmacological closure: indomethacin, ibuprofen,
      • absolute contraindication: heart defects in which an open trachea is necessary for survival (e.g. coarctation of the aorta),
      • side effects: oliguria, fluid retention and hyponatremia due to reduced renal blood flow, reduced cerebral blood flow, gastrointestinal complications (bleeding, ulceration), bleeding (impaired platelet function), [[icterus] ],
    • surgical treatment (ligature, transection)[2].
    • cardiac catheterization (Amplatz occluder)


Links[edit | edit source]

Related Articles[edit | edit source]

External links[edit | edit source]

References[edit | edit source]

  1. a b {{#switch: book |book = Incomplete publication citation. GOMELLA, TL, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2013. pp. 800-804. 978-80-7262-438-6. |collection = Incomplete citation of contribution in proceedings. GOMELLA, TL, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2013. pp. 800-804. {{ #if: 978-0-07-176801-6 |978-80-7262-438-6} } |article = Incomplete article citation.  GOMELLA, TL, et al. 2013, year 2013, pp. 800-804,  |web = Incomplete site citation. GOMELLA, TL, et al. Lange, ©2013.  |cd = Incomplete carrier citation. GOMELLA, TL, et al. Lange, ©2013.  |db = Incomplete database citation. Lange, ©2013.  |corporate_literature = GOMELLA, TL, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2013. 978-80-7262-438-6} }, s. 800-804.
  2. a b c d
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  3. a b c {{#switch: book |book = Incomplete publication citation. GOMELLA, T. L, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2009. 978-80-7262-438-6. |collection = Incomplete citation of contribution in proceedings. GOMELLA, T. L, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2009. {{ #if: 0071638482 |978-80-7262-438-6} } |article = Incomplete article citation.  GOMELLA, T. L, et al. 2009, year 2009,  |web = Incomplete site citation. GOMELLA, T. L, et al. Lange, ©2009.  |cd = Incomplete carrier citation. GOMELLA, T. L, et al. Lange, ©2009.  |db = Incomplete database citation. Lange, ©2009.  |corporate_literature = GOMELLA, T. L, et al. Neonatology : Management, Procedures, On-Call Problems, Diseases, and Drugs. Lange, 2009. 978-80-7262-438-6} }
  4. http://int-prop.lf2.cuni.cz/zof/vysetreni/srdceva_n.htm#od

Taken from[edit | edit source]

  • {{#switch: web

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  Incomplete publication citation. BENEŠ, George2009. Also available from <http://jirben.wz.cz>. 

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  #if:  |978-80-7262-438-6} }
  |article = 
  Incomplete article citation.  BENEŠ, George. Study Materials. 2009, year 2009, also available from <http://jirben.wz.cz>. 

|web =

  BENEŠ, George. Study Materials [online]. ©2009. [cit. 2009]. <http://jirben.wz.cz>.

|cd =

  BENEŠ, George. Study Materials [CD/DVD]. ©2009. [cit. 2009]. 

|db =

  Incomplete database citation. Study Materials [database]. ©2009. [cit. 2009]. <http://jirben.wz.cz>.

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  Incomplete citation of company literature. BENEŠ, George. 2009. Also available from <http://jirben.wz.cz>. legislative_document = 
  Incomplete citation of legislative document.  2009. Also available from URL <http://jirben.wz.cz>.

References[edit | edit source]

  • {{#switch: book

|book =

  Incomplete publication citation.  and Carlo L. ACERINI. Oxford Handbook of Paediatrics. New York : Oxford University Press, 2008. pp. 175. 978-80-7262-438-6.

|collection =

  Incomplete citation of contribution in proceedings.  and Carlo L. ACERINI. Oxford Handbook of Paediatrics. New York : Oxford University Press, 2008. pp. 175. {{
  #if: 978-0-19-856573-4 |978-80-7262-438-6} }
  |article = 
  Incomplete article citation.   and Carlo L. ACERINI. 2008, year 2008, pp. 175, 

|web =

  Incomplete site citation.  and Carlo L. ACERINI. Oxford University Press, ©2008. 

|cd =

  Incomplete carrier citation.  and Carlo L. ACERINI. Oxford University Press, ©2008. 

|db =

  Incomplete database citation. Oxford University Press, ©2008. 

|corporate_literature =

   and Carlo L. ACERINI. Oxford Handbook of Paediatrics. New York : Oxford University Press, 2008. 978-80-7262-438-6} }, s. 175.