Surgery of the Ductus Arteriosus. Botalli Related Diseases in Smalls Flashcards
Anatomy
Remember- no gas exchange before birth!! therefore more blood must go through the aorta to be exchanged by the mother (via Botalli)
First few breaths trigger the pum circuit
Within 10 days- the duct shrinks and becomes a ligament
The Related diseases
- PRAA and LLA: botalli is not the primary cause
- PDA: botalli is the primary cause
PRAA and LLA
Diagnosis of PRAA: history
vomiitting (always after the swelling) regurg-usually after eating
Retained/incr appetite (sure sign that there is an obstruction)
Weight loss
Retarded development
Diagnosis of PRAA: phys exam
no pathognomic signs
Cachexia
Retarded development
Dilated neck- palpable esophageal distension
Diagnosis of PRAA: radio and endoscopy
Radio:Always do plain before contrast!
use high vol of barium sulphate
Megaesoph cranial to the base of the heart
Endo: esophageal: dilation, stang, ulcer
Diff of PRAA
Idiopathic congenital total megaesophagus
Congenital NM disease, abnormal vagus innerv of the muscular layer of the esoph– causes dilation!
PRAA therapy
Conservative: cant really do– asp pneumonia
Symptomatic
Soft dies, small meals many times fed at a height!
Prokinetics eg metoclopromide?? because incr the contractions of the cardia
Gastric protectants
Surgery
Surgery for PRAA
Indications need to be there!
- Inhalation anaesth- v high level
- Left lat thoracotomy at 4 ICS (this is the level of the botalli)
- Ligature and transection of the botalli:
* Mixtor dissector , Ao is behind the lig, put prox and dist ligatures around the ligament and then bisect– esophagus immediately widens and has more room- can be seen by the fact the the intubation tube now has more room! - Dissection and balloon dilation of the esophagius- to dilate the lumen!
PDA and its pathogenesis
When the ductus doesn’t close- it creates a huge P gradient btw the Ao (high P) and the puml A (low P)… blood from the Ao enters the pulm A– overwhelming hydrostatic P— hyperT of the chest and lungs— pulm edema
Incidence of PDA
Most common congenital heart disease in dogs!
Puppies: 2 mnths-1 yr (older than this the lig could be small/atrophied)
Female
Rare in cats
Diagnosis of PDA
L to R shunt (because this is the direction of the P gradient, from Ao (L) to pulm a (R)
Retarded development
Exercise intolerance
L phremitus: murmur in 3/4 ICS because of constant “ machonery”
Femoral a: water hammer pulse- because (+) inotropic damage in the heart
Enlarged L… then R ventricle
Decomp hyperT and edema
Coughing
eCG: wide P tall R
Doppler echo: pathognomic patency signs
X-ray: dilated LV
R to L shunt diagnosis
**don’t get confused, it is L to R for PDA**
Polycythaemia because incr erythropoetin
SEVERE pulm hyperT (massive resist from pulm area)
Blood flows from pulm trunk to the Ao
Differential cyanosis!!! vessels from ASC Ao are still filled with oxygenated blood
Desc Ao brings blood towards the rest of the body which is high in CO2
When check mm/interdigital/conjunctiva- they are ok (pink) BUT the more caud mm of vagina/prepuce will be cyanotic
Treatment of PDA: surgical
Indiaction and the patient must be <1 yr
High level of IV anaesth
- Left lat thoracotomy in 4th ICS (same as PRAA)
- Double/triple ligation of ductus botalli
Nemeth’s description: go through latiss– scaleneus– ventr serratus into chest- creating PTX
Separate the IC muscles right in the middle of 2 ribs
Reflect cran lobe caud
Use Finietteo? retractor
The ligature should cause and incr in BP BUTTT the brennan reflex once the stretch receptors are triggered- signals to the brainstem to decr Ao BP by bradycard– control with atropine/glycopyrrolate
He doesn’t put in chest drain after
Treatment of PDA: non-surgical
- Gianturco “occlusion coil” into lumen of PDA under fluoroscopic guidance! introduce the coil with a catheter- coil unravels– thrombositisation!! but there is a danger if the coil migrates to the pulm A
- Amplatzer vascular plug
- Gianturco-Grifka occlusion device
