POSTOPERATIVE CARE OF THE PATIENTS WITH TOF, CHĂM SÓC BỆNH NHÂN TỨ CHỨNG FALLOT SAU PHẪU THUẬT

POSTOPERATIVE CARE
OF THE PATIENTS WITH
TOF


BACKGROUND:
 Minimal monitoring standards for

children a pediatric cardiac ICU include:
1.ECG, arterial line, CVP.
2.Central and peripheral temperature.
3.Pulse oximetry, temporary pacing
wires.
4.Typically a left atrial line.
5.Pulmonary artery catheters
 The monitoring requires a 1:1
nurse:patient.


BACKGROUND (CONTINUE):
Post-op care of patients with TOF is

typically uneventful with most
patients being extubated within 24
hours of surgery.
Patients with TOF increase their
interstitial, pleural, and peritoneal
fluids early postoperatively.
Like other cyanotic individuals,
they can be sensitive to the
damaging effects of CPB.

THE DAMAGING EFFECTS OF CPB: ( BACKGROUND )
 Vascular access:

♦Monitoring of arterial blood pressure and intermittent
blood gas by arterial cannulae.
 Retention and bleeding:
♦ Checking coagulation times and platelet count.
♦ Bleeding into the pericardium results in the
pericardial tamponade. So, an ECHO should be obtained
soon after line removal. Two common causes of cardiac
tamponade:
1.The presence of blood .
2.Compression of the heart by adjacent structures.
♦ Cardiac tamponade: gradual onset of hypotension,
elevated heart rate, left atrial and CVP and reduction in
CO and hence pulse volume with inspiration(pulsus
paradoxus).


Nutrition: ( CPB continue)
♦The

goals of metabolic and nutritional
support in the paediatric cardiac ICU are first.
♦ Allowance must be made in planning postop feeding, to provide sufficient calories for
ongoing needs and “catch-up” requirement.

.

Age
(years)

Weight
(kg)

Caloric
requirement
(kcal/kg)

<1
>1-6
7-12
12-18

3-10
11-20
21-40
40-70

90-120
75-90
60-75
25-30


I.REPAIR:

1.Residual hemodynamic problems:

* Residual VSD
*RV outflow tract obstruction.
*PV and/or annular stenosis.
*Supravalvar PA stenosis.
*PR
*TR
*RV dysfunction.
*RV outflow tract aneurysm.
*LV dysfunction.
*PHTN.
2.Arrhythmia and conduction disturbance:
*SVT.
*VT.
*Complete heart block.


REPAIR:(continue)
Assessing of the hemodynamic continuously
Measurement of cardiac output.

 Identifying of an important right-to-left or left-to-right

shunt by ECHO.
Following arterial desaturation in the early hours after
operation. (Desaturation from right-to-left shunting usually
decreases within 48 hours as RV function improves).
In the absence of shunt, values of PLA and PRA relate the
function of 2 ventricular. (After repair, these are usually
similar).
If PLA is 5 to 10mmHg higher than P RA, a residual left-toright shunt at ventricular or great artery sought promptly

closed by reoperation.
If no shunt, elevated PLA indicates LV hypoplasia or severe
impairment of LV systolic or diastolic function (inotropic
agent and afterload reduction).


REPAIR : (continue)

PRA is rarely 5 to 10 mmHg higher than

PLAindicating important volume or pressure
overload of the RV or RV dysfunction
(Precarious).
PRA /PLA is greater than 0.7, the patient should
reoperate (if a transannular patch was not
used). If a transannular patch is in place,
catecholamine is indicated.
Bleeding (Preoperative polycythemia and
depletion of many clotting factors, extensive
collateral circulation, and damaging effects of
CPB tendency to bleed. (platelet-rich-plasma
and reoperated).


Residual VSD: ( REPAIR : continue.)

Residual VSD may be poorly tolerated:

►The normal LV pre-op without
significant ventricular hypertrophy.

► Present early postoperatively of
congestive HF.
► Cardiac catheterization.
Most residual VSDs are small and important
only in terms of the potential for infective
endocarditis.
If hemodynamic instability occur after
repair, the present of residual VSD should
be promptly and thorough investigated.


REPAIR: (continue)
After the patients leave the ICU,

body weight is followed closely.
(Transient fluid retention is common).
 Digoxin is useful in a volume
overload RV for 6 weeks.
Diuretics are used as indicated.


REPAIR: (continue)
Residual right ventricular outflow tract
obstruction ( RRVOTO):
Residual narrowing in the infundibulum, at the

RV pulmonary trunk junction ( with or without a
transannular patch) or more distally.
Stiffening, thickening, and eventually even
calcification of PV cusps cause RV hypertention.

RRVOTO occurred uncommonly, lately.
It includes: valvar stenosis, annular stenosis, and
supravalvar main pulmonary arterial obstruction
The site and severity of them determined by
ECHO
Balloon valvuloplasty or reoperate.


RRVOTO (continue):
Pulmonary artery branch stenosis is

relatively common post-op.
The left pulmonary artery at the site of
prior ductus insertion .
It can be treated by using transcatheter
balloon arterioplasty with or without the
use of stents.


REPAIR: (continue)
Right ventricular dysfunction:
 RV systolic hypertention and PR after repair.
 RV systolic function and end-diastolic volumn Post-op RV
systolic and diastolic function and a resting systolic pressure up
to 60 to 70 mmHg have little adverse effect.
Higher systolic pressures produce dysfunction.
Low CO may be attributable to RV dysfunction. (Elevated CVP
hepatomegaly, edema, pleural effusion…).
RV dysfunction assessed by ventricular size and EF and severe
PR (3 to 5 days to recover).

The mainstays of therapy are inotropic support, digoxin,
diuretics and ventilatory maneuvers to decrease the P vascular
resistance can reduce RV afterload.
Negative pressure ventilation improve CO well to avoid
secondary organ damage.
TR usually occurs with moderate to severe right ventricular
dilatation secondary to PR and/or right ventricular dysfunction.
When operation is required for P V replacement or correction of
residual outflow obstruction, TV annuloplasty can be a useful
adjunctive procedure.


REPAIR: (continue)
PR commonly accompanies TOF

repair b/c of the frequent need for
transannular patching for adequate
relief of right ventricular outflow tract
obstruction.
PR is usually well tolerated when PA
and RV pressures are low.


REPAIR:(continue)
Right ventricular aneurysms:
 Prominent outflow patches were too large to begin with.
The aneurysms may be a false one. ( true aneurysms as
usual)
 excessive thinning or devascularization of the RV free wall
or thinning and bulging of pericardium if it has been used

as an infundibular or transannular patch.
 Most RV aneurysms develop within 6 months of operation,
and true ones stabilize and rarely progress, whereas false
ones may progress rapidly and rupture.
These patches are akinetic, can contribute to RV
dysfunction.
 They should be resected and retailored.
Only 0.9% of patients of TOF underwent reoperation for RV
aneurysms.


REPAIR: (continue)
LV ventricular function:

1.LV systolic and diastolic function are
variable late post-op.
2.Risk factors for poor LV function
include:
►Older age at repair,
► Pre-repair status of LV
► Residual or recurrent defects.
Infective endocarditis: it is rare after
repair.


REPAIR:(continue)
Arrhythmia and conduction disturbance:
Arrhythmia death was 5% to 10% when the patients

underwent repair in adult life.

 While it occur 1% of the patients younger than age 5
years at operation.
The RV scar may be arrhythmogenic. Excising the scar
and inserting a patch graft.
Heart block:
Complete heart block is common after repair. It
occurred in 1,3%
Junctional ectopic tachycardia: It occurs
infrequently after repair of TOF. Survival depends
on aggressive treatment in ICU with core cooling
and amiodaron. Thereafter, there is probably little
risk of complete heart block.


II.SYSTEMIC-PULMONARY ARTERIAL SHUNTING:
Careful intraoperative monitoring and control of

PaO2, pH, and buffer base are required.
An intraarterial needle may have been placed
preoperatively, and the baby is returned to the ICU
still intubated.
Using dopamine and epinephrine to establish arterial
blood pressure is 10% to 20% greater than normal to
ensure good flow through the shunt.
Recommending a heparin drip for 24 hours.
A chest radiograph is obtained after procedure and
every 4 hours later.
Hemorrhagic pulmonary edema produces hypoxia
and clinical deterioration. So, many patients died a
few days after shunting operations for TOF.

SYSTEMIC-PULMONARY ARTERIAL
SHUNTING:
Mild renal failure, rarely acute renal failure and

anuria develop after a simple shunting procedure.
A surgically created shunt must function.
If is poorly functioning, prompt reoperation is
indicated. So, auscultation ( excepting large AP
collateral arteries, a continuous murmur is present
pre-operatively) for assessing its patency during
the entire post-op.
If cyanosis has not improved, ECHO or aortography
is indicated.
a hospital mortality approaching zero. Even in the
first month of life, hospital mortality was 0.6%.


SYSTEMIC-PULMONARY ARTERIAL SHUNTING:
The most important risk factor for early death after classic

shunting procedures is PA problems and young age.
Early (less than 30 days) nonfatal shunt closure or narrowing
occurs uncommonly (7%) in patients undergoing classic B-T or
PTEE shunt operations.
Intermediate-term shunt closure or narrowing requiring
reoperation is more common in neonates and young infants than
older patients occuring in 3% to 20%.
Reduced blood flow in the arm on the side of a classic B-T shunt .

 Severe blood flow reduction cause gangrene of the hand occur.
Sudden death, without explanation or autopsy is common after
classic shunting procedures (4 months after operation).
Nonfatal brain absess is also common.
Iatrogenic PA problems:Angiographic evidence of PA distortion is
fairy common late post-op.
Beneficial interim results of shunting procedures are increased
Qp, with consequent reduction in cyanosis and polycythemia,
and improved functional capacity.


SYSTEMIC-PULMONARY ARTERIAL
SHUNTING:
NYHA functional class is usually I or II after shunting. SaO2 at

rest is about 80% to 90%, but always decrease with exercise,
at times to as low as 50%.
These benefits are obtained at the expense of increased LV
stroke volumn, a stimulus to gradual development of LV
dysfunction.
Diffuse increase in size of the RPA and LPA.
Severe infundibular or valvar stenoses becomes complete
atresia after a palliative shunting operation.
Important pulmonary vascular disease may develop after a
classic B-T shunt but rarely before 7 years.
The proportion of patients developing hypertention pulmonary
vascular disease increases with increasing shunt duration
(before 5 years).