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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3612_Библиотеки_им_академика_М_И_Перельмана
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290
Key Questions in CONGENITAL CARDIAC SURGERY
c) cardiac surgery, including:
i) temporary shunt insertion, such as a modified BT shunt;
ii) partial correction of the defect, such as using a
transannular patch;
iii) primary correction of the defect, such as tetralogy of
Fallot repair;
iv) extracorporeal life support pending further decisions.
9 What are the principles of pre-operative management
of a neonate or infant with transposition of the great
arteries?
In transposition of the great arteries (TGA), there are two parallel
•
circulations, with the morphological right ventricle giving rise to the
aorta and the morphological left ventricle giving rise to the main
pulmonary artery. Without any mixing, this circulation is incompatible
with life.
Mixing in TGA can occur at:
•
a) atrial level (interatrial communications);
b) ventricular level (ventricular septal defect);
c) arterial level (patent ductus arteriosus).
TGA is usually an antenatal diagnosis.
•
Many neonates with TGA are born with an adequate PFO and a PDA
•
which can be maintained with prostaglandin, allowing adequate
mixing. In these patients, critical care is not usually required.
Some neonates with TGA, however, will have profound cyanosis
•
requiring critical care intervention because of a combination of
reasons, including:
a) associated pulmonary hypertension during foetal transition;
b) restrictive or an intact atrial septum;
c) delayed diagnosis with closure of the PDA;
d) associated cardiac lesions, such as pulmonary artery stenosis.
The aim of PICU management is to improve oxygen saturation levels
•
by increasing mixing between the two circulations and treating any
additional pathology, such as congenital infections.
Strategies to improve mixing in this cohort include:
•
a) ensuring ductal patency with prostaglandin;
8 Paediatric cardiac intensive care
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b) ensuring unrestricted atrial shunting by:
i) percutaneous balloon atrial septostomy (BAS), to
remove any mechanical obstruction to mixing;
ii) prostaglandin, which is administered to increase
pulmonary venous return to elevate the left atrial
pressure in order to encourage mixing through the atrial
septum;
c) reducing pulmonary vascular resistance with:
i) oxygen therapy;
ii) sedation and muscle relaxation;
iii) ventilation to achieve a normal or lower PaCO
iv) inhaled nitric oxide therapy;
d) increasing systemic vascular resistance with noradrenaline or
vasopressin;
e) treating other associated problems, such as sepsis with
antibiotics.
Acute surgery for TGA is rarely indicated as an unrestrictive atrial
•
septum and a PDA usually provides adequate mixing. In cases of
poor response to balloon septostomy and ongoing reduced cardiac
output and desaturation, emergency surgery may be indicated.
Ideally, the neonate will be extubated following the BAS to allow for
•
the normal reduction in PVR to occur in the first week of life, prior to
undergoing surgical repair.
;
2
291
10 What are the principles of management of a child
presenting with left ventricular failure and dilated
cardiomyopathy?
Children can present with left ventricular (LV) failure as the primary
•
cardiac pathology (such as myocarditis, cardiomyopathy or
congenital heart disease) or as the condition secondary to another
critical illness, such as septic shock.
Children with LV failure will present with varying degrees of low
•
cardiac output states and cardiogenic shock. Acute decompensation
can either occur due to worsening of LV function or intercurrent
illness, such as lower respiratory tract infections.
Any critically unwell child with shock or respiratory distress should
•
have a basic bedside assessment of the left ventricle, including:
a) echocardiography — which can provide a detailed assessment
of LV function, rule out structural heart disease and ensure the
coronary arteries are assessed, particularly ruling out
anomalous coronary artery origins;
292
Key Questions in CONGENITAL CARDIAC SURGERY
b) electrocardiography (ECG) — which can rule out
tachyarrhythmia as the cause of LV dysfunction and assess for
signs of active or previous ischaemia or infarction (Q waves,
ST segment and T wave changes);
c) blood results — which can assess for end-organ perfusion
(such as renal function), signs of myocardial infarction (such as
troponin) and tissue oxygen delivery (such as lactate or mixed
venous oxygen saturation levels);
d) cardiomyopathy ‘screen’ — which may be indicated to identify
any causes of cardiomyopathy, including genetic testing,
metabolic assessment and endocrine evaluation.
Treatment strategy for severe LV dysfunction is aimed at ensuring
•
adequate oxygen delivery to tissues, whilst treating any reversible or
underlying causes.
The medical management strategy specifically for LV failure can be
•
considered in terms of the factors determining cardiac output (Figure
4).
Figure 4. Intensive care unit medical management strategies for the
failing left ventricle. ACE = angiotensin-converting enzyme.
8 Paediatric cardiac intensive care
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Rapid resolution of LV function with good critical care management
•
usually implies a secondary cardiac cause (e.g. sepsis). Ongoing LV
dysfunction in the absence of structural congenital heart disease
suggests a primary cardiomyopathy/myocarditis.
If medical management fails, consideration must be given to the use
•
of mechanical support, either ECMO or ventricular assist devices.
The aim of this therapy is to bridge the child to recovery, definitive
treatment or transplant. Early discussion with a cardiac
transplantation centre is recommended.
11 What are the main complications seen post-
cardiotomy and thoracotomy?
A systematic approach can be taken to consider the potential
•
common postoperative complications and it can be helpful when
identifying and acting upon them on the PICU, including:
a) airway:
i) iatrogenic pathology from airway management (such as
endobronchial intubation or airway oedema);
ii) vocal cord palsy (recurrent laryngeal nerve palsy);
iii) iatrogenic compression of central airways, especially the
main bronchi and trachea, resulting from the operation
(especially arch surgery);
b) breathing:
i) acute lung injury;
ii) pneumothorax;
iii) pleural effusion;
iv) chylothorax (thoracic duct injury);
v) atelectasis/collapse;
vi) pulmonary oedema;
vii) diaphragm palsy (phrenic nerve injury);
c) circulation:
i) systemic inflammatory response;
ii) low cardiac output state;
iii) myocardial dysfunction;
iv) arrythmias and heart block;
v) coagulopathy and bleeding;
vi) cardiac tamponade (either from bleeding or myocardial
oedema);
vii) residual untreated cardiac lesions;
viii) new iatrogenic cardiac lesions;
ix) thrombosis;
293
294
Key Questions in CONGENITAL CARDIAC SURGERY
d) disability:
i) pain;
ii) stroke (ischaemic or haemorrhagic);
iii) anxiety;
iv) delirium/withdrawal;
e) miscellaneous:
i) sepsis — such as line sepsis, mediastinitis, wound
infection;
ii) scarring;
iii) pyrexia;
iv) hypoglycaemia;
v) fluid overload;
vi) electrolyte disturbances;
vii) acid-base disturbances;
viii) renal impairment;
ix) multi-organ dysfunction;
x) ischaemic colitis;
xi) feed intolerance.
12 What is the management strategy for patients with
postoperative bleeding?
Many children bleed following cardiopulmonary bypass. The
•
common causes include:
a) coagulopathy secondary to an inflammatory and immunological
response to surgery and exposure to the extracorporeal circuit, with
bypass times >90 minutes associated with a greater risk of bleeding;
b) major transfusion intra-operatively;
c) consumption of platelets and coagulation factors during
cardiopulmonary bypass;
d) inadequate heparin reversal;
e) haemodilution;
f) hypothermia;
g) surgical bleeding.
The management requires a multidisciplinary, systematic approach
•
which can improve patient outcomes, avoid unnecessary use of
blood products and prevent surgical re-exploration. Most units use
institution-based protocols and major haemorrhage policies.
The level of intervention needed is dependent on the severity of
•
bleeding and level of cardiovascular compromise. Haemorrhagic
shock is a clinical emergency and needs to be managed aggressively
and promptly.
Although the severity of bleeding definition varies, a general rule can
•
be based on chest drain losses in relation to body weight (Table 3).
8 Paediatric cardiac intensive care
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Table 3. Classification for severity of bleeding post-cardiopulmonary
bypass.
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Nil — check drains are not blocked
Minimal
Moderate
High
Very severe — assume surgical bleeding
The management of bleeding on the PICU includes:
•
a) resuscitation — to ensure adequate oxygen delivery to tissues
despite blood loss;
b) replacement of lost blood volume — which needs to be
warmed and a mix of red blood cells, platelets, fresh frozen
plasma and cryoprecipitate to replace the whole blood lost.
Pump blood or cell-saved blood can also be used;
c) correction of any residual coagulopathy;
d) early antifibrinolytic treatment (tranexamic acid) — which has
been shown to significantly reduce the need for transfusion
with minimal risk of venous thrombosis;
e) ensuring normothermia;
f) restore ionised calcium to normal levels;
g) further reversal of heparin with protamine;
h) correcting acidosis;
i) considering the possibility of surgical bleeding or cardiac
tamponade, which may require chest re-exploration.
0
1-2mL/kg/hr
2-5mL/kg/hr
5-10mL/kg/hr
>10mL/kg/hr
295
If initial resuscitative measures have failed to control a major
•
haemorrhage, then more potent thrombin generators can be
considered including recombinant factor VIIa (rFVIIa). The
administration of rFVIIa should only be used in extreme
circumstances and where all surgical sources of bleeding have been
corrected. As the use of rFVIIa has been associated with increased
adverse events, including arterial thrombi, it should be used with
caution.
Although coagulation studies are useful to direct a focused
•
transfusion strategy, resuscitation should not be delayed waiting for
results.
Only few coagulation tests will provide meaningful information on
•
whole blood function, as the majority of them look at specific parts of
the coagulation cascade (e.g. INR, APTTR).
Key Questions in CONGENITAL CARDIAC SURGERY
Two bedside examples of whole blood coagulopathy screens include:
•
a) activated clotting time (ACT) — a bedside test of fibrin
formation in whole blood that is used to monitor heparin
anticoagulation but not specific to it. It provides a limited
amount of information about clotting. The normal range for the
ACT is 100-140 seconds;
b) thromboelastogram (TEG®) (Figure 5) — which can provide a
detailed whole blood clotting test to help determine the cause
of coagulopathy and thereby guide which blood product to
administer. It can be difficult, however, to differentiate between
thrombocytopaenia and hypofibrinogenaemia.
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ivPM
296
α
j^
o=íáãÉ
h
`дзннбеЦ=нбгЙ `дзн=вбеЙнбЕл `дзн=лн~Дбдбну
Time
zero
Time to MA 30 mins Clot lysis time
Parameter Description Clinical implications
Reaction time (R time)
Normal 5-10 minutes
K value
Normal 1-5 mins
α
-angle
53-72°
Maximal amplitude (MA)
55-73mm
Lysis at 30 minutes (LY30)
0-8%
Time to first significant clot
formation/fibrin initiation
Clot formation/time to clot
firmness of 20mm amplitude
Speed of fibrin accumulation
Maximum clot strength
Highest vertical amplitude
of TEG
Degradation of clots 30 mins
after MA/indicator of excess
fibrinolysis
áR time = âcoagulation factors
Affected by anticoagulation
FFP or protamine
áK time = âplatelets and/or
fibrinogen
Affected by anticoagulation
âα-angle = âfibrinogen and/or
platelets
Affected by anticoagulation
âMA = âplatelets
Affected by antiplatelet drugs
áLY30 = áclot breakdown
Consider antifibrinolytics,
e.g. tranexamic acid (TXA)
Figure 5. Thromboelastogram (TEG
®
) and its interpretation.
8 Paediatric cardiac intensive care
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13 What are the characteristic findings and management of
a patient with post-cardiotomy low cardiac output state?
Low cardiac output state (LCOS) describes a common phenomenon
•
seen on the PICU following congenital cardiac surgery. The cardiac
output falls, causing a significant impairment of delivery of oxygen to
the tissues.
LCOS occurs in approximately 25% of children following cardiac
•
surgery. One major study involving 122 neonates undergoing the
arterial switch procedure for transposition of the great arteries,
showed that 25% had a cardiac index <2L/min/m
this occurred 6-12 hours following admission to the PICU (often
postoperative night one), before returning to baseline after 24 hours.
LCOS occurs because of:
•
a) inflammatory response due to cardiopulmonary bypass;
b) myocardial ischaemia due to the presence of the aortic cross-clamp;
c) reperfusion injury;
d) ventricular injury — such as from the ventriculotomy;
e) residual cardiac lesions;
f) hypovolaemia — such as from bleeding or third space fluid
loss;
g) cardiac tamponade;
h) pulmonary hypertension;
i) arrhythmia — such as junctional ectopic tachycardia (JET);
j) drug delivery issues — such as inotropes.
2
. The majority of
297
The clinical features of LCOS include:
•
a) examination findings — cool peripheries, weak pulses and a
grey/mottled appearance;
b) observation findings — tachycardia, hypotension, reduced
urine output and a fall in renal and cerebral near-infrared
spectroscopy (NIRS) monitoring;
c) investigation findings, including:
i) raised lactate;
ii) widening arteriovenous oxygen saturation difference (low
SvO2);
iii) end-organ injury — such as acute kidney injury;
iv) fall in cardiac index.
Many children return from the operating room on a milrinone infusion,
•
based on the PRIMACORP study (PRophylactic Intravenous use of
Milrinone After Cardiac OpeRation in Pediatrics), which demonstrated
298
Key Questions in CONGENITAL CARDIAC SURGERY
that the use of milrinone when compared to placebo reduced the
incidence of LCOS and that the reduction in LCOS was more
significant with a higher dose of milrinone.
Upon identifying LCOS, the intensivist must ensure that there is no
•
obvious reversible cause that needs correcting, such as tamponade
or a residual lesion. Often, LCOS is a gradual process that is seen
over several hours before resolving.
The general management of LCOS in the absence of reversible
•
causes are focused around ensuring adequate oxygen delivery to the
tissues.
The overall strategy is based on the recognition and correction of the
•
factors determining the oxygen delivery (DO2), which is measured in
mL/kg/min, and is directly proportional to CO (cardiac output) and
arterial content of oxygen (CaO2) (Figure 6). Therefore, optimising
CO and CaO2directly increases oxygen transport, although it does
not affect oxygen uptake at tissue level.
Figure 6. Factors determining oxygen delivery. CaO
of oxygen; Hb = haemoglobin; SaO
partial pressure of oxygen; DO
HR = heart rate; SV = stroke volume; EDV = end-diastolic volume; ESV =
end-systolic volume.
When looking at CaO2, interventions aimed at affecting the
•
proportion of oxygen dissolved in plasma (PaO2) are not significant,
given that the factor of 0.003 by which this is calculated in the overall
equation.
Conversely, haemoglobin (Hb) and oxygen saturation (SaO2)
•
interventions are important in increasing transport.
2
= oxygen saturation levels; PaO2=
2
= oxygen delivery; CO = cardiac output;
= arterial content
2
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Heart rate (HR) is the most important factor in regulating cardiac
•
output, given the small dimensions of the ventricular cavities and the
poor compliance of the infant myocardium.
Manipulations of preload and afterload are very important given the
•
reduced contractility of the young heart, especially in the
postoperative setting. Inotropic support is often required after
cardiotomy.
Interventions aimed at regulating the oxygen delivery formula should
•
be considered in a systematic way in every patient after surgery to
maximise their effects, including:
a) sedation and muscle relaxation (reduces metabolic demand);
b) optimising ventilation and oxygenation;
c) optimising preload by correcting bleeding, ensuring an
adequate haemoglobin, use of fluid boluses according to
response;
d) optimising contractility — using inotropes (such as adrenaline,
dopamine), inodilators (such as milrinone) or a calcium infusion;
e) optimising afterload — by achieving normothermia and using
inodilators (such as milrinone) or vasopressors (such as
noradrenaline or vasopressin), depending on the SVR;
f) supporting end-organ function — such as with renal
replacement therapy;
g) considering steroid therapy — such as with hydrocortisone.
Glucocorticoids have been used in inotrope-resistant shock in
the PICU for many non-cardiac causes. In cardiac children, the
baseline cortisol level does not seem to be associated with the
response seen. Whilst steroids may improve blood pressure and
inotropic requirement, their use has not been associated with
improved mortality but does increase morbidity, such as
infections;
h) extracorporeal life support — if LCOS is refractory to medical
management.
299
14 How is postoperative junctional ectopic tachycardia
managed?
Arrhythmias occur in around 5-15% of all children undergoing
•
congenital cardiac surgery. Of those, junctional ectopic tachycardia
(JET) is the most common and problematic.
The aetiology of JET is believed to be oedema or damage to the
•
bundle of His and surrounding tissues. It generally occurs within the
first 24-72 hours following surgery and is self-limiting, often
terminating within 7-10 days.
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