Open chest

Cite this article as:
Marc Anders. Open chest, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3705

Negative impact on haemodynamics and respiratory parameters after median sternotomy was first described in 1975, with emphasis on “compression of the heart and producing a cardiac tamponade”.


Indications for delayed sterna closure and open chest:

  • ‘Large’ heart syndrome
  • Haemodynamic instability after temporal sternal approximation
  • Low cardiac output post CPB
  • ECMO or VAD cannulation
  • Severe arrhythmia
  • Severe bleeding complications
  • Severe contamination requiring frequent reexploration

Potential complications due to delayed sterna closure with increased rate of infection, longer PICU stay.

Effects of sternal closure:

  • Increase in intrathoracic pressure
  • Decrease in total lung compliance
  • Decrease in systolic/mean BP
  • Decrease in SV, leading to a decrease in CO
  • Decrease in cerebral oxygenation

Indication for chest closure:

  • When the patient is ready!
  • Haemodynamically stable (age appropriate MAP with minimal inotropic support, stable CVP, LA, PAP, stable heart rat and rhythym, appropriate CRT)
  • Respiratory stable (acceptable ventilation settings, FiO2 requirements)
  • Stable fluid status (oedema, fluid balance over last 12/24 hrs)

Preparation for sterna closure in PICU:

  •  Sterile surgical field (gown, mask)
  • Standard monitoring (ECG, invasive BP, CVP (LA, PAP, pacemaker, SaO2, etCO2, ventilation parameters)
  • Standard setup: standby for inotropic support with adrenaline or dobutamine (noradrenaline infusion), adrenaline 10 mcg/kg bolus, fluid resuscitation with NaCl 0.9%, human albumin and PRBC (minimum 2 units crossmatched), good floating fluid line and separate inotropic line, accessible outside the surgical field
  • Cephazolin 25-50 mg/kg IV minimum 30 mins preceding the surgical procedure
  • Fentanyl 5 mcg/kg IV bolus and midazolam 100 mcg/kg IV Bolus plus vecuronium 0.1 mg/kg IV bolus to provide adaequate anaesthesia and muscle relaxation

Observe during and post sternal closure: haemodynamic/respiratory/fluid and metabolic stability


References:

[1] J Thorac Cardiovasc Surg. 2010 Apr;139(4):894-900: Horvath et al: Cerebral and somatic oxygen saturation decrease after delayed sternal closure in children after cardiac surgery

[2] Cardiol Young. 2009 Dec;19(6):573-9. Vojtovic P et al: Haemodynamic changes due to delayed sternal closure in newborns after surgery for congenital cardiac malformations

[3] J Thorac Cardiovasc Surg. 1997 May;113(5):886-93: Tabbutt et al: Delayed sternal closure after cardiac operations in a pediatric population


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Nutrition

Cite this article as:
Marc Anders. Nutrition, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3905

Facts:

1. Nutritional support for children in PICU is important to prevent deficiency and remain in a positive or neutral neutrogen balance

2. Overfeeding is associated with adverse effects

3. There is no clear evidence supporting PN over TPN

4. If the bowel works, use it !

5. Always slowly introduce lipids !

5. Cautiously introduce enteral feeding where there is low CO!

Energy requirements in healthy children
premature 110 – 120 kcal/kg/d
0 < age < 1 90 – 100 kcal/kg/d
1 < age < 7 75 – 90 kcal/kg/d
7 < age < 12 60 – 75 kcal/kg/d
12 – 18 30 – 60 kcal/kg/d
Feeding the healthy neonate
Day Dextrose Protein Lipids
g / kg /d
1 4 – 8 1 ( – 3) 1
2 4 – 8 1 ( – 3) 2
3 5 – 10 1 ( – 3) 3
4 5 – 12 2 ( – 3) 3
5 6 – 15 2.5 ( – 3) 3
6 7 – 16 2.5 ( – 3) 3
Feeding the healthy child
Age Dextrose Protein Lipids
g / kg /d
< 1 mo 7 – 16 2.7 1 – 3
< 6 mo 7 – 16 1.5 1 – 3
< 1 y 7 – 16 1 – 1.5 1 – 3
< 7 y 5 – 15 0.9 1 – 2
< 12 y 5 – 15 0.9 1 – 2
> 12 y 5 – 10 0.9 1 – 2

 

  • 1 Kcal = 1 calorie = 1000 cal = 4184 joules
  • 1 g dextrose = 3.8 Kcal
  • 1 g protein = 4 Kcal
  • 1 g lipid = 9 Kcal

References:

[1] Intensive Care Med, 2004, 30(9), 1807-13: van der Kuip M: Nutritional support in 111 pediatric intensive care units: a European survey

[2] Cochrane Database Syst Rev. 2009, 15;(2):Joffe et all: Nutritional support for critically ill children

[3] Ger Med Sci, 2009 Nov 18;7, Doc15: Fusch et all: Neonatology/Paediatrics – Guidelines on Parenteral Nutrition, Chapter 13

[4] J Parenter Enteral Nutr. 2009 May-Jun;33(3):260-76: A.S.P.E.N. Clinical Guidelines: Mehta et al: nutrition support of the critically ill child

[5] J Parenter Enteral Nutr. 2010 May-Jun;34(3):247-53: Jaksic et al: A.S.P.E.N. Clinical guidelines: nutrition support of neonates supported with extracorporeal membrane oxygenation JPEN


Table: nutrition in EBM/formula:

Formula / Additive

kCal

/ml

Prot (g)

/ 100ml

Fat (g)

/ 100ml

CHO (g)

/ 100ml

INFANT FEEDS 0 – 12 MONTHS or < 8kg
Human Milk/ EBM 0.69 1.0 4.3 7.2
Human Milk + 2 blue scoops Karicare 0.83 1.3 4.9 8.8
Karicare Gold Plus 1 ¼ strength 0.83 1.7 4.4 9.1
Infatrini FS 1.0 2.6 5.4 10.3
Pepti-junior Gold FS (partially hydrolysed) 0.67 1.8 3.6 6.9
Pepti-junior Gold 1 ¼ strength 0.84 2.25 4.5 8.6
Neocate LCP FS (extensively hydrolysed) 0.70 1.9 3.4 7.9
Neocate LCP 1 ¼ strength 0.87 2.4 4.2 9.9
Monogen FS (MCT based feed – chylothorax) 0.75 2.0 2.1 12.0
Monogen 1¼ Strength 0.93 2.5 2.6 15
Kindergen FS (renal) 1.0 1.5 5.3 11.8
Kindergen 1¼ Strength 1.25 1.9 6.6 14.8
Neocate advance FS (>12months) 1.0 2.9 5.1 10.5
PAEDIATRIC FORMULAE 1-6 YEARS
* Nutrini Multi-fibre
(0.8g fibre per 100ml)
1.0 2.8 4.4 12.3
Nutrini 1.0 2.8 4.4 12.3
Nutrini Energy 1.5 4.1 6.7 18.5
ADULT FORMULAE >12 YEARS or 45kg
* Nutrison multi-fibre (1.5g per 100ml) 1.0 4.0 3.9 12.3
Nutrison Standard 1.0 4.0 3.9 12.3
Nutrison Energy 1.5 6.0 5.8 18.5
Nutrison Energy multi-fibre (1.5g per 100ml) 1.5 6.0 5.8 18.5
ADDITIVES (per 100ml) – per gram or ml
Duocal 1x Blue Scoop (1.2g) 5.9 0 0.27 0.87
Polyjoule 1x Blue Scoop (1.2g) 4.6 0 0 1.1
Protifar 1x Blue Scoop (0.85g) 3.1 0.75 0.014 0.013
Per ml MCT oil 8.4 0.95
Karicare Gold 1x Blue Scoop 6.9 0.15 0.37

0.72

 


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Maintenance fluids

Cite this article as:
Marc Anders. Maintenance fluids, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3901

Maintenance fluid [ml/hr] requirements for ≤10 kg:

Wt / kg 3 5 7 9 10
Active 12 20 28 36 40
Inactive 6 10 14 18 20
Fever add 10 % for every 1 o Celsius
Hypothermia deduct 12 % for every 1o Celsius
30 % post OP Cardiac Day 1 4 6 9 12 13
50 % post OP Cardiac Day 2 6 10 14 18 20
Burns add 4 % for every 1 % burnt (day 1)
add 2 % for every 1 % brunt (day 2)

Maintenance fluid [ml/hr] requirements for ≥11 kg & <20 kg

Wt / kg 11 13 15 17 20
Active 42 46 50 54 60
Inactive 21 23 25 27 30
Fever add 10 % for every 1 o Celsius
Hypothermia deduct 12 % for every 1o Celsius
30 % post OP Cardiac Day 1 14 15 17 18 20
50 % post OP Cardiac Day 2 21 23 25 27 30
Burns add 4 % for every 1 % burnt (day 1)
add 2 % for every 1 % brunt (day 2)

Maintenance fluid [ml/hr] requirements for ≥21 kg:

Wt / kg 21 30 40 50 60
Active 61 70 80 90 100
Inactive 30 35 40 45 50
Fever add 10 % for every 1 o Celsius
Hypothermia deduct 12 % for every 1o Celsius
30 % post OP Cardiac Day 1 20 23 27 30 33
50 % post OP Cardiac Day 2 30 35 40 45 50
Burns add 4 % for every 1 % burnt (day 1)
add 2 % for every 1 % brunt (day 2)

 


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Fluids

Cite this article as:
Marc Anders. Fluids, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3689

Anion gap = Na+ + K+ – (Cl + HCO3). normal 8-12 mEq/l.

Total body water (TBW) = intracellular fluid (ICF) plus extracellular fluid (ECF). [Weight x 600 ml in adults (500 ml in female), Weight x 650 ml in paeds, Weight x 700 ml in neonates]

ECF = intravascular fluid (plasma and lymph in the vessels) plus interstitial fluid (between cells)

Osmolality = 2 x Na+ + K+ + Glucose (mmol/l) + Urea (mmol/l).

Osmotic gap = measured osmolality – calculated osmolality

Na+ deficit [mmol/l] = (Na+Target – Na+Current) x TBW / 1000

Cl deficit [mmol] = (ClTarget – ClCurrent) x 0.2 x Weight

Water deficit = 4 ml x Weight x (Na+Target – Na+Current)

Maximum change in osmolality in hyper- or hypoosmolaric: 1 mmosmol/l per hour. Cave central pontine myelinolysis


Body water and blood volume composition with age

Adult bodies are 60% water (20% ECF, 40% ICF). Blood volume 70 ml/kg.

Term neonate bodies are 75% water (40% ECF, 35% ICF), and term neonates usually lose 5-10% of their weight in the first week of life, almost all of which is water loss. Blood volume 80 ml/kg.

Preterm neonates have more water (at 23 weeks gestation, 90% water composed of 60% ECF and 30% ICF), and they may lose 10-15% of their weight in the first week of life.

Small for gestational age (SGA) preterm infants may have a higher proportional body water content (90% for SGA infants vs 84% for appropriate for gestational age [AGA] infants at 25-30 weeks gestation).

Maintenance Fluid [ml/hr] for active Children > 2 days
≤ 10 kg: 11 kg & < 20 kg ≥ 21 kg
4 ml/kg/hr 40 ml/hr +
2 ml/kg/hr
60 ml/hr +
1 ml/kg/hr

 

Day 1 Day 2 Day 3
Maintenance Fluid [ml/hr] active Neonates ≤ 3 days
2 ml/kg/hr 3 ml/kg/hr 4 ml/kg/hr
NaRequirements for active Neonates ≤ 3 days
1 – 3 mmol/kg/d 3-5 mmolk/kg/d 2-4 mmol/kg/d
K+ Requirements for active Neonates ≤ 3 days
1 – 2 mmol/kg/d 2-3 mmol/kg/d 1-2 mmol/kg/d

 

Normal maintenance fluid:
NaCl 0.9 % or NaCl 0.9 % in 5 % Dextrose or NaCl 0.9 % in 2.5 % Dextrose or Ringer Lactate or Hartmann Solution

References:

[1] Pediatrics, 1957, May;19(5):823-32: Holliday at all: The maintenance need for water in parenteral fluid therapy.

[2] Kidney Int., 2005, Jan;67(1):380-8: Friedman: Pediatric hydration therapy: historical review and a new approach.

[3] Pediatr Nephrol. 2005, Dec;20(12):1687-700: Moritz ML at all: Preventing neurological complications from dysnatremias in children.

[4] Arch Dis Child, 2006, 91(3):226-32: Neville at all: Isotonic is better than hypotonic saline for intravenous rehydration of children with gastroenteritis: a prospective randomised study.

[5] N Engl J Med 2011;364:2483-95: Maitland et al: Mortality after Fluid Bolus in African Children with Severe Infection


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Chest drains

Cite this article as:
Marc Anders. Chest drains, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3699

If losses >10 ml/kg/hr in a postoperative patient, notify surgeon immediately.

In the first two hours, losses may be up to 5 ml/kg/hr, thereafter it should be less than 2 ml/kg/hr. If losses exceeds these levels, check ACT, aPTT, PT, fibrinogen, platelets and TEG, and transfuse accordingly.

If significant losses continue, notify surgeons.


Insertion of chest drains:

Preparation and equipment:

1. Chest tube set and tray.

2. Choose appropriate size.

3. CXR before procedure.

4. Identify insertion site via ultrasound (ensure distance from liver, kidneys, spleen or heart).

5. Prepare chest tube insertion site with antiseptic solution and sterile drapes in standard fashion (sterile gown, gloves, head and face mask).

6. Consider local anaesthetic (i.e. lignocaine; remember: 1% = 10mg/ml, maximum lignocaine dose 5 mg/kg without adrenaline).

7. Attach introducer needle to syringe and advance slowly and carefully needle over the superior border of the rib into the pleural space. Fluid or air should be aspirated to verify intrapleural position.

8. When the appropriate drainage site and depth has been identified, de-attach syringe and slowly introduce the J-tip of the guidewire: the guidewire should pass through and into the pleural space without any resistance!

9. Remove the needle, but leave wire in situ.

10. While maintaining the wire position, dilate the tract by supplied dilator (hold dilator always at the tip, next to the skin, rotate it carefully to prevent the wire from kinking)

11. Remove dilator, keep the guidewire in situ, advance the chest tube slowly into the pleural space (if any resistance, ensure the guidewire is still in situ, re-dilate skin/pleural opening, if necessary).

12. Remove guidewire, leaving the chest tube in situ.

13. Use sutures or steri-strips to secure the chest tube.

14. Attach 3-way tap and connect the tip of the chest tube via connector to a chest tube (use minimal suction – 10 cmH2O)

15. CXR to confirm position and success!

16. Observe ventilation pressures and FiO2 always before, during and after the procedure.


Removal of chest drains:

Preparation and equipment:

1. Keep patient fastened. Food/formula 6 hours, breast milk 4 hours, clear fluids 2 hours.

2. Continue monitoring: ECG, SpO2, BP.

3. All emergency equipment available.

4. Appropriate analgesia.

Age < 6 month > 6 month
Morphine 20 mcg/kg
Ketamine 0.5 mg/kg
if dysphoric response with Ketamine, consider
midazolam 0.1 mg/kg, can be repeated once

 

5. Remove drain in aseptic technique during expiration.

6. Repeat CXR 30 mins after drain removal to exclude pneumothorax.


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Blood products

Cite this article as:
Marc Anders. Blood products, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3678

Pump blood

Pump blood is the blood remaining in the bypass circuit on the completion of bypass. It is a mixture of the patient’s own blood, other fluids and any bank blood used to prime the bypass circuit.

Unfiltered pump blood has a low Hct and contains large amounts of heparin and inflammatory cytokines. The use of CUF (continuous ultrafiltration) during bypass or MUF (modified ultrafiltration) after bypass, concentrates the pump blood and removes some heparin and cytokines. If pump blood is used, additional heparin reversal will be needed. It should not be used if there is excessive bleeding or if the Hb is low.

Protamine sulphate is used to reverse the heparin in pump blood. The dose is 1 mg per 25 ml of pump blood. Recheck ACT after 10 ml/kg pump blood. Rapid infusion may cause pulmonary hypertension.


Packed red blood cells (PRBC)

Each unit of pack cells contains ~ 300ml and has an Hct of 0.5-0.7 (Na+ ~20, K+ up to 2 0mmol/l, especially if irradiated)

Warning: Neonates should be transfused with blood which is as fresh as possible, and sufficiently slowly to minimise any adverse effect from hyperkalaemia and citrate toxicity (hypocalcaemia).

Used for treatment of anaemia and the management of active bleeding. Must be compatible with recipients ABO and Rh groups and clinically significant red cell antibodies.

Transfusion of 4 ml/kg increases Hb by approximately 1 g/dl. In rapid transfusion situations alternate red cell units with colloid solutions e.g. FFP.

Store only in a designated blood refrigerator (2 to 6°C). Use within 4 hours of removing from refridgerator and always use a leucocyte filter.

Request irradiated products if suspicion of immunodeficiency (e.gg Di George anomaly) or in any neonate <1 month undergoing cardiac surgery.

Donor blood exposes the patient to risk of infection and transfusion reaction. Pump blood, however is blood to which the patient has already been exposed.


Platelets

Cardiopulmonary bypass frequently leads to both thrombocytopenia (dilutional) and more importantly platelet dysfunction (early onset). Platelet transfusion should be considered for excessive bleeding, irrespective of the absolute platelet count. Transfused platelets have a storage (function) defect lasting 2-4 hrs.

Platelet transfusion should not be used for “routine” volume expansion. Should be ABO compatible to prevent haemolysis caused by donor anti-A and anti-B. Female infants and children (all females <45 years) should receive RhD negative platelets. The dose is 10 ml/kg – repeat platelet count and/or TEG.


Fresh frozen plasma

Plasma separated from one donation of blood. Contains normal levels of stable clotting factors, albumin and immunoglobulin. Factor VIII levels are ~70% normal while plasma proteins (immunoglobulins and clotting factors) are slightly diluted.

It should be ABO compatible to prevent haemolysis by donor anti-A or anti-B.

Should be used for microvascular bleeding following massive transfusion or cardiopulmonary bypass, emergency reversal of warfarin effect (in addition to Vitamin K), bleeding resulting from hepatic failure and proven coagulopathy (factor deficiency or DIC).

Loss of clotting factors may occur as a result of excessive loss of peritoneal, pleural fluid or ascites (via PD catheter). If replaced with NaCl 0.9% alone this may lead to a dilutional coagulopathy.

Dose is 10-20 ml/kg IV. FFP should ideally administered slowly (<40 ml/kg/hr) as rapid administration can result in cardiovascular collapse by several mechanisms including calcium chelation by citrate (check patient iCa if concerned).Infection risk similar to other blood components. Transfusion should not be used for ‘routine’ volume expansion.


Cryoprecipitate

The cold precipitated fraction derived from FFP. Contains factor VIII, fibrinogen, von Willebrand factor and factor XIII.

Should be used for significant fibrinogen deficiency associated with clinical bleeding, DIC, trauma or during invasive procedures. Suitable for haemophilia and von Willebrand disease. Dose is 5 ml/kg IV. One bag is usually 20-30 ml. Infection risk is similar to other blood components.


Human albumin solutions

Albumex 4% Albumex 20%
Protein 40 g/l Protein 200 g/l
Na 140mmol/l Na 48 – 100mmol/l
Volume expansion Hypoproteinaemia
50, 250, 500ml bottle 10, 100ml bottle
5 – 10ml/kg aliquots 5ml/kg aliquots

Albumex 20% is hyperoncotic and in an ideal situation (ie. normal capillary permeability) should expand circulating volume by a factor of 5.


References:

[1] Cochrane Database Syst Rev. 2011 Mar 16;3: Perel et al: Colloids versus crystalloids for fluid resuscitation in critically ill patients

[2] SAFE Study Investigators, Finfer et al: Effect of baseline serum albumin concentration on outcome of resuscitation with albumin or saline in patients in intensive care units: analysis of data from the saline versus albumin fluid evaluation (SAFE) study

[3] Pediatr Crit Care Med. 2007 Sep;8(5):459-64: Jatana et al: Deletion 22q11.2 syndrome–implications for the intensive care physician

[4] Peditar Crit Care Med 2011 Vol.12, No2: Isthaphanous: Red blood cell transfusion in critically ill children: A narrative review


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Anticoagulation

Cite this article as:
Marc Anders. Anticoagulation, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3723

UNFRACTIONATED HEPARIN (UFH)

Indications:

Low dose heparin infusions are used in the maintenance of central venous lines, arterial lines and the prevention and treatment of deep vein thromboses.


Administration:

Heparin can be administered by intravenous and subcutaneous routes. This protocol applies to the intravenous route only.

Heparin is compatible with 5% dextrose, 0.9% NaCl and 0.45% NaCl.

  • Obtain patient weight and baseline FBC, aPTT, INR
  • For maintenance of central line in infants less than 5 kg commence 10 U/kg/hr
  • For shunt prophylaxis in any patient commence 10 U/kg/hr once no major postoperative bleeding
  • The need for monitoring will be individualised for each patient. In general it is recommended an aPTT be obtained at 24 hours, and some stable patients may require aPTT only every 2-3 days
  • Twice weekly FBC must be obtained to monitor for heparin induced thrombocytopaenia (consider HIT ELISA screen)
  • Coagulation studies required for other reasons should not be obtained from a line containing heparin

 

Adverse events:

Bleeding whilst on low dose heparin is uncommon, but can occur. If bleeding occurs, cease heparin infusion. Check FBC, clotting and TEG. Consider seeking haematology consult.

Antidote: protamine

 

Precautions:

In patients with renal failure this low-dose heparin infusion may result in therapeutic anticoagulation.

Standard Therapeutic IV UFH Protocol
Age < 1year > 1year Adult
Loading 75U/kg 75U/kg 5000U
Maintenance 25U/kg/hr 20U/kg/hr 1500U/hr

Obtain venous blood sample for aPTT 4 hours post completion of loading infusion (NOT earlier). Adjust heparin infusion rate to maintain aPTT 60-85 s.

Normogram for adjusting UFH IV Dose
aPTT (sec) Bolus (U/kg) Hold (min) Rate Change (U/hr) repeat aPTT
< 50 50 0 + 20% 4hrs
50 – 59 0 0 + 10% 4hrs
60 – 85 0 0 No change 24hrs
86 – 95 0 0 – 10% 4hrs
96 – 120 0 30 – 10% 4hrs
>120 0 60 -15% 4hrs

 

Monitoring of therapy: 

Heparin is usually monitored by aPTT. However, this may be inaccurate in certain clinical circumstances. An alternative is an anti-Xa assay.

 

Heparin antidote:

If anticoagulation with heparin needs to be discontinued for clinical reasons, termination of the heparin infusion will usually suffice. If an immediate effect is required, consider administering protamine sulfate.

Protamine is a medication that requires a high level of caution when being prescribed and administered. Outside cardiac surgery and ICU, consultant or fellow approval is required for the use of protamine – do not allow this to lead to delayed administration in the case of bleeding. Contact the appropriate senior person immediately.

Protamine sulfate neutralises heparin by virtue of its positive charge. Following IV administration, neutralisation occurs within 5 minutes.

The maximum dose of protamine sulfate, regardless of the amount of heparin received is 50 mg except for reversal of heparin following cardiopulmonary bypass.

Protamine sulfate is usually administered in a concentration of 10 mg/ml at a rate not to exceed 5 mg/minute. If administered too quickly, protamine sulfate may cause cardiovascular collapse (severe pulmonary hypertension).

Patients with known hypersensitivity reactions to fish, and those who have received protamine-containing insulin or previous protamine therapy may be at risk of hypersensitivity reactions to protamine sulfate.

Obtain blood for PT and aPTT 15 mins after the administration of protamine sulfate.

The dose of protamine sulfate is based on the amount of heparin received in the previous 2 hrs as follows:

Time since last
Heparin dose
Protamine dose (mg) per 100U Heparin received
< 30min 1mg
30 – 60min 0.5 – 0.75mg
60 – 120min 0.375 – 0.5mg
> 120min 0.25 – 0.375mg

LOW MOLECULAR WEIGTH HEPARIN (LMWH)

Indications:

Low molecular weight heparins are used for the prophylaxis or treatment of deep vein thrombosis. The decision to use LMWH instead of standard heparin (or warfarin) will depend upon the clinical scenario and individual patient factors such as risk of bleeding or availability of venous access.

The following are guidelines only and may need to be adapted in individual circumstances.

 

Administration:

  • Obtain patient weight and baseline FBC, aPTT, PT.
  • Dose as follows, administering via subcutaneous route, either via an insuflon catheter, or by rotating sites of subcutaneous injections.
  • Timing of commencement of therapy (especially post-procedural) should be individualised.
  • Duration of therapy is determined on an individualised basis, based up on indication for treatment.
LMWH (Enoxaparin) in infants and children
Age < 2mths 2 mth – 18 yrs
Treatment 1.5 mg/kg/dose BD 1mg/kg/dose BD
Prophylaxis 0.75 mg/kg/dose BD 0.5mg/kg/dose BD
LMWH (Dalteparin) in adults (100U = 1mg)
Treatment 100 U/kg/dose BD
Prophylaxis 2500-5000U OD
Normogram for LMWH therapy
Anti-Xa level (U/ml) ? Hold next dose Dose change ? repeat Anti-Xa level
< 0.35 No + 25% 4hrs post next dose
0.35 – 0.49 No + 10% 4hrs post next am dose
0.5 – 1.0 No No change Once per week / 4hrs post am dose
1.1 – 1.5 No – 20% 4hrs post next am dose
1.6 – 2.0 3hrs – 30% Trough level pre next dose, then 4hrs post next am dose
> 2.0 Until Anti-Xa < 5U/ml – 40% Trough level pre next dose and if not <0.5U/ml repeat BD

 

Adverse events:

The major adverse event related to treatment with LMWH is bleeding.

If a patient on LMWH develops a major bleed, withhold further doses and seek an urgent haematology consult.

HIT is rare in LMWH treatment, but consider if rapid fall in platelet count.

Antidote: protamine

 

Precautions:

In patients with renal failure this low-dose heparin infusion may result in therapeutic anticoagulation. It is recommended that prior to any surgery or spinal or epidural procedure, 2 doses of LMWH be omitted. Haematology consult to advise on management around such procedures is advised.

 

Heparin antidote:

If anticoagulation with LMWH needs to be discontinued for clinical reasons, termination of the heparin infusion will usually suffice. If an immediate effect is required, consider administering protamine sulfate. Protamine is a medication that requires a high level of caution when being prescribed and administered. Outside cardiac surgery and ICU, consultant or fellow approval is required for the use of protamine – do not allow this to lead to delayed administration in the case of bleeding. Contact the appropriate senior person immediately.

Protamine sulfate neutralises heparin by virtue of its positive charge.

  • If protamine is given within 8 hrs of the LMWH then a maximum neutralizing dose is 1 mg protamine/1mg (or 100U)) of LMWH given in the last dose.
  • If more than 8 hours have passed since the dose of LMWH was given, administer 0.5 mg protamine per 1mg (or 100U) of LMWH given.

Protamine is administered by slow IV infusion (over 10 mins) to avoid a hypotensive reaction.


ASPIRIN

Aspirin is a medication only available for oral administration (in Australia). Tablets are available in enteric and non-enteric coating. Dispersible tablets are also available. For infants and small children it may be necessary to either crush tablets or use a dispersible tablet and administer the aspirin in liquid form. These guidelines are for the use of aspirin for its antiplatelet activity.

 

Indications:

Aspirin is commonly used in patients with cardiac disease and those with a history of arterial stroke. There are also certain indications for the use of aspirin in pregnancy. It is more commonly used in patients with or at risk of arterial thrombosis. There is no data to support the use of aspirin in the treatment/prevention of venous thromboembolism.

 

Administration and maintenance:

  • Aspirin is commenced only when patients are permitted oral intake
  • Commence 3-5 mg/kg/day to a maximum of 100mg
  • Continue aspirin therapy as clinically indicated. For primary and secondary prophylaxis at least 3 months therapy is recommended.
  • Post Norwood procedure or in patients with shunt., prophylaxis is required until surgical correction.

 

Therapeutic monitoring is not required!

 

Precautions:

A significant association between Reyes syndrome and the ingestion of aspirin by children with influenza-like illness or chicken pox has been reported in the literature.

Parents should be educated regarding the risk of developing Reyes Syndrome secondary to aspirin therapy. It should be clearly explained that aspirin therapy must be stopped in the presence of fever and/or chicken pox or measles. Paracetamol is permitted in this scenario.

The concurrent use of non-steroidal anti-inflammatory medications and aspirin is not recommended.

 

Mechanism:

Irreversible platelet inactivation. Once therapeutic doses are taken, antiplatelet effect remains for the lifespan of the platelet population which is 7-10 days. Patients scheduled to undergo surgical procedures should in general, stop aspirin 7-10 days prior to surgery.

Perioperative aspirin therapy may increase the risk of perioperative bleeding. The timing of cessation of aspirin therapy is the decision of the primary physician.

 

Adverse effects:

Patients on aspirin therapy are at a slightly increased risk of bleeding and bruising. Usually this is not significant. If a patient develops significant bleeding or bruising whilst on aspirin, prompt referral to a haematologist is required.


CLOPDIOGREL

Clopidogrel is a theinopyridine derivate that produces its antiplatelet effect through an active metabolite, which irreversibly modifies the ADP purinergic P2Y12 platelet receptor.

 

Indications:

Clopidogrel is widely used in adult cardiac and cardiovascular ischaemic disease (MATCH Trial), however the use in children is based on single centre experience or safety trials (PICOLO Trial)

 

Administration and maintenance:

  • Clopidogrel is commenced only when patients are permitted oral intake
  • Commence 0.2 mg/kg/day
  • Continue aspirin therapy as clinically indicated. For primary and secondary prophylaxis at least 3 months therapy is recommended
  • Post Norwood procedure or in patients with shunt after surgical consultation. Prophylaxis is required until surgical correction

 

Adverse effects:

Patients on clopidogrel therapy are at a slightly increased risk of bleeding and bruising. Usually this is not significant. If a patient develops significant bleeding or bruising whilst on clopidogrel, prompt referral to a haematologist is required


THROMBOLYSIS WITH R-TPA (ALTEPLASE)

These guidelines are for systemic thrombolytic therapy. There is no data to support the use of local thrombolytic therapy in infants and children except for line blockages.

Indications:

Massive pulmonary embolism/pulmonary embolism not responding to heparin/arterial occlusions /potential for acute, extensive DVT threatening organ or limb viability.

 

Contraindications:

Active bleeding/significant potential for serious local bleeding/general surgery within the previous 2 days/neurosurgery within the previous 3 weeks/AV malformations/recent severe trauma.

 

Preparation for infusion:

  • Obtain patient weight, FBE, INR/PT, aPTT and fibrinogen. Platelet count must be 100. Fibrinogen must be >2.0. Administer FFP infusion 20 ml/kg (plus frusemide) if clinically indicated, especially in neonates <1 month (low plasminogen levels). Consider appropriate staffing requirements are in place to monitor infusion.
  • Ensure adequate venous access to: infuse thrombolytic therapy and obtain blood specimens during infusion.
  • Establish heparin infusion of 10 U/kg/hour to be administered continuously throughout thrombolytic infusion. If possible heparin should be administered for 6 hours prior to lysis as this may be advantageous for thrombolytic action.
  • Premedicate with paracetamol and/or promethazine due to potential for allergic reactions.

 

Administration:

Loading Infusion
FFP 20ml/kg in neonates< 1month
Heparin Preferably commence 10U/kg/hr,6hrs prior r-TPA 10U/kg/hr during r-TPA treatment
r-TPA No 0.5mg/kg/hrfor 6hrs

 

Monitoring:

  • HR and BP hourly
  • All puncture sites hourly during infusion and for 4 hours post infusion
  • Check fibrinogen at 3 hours into infusion and at completion
  • If any signs of bleeding and/or bruising occur – cease infusion, check FBC, clotting and TEG and seek urgent haematology consult
  • If treating a peripheral artery thrombosis, observe limb hourly for pulse, colour, temperature and capillary return

After r-TPA: cease lytic therapy at 6 hours and increase heparin to 20 U/kg/hour aiming for aPTT 60-85 s (no bolus). Arrange clinical review (e.g. Doppler ultrasound) to determine response or need for further thrombolysis.

 

Complications:

In 30-50% of patients a bleeding event will occur. This is usually in the form of oozing from a wound or puncture site. Treatment with local pressure is usually sufficient. Major bleeding (intracranial, retroperitoneal, external) can develop in up to 10% of patients. If bleeding occurs, cease infusion and seek an urgent haematology consult.

 

Precautions:

  • No IM injections during thrombolytic therapy
  • Minimise patient handling during infusion
  • Avoid concurrent use of warfarin and antiplatelet agents
  • Delay any invasive procedures such as urinary catheterisation, resiting venous/arterial access, or perform such procedures pre-thrombolytic infusion.

BLOCKED CVL LINES

Indications: CVLs that will not infuse properly or CVLs that will not allow for the withdrawal of blood samples when this is an essential function of that line. (e.g. haemodialysis, oncology patients).

Initial Management: obtain CXR to confirm line placement and absence of kinking. Ultrasound to rule out major vessel thrombosis.

 

Initial action if blood related blockage:

If unable to draw blood sample, unable to infuse blood or there is blood back-up in infusion line:

  • Attempt to aspirate
  • Flush with 0.9% N saline
  • If unsuccessful flush with strong heparin solution (100 U/ml) to a maximum of 5 ml
  • Give r-tPA in each obstructed lumen: <10 kg (0.5 mg r-TPA each lumen) or >10 kg (2.0 mg r-TPA each lumen) and leave for 2-4 hrs. Try to withdraw thereafter and flush with NaCl 0.9%
  • If able to flush line but no blood return, arrange diagnostic imaging as clinically indicated
  • If unable to flush line obtain surgical consult or consider venography and/or ultrasound

References:

[1] CHEST 2008; 133:887S-968S: Monagle P. et al: Antithrombotic Therapy in Neonates and Children. American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)

[2] CIRCULATION 2008, 117:553-559: Li et al: Dosing of Clopidogrel for Platelet Inhibition in Infants and Young Children: Primary Results of the Platelet Inhibition in Childen On cLOpridogrel (PICOLO) Trial


All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Weaning opioids and steroids

Cite this article as:
Marc Anders. Weaning opioids and steroids, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3890

Withdrawal from drugs (principally opioids) prolongs hospital admissions and causes morbidity!

Gradual weaning of drug dosing aims to prevent the onset of withdrawal abstinence syndromes:

  • regime one: 10% reduction in original dose per day weaning over 10 days or
  • regime two: 20% reduction in original dose per day weaning over 5 days
  • regime three: 20% reduction in original dose every 2nd day weaning over 10 days

All are equally effective and the shorter 5-day wean is not associated with any increased withdrawal symptoms requiring reinstitution of drug therapy 

The choice of regime is typically arbitrary based on length of therapy and clinician choice.


Dose conversion of IV and enteral:

Dose escalation and/or opioid rotation are both effective ways to combat tolerance (although there is an inevitable amount of cross tolerance) but not physical dependence.

Converting between opioids and route of administration involves documenting the total 24-hour dose being administered and then using the conversion table and calculating a total daily dose of the new drug via the new route.

Drug IV equivalent IV : morphine ratio enteral equivalent IV : enteral ratio
Morphine 10mg 1 : 1 30 mg 1 : 3
Codeine 100mg 10 : 1 200mg 1 : 2
Oxycodone 10mg 1 : 1 20mg 1 : 2
Fentanyl 100mcg 0.01 : 1 n/a n/a
Methadone 10mg 1 : 1 20mg 1 : 2

Dose conversion for IV midazolam into oral diazepam:

[Midazolam IV [rate in mcg/kg/min] x weight x 24 ] x 0.5 = Diazepam oral

References:

[1] Brunton, L et al (2010), Goodman and Gillman’s the Pharmacological Basis of Therapeutics 12th Edition, McGraw Hill Medical, New York

[2] Macintyre, PE et al (2010), Acute Pain Management: Scientific Evidence 3rd Edition, Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, Melbourne

[3] Miller, RD et al (2009), Miller’s Anesthesia 9th Edition, Churchill Livingstone Elsevier, Philadelphia

[4] Peck, TE & Hill, S (2008), Pharmacology for Anaesthesia and Intensive Care 3rd Edition, Cambridge University Press, Cambridge

[5] Sasada, M & Smith, S (2003), Drugs in Anaesthesia and Intesive Care 3rd Edition, Oxford University Press, Oxford

[6] Stoelting, RK & Hillier, SE (2005), Pharmacology and Physiology in Anesthetic Practise 4th Edition, Lippincott, Williams and Wilkins, Philadelphia

[7] Pediatrics 2010 May;125(5):e1208-25: Anand et al: Tolerance and withdrawal from prolonged opioid use in critically ill children.


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Muscle relaxation

Cite this article as:
Marc Anders. Muscle relaxation, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3883

Definition:

Muscle relaxants block transmission at the neuromuscular junction (NMJ) by interfering with nicotinic cholinergic receptors (AChRs). They are large polar molecules with small volumes of distribution that are not orally bioavailable and do not cross the placenta or blood-brain barrier.

They have no analgesic, anaesthetic or amnestic properties and so should never be given without appropriate sedative/anaesthetic drugs.

The clinical indications for muscle relaxation are:

  • to facilitate intubation of the trachea
  • to improve surgical and/or procedural working conditions
  • to facilitate intra-hospital and inter-hospital transfers
  • to prevent shivering in patients being therapeutically cooled
  • to facilitate mechanical ventilation including using mechanical ventilation to manipulate PaCO2 and acid-base status
  • to improve post-operative stability (especially in high-risk cardiac surgery and laryngo-tracheal surgery with or without complex / abnormal airway anatomy)

Drugs are classified as depolarising (mimic the actions of ACh) and non-depolarising (interfere with the actions of ACh).

Suxamethonium is the only depolarising neuromuscular blocking drug still in clinical use.

Non-depolarising neuromuscular blocking drugs are classified as long-acting (pancuronium), intermediate-acting (rocuronium, vecuronium, atracurium & cisatracurium) and short-acting (mivacurium).

Drug selection is influenced by desired speed of onset, duration of action and the possibility of drug induced side effects (see table of drugs).

Among suxamethonium’s myriad of adverse effects it is also a known trigger for malignant hyperthermia (genetically abberant muscle sarcoplasmic reticulum calcium channels) – the treatment is active cooling and dantrolene 1 mg/kg up to 10 mg/kg.

Patients with genetically abdnormal pseudocholinesterase will have prolonged neuromuscular blockade with suxamethonium (choline apnoea) – they need supportive care until it is cleared (severe cases require dialysis to clear the drug) and an assessment of their pseudocholinesterase function (dibucaine number).

Suxamethonium and rocuronium (see table: muscle relaxants rapid onset) are the only drugs capable of producing intubating conditions in 60-90 seconds and so are the only drugs used for rapid sequence induction (RSI). Suxamethonium has a brief duration of action where as an RSI-dose of rocuronium will have a prolonged duration of action.

The duration of action of non-depolarising neuromuscular blocking drugs is prolonged by hypokalaemia, hypocalcaemia, hypoproteinaemia, hypermagnesaemia, dehydration, acidosis and hypercapnoea.


Potency of neuromuscular blocking drugs is described by the effective dose (ED) necessary to depress single-twitch depression by 95% in the adductor pollicis muscle – ED95 (intubating doses are generally two times the ED95 dose; the RSI-dose for rocuronium is four times its ED95); potency is centrally located, and central muscles (larynx, jaw and diaphragm) develop neuromuscular blockade faster, experience less profound block and recover more quickly than in more peripherally located muscles (adductor pollicis). Eyelash reflex and orbicularis inversely related to onset time.


Monitoring of depth of neuromuscular blockade:

Nerve stimulators are used to monitor the depth of neuromuscular blockade.

There is a margin of safety regarding nAChRs at the NMJ and the generation of a myocyte action potential such that >75% of nAChRs must be occupied by drug before clinically significant (and detectable) blockade is apparent.

Neuromuscular blocking drugs must occupy at least 75% of nAChRs before there is clinically significant and detectable blockade (this is the margin of safety with regard to nAChR numbers and transmission at the NMJ).

The ulnar or radial nerves are commonly used with the negative electrode on the volar surface of the wrist directly over the nerve to be stimulated and the positive electrode at least 3 cm distal where it cannot interfere with the relevant muscle groups.

A current of 60 mA (maximum 80 mA) is applied for 0.1 ms (maximum 0.3 ms) per stimulation; the patterns of stimulation used in PICU are the train-of-four (TOF) count, tetanic (>30 Hz) stimulation and post-tetanic count.

The TOF ratio is the ratio of the height of the first twitch (T1) to the fourth twitch (T4) – this is not easily interpretable if only using visual and tactile evaluation of the response. The TOF count (absolute number of twitches) is easier to detect and interpret:

  • T4 begins to reduce in height at >70% receptor occupancy;
  • T1 starts to reduce in height at >80% occupancy;
  • T4 disappears at >90% occupancy;
  • T1 disappears at >95% occupancy.

Tetanic stimulation (usually 50 Hz) is known to increase subsequent twitch height either by mobilising ACh stores and/or increasing calcium influx into the nerve ending; When the TOF count is zero (>95% blockade) then a tetanic stimulation and a post-tetanic (TOF) count can help define deep neuromuscular blockade.

  • The effects of tetany last for up to 6 minutes and this must be taken into consideration if repeat testing occurs
  • If the TOF-count is zero and the post-tetanic count is also zero – this signifies either very deep neuromuscular blockade or a malfunctioning nerve stimulator (test it on yourself)

Reversal of neuromuscular blockade:

  • Antagonist-assisted reversal of neuromuscular blockade using anticholinesterases (edrophonium, neostigmine or pyridostigmine) reflects their inhibition of acetylcholinesterase (AChE) and the resulting increased ACh at the NMJ to compete for nAChR binding sites.
  • Neostigmine is generally used at a dose of 4-7 mcg/kg and is more suitable for reversing deeper levels of block.
  • Anticholinesterases produce typical and expected muscarinic side effects (mainly bradycardia, bronchoconstriction, increased secretions & GI hyper-peristalsis) and so should be given with an antimuscarinic anticholinergic drug such as atropine (20 mcg/kg) or glycopyrrolate (10 mcg/kg).
  • Sugammadex is a cyclodextrin that encapsulates rocuronium and vecuronium and effectively neutralises them; remaining drug diffuses away from the NMJ and its effects are reversed.
  • It acts within 2 minutes and has no other effects (as yet). The complex is excreted in the urine. The dose for routine reversal is 2-4 mg/kg; the dose for emergent reversal in a cant intubate-can’t ventilate scenario is 16 mg/kg.

Table: Muscle relaxants rapid onset

Suxamethonium Rocuronium
Type/class Dicholine ester Aminosteroid(intermediate acting)
ED95 0.3mg/kg 0.3mg/kg
Intubating dose 1mg/kg (adults)
2mg/kg (children)
3mg/kg (neonates)
0.6mg/kg
1.2mg/kg (RSI)
Onset time 30-60seconds 30-90seconds
Recovery time 3-5minutes 20-35minutes
Infusion dose n/a 5-15mcg/kg/min
VD 0.17L/kg 0.3L/kg
Protein binding 99% 30%
Clearance 40mL/kg/min 4mL/kg/min
t½-elim 3-5minutes 80minutes
Metabolism Plasma pseudocholinesterase No significant metabolism
Excretion Resulting choline is taken up into nerves<5% unchanged in urine Bile (50% unchanged)Urine (30% unchanged)
Hepatic failure No effect t½-elim up to 100 minutes
Renal failure No effect t½-elim up to 100 minutes
Pros Rapid onset & intense paralysis make it suitable for RSI

Suitable for RSI due to shorter onset timeNo histamine releaseMinimally affected by renal & hepatic impairment

May be reversed with sugammadex

Cons

Raised intra-gastric, intra-ocular & intra-cranial pressuresFasciculations that can lead to severe myalgia & even rhabdomyolysisBradycardia (muscarinic) +/- brady-arrhythmias

Hyperkalaemia (more so with neuromuscular disease & burns)

Malignant hyperthermia

Choline apnoea

Anaphylaxis

Will accumulate with prolonged infusions (ensure monitoring of depth of blockade)
Other points 80% of an administered dose is hydrolysed before reaching the NMJsRepeat doses should always be accompanied by an anticholinergic (consider routine anticholinergic administration in infants) There are rare reports of anaphylaxisIt does cause a small increase in intra-occular pressure

Table: Muscle Relaxans slow onset

Vecuronium Pancuronium Cisatracurium
Type/class Aminosteroid(intermediate acting) Aminosteroid(long acting) Benzylisoquinolinine(intermediate acting)
ED95 0.05mg/kg 0.06mg/kg 0.05mg/kg
Intubating dose 0.1mg/kg 0.1mg/kg 0.1mg/kg
Onset time 3-5minutes 3-5minutes 3-5minutes
Recovery time 20-35minutes 60-90minutes 20-35minutes
Infusion dose 0.5-2mcg/kg/min n/a 1-10mcg/kg/min
VD 0.27L/kg 0.26L/kg 0.2L/kg
Protein binding 60-90% 15-30% unknown
Clearance 5mL/kg/min 2mL/kg/min 5mL/kg/min
t½-elim 60minutes 132minutes 25minutes
Metabolism Hepatic with some active metabolites Hepatic with some active metabolites Hoffman elimination (no active metabolites)
Excretion Urine (25% unchanged)Bile (25% unchanged) Urine (80% unchanged)Bile (10% unchanged) Urine
Hepatic failure t½-elim up to 3 hours t½-elim up to 6 hours No change
Renal failure t½-elim up to 2 hours t½-elim up to 48 hours No change
Pros Commonly used medication with predictable onset & duration of actionNo histamine releaseMay be reversed with sugammadex Long acting
(decreased dosing requirements)
Non-organ clearance makes it unaffected by renal and/or hepatic impairmentStable offset time after prolonged infusions due to rapid Hoffman eliminationNo histamine release
Cons Will accumulate with prolonged infusion (ensure monitoring of depth of blockade) Minimally metabolized so sensitive to effects on hepatic & renal functionRisk of arrhythmias in patients on digoxin Potent drug with prolonged onset time
Other points Large doses may cause a slight (10-15%) drop in SVR and BP

10-15% increase in HR (mainly anticholinergic effect)Mild increase in BP secondary to increased HR (no inotropy)Useful for obviating HR effects of induction doses of narcotics

It may decrease the PT and APTT

One of 10 stereoisomers of atracurium (atracurium is not used often anymore due to histamine release and has a metabolite that can cause convulsions).

 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Intubation

Cite this article as:
Marc Anders. Intubation, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3880

Indication:

  • to secure the airway: severe airway obstruction/inadequate protective reflexes (coma or prolonged seizures)
  • to facilitate ventilation: hypoxaemic and/or hypercarbic respiratory failure

Intubation should NOT be attempted by the inexperienced if more skilled personnel are available. Two doctors always present if possible!


Assessment:

  • how urgent is the intubation?
  • anatomical abnormality, which would suggest difficult intubation?
  • any evidence of airway obstruction?
  • cardiovascular status – any hypovolaemia/hypotension?
  • is the patient fasted?

 Preparation equipment:

  • intubation drugs
  • volume replacement (10ml/kg NaCl 0.9%)
  • ETT (size = age/4 + 4 – for uncuffed ETT for cuffed ETT size = age/4 + 3.5), one size above and one size below calculated ETT
  • styllete, gum elastic bougie
  • laryngoscope with blade (check light bulb and battery)
  • Magill’s forceps
  • face mask
  • Guedel and nasopharyngeal airways
  • self inflating bag and anaesthetic circuit
  • suction equipment: Yankauer’s sucker and suction catheters
  • connector, cuff inflating syringe, tape
  • CO2 detector

Procedure:

  • monitor cardiovascular and respiratory status (ECG, SpO2, BP non-invasive/invasive)
  • explain to patient/parents
  • empty stomach if nasogastic tube is in situ
  • position patient: neutral position in neonates, young children – sniffing position in older children, adolescents
  • preoxygenation for minimum two minutes
  • consider atropine 20 mcg/kg IV
  • give analgesic agent
  • give sedative agent
  • apply gentle pressure to the cricoid
  • check for bag and mask ventilation possible with appropriate visual inflation/deflation and chest wall movement
  • give paralysis agent
  • continue bag and mask ventilation, while continuing to apply gentle cricoid pressure, except in circumstances where bag and mask ventilation is contraindicated (see rapid sequence induction)
  • intubate orally, release cricoid pressure
  • check ETT position: chest wall rise, auscultation and CO2 detector
  • once patient stabilised and appropriate ventilation, consider to change to a nasal ETT
  • once ETT position confirmed, tape ETT
  • insert nasogastric tube, empty stomach
  • CXR to confirm position of ETT and nasogastic tube
  • consider ongoing analgesia and sedation
  • document event

Intubation drugs:

see analgesia and sedation in PICU

Analgesia Sedation Paralysis
cardiovascular stable, no airway obstruction > 1 year

Fentanyl1 – 2mcg/kg

or

Morphine

100mcg/kg

Propofol1 – 2.5mg/kg Vecuronium 0.1mg/kg
cardiovascular stable, with airway obstruction > 1 year

Fentanyl1mcg/kg

or

Morphine

100mcg/kg

Ketamine1 – 2mg/kg Vecuronium 0.1mg/kg
cardiovascular stable, no airway obstruction < 1year

Fentanyl1 – 2mcg/kg

or

Morphine

100mcg/kg

Midazolam50 -100mcg/kg Vecuronium 0.1mg/kg
cardiovascular stable, with airway obstruction < 1 year Always seek senior assistance!Consider induction with volatile anaesthetic!
cardiovascular unstable, any age

Fentanyl1 – 2mcg/kg

or

Morphine

100mcg/kg

Vecuronium0.1mg/kg
rapid sequence induction

Fentanyl1 – 2mcg/kg

or

Morphine

100mcg/kg

Midazolam50 -100mcg/kg Rocuronium1mg/kg
patients with raised ICP

Fentanyl1 – 2mcg/kg

or

Morphine

100mcg/kg

Thiopentone2 – 7mg/kg Rocuronium1mg/kg
anticipated difficult airway Always seek senior assistance!Consider induction with volatile anaesthetic!

 


Unexpected difficult intubation:

  • call for help!
  • restart bag and mask ventilation with gentle cricoid pressure
  • optimise patient position
  • consider bougie or stylete
  • consider different laryngoscope blade

Cannot ventilate – cannot intubate:

  • call for help!
  • consider reposition of head
  • jaw thrust
  • insert Guedel/nasopharyngeal airway
  • use both hands to hold mask
  • release cricoid pressure
  • consider laryngeal mask (LMA)

    All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Inotropes and vasopressors

Cite this article as:
Marc Anders. Inotropes and vasopressors, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3876

Definition:

Inotropes: sympathomimetic agent which act on the sympathetic (or adrenergic) nervous system (β-receptors) resulting in positive inotropic (increase in contractility), chronotropic (increase in heart rate), dromotropic (increase in conduction of impulse) and lusitropic effect (improved diastolic relaxation)

Vasopressors: sympathomimetic agent which act on the sympathetic (or noradrenergic) nervous system (α-receptors) resulting in vasoconstrictor effect

The ideal vasoactive support agent: effect on cardiac output/effect on SVR/effect on myocardial oxygen consumption/no tachyphylaxis does not exist!


a) Sympathomimetics: endogenous catecholamines:

Adrenaline (β1 >> β2 and α1 > α2 agonist) via cAMP

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
– 0.05 ++ ++

↑ HR, SV, CO

(↓) SVR

0.05 – 0.10 +++ ↑ HR, SV, CO
0.10 – 0.20 +++ +++ +++

↑ HR, SV, SVR

(↓) CO

Side effects: increasing myocardial oxygen requirement, tachyarrhythmias, worsening diastolic function, tachyphylaxis, hyperglycaemia, lactate increase

Noradrenaline (α1 > α2 and β1 >> β2 agonist) via cAMP ?

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
– 0.10 +++ ++ +++

↑ SVR, HR

(↓) CO

0.10 – 0.20 ++++ +++ +++

↑ SVR, HR, SV

↓ CO

Side effects: increasing myocardial oxygen requirement, can cause decrease in CO, tachyphylaxis, hyperglycaemia

Dopamine (D1 and D2, higher doses: β1 >> β2 and α1 > α2 agonist) via cAMP. Precursor of norepinephrine

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
0.5 – 2 ↑ increased splanchnic perfusion
2 – 5 ++ ↑ HR, SV, CO
5 – 10 ++ ++

↑ HR, SV, SVR

(↓) CO

> 10 +++

↑ SVR

↓ CO

Side effects: increasing myocardial oxygen requirement, can cause decrease in CO, tachyarrhythmias, tachyphylaxis, hyperglycaemia, immunsuppressive effect, inhibition of thyrotropin releasing hormone

b) Sympathomimetics: synthetic catecholamines:

Dobutamine (β1 >> β2)via cAMP

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
2.5 – 10 ++ ++

↑ HR, SV, CO

(↓) SVR

> 10 +++ ↑ HR, SV, CO
Side effects: increasing myocardial oxygen requirement, tachyarrhythmias, worsening diastolic function, tachyphylaxis, hyperglycaemia

Isoprenaline (β)via cAMP

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
0.01 – 1 +++ + ↑ HR, SV, CO
Side effects: increasing myocardial oxygen requirement, tachyarrhythmias, worsening diastolic function, tachyphylaxis, hyperglycaemia

c) Sympathomimetics: synthetic noncatecholamines:

Phenylephrine (α1 >> α2 agonist) – resuscitation in Fallot spells

Dose

mcg/kg/min

α1 α2 β1 β2 Clinical effect
0.1 – 5 +++ ++ +++

↑ SVR

↓ HR (reflex), CO

Side effects: increasing myocardial oxygen requirement,

can cause decrease in CO, tachyphylaxis, hyperglycaemia


d) Phosphodiestarase inhibitors:

Milrinone via cAMP

Dose

mcg/kg/min

Clinical effect
Load: 50mcg/kg
0.2 – 1

↑ CO (positive inotropic and lusitropic effect)

↓ PVR, (SVR)

Side effects: arrhythmia, hypotension (ensure appropriate volume load)

e) Myofilament calcium sensitisers:

Levosimendan via increasing sensitivity to calcium

Dose

mcg/kg/min

Clinical effect

Load: 1.25mcg/kg

over 10min

Infusion: 0.2 ↑ CO (positive inotropic and lusitropic effect)
Side effects: arrhythmia, hypotension in the first hours

f) Vasoregulatory agents:

Vasopressin (V1 – arterial and V2 – tubular agonist)

Dose

IU/kg/hr

V& V2 Clinical effect
0.01 – 0.06 +++ ↑ SVR
Side effects: increasing myocardial oxygen reqirement, can cause decrease in splanchnic perfusion

References:

[1] Am Heart J 2002 Jan; 143(1) : 15-21: Hoffman TM et al: Prophylactic intravenous use of milrinone after cardiac operation in pediatrics (PRIMACORP) study.

[2] Lancet 2002, 306: 196-202: Follath F et al: Efficacy and Safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (the LIDO study); a randomised double-blind trial.

[3] Curr Opin Crit Care. 2010 Oct;16(5):432-41: Parissis et al: Inotropes in cardiac patients: update 2011

[4] Curr Opin Anaesthesiol. 2009 Aug;22(4):496-501: Salmenperä et al: Levosimendan in perioperative and critical care patients.

[5] Pediatr Cardiol. 2004 Nov-Dec;25(6):623-46: Barnes et al: The pediatric cardiology pharmacopoeia: 2004 update

[6] Pediatr Crit Care Med. 2006 Sep;7(5):445-8: Namachivayam P et al: Early experience with Levosimendan in children with ventricular dysfunction.

[7] N Engl J Med. 2008 Feb 28;358(9):877-87: Russel et al: Vasopressin versus norepinephrine infusion in patients with septic shock


 All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.