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Fig. 35.3. An infant with CPAP properly attached to the head.

(1) Head cap (cap fit well on head covering down to eye brows,

almost entire ears and back of head); (2) breathing circuit tubes

attached to side of hat while avoiding both eyes; (3) three-way

elbow on expiratory limb allows the attachment of pressure

manometer or could be capped to preserve pressure within circuit;

(4) orogastric tube attached to lower lip and chin with Tegaderm;

(5) neck roll allowing slight neck extension (sniff position); (6)

nasal prongs applied to baby—prongs inserted into nares allowing

a space between the transverse arm of the nasal prongs and nose to

avoid damage to nasal columella; (7) supporting chin strip.

Infant should be assessed during the trial for any

tachypnea, retractions, oxygen desaturation, or

apnea. If any of these signs are observed, the trial is

considered failed. Infant should be restarted immediately on CPAP, for at least 24 hours, before

another trial is undertaken.

b. There is no need to change the level of positive pressure during the weaning process. Infant is either on

b-CPAP 5-cm H2O or off CPAP.

c. Do not wean the infant off b-CPAP if there is any

likelihood of respiratory compromise during the

weaning process. It is wise to anticipate and prevent

lung collapse, rather than risk having to manage collapsed lungs.

d. Do not wean infants off b-CPAP if they require supplemental oxygen. (13)

4. Potential Complications

a. Nasal obstruction: From secretions or improper

positioning of b-CPAP prongs. To avoid obstruction,

nares should be suctioned frequently and prongs

checked for proper placement. Never use a nasal–

pharyngeal tube to supply b-CPAP, because of significant risk of nasal airway obstruction.

b. Nasal septal erosion or necrosis: Due to pressure

on the nasal septum. This can be avoided by maintaining a small space (use DuoDERM 2 to

3 mm) between the bridge of the prongs and the

septum. Choosing the proper-sized snug-fitting

nasal prongs, using a Velcro mustache to secure

the prongs in place, and avoiding pinching of the

nasal septum, will minimize the risk of septal

injury. Significant nasal septal erosion may require

consultation with the ENT or Plastic Surgery

team.

c. Gastric distention: From swallowing air. Gastric distention is a benign finding and does not predispose

the infant to necrotizing enterocolitis or bowel perforation (14). It is important to ensure patency of the

indwelling orogastric tube because secretions may

block the tube and lead to distention.

d. Pneumothorax: During the first 2 days of life, premature infants usually will require intubation for this

complication.

e. Unintended increase/decrease in positive end pressure: The tubing that is placed under water to provide positive end pressure must be firmly fixed in

place so that it cannot be displaced to produce

unwanted pressure changes.

Acknowledgement

We thank Aser Kandel, MD for drawing the illustrations in

this chapter.

 


Chapter 35 ■ Bubble Nasal Continuous Positive Airway Pressure 233

c. Fixing corrugated tubes in place

(1) Use appropriate-sized hat and fold rim back 2 to

3 cm.

(2) Place the hat on the infant’s head so that the rim

is just over the top of the ears.

(3) Hold the corrugated tubing to one side of the head.

(4) Tape the tube to the hat at the side of the head.

(5) Repeat the same procedure for the tubing on

the other side of the head.

d. Draining excess air from the stomach

(1) Pass an orogastric tube and aspirate the stomach

contents.

(2) Fix tube at appropriate position.

(3) Leave tube open to air to ventilate excess air

from stomach.

e. Maintaining a good seal for CPAP pressure

(1) Gently apply a chin strip to minimize air leak

from the mouth.

1 2

3

5b

6

4

5a

Fig. 35.2. Components of the CPAP attachment device.(1)Infant’s nose before applying b-CPAP; (2)

protective DuoDERM applied to upper lip and nose; (3) thin Velcro moustache piece: applied to upper

lip on top of DuoDERM with sharp edges not touching nose; (4) nasal prongs (prongs are slightly curved

to better fit within anatomy of nasal passages); (5a,b) thick Velcro ring pieces: wrapped around both sides

of the transverse arm; (6) nasal prongs applied to baby—prongs inserted into nares with thick Velcro rings

attached to thin Velcro moustache (allow a space between the transverse arm of the nasal prongs and nose

to avoid damage to nasal columella).


234 Section VI ■ Respiratory Care

2. Maintenance of b-CPAP

a. Check the integrity of the entire CPAP system every

3 to 4 hours (Appendix F) (12)

b. Suction nasal cavities, mouth, pharynx, and stomach every 3 to 4 hours, and as needed.

c. Keep CPAP prongs off nasal septum at all times.

d. Change the infant’s position every 4 to 6 hours, to

allow postural drainage of lung secretions.

3. Weaning off b-CPAP

a. A trial off CPAP should be given when the infant’s

weight is more than 1,200 g and he or she is breathing

comfortably on b-CPAP without supplemental oxygen.

The nasal prongs should be separated from the

corrugated tubing, keeping the tubing in place.

5

1

2

3 6

7 4

 



232 Section VI ■ Respiratory Care

a. Short binasal prongs

b. Velcro (to make attachment circles and moustache

for upper lip)

c. DuoDERM (to make nasal septum protective layer)

d. CPAP head cap

e. Adhesive tape

E. Technique (See Procedures Website

for Video)

1. Starting b-CPAP

Nonventilator-derived b-CPAP apparatus involves

making a simple water seal device that can be put

together in neonatal units. It consists of a container of

water, through which the expiratory gas from the baby

is bubbled at a measured level below the surface (e.g.,

5 cm below the surface = 5cm H2O CPAP). The lower

the level of the tip of the expiratory tubing below the

surface of the water, the higher the CPAP (Fig. 35.1). It

is important to fix the water bottle to an IV pole at or

below the level of the baby’s chest to avoid any accidental displacement or water spills. The recent, commercially available, preassembled circuits rely on the same

basic principle.

a. Before attaching the device to an infant

(1) Position the infant with the head of the bed elevated 30 degrees.

(2) Gently suction the mouth, nose, and pharynx.

Whenever possible, use size 8-Fr suction

catheter. Smaller-sized catheters are not as efficient.

(3) Place a small roll under the infant’s neck/shoulder.

Allow slight neck extension to help maintaining

the airway open.

(4) Clean the infant’s upper lip with water.

(5) Place a thin strip of DuoDERM (or Tegaderm)

over the upper lip. That should also cover the

nasal columella and both sides of nasal apertures (Fig. 35.2).

(6) Cut a Velcro moustache and fix it over the

DuoDERM.

(7) Cut two strips of soft Velcro (8 mm width) and

wrap them around the transverse arm of the

device, about 1 cm away, on each side, from the

nasal prongs.

b. Placing nasal prongs into infant’s nostrils (Figs. 35.2

and 35.3)

(1) Use appropriate-size CPAP prongs. The correct

size nasal prongs should snugly fit the infant’s

nares without pinching the septum. If prongs

are too small, they will increase airway resistance and allow air to leak around them, making it difficult to maintain appropriate pressure.

If prongs are too large, they may cause mucosal

and septal erosion.

(2) Curve prongs gently down into the infant’s

nose.

(3) Press gently on the prong device until the soft

Velcro strips adhere to the moustache.

(4) Make sure of the following points

(a) Nasal prongs fit well in the nostrils

(b) Skin of nares is not stretched (indicated by

blanching of the rim of the nostrils)

(c) Corrugated tubes are not touching the

infant’s skin

(d) There is no lateral pressure on the nasal septum

(e) There is a small space between the nasal

septum and the bridge between the prongs

(f) Prongs are not resting on the philtrum

5

4

3

2

1

Manometer

Distal

tubings

Flowmeter

Oxygen

blender

The

CPAP

bottle

Nasal

CPAP

canula Proximal

tubings

Thermometer

Heated

humidifier

Fig. 35.1. Bubble CPAP circuit. This simplified

diagram demonstrates the components of the b-CPAP

device that is either assembled at the bedside or commercially manufactured. Gas mixture flows to the

infant from the wall source after it is warmed and

humidified. The free expiratory limb of the tube is

immersed under the surface of sterile water to produce

the required CPAP (usually 5 cm H2O).


 


231

Hany Aly

M.A. Mohamed

Bubble Nasal Continuous

Positive Airway Pressure

35

A. Definition

Continuous positive airway pressure (CPAP) is a noninvasive, continuous flow respiratory system that maintains positive pressure in the infant’s airway during spontaneous

breathing. CPAP was developed by George A. Gregory in

the late 1960s (1). Positive pressure was originally applied

by placing the neonate’s head into a semiairtight “box” (the

Gregory box) and, subsequently, by a fitted face mask covering the mouth and nose (2). A major problem with both

these methods of application was the fact that it was difficult

to feed the baby without discontinuing the CPAP, thus the

evolution to the current method of applying CPAP through

bilateral nasal prongs (3). “Bubble CPAP” (b-CPAP) is a

modern resurgence of the original method of supplying

CPAP, wherein pressure is generated in the breathing circuit by immersing the distal end of the expiratory limb of

the breathing circuit under a water seal (4–6) (Fig. 35.1).

Bubble CPAP allows provision of CPAP without use of

a ventilator, and it is currently primarily used for early treatment of low-birthweight premature infants with or at risk for

respiratory distress syndrome and/or with frequent apnea/

bradycardia (7). In addition to cost considerations, there is

early evidence that b-CPAP may be more effective in small

premature babies than ventilator-derived CPAP (8).

CPAP has the Following Physiologic Actions

1. Prevents alveolar collapse and increases functional

residual capacity

2. Splints the airway and diaphragm

3. Stimulates the act of breathing and decreases apnea

4. Conserves surfactant via decreased inflammatory

responses (9)

5. Stimulates lung growth when applied for extended

duration (10)

B. Indications

1. Premature infants with/at high risk for respiratory distress syndrome

2. Premature infants with frequent apnea and bradycardia

of prematurity

3. Infants with transient tachypnea of the newborn

4. Infants who have weaned from mechanical ventilation

5. Infants with paralysis of the diaphragm or tracheomalacia

When to Start b-CPAP?

a. Premature infants with a birthweight <1,200 g can

be supported with b-CPAP starting in the delivery

room, before any alveolar collapse occurs

b. Infants ≥1,200 g may benefit from b-CPAP in the

following conditions

(1) Respiratory rate >60 breaths/min

(2) Mild to moderate grunting

(3) Mild to moderate respiratory retraction

(4) Preductal oxygen saturation <93%

(5) Frequent apneas

C. Contraindications

1. Choanal atresia

2. Congenital diaphragmatic hernia

3. Conditions where b-CPAP is likely to fail in the delivery room such as

a. Extremely low gestational age infants (≤24 weeks)

b. Floppy infants with complete apnea due to maternal anesthesia

4. Relative contraindication: Infants with significant apnea

of prematurity may require the introduction of nasal

intermittent positive pressure ventilation via a variable

flow device (11).

D. Equipment

B-CPAP System Consists of Two Components

1. A breathing circuit of light-weight corrugated tubing

that has two limbs

a. Inspiratory limb to provide a continuous flow of

heated and humidified gas

b. Expiratory limb with its terminal end immersed

under water seal to create positive pressure

2. A device to safely connect the circuit to patient’s nares

that includes (Fig. 35.2)

 



Chapter 34 ■ Management of Vascular Spasm and Thrombosis 229

5. Roy M, Turner- Gomes S, Gill G, et al. Accuracy of Doppler

ultrasonography for the diagnosis of thrombosis associated with

umbilical venous catheters. J Pediatr. 2002; 140: 131.

6. Manco- Johnson MJ, Grabowski EF, Hellgreen M, et al.

Laboratory testing for thrombophilia in pediatric patients. On

behalf of the Subcommittee for Perinatal and Pediatric

Thrombosis of the Scientific and Standardization Committee of

the International Society of Thrombosis and Haemostasis (ISTH).

Thromb Haemost. 2002;88:155.

7. Raffini L. Thrombophilia in children: who to test, how, when

and why? Hematology Am Soc Hematol Educ Program. 2008:

228.

8. Yang JYK, Chan AKC. Neonatal systemic venous thrombosis.

Thrombosis Res. 2010;126:471.

9. Wong AF, McCulloch LM, Sola A. Treatment of peripheral tissue

ischemia with topical nitroglycerine ointment in neonates.

J Pediatr. 1992;121:980.

10. Vasquez P, Burd A, Mehta R, et al. Resolution of peripheral artery

catheter induced ischemic injury following prolonged treatment

with topical nitroglycerine ointment in a newborn: a case report.

J Perinatol. 2003:23:348

11. Baserga MC, Puri A, Sola A. The use of topical nitroglycerine

ointment to treat peripheral tissue ischemia secondary to arterial

line complications in neonates. J Perinatol. 2002;22:416.

12. Monagle P, Chalmers E, Chan A, et al. Antithrombotic therapy

in neonates and children: American College of Chest Physicians

Evidence Based Clinical Practice Guidelines (8th edition). Chest.

2008;133:887S.

13. Saxonhouse MA. Management of neonatal thrombosis. Clin

Perinatol. 2012;39:191.

14. Albisetti M. Thrombolytic therapy in children. Thromb Res.

2006;118:95.

15. Kumar P, Hoppensteadt DA, Prechel MM, et al. Prevalence of

heparin- dependent platelet activating antibodies in preterm newborns after exposure to unfractionated heparin. Clin Appl Thromb

Hemost. 2004;10:335.

16. Streiff W, Goebel G, Chan AKC, et al. Use of low molecular

weight heparin (enoxaparin) in newborn infants: a prospective

cohort study of 62 patients. Arch Dis Child Fetal Neonatal Ed.

2003;88:F365.

17. Malowany JI, Monagle P, Knoppert DC, et al. Enoxaparin for

neonatal thrombosis: a call for a higher dose for neonates. Thromb

Res. 2008;122:826.

18. Wiernikowski JT, Chan A, Lo G. Reversal of anti- thrombin activity using protamine sulphate. Experience in a neonate with a 10

fold overdose of enoxaparin. Thromb Res. 2007;120:303.

19. Raffini L. Thrombolysis for intravascular thrombosis in neonates.

Curr Opin Pediatr. 2009;21:9.

20. Williams MD. Thrombolysis in children. Br J Haematol. 2009;

148:26.

21. Zenz W, Arlt F, Sodia S, et al. Intracerebral hemorrhage during

fibrinolytic therapy in children. A review of literature of the last

thirty years. Semin Thromb Hemost. 1997;23:321.

22. Nowak- Gottl U, Auberger K, Halimeh S, et al. Thrombolysis in

newborns and infants. Thromb Haemost. 1999;82(suppl):112.

23. Yang JY, Williams S, Brando LR, et al. Neonatal and childhood

right atrial thrombosis: recognition and a risk-stratified treatment

approach. Blood Coagul Fibrinolysis. 2020;21:301.

24. Coombs CJ, Richardson PW, Dowling GJ, et al. Brachial artery

thrombosis in infants: an algorithm for limb salvage. Plast Reconstr

Surg. 2006;117:1481.

25. Ade-Ajayi N, Hall NJ, Liesner R, et al. Acute neonatal arterial

occlusion: is thrombolysis safe and effective? J Pediatr Surg.

2008;43:1827.


230

35 Bubble Nasal Continuous Positive Airway Pressure

36 Endotracheal Intubation

VI Respiratory Care


 



228 Section V ■ Vascular Access

procedure such as lumbar puncture is

required, skip two doses of LMWH, and

measure anti-FXa level prior to the procedure.

(g) If an immediate antidote is required, protamine may be administered. The dose is usually a 1:1 ratio with LMWH; administration

of the dose may be done in 2 to 3 aliquots

with monitoring of anti-FXa levels (18).

(3) Thrombolytic agents

(a) Thrombolytic agents should be considered

in the presence of extensive or severe thrombosis when organ or limb viability is at risk.

(b) The use of streptokinase and urokinase has

been superseded by rTPA.

(c) rTPA acts by converting fibrin-bound plasminogen to plasmin, which then proteolytically cleaves fibrin within the clot to fibrin

degradation products. rTPA is nonantigenic

and has a short half-life. Supplementation

with plasminogen in the form of fresh frozen

plasma enhances the thrombolytic effect.

(d) Thrombolysis does not inhibit clot propagation, so anticoagulation may be necessary.

The administration of heparin, either concomitantly or following thrombolytic therapy, has not been adequately evaluated in

neonates.

(e) Dosage: A wide variety of dosage protocols

have been used (3,12,14,19,20).

 i. High-dose protocol: Continuous infusion

of rTPA 0.1 to 0.6 mg/kg/h for 6 hours.

 ii. Low-dose protocol: Continuous infusion

of rTPA 0.01 to 0.06 mg/kg/h over 24 to

48 hours. Simultaneous infusion of

UFH at 10 U/kg/h.

iii. Catheter-directed thrombolysis: Infusion

of low doses of rTPA through a catheter

with the tip adjacent to or within the

thrombus. Initial bolus dose ranges

from 0 to 0.5 mg/kg, followed by infusion of 0.015 to 0.2 mg/kg/h.

(f) Monitoring

 i. Measure thrombin time, fibrinogen

and plasminogen levels, and fibrin split

products or d-dimers prior to therapy, 3

to 4 hours after initiation of fibrinolytic

therapy, and one to three times daily

thereafter.

 ii. Imaging studies every 4 to 12 hours during fibrinolytic therapy to allow discontinuation of treatment as soon as clot

lysis is achieved.

iii. Fibrinolytic response is measured by a

decrease in fibrinogen concentration

and increase in levels of fibrindegradation products, but the correlation between these hemostatic parameters and efficacy of thrombolysis is poor.

Maintain fibrinogen levels of at least

100 mg/dL.

E. Complications of Anticoagulation/

Fibrinolytic Therapy

1. Hemorrhagic complications (1,21,22)

a. Intracerebral hemorrhage: Incidence approximately

1% in term neonates, 13% in preterm neonates,

increasing to 25% in preterm infants treated in the

first week of life. Data in preterm infants is confounded by the risk of “spontaneous” intraventricular hemorrhage (21).

b. Other major hemorrhage: Gastrointestinal, pulmonary

c. Bleeding from puncture sites and recent catheterization sites: Bleeding and hematoma at the site

of the indwelling catheter for LMWH has been

noted (1)

d. Hematuria

2. Embolization

Dislodgement of intracardiac thrombus, causing

obstruction of cardiac valves or main vessels, or pulmonary or systemic embolization (23).

F. Surgical Intervention (24,25)

Early consultation is recommended because surgical management may be required concomitantly, particularly for

life- or limb-threatening emergencies.

1. Thrombectomy

2. Microvascular reconstruction

3. Decompressive fasciotomy

4. Mechanical disruption of thrombus, using soft wires

and balloon angioplasty in conjunction with continuous site-directed thrombolytic infusion into the clot.

5. Amputation

References

1. Van Elteren HA, Veldt HS, te Pas AB, et al. Management and

outcome in 32 neonates with thrombotic events. Int J Pediatr.

2011; 2011:217564.

2. Brotschi B, Hug MI, Latal B, et al. Incidence and predictors of

indwelling arterial catheter related thrombosis in children.

J Thromb Haemost. 2011;9:1157.

3. Saxonhouse MA, Burchfield DJ. The evaluation and management of postnatal thromboses. J Perinatol. 2009;29:467.

4. Haase R, Merkel N. Postnatal femoral artery spasm in a preterm

infant. J Pediatr. 2008;153:871.

 


(b) Check complete blood count, platelet

count, activated partial thromboplastin time

(aPTT), prothrombin time and fibrinogen

levels before starting UFH therapy.

(c) Dosage: Is adjusted according to gestational

age (12).

<28 weeks GA: Loading dose 25 U/kg IV

over 10 minutes

Maintenance dose 15 U/kg/h

28 to 37 weeks GA: Loading dose 50 U/kg

IV over 10 minutes

Maintenance dose 15 U/kg/h

>37 weeks GA: Loading dose 100 U/kg IV

over 10 minutes

Maintenance dose 28 U/kg/h

(d) Monitoring

i. Maintain anti–factor Xa (anti-FXa) level of

0.03 to 0.7 U/mL (aPTT 60 to 85 seconds)

ii. Check anti-FXa level 4 hours after loading dose and 4 hours after every change

in the infusion rate.

iii. Check platelet counts and fibrinogen

levels daily for 2 to 3 days once therapeutic levels are achieved and at least

twice weekly thereafter, while on UFH.

iv. Monitor thrombus closely both during

and following treatment.

(e) Complications

i. Bleeding: Discontinue UFH infusion;

consider protamine sulphate if anti-FXa

level is >0.8 U/mL and there is active

bleeding. Dosage: 1 mg/ 100 U heparin

received if the time since the last heparin dose is <30 minutes. Use protamine

conservatively, starting with a smaller

dose than calculated.

ii. Heparin-induced thrombocytopenia (rare

in neonates) (15)

(2) LMWH (16,17)

(a) LMWHs have specific activity against factor

Xa and less activity against thrombin, so

therapy is monitored by anti-FXa assay and

not by aPTT.

(b) Different LMWHs preparations (e.g.,

enoxaparin, dalteparin, reviparin) differ in

their molecular weights and dosage regimens. Enoxaparin is the LMWH most commonly used.

(c) Advantages: Subcutaneous administration

(d) Dosage: Administered either by subcutaneous injection or through an indwelling subcutaneous catheter (Insuflon, Unomedical,

Birkerod, Denmark)

Term neonates: 1.7 mg/kg every 12 hours.

Preterm neonates: 2 mg/kg every 12 hours.

(e) Monitoring

i. Adjust dose to maintain anti-FXa level

between 0.5 and 1 U/mL.

ii. In neonates, prematurity, rapid growth,

and liver and kidney dysfunction make

LMWH dosage less predictable.

Frequent adjustment of the dose is

required to attain target anti-FXa levels.

iii. Draw blood sample for testing from

fresh venipuncture. There must be no

contamination from standard heparin

(e.g., from an arterial line).

iv. Check levels 4 hours after subcutaneous

administration of LMWH on days 1 and

2 of treatment.

v. If therapeutic, a weekly check of antiFXa levels is adequate.

(f) To discontinue anticoagulation, simply discontinue LMWH therapy. If an invasive

 


Fig. 34.2. Skin necrosis associated with an umbilical artery catheter. Such lesions develop after vasospasm or embolism. A: Spinal injury may be present when ischemia involves this region. B: The distal part

of an extremity is a common site for embolic arterial loss. The full extent of loss is unpredictable at this

stage. (From Fletcher MA. Physical Diagnosis in Neonatology. Philadelphia: Lippincott-Raven; 1998:127.)

Table 34.2 Laboratory Tests for Suspected Prothrombotic Disorders

Laboratory Test Collection Tube

Antiphospholipid antibody panel, anticardiolipin, lupus anticoagulant

(IgG, IgM)

Citrated plasma

Fibrinogen Citrated plasma

Protein C activity

Protein S activity

Antithrombin (activity assay)

Citrated plasma

Factor V Leiden

Prothrombin G

Methylenetetrahydrofolate reductase

Ethylenediaminetetraacetic acid

Homocysteine

Lipoprotein(a)

Citrated plasma

From Saxonhouse MA. Management of neonatal thrombosis. Clin Perinatol. 2012;39:191,with permission.


Chapter 34 ■ Management of Vascular Spasm and Thrombosis 227

c. Anticoagulation for at least 10 days; UFH or LMWH

is recommended for neonates with UAC-related

thrombosis.

d. If there are potentially life-, limb-, or organ-threatening signs in neonates with UAC-related thrombosis,

thrombolysis with rTPA should be considered.

e. If there are contraindications to thrombolysis, surgical thrombectomy may be indicated.

4. Anticoagulant/thrombolytic therapy

a. Contraindications

(1) Major surgery within the last 10 days

(2) Active or major bleeding: Intracranial, pulmonary, or gastrointestinal

(3) Preexisting cerebral ischemic lesions

(4) Seizures within 48 hours

(5) Relative contraindications (anticoagulant/

thrombolytic therapy may be given after correction of these abnormalities)

(a) Thrombocytopenia (platelet count <100 ×

109

/L)

(b) Hypofibrinogenemia (fibrinogen <100 mg/

dL)

(c) Severe coagulation factor deficiency

(d) Hypertension

b. Precautions

(1) No arterial punctures

(2) No subcutaneous or intramuscular injections

(3) No urinary catheterizations

(4) Avoid aspirin or other antiplatelet drugs.

(5) Monitor serial head ultrasound scans for intracranial hemorrhage.

c. Anticoagulants

(1) UFH

(a) Anticoagulant, antithrombotic effect limited by low plasma levels of antithrombin in

neonates.

 



h. Anticoagulation therapy with unfractionated heparin (UFH) or low-molecular-weight heparin

(LMWH) is used for clinically significant clots with

the goal of preventing clot extension or embolization.

i. Recombinant tissue plasminogen activator (rTPA) is

reserved for thrombolysis of severe life-, organ-, or

limb-threatening thrombosis.

j. The International Children’s Thrombophilia

Network, which is based in Canada, is a free

consultative service, maintained 24 hours a day, for

Fig. 34.1. Vasospasm following attempted radial artery catheterization in extremely preterm infant.

Table 34.1 Diagnosis of Vascular Thrombosis

Site Clinical Signs Diagnostic Imaging

CVL-associated venous thrombosis Malfunction of CVL, SVC syndrome, chylothorax, swelling and

livid discoloration of extremity, dilatation of collateral veins

over trunk or abdomen in chronic cases

Inferior vena cava thrombosis Lower limbs cool, cyanotic, edematous Contrast angiography

Doppler ultrasonography

Real-time 2D ultrasonography

Superior vena cava thrombosis

Renal vein thrombosis

Swelling of upper limbs and head, chylothorax

Flank mass, hematuria, thrombocytopenia, hypertension

Aortic or renal arterial thrombosis Systemic hypertension, hematuria, oliguria

Peripheral or central (aorta or iliac) arterial

thrombosis

Pallor, coldness, weak or absent peripheral pulse(s),

discoloration, gangrene

Right atrial thrombosis Congestive heart failure Echocardiography

Pulmonary thromboembolism Respiratory failure Lung perfusion scan

CVL, central venous line; SVC, superior vena cava.

}


226 Section V ■ Vascular Access

physicians worldwide who are caring for children

with thromboembolic disease. The toll-free number

in the North America is 1-800-NO-CLOTS; the

number for physicians elsewhere is 1-905-573-4795

(Web site http://www.1800noclots.ca/) The service

provides current management protocols as well as

links to the network and its services.

2. Management of catheter-related venous

thrombosis (12)

a. Either initial anticoagulation or supportive care

with radiological monitoring may be appropriate.

However, anticoagulation is recommended if extension of the thrombus occurs during supportive care.

b. Remove central venous lines (CVL) or umbilical

venous lines associated with confirmed thrombosis, preferably after 3 to 5 days of anticoagulation.

This recommendation has been made to reduce

the risk of paradoxical emboli at the time of CVL

removal.

c. Intravascular catheters are occasionally left in place

if local thrombolysis through the catheter is planned

(14).

d. Anticoagulation may be with LMWH or UFH for 3

to 5 days followed by LMWH.

e. Total duration of anticoagulation is between 6 and

12 weeks.

f. Thrombolytic therapy is not recommended for neonatal venous thrombosis unless major vessel occlusion is causing critical compromise of organs or limbs.

3. Management of arterial thrombosis (12)

a. Initiate management as for vasospasm if there are

peripheral signs of ischemia.

b. Remove catheter unless catheter-directed thrombolysis is planned (14)

A B

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