case studies - neonates by: nicole stevens. case studies - neonates haemolytic disease of the...

Case Studies - NeonatesBy: Nicole Stevens

Case Studies - Neonates•Haemolytic disease of the newborn (Baby

Eric)•Hyperbilirubinaemia•Hypoglycaemia (Case 1 and 2)•Birth asphyxi/HIE•Sepsis•RDS/pneumothorax•The undiagnosed cardiac abnormality in a

level 2 facility•The 24-26wker born in a non-tertiary facility

1. Case Study: Baby Eric

Maternal history:•Gravida 5, Para 4 (after birth of Eric)•Blood group O+ve; anti-c, anti-e

antibodies pos•GBS neg, Hep B/syph/HIV neg•Hep C pos•Smoker (15 day)•Normal morphology scan; 32/40 scan

showing asymmetrical growth restriction


•Induction of labour for IUGR & polyhydramnios

•16/5 @ 1225hrs, Normal vaginal birth•Live born male, Apgars 9@1, 9@5mins•36.6wks, Birth weight: 2600gs•Transferred to postnatal ward for ongoing

care•Mother planning to breastfeed


•17/5 On examination by midwife at 33hrs of age, noted to be jaundiced.

•Had been feeding 2-3/24; had not passed mec since birth

•SBR taken: 228 micromol/L (in exchange range); paediatric team notified

•Seen by paed, admitted to SCN, quadruple phototherapy lights commenced

4. Case Study: Baby EricPlan (17/5):•Feed to maintain TFI at 80mL/kg;

EBM/formula 3x8•Bloods to be taken in 4hrs (Blood group,

coombs and repeat SBR) •Monitor abdomen, notify paeds of

distention or feed intolerance.Note: large mec stool passed shortly after

admission to SCN

5. Case Study: Baby Eric•SBR 4 hrs later (37hrs): 212 (out of exchange

range); passing concentrated urinePlan:•Continue quadruple lights, remain in isolette•Repeat SBR in 6hrs: 178 (out of phototherapy

range)Plan (18/5):•Feeds increased to 100mL/kg•Reduce to double phototherapyNote results back from group and coombs: O

Pos, pos coombs, anti-IgG pos, anti-C3 neg


Plan 19/5 – 20/5 (day 4 – 5):•Increased TFI to 120mLs/kg•Out of isolette for feeds•Mum suppressed lactation, bottle feeding

on NanHa•Daily blood tests continuing•Baby examining well, alert vigorous, fully

suck feeding. Normal weight loss post birth


•Day 6 down to single lights. Continue daily bloods, regular feeds

•Day 10 back up to triple lights.•Day 11 back to birth weight. •Day 12 decrease to double lights


•Day 13 continuing decrease in Hb, pale, slightly lethargic, but haemodynamically stable

•Given blood transfusion. IV bung inserted and given 50mLs PRBC (19mL/kg), expected to raise Hb by 4.7g/dL

•6 grams intragram P also given, IV, over several hours


•Day 14 reduced to single lights•Day 15 phototherapy ceased•Home day 18 with paediatric clinic follow

up with repeat Hb and retics prior to this appointment

•Discharge wt: 2790g, 39.3wks CA•Discharge medications: Folate and

ferrous suphate daily.

11. Pathology summaryDate Time SBR Hb other17/5 0945 228/618/5 0500 212/6 16.8 Hct 48.8%, plat 22518/5 1220 178/6 Opos, coombs pos, anti-

IgG: pos19/5 1030 192/12 anti-C3:neg

20/5 0930 291/821/5 1143 233/722/5 0910 207/723/5 0805 263/724/5 0945 244/10 11.625/5 1130 262/2926/5 1050 294/33 10.1

12. Pathology summaryDate Time SBR Hb other27/5 0800 280/828/5 0830 258/16 8.629/5 1200 233/35 6.9 PRBC transfusion30/5 1000 182/8 10.91/6 1155 101/14 10.43/6 0730 84/8 10.8 DISCHARGED

HOME 19/6 (outpt f/up) 8.4 retics 3.1%6/7 8.6 retics 2.6%25/8 11.419/9 13.5

13. Considerations• Communication from antenatal care providers to

paediatric team regarding maternal anti-e, anti-c antibodies

• Early screening of SBR (cord blood)• Closer monitoring and awareness in first 24 hrs• Physiological v’s Pathological jaundice• Early onset jaundice can be a neonatal

emergency• Haemolytic disease of the newborn• Action of phototherapy

CASE STUDY: CASE STUDY: HYPERBILIRUBINAEMIAHYPERBILIRUBINAEMIA

BY: NICOLE STEVENS

Case studyCase study•Multipara•G3P2, 39+2wks gestation•Repeat elective caesarean section booked•O+ve, antibodies neg, rubella immune•GBS –ve, well through pregnancy•No other history of note

Case StudyCase Study•Date of birth 29/7/11•Time of birth 0930hrs•Live female infant•Born via EL LUSCS•Apgars 6@1min, 10@5mins•To postnatal ward for routine care•Weight 3590g

Case StudyCase Study•Noted to be jaundiced at 26 hrs of age•SBR taken: 188/12 (30/07/11 @ 1130hrs)• Just at treatment line•Double phototherapy commenced•Breast feeds + 90mL/kg topups•Further bloods taken at 2020hrs (35hrs

old):SBR: 186/12. Going away from treatment line (below)

•Blood group: A+ve, DAT: positive, Hb: 12.9, WCC: 25.5, Platelets: 267

Case StudyCase Study• Double lights continued• Bloods repeated 31/7 @ 0615hrs (45hrs

old): SBR: 158/9• Phothotherapy ceased• Bloods repeated 12 hrs later: SBR 168/11• Remained out of lights• Bloods repeated 24 hrs later (69hrs old): SBR: 171/12, Hb: 12.7• Minimal rise, unconcerning

Case StudyCase Study•Mum suppressed lactation•Discharged home Day 4, bottle feeding•Followed up by DOM service•No further issues

•NICE guidelines currently the tool in use in SCN at BHS, other places will have different tools which will slightly alter the treatment ranges. (National Institute for Health and Clinical Excellence: treatment threshold graphs for babies with neonatal jaundice).

ABO incompatabilityABO incompatability•A common and generally mild type of

haemolytic disease in babies•Occurs, usually, with an O group mum

and an A or B group baby•Prem babies will be more severely

affected than healthy term babies.•Does not become more severe in future

pregnancies (such as with the negative blood group mothers)

ABO incompatabilityReview of blood types:• The genes you inherit from your parents determine

your blood group; there are 4 (major) types:A, B, AB & O

• Each type has an individual collection of chemicals on the blood cell surface, known as antigens

• A has A antigen, B has B antigen, AB has both and O has none

• If different blood types mix, an immune response occurs and antibodies will be produced to attack the foreign antigen

ABO incompatability•Generally during pregnancy mother and

fetus’ blood doesn’t mix, but it can (miscarriage, trauma, birth and sometimes for unknown reasons)

•The O group mum may produce antibodies against an A, B or AB group baby, these antibodies can cross the placental membrane and increase the rate of haemolysis (cause red blood cell destruction), hence increasing the production of bilirubin – a waste product

Jaundice and length of stay• Readmit from home, dehydrated, no underlying haemolytic

disease – if treated and fed usually only 24 – 48 hrs stay required. Increase education to parents, if breastfeeding, provide lactation support

• Premature baby, may be a reoccurring problem over first 1 – 2 weeks of life, usually resolved by the time baby otherwise ready for home

• Pathological/haemolytic cause: can be protracted length of treatment over 1 – 2 wks (sometimes longer), with rebounds. Long term anaemia may result in need for top up transfusions.

• Breast milk jaundice: months, low levels persisting over prolonged period of time, not usually requiring treatment beyond the first 1 – 2 weeks. Diagnosed by exclusion after several weeks.

Nursing Care• Educate parents• Maximise time under lights and surface area

exposed (lights above and below in more severe cases). Big nappies covering half the body need to be folded down/minimised; don’t over nest and reduce exposure to lights.

• Consider nappy off & staying in incubator to feed in pathological cases (in early days if levels high)

• If coming out for feeds, keep it brief. • Eye care• Skin care• Feeding support/establishment of lactation

Case study 1 continued

•Neonate of gestational diabetic mother•Poor control of diabetes in pregnancy•Prematurity•Large for gestational age (? High levels of

circulating insulin): above the 97th centile for a baby of this gestation

•Respiratory distress•Sick baby/anaemic

Case 1•32 yr old multi presented to hospital in

the Gippsland region, with history of decreased fetal movements (32.4wks gestation), CTG showed sinusoidal trace – EM LUSCS performed

•Antenatal history: poorly controlled GDM on insulin; pregnancy induced cholestasis; antenatal depression (medicated); fetus estimated to be on the 98th centile and polyhydramnios evident

•Steroids given just prior to delivery

Case study 1 cont…•Baby Beau born at 1530hrs via EM LUSCS

(3300gs)•Noted to be pale, irregular

respirations/periods of apnoea – CPAP/IPPV given intermittently until breathing regularly.

•Nasal CPAP commenced at 40 mins of age with a PEEP of 5cm H20, FiO2: 45%

•Umbilical pH 7.13 venous, 7.21 arterial•FBE, CRP, BC, electrolytes, ABG and BSL

taken•APGARS: 5, 4, 4, 4 @ 1, 5, 10 & 15mins

Case study 1 cont…• Results of interest: (at 1&1/2 hrs of age) Hb 64, ph

7.12, CO2 75 PEEP increased to 10 at this point• Initial BSL’s: 1.5 & 1.8 (received 2 x 2.5mL/kg of

10% dextrose bolus’), BSL 1 hour later 2.6mmol/L. Infusion of 45mL/kg 10% dextrose commenced.

• Issues: anaemia, prematurity, hypoglycaemia, LGA, respiratory distress requiring CPAP

• NETS called and t/f planned to RWH• Mother and baby both A+ve, Kleihauer positive

(fetal-maternal haemorrhage)

Case study 1 cont…

•12.5% dextrose commenced by NETS•Transferred to RWH (at 6 hrs of age) with

NETS intubated, received x1 dose surfactant before t/f and one at RWH – extubated the following day.

•Received a transfusion of PRBC’s•TBG’s stabilised 3.5, 3.8, 2.9,3.4, 4.4, 4.4,

4.0 etc•Hb checked post transfusion 145, next day

158

Case study 1 cont…

•What were this babies risk factors for hypoglycaemia?

Case study 1 continued

•Neonate of gestational diabetic mother•Poor control of diabetes in pregnancy•Prematurity•Large for gestational age (? High levels of

circulating insulin): above the 97th centile for a baby of this gestation

•Respiratory distress•Sick baby/anaemic

Case study 1 cont...

Other issues for this baby??•Low apgars, hypoxic episode, ?HIE (will

discuss in later case study)•Anaemia (fetomaternal haemorrhage)•RDS (CPAP initially 5cm, then up to 10cm)•Too high?? What was the reason for this?

What was another option?• Intubated and given surfactant prior to

transfer

Case study 1 cont...•Fetomaternal hemorrhage refers to the

entry of fetal blood into the maternal circulation before or during delivery

•Is a pathological condition with a wide spectrum of clinical variation

•Secondary to the resultant anaemia, it may have devastating consequences for the fetus, such as: neurologic injury, stillbirth or neonatal death

•The most common antenatal presentation is reduced fetal movements

Case study 1 cont...

Management•Immediate delivery if acute presentation

and fetal compromise evident•Consider intrauterine transfusion versus

delivery based on: GA, status of fetus, availability of personnel to perform transfusion, procedural difficulty, rapid/large haemorrhage v’s slow haemorrhage

•Administer steroids if < 34 weeks GA

Case study 1 cont...• The Kleihauer-Betke test is a quantitative assay

for fetomaternal hemorrhage that detects fetal red blood cells in the presence of maternal red blood cells by staining of a blood smear following acid elution. It is based on the relative resistance of fetal hemoglobin (HbF) for acid treatment compared to maternal adult hemoglobin (HbA). The results are used to calculate the dose of Rh immune globulin (RhIg) to administer to an Rh negative woman for post-natal prophylaxis of Rh alloimmunization.

• Sample Required: 7 ml EDTA(If postnatal sample, draw > 1 hour after delivery)

• Normal Test Values: The percentage of fetal hemoglobin in adults is normally < 1%

Reference List

•www.ncbi.nlm.nih.gov/pubmed/20410781 Wyle BJ & D’Alton ME. Fetomaternal hemorrhage

www.psbc.org/lab_redcell/test11.htm

Case Study No. 2•Multipara, NVB at 40wks gestation, born

at 2044hrs. Mec liquor present, but baby vigorous, nil resus required

•Apgars of 9 and 9•Birth weight: 4090gs•Mother planning to breastfeed•Transferred to postnatal ward, good

breast feed noted at 2130hrs•Baby normothermic•Hep B and Vit K given

Case study 2 cont..•On commencement of day shift, midwife

noted that baby had not fed since 2130hrs in the evening, mother confirmed same

•BSL taken at 0845hrs: 1.2, TBG performed in SCN: 2.3

•Baby breastfed and topped up, received 0.5mL EBM and 8mL Nan via syringe

•TBG repeated at 1045hrs: 1.5; baby admitted to SCN

•Attempt made at suck feed, too sleepy, NGT inserted and 60mL/kg feed given.

Case study 2 cont…• TBG at 1210hrs: 2.1; d/w paeds further

30mL/kg feed given via NGT• TBG at 1315hrs: 2.1; d/w paeds, for insertion of

IV bung• 1400hrs IVB inserted 2mL/kg bolus of 10%

dextrose given and IVT commenced at 60mL/kg• Baby made NBM• 1445hrs TBG 2.6, NBM infusion continued• 1600hrs TBG 3.6, NBM infusion continued• 2000hrs TBG 3.5, baby breast fed, IVT

continued

Case study 2 cont…• Plan from this point would be to continue

breastfeeding on demand, or 3-4/24• Continue dextrose infusion overnight• Plan to wean dextrose next day and continue to

establish breastfeeding/supply• No set rules on how to wean the dextrose, could go

down by 2mL/hr with each feed, checking an AC BSL; or could be more ‘aggressive’ and half it initially, half again and then cease. Each hospital and doctor will be different, but as long as the BSL’s are monitored as the dextrose is weaned either option above would be acceptable, or variations of the same.

Case study 2 cont..

•What are the risk factors for hypoglycaemia for this baby?

Case study 2 cont..

•Large for gestational age•Did not have blood sugar monitoring, and

any baby who is greater than 4kgs or > than the 90th centile should have monitoring of BSL’s initially until stable

•Did not receive a feed for 12hrs

1. KHG1P0

O+ve, nil antibodies

Serology negative, rubella immune

No abnormalities noted on US at 19+5/40

Hypertension during pregnancy

SROM at 35+1 (8hrs pre delivery), NVD, Apgars 8,9,9, BW 2585g

Admitted to SCN due to prematurity

NG feeds commenced

2. KHDay 9

•Increased WOB and RR noted (60)•FBE CRP benign •CXR NAD•Multiple attempts at IV access unsuccessful. IM benpen/gent

Day 10•RR up to 80. SaO2 91%. Temp 37.7•Bright red PR blood noted at nappy change 0940 •Lethargic with poor tone•Multiple attempts at IV access – scalp vein •Systolic murmur noted. Palpable femoral pulses.

3. KH

•What’s your guess at a diagnosis?•Why the increased work of breathing?•Doesn’t appear to be a sepsis issue –

blood tests are normal•Difficult IV access – shutdown?•PR bleeding – odd•Murmur heard•What tests, investigations are you

thinking need to be done?

4. KHDay 10 22/8•Transferred to MMC•Echo: coarctation + PDA. Prostin commenced •Treated for suspected NEC

•Normal AXR

•Surgical review

•NBM, triple antibiotics

•PR bleeding likely secondary to gut ischaemia

26/8•Transferred to RCH•28/8 – coarctation repair, PDA ligation•Small-mod perimembranous VSD + 2 apical muscular VSDs

5. Coarctation of the Aorta• Suspected congenital heart disease in the

newborn is a medical emergency• Coarctation of the aorta is the most commonly

missed congenital heart disease• It is a narrowing, or stricture of the aorta• Remain alert for this condition, especially in a

neonate presenting with poor feeding, failure to thrive, or signs of heart failure

• Specific physical findings include a systolic murmur, weak or absent femoral pulses, and upper body hypertension

6. Coarctation of the aorta

7. Coarctation of the Aorta• Accounts for 7% of congenital heart defects • Leads to restricted blood flow to the lower part

of the circulation• Heart failure may develop• In most cases surgical repair is required,

sometimes in the early weeks of life• Detection and treatment reduces the morbidity

and mortality from heart failure and improves long term outcomes

BEWARE: a normal result on a newborn examination

does not rule out congenital heart disease

8. Diagnosis note• A harsh systolic murmur over the left sternal

border indicates a 54% change of an underlying cardiac malformation

• Weak or absent femoral pulses are found in 92% of infants with coarctation of the aorta, if this is noted a paediatrician should be consulted and ideally, four limb BP’s taken.

• Upper limb HT has been found in 97% of infants with coarctation and a systolic BP that is > 20mmHg higher in the arms than the legs is evidence of coarctation

• However, a negative finding on the four limb PB measurement does not exclude the condition

9. Coarctation of the AortaRepair:•Removal of the section with the stricture

and rejoin the ends back together•Or, use the artery to the left arm to create

a flap, which is turned down to enlarge the narrow section (subclavian flap)

•Or, it may be possible to manage with a balloon catheter (balloon angioplasty)

Conventional method is the end-end reanastomosis

10. Coarctation of the Aorta• Coarctation may also occur with other other cardiac

defects, typically involving the left side of the heart. The defects most commonly seen with it are: bicuspid aortic valve and ventricular septal defect (VSD)

• Coarctation is common in patients with some chromosomal abnormalities, such as Turner’s syndrome

• In the presence of a coarctation, the left ventricle has to work harder (increased afterload), since it must generate a higher pressure than normal to force blood through the narrow segment of the aorta to the lower part of the body.

• If the narrowing is severe, the ventricle may not be strong enough and congestive cardiac failure may occur or inadequate blood flow to the organs of the body.

11. Methods of repair of a coarctation

12. Coarctation of the aorta & PDA• Coarctation occurs most commonly in a short

segment of the aorta just beyond where the arteries to the head and arms take off, as the aorta arches inferiorly toward the abdomen and legs

• This portion is called the juxtaductal part of the aorta (or the part near where the ductus arteriosus (DA) attaches

• The DA is a vessel normally present in the fetus, it has a special tissue in its wall that helps it close in the first hours of life; it is thought that a coarctation may be caused by the presence of extra ductal tissue extending into the adjacent aorta which results in aortic narrowing as the ductal tissue contracts after birth

13. PDA Coarctation

14. Management of Coarctation• Goals are to improve ventricular function and

restore blood flow to the lower body• Commence a prostaglandin infusion to open up

the PDA if it had closed, and maintain it in an open state until surgery can be performed

• This will allow blood to areas beyond the coarctation

• It may be necessary to also begin medications to improve cardiac contractility (an inotrope)

• Babies will need to be intubated and ventilated prior to surgery, if not earlier, during the period of stabilisation

15. Managing cardiac conditions in SCN’s• In the ideal world all cardiac conditions would be

diagnosed antenatally and the babies would be birthed in an appropriate centre with staff prepared to manage the situation in a controlled manner

• In Victoria this would mean being booked in to one of the tertiary hospitals with a NICU facility, stabilised and then transferred (usually) to RCH if it is a lesion that requires surgical repair

• But… the ideal doesn’t always occur. Babies with some congenital cardiac abnormalities (that are undetected antenatally) can present well initially, even up until time of discharge may not have raised alarm bells; be sent home, and may be the baby that ‘crashes’ at home several days later (when the PDA closes) and they are in a life threatening crisis and rushed in by ambulance

16. Managing cardiac conditions in SCN’sScreening:• Morphology scan at the 20 wk mark that results in clear

views of all chambers of the heart and the vessels surrounding

• If suspicions raised postnatally (by murmurs, respiratory status, colour, SaO2, 4 limb BP’s), consult a paediatrician

• Echocardiogram• Routine screening of all babies: BHS has recently

commenced routing screening of all babies of pre & post ductal SaO2 prior to discharge, discrepancies are reported to a paed and management plan made.

17. Managing cardiac conditions in SCN’sProstaglandin infusions• Suspicion of a duct dependent lesion or confirmed diagnosis,

discuss with NETS and start prostaglandin if required• Will require a separate line, can be peripheral or centralEg. Of how to prepare (alprostadil 500mcg/1mL amp)• Draw up 60 mcg/kg (3.3kg baby = 198mcg = 0.4mL)• Add this to 50mL’s of solution, such as 0.9% NaCl (follow

own units guidelines), in a 50mL syringe; once the syringe is made applicable to the individual babies weight the following doses apply:

• 1mL/hr =0.02mcg/kg/min or (20nanogram/kg/min)• Dose range is 0.01(0.5mL/hr)-0.05(2.5mLs/hr) = 10 – 50 nanogram/kg/min

18. Nursing management• Weight • Observations• Paperwork • Setting up respiratory support if required (CPAP or

Ventilator)• Remember in duct dependent lesions oxygen usually has a

detrimental effect (PDA will constrict in response to exposure to higher levels of oxygen)

• SaO2 in the 70% + range are OK• Gases and respiratory effort will determine need for

respiratory support• Term babies, ventilated, may need infusions such as

morphine or midazolam and potentially muscle relaxation (pancuronium) to ‘accept’ ventilation; they can be vigorous and difficult to manage otherwise and are at heightened risk or accidental extubation and/or ineffective ventilation

19. Reference list

•www.rch.org.au/cardiology•www.bmj.com/content/343/bmj.d6838

1. MJ•14yo mother, 18yo father. Living with partner’s grandmother.•O+ve, serology negative•Seen at 15 and 21/40•20/40 US NAD

•Presented to ED at 25/40 with PV bleeding and back pain•Arrived 1720•Examined by O&G at 1731•Transfer to birth suite at 1738•Magnesium infusion commenced 1744, celestone given

2. MJ•Born at 1805 – placed in plastic zip lock back and hat put on•To resuscitaire, 2 consultants and SCN NUM present•Initial HR 60 on monitor, improved with IPPV•Successfully intubated at 11mins (after 6 attempts)•Transferred to SCN at 20mins•750g•Apgars 4, 6, 10•Ventilated ACVG 4mL/kg•Bag removed as oozing thick, bloody mec into it, nappy applied•Some issues with temp control, while central lines being inserted

3. MJ•Central line insertion commenced•NETS arrived 1930hrs, lines completed•Placed onto heated gel mattress•Caffeine loaded•Surfactant given•Transferred to Mercy•Honey moon period

•Extubated day 6 to CPAP, reintubated 5hrs later•Day 7 – abdominal distension, AXR revealed perforation•Transferred to RCH 6/9/12

DIAGNOSIS???

•RIP 24/9/12

4.Management of the extreme premature infant born in a non-tertiary facility• If at all possible transport in utero!!!If not possible: CALL NETS IMMEDIATELY• Temperature management• Assisting with intubation/suction/pedicap/ taping of ET tube (protect skin with a hydrocolloid)• Ventilation• Humidity/insensible water loss• Weight/Observations (including blood pressure)• Blood glucose management• Blood gases and other tests (usually BC, FBE, CRP)• Central access (UVC’s and UAC’s): if able to do this

5. Management of the extreme premature infant born in a non-tertiary facilityFluids for central lines• Sterile technique should be used for the

preparation of all fluids going into central lines• Heparinised saline for UAC • 10% Dextrose for UVC until position confirmed

with XRAY• Xray will be required for ET tube placement, and

for central line placement before drugs can be run through the UVC.

• In a tertiary hospital parenteral nutrition would be commenced as soon as line placement confirmed as OK in a baby of this gestation/size

• If unable to do central lines a peripheral line will suffice in the short term while waiting for NETS

6. Management of the extreme premature infant born in a non-tertiary facility• Inotropes•Antibiotics•Caffeine loading•Hep B, Vit K•Communicate with Hospital coordinator•Communicate with NETS/paperwork ,

consent•Paperwork (vital: drug charts, fluid charts,

birth details, child health book)•Counsel parents

7. Necrotising enterocolitis (NEC)•Statistics•Risk factors•Signs and symptoms•Differential diagnosis•Radiographic findings•Management•Complications•Prevention

8. NEC: Statistics• The most common gastrointestinal emergency in

neonates• 90% of babies with NEC are preterm• Predominantly a disease of the VLBW infant• Most common in babies < 1000g, or those that

are both preterm and growth restricted• The incidence of NEC is inversely proportional to

birthweight• Usually the age of onset is inversely proportional

to gestation, ie. Smaller babies present later

9. NEC: Statistics• Approx. 50% of babies that develop NEC require

surgery• The mortality rate is 20 – 40%• Of those who survive, approximately 25% develop

long term sequelae• Early, or suspected, NEC is often difficult to

diagnose as the clinical signs and symptoms are often non-specific, as are the radiological and laboratory findings

• Babies with definite NEC should be transferred to a NICU facility

• Staff working in SCN facilities need to be able to recognise suspected NEC, and be aware of management of babies transferring back who have had previous NEC

10. NEC: Risk factors• Prematurity, low birth weight• Enteral feeding (although approx. 10% of cases

have never fed)• Formula feeding (6 times more likely than EBM)• Often occurs in clusters (although organisms

vary)• Bowel ischaemia

In term infants: polycythaemia, cardiac surgery, abdominal surgery (esp. gastroschisis, intestinal atresia) and endocrine abnormalities

11. NEC: Signs & symptomsGastrointestinal dysfunction:• Abdominal distention• Vomitting• Bilious drainage from enteral feeding tubes• Blood in stoolSystemic• Temperature instability• Apnoea’s and/or bradycardias• Lethargy• Hypotension

12. NEC: Differential diagnosis

•Dysmotility of prematurity•Septic ileus•Bowel obstruction•Gastroenteritis•Anal fissure•Cows milk protein sensitive enterocolitis

13. NEC: Radiographic findingsNon specific:• Diffuse gaseous distension• Asymmetric, disorganised bowel pattern• Featureless loops• Dilated bowel loops• Bowel wall thickening• Increased peritoneal fluid

14. NEC: Management• Nil by mouth• Gastric tube on free drainage, and aspirate

regularly• Blood culture, +/- other bloods such as FBE, CRP• Antibiotics (‘triple’, such as vancomycin,

gentamycin and metronidazole – for definite)• May require gut rest for 10-14 days, therefore

TPN and fluid management and analgesia• Maybes: Inotropes, ventilation• Frequent Xrays• Surgery (in up to 50% of cases)

15. NEC: complicationsSurgery requiring ileostomy results in long term

issues:• Require supplemental Na even when well• High risk of rapid dehydration with

gastroenteritisStricture:• 20-30%• Most commonly in large bowel• 80% on left side• May not develop for weeks to months post-NEC• Presents with recurrent abdo distention• Surgical consultation and contrast enema

required

16. NEC: Prevention

•Antenatal corticosteroids•Early intervention (nil orally) for

suspected NEC•Breast milk in preference to formula (donor milk bank established at MHW)•Infection control practices may limit the

size of disease clusters.

17. Reference List

•www.netsvic.org.au/nets/handbook

1. Baby BJ •Antenatal hx: 26yr old, G2P1, previous

LUSCS (breech); bld grp O +ve, serology neg. GDM on insulin; gestational ITP (platelets on day of delivery 82)

•Delivery hx (30/7/12): APH, breech until 2/52 ago, decision to perform LUSCS, no labour. Pink liquor.

•Baby: cried at 20 secs, then apnoeic, IPPV for 1 min, then good respiratory effort

•Apgars 9 & 9. Birth weight: 2670g

2. Baby BJ• For admission to SCN from theatre,Issues:• Prematurity• Risk of hypoglycaemia• ? RDS• Maternal ITP• Breech until late in pregnancyPlan:• Observe resp. status, aim SaO2 above 88%; BSL

at 1 hr, feed if able then (dependent on resp effort); otherwise IV insertion, 10% dextrose and antibiotics

3. Baby BJ• Admitted to SCN at 1840hrs. Hep B, Vit K given • Initial Gas: pH: 7.136, PCO2: 78.9, HCO3: 26.6, BE:

-2, Lactate: 1.6; TBG: 1.7. CRP: <3, FBE: NAD (plt: 200)

Plan:• IV bung inserted, 10% dextrose commenced and

2mL/kg bolus given (recheck TBG in 30mins)• Hypoglycaemia resolved and not an ongoing issue• IV antibiotics commenced (Benpen 12/24, 60mg/kg

& Gent 36/24, 5mg/kg)• Commenced CPAP of 6cm/H2O; FiO2: 25% at

2000hrs• NETS notified of baby on CPAP – keep for now• CPAP increased to 7 at 2245hrs, grunting

4. Baby BJ• Remained stable in a CPAP of 7 overnight,

intermittent grunt and mild work of breathing. FiO2 at 21-23%.

• CXR and bloods done 1630hrs (CRP 4.7, FBE NAD, plt: 167)

• Reduced to CPAP of 6, in air• Parents and sibling visiting• Urine output at 1mL/kg/hr• Overnight: increased WOB, ? Apnoeic episode,

febrile, tachypnoeic, no increase in O2 requirement

6. XRAY interpretation (31/8/12 @ 1643hrs)

•Bilateral but diffuse reticular granular densities

•Lungs do not appear hyperinflated•No pleural effusions•Heart is not enlarged•NG tube is noted, tip below L)

hemidiaphragmImpression: findings would favour hilar

membrane disease (RDS), with infection also in the differential

7. Baby BJ (1/7/12)• CPAP increased to 7 in the AM (CapG pH: 7.16, CO2:

77)• Excessive handling around time gas collected, GNC,

bloods etc.• CPAP reduced to 5 later in the afternoon, in air mild

WOB (pH 7.34, pCO2 47)• Generalised oedema noted; Urine output increasing

(3.5)• Phototherapy commenced (SBR 158 at 40 hrs of age)• OPos group, coombs neg• Hungry, irritable at times, having small amounts of

EBM as available for comfort, taking well.• Had been febrile overnight (? Environmental), CRP 3.0

8. Baby BJ (1/7/12 cont…)• Genta level taken prior to the 2nd dose because of

concerns regarding renal function (urine output still low in the morning when dose due, significant oedema still present and Na level 135)

• Genta trough level: 1.4 so dose withheld.Nursing issues:• Weigh nappies of babies on CPAP especially in first

couple of days, once diuresis evident and baby stable consider discontinuing

• Be mindful of renal function when giving genta as it is metabolised in the kidneys and levels may stay high.

9. Baby BJ (1/7/12 cont..)• Very unsettled 1700hrs, crying++, not able to settle.• Increased WOB noted and slight O2 requirement

(25%)• Asked paed to r/v• Significant deterioration (colour change,

desaturation, O2 up to 100%) at approx. 1900hrs, following an unsettled period. Registrar in attendance, transilluminated appeared to be a pnuemothorax, CXR attended to – confirmed pnuemothorax, consultant called.

• Preparation for insertion of intercostal catheter• Morphine bolus given & sucrose given• Pigtail catheter inserted by registrar at 1945hrs

11. Xray interpretation (1/8/12 @ 1914hrs)

•Large right sided pneumothorax•Displacement of the mediastinal contents

towards the left•Air space opacity in the left lung is

increased likely to be due to a degree of compression from the pnuemothorax

THIS BABY CLINICALLY VERY UNSTABLE, ALL HANDS ON DECK FOR ICC INSERTION!!


• R) pneumocath noted (pigtail catheter used)• No residual pneumothorax• Heart not enlarged, and cardiothymic contour

normal• NG tube seen with tip below the level of the

diaphragm• Bilateral air space opacities in both lungs are

unchanged from previous

SIGNIFICANT IMPROVEMENT INSTANTLY AS CHEST DRAIN INSERTED – AUDIBLE HISS HEARD!

14. Baby BJ

•NETS called to retrieve, on their way•Gas (pH 7.17, CO2 78)•2205 hrs NETS arrived•Morphine infusion commenced•Still on CPAP, apnoeic episode when

being examined by NETS doctor•Decision to intubate for safety for

transport•Intubated/ventilated


•R) sided pleural catheter insitu•Air space opacity in both lungs unchanged•ET tube is seen with tip at the level of the

clavicle•NG tube is seen with tip below diaphragm•Heart size normal•No residual pneumothorax

17. Baby BJ•Gas (after intubation/ventilated): pH: 7.32,

pCO2: 48, HCO3: 25, BE: -1.7, Lact: 2.5•Prepared for transport•Left at 0100hrsOutcome:•Returned to BHS the next day, self

ventilating in air, ICC out, NGT for feeds, IVT weaning.

•Established feeds over the next 2 weeks and went home doing very well.

18. Pnuemothorax

•Signs & symptoms•Diagnosis•Nursing management•Medical management

19. Signs & Symptoms

•Irritability•Sudden deterioration with desaturation•Increase in respiratory distress•Diminished chest movements•Drop in blood pressure•Colour change•Blood gases may reflect hypoxia,

respiratory and/or metabolic acidosis

20. Signs & Symptoms & diagnosis•Unequal or decreased air entry•Displaced apex beat•Transillumination (not always reliable

especially in term/oedematous infants)•CXR will confirm diagnosis (but not

always a quick turn around time to have performed)

21. ManagementPain relief:• Oral sucrose• Infiltration of insertion site with 1% lignocaine

before preparing and draping the field• IV morphine bolus and/or infusionIn an emergency can do a needle aspiration:• 21g butterfly needle, 3 way tap, 10mL syringe,

alcohol swab, sterile gloves• Infant supine, insert over the top of the rib in the

2nd or 3rd intercostal space (mid clavicular). Aspirate air into syringe, expel using 3 way tap, repeat as required until air all removed.

22. Management• Following needle aspiration an ICC will need to be

inserted for ongoing management• See neonatal handbook, or own hospitals clinical

practice guidelines for procedure instructions.• Under controlled circumstances effort is generally

made to perform the insertion in line with the auxilla (for cosmetic reasons).

• The ICC will need to be connected to a Heimlich valve or an underwater seal drainage set.

• Familiarise yourself with what equipment your units have because in a high anxiety situation you don’t want to be playing guessing games on what goes where!!

23. Nursing management• Have equipment ready to attach to ICC• Keep end sterile and hand to doctor when they

are ready to attacn• Set suction as required if using underwater seal

drainage (until water bubbling gently in chamber – may not need suction on to achieve this). Appropriate volume of water needs to be added to chamber as indicated in instructions.

• Continue with observations• Ensure pain relief is adequate• Counsel parents• Handover to NETS nurse• Copy appropriate paperwork for transfer

24. Reference

•NETS handbook (pneumothorax drainage)www.netsvic.org.au/nets/handbook

1. HIE: A Case Study•Baby M was born limp, blue, and without

respiratory effort at 38 wks GA to a 38yr old, G5P1 woman.

•NVB after a precipitate labour•A uterine rupture was later diagnosed•Apgar scores were 1, 2 and 4 at 1, 5 and 10

mins•Resuscitated in delivery room, intubated and

transferred to the NICU at the birth hospital•Initial cord pH was 6.7, arterial blood gas

after resus showed pH of 7.17

2. HIE: a case study cont...• Neurological exam notable for dilated and

unresponsive pupils, no spontaneous movements, and diminished reflexes and tone – consistent with moderate to severe encephalopathy

• Seizure activity (lip smacking) commenced at 1hr of age; confirmed on electroencephalogram (EEG/brainz monitor)

• Central access was gained for fluids, medications, blood taking and continuous monitoring

3. HIE: a case study cont...•Criteria met to cool (respiratory depression

at birth requiring intubation and continued need for ventilation, concern for placental abruption, cord pH less than 7, clinical encephalopathy and on EEG

•Cooling commenced at 4 hrs of age (criteria to achieve this by 6 hrs of age met)

•Anticonvulsants given to control seizures and continued for several days

4. HIE: a case study cont...•Remained intubated for airway protection

for several days•Fluid restricted to prevent further injury

to the brain•Kidneys were affected by the hypoxic

events at birth as evidenced by poor urine output and electrolyte disturbances requiring fluid restriction and electrolyte boluses

•Liver enzymes were mildly elevated but there was no evidence of coagulopathy

5. HIE: a case study cont...•Began rewarming after 72 hrs cooled•EEG tracings on day 5 showed no evidence of

seizure activity•Phenytoin ceased, phenobarbitone continued•MRI on same day showed minor changes in

occipital cortex, but no significant abnormalities

•Sedation lightened, extubated to room air day 6

• IV fluids liberalised and NGT feeds commenced day 7

6. HIE: a case study cont...•Neurological exam continued to improve –

pupils became reactive, suck and gag reflexes were present and she began to move spontaneously

•Normal MRI noted on day 12•Discharged home day 15 fully suck

feeding and off all anticonvulsants•Followed up 6 monthly in neurology clinic

– meeting developmental milestones with no neurological deficits evident

7. HIE• Definition & Diagnosis• Etiology & Risk Factors• Incidence• Pathophysiology• Diagnosis• Assessment• Multisystem involvement • Hypothermia management• Nursing management• Outcomes

8. Definitions• Hypoxia or Anoxia: A partial (hypoxia) or complete

(anoxia) lack of oxygen in the brain or blood• Asphyxia: The state in which placental or

pulmonary gas exchange is compromised or ceases altogether

• Ischemia: The reduction or cessation of bloodflow to an organ which compromises both oxygen and substrate delivery to the tissue

• Hypoxic-Ischemic Encephalopathy: Abnormal neurologic behavior in the neonatal period arising as a result of a hypoxic-ischemic event.

9. Etiology of HIE• Maternal:

▫ Cardiac arrest▫ Asphyxiation▫ Severe anaphylaxis▫ Status epilepticus▫ Hypovolemic shock

• Uteroplacental:▫ Placental abruption▫ Cord prolapse▫ Uterine rupture▫ Hyperstimulation with

oxytocic agents

• Fetal:▫ Fetomaternal hemorrhage▫ Twin to twin transfusion▫ Severe isoimmune hemolytic

disease▫ Cardiac arrhythmia

10. Incidence of HIE•Occurs in 1-6 per 1000 live term births in

developed countries▫25% die or have multiple disabilities▫4% have mild to moderate forms of

cerebral palsy▫10% have developmental delay (this is

similar to the control population!)

11. Pathophysiology•Acute HIE leads to primary and secondary

events:▫Primary neuronal damage: cytotoxic changes

due to failure of microcirculation inhibition of energy-producing molecular processes ATPase membrane pump failure cytotoxic edema and free radical formation compromised cellular integrity

▫Secondary neuronal damage: May extend up to 72 hours or more after the acute insult and results in an inflammatory response and cell necrosis or apoptosis (fueled by reperfusion)

12. Diagnosis•There is no clear diagnostic test for HIE•Abnormal findings on the neurologic exam

in the first few days after birth is the single most useful predictor that brain insult has occurred in the perinatal period

•Essential Criteria for Diagnosis of HIE:▫Metabolic acidosis (cord pH <7 or base deficit

of >12)▫Early onset of encephalopathy▫Multisystem organ dysfunction

13. Clinical Staging of HIE (Sarnat and Sarnat, 1976)

HIE can be divided into Mild, Moderate, and Severe

14. Assessment Tools in HIE•Amplitude-integrated EEG (aEEG)

▫When performed early, it may reflect dysfunction rather than permanent injury

▫Most useful in infants who have moderate to severe encephalopathy Marginally abnormal or normal aEEG is very

reassuring of good outcome Severely abnormal aEEG in infants with

moderate HIE raises the probability of death or severe disability from 25% to 75%

15. Assessment Tools in HIE•Neuroimaging

▫Cranial ultrasound: Not the best in assessing abnormalities in term infants. Echogenicity develops gradually over days

▫CT: Less sensitive than MRI for detecting changes in the central gray nuclei

▫MRI: Most appropriate technique and is able to show different patterns of injury. Presence of signal abnormality in the internal capsule later in the first week has a very high predictive value for neurodevelopmental outcome

16. CNS complications

•Most widely reported and best known sequelae

•Major findings include: intracranial haemorrhage, cerebral infarction, cerebral oedema & gross brain swelling

•Clinical manifestations: abnormal states of consciousness and tone, full or tense anterior fontanel, irritability, tremors, convulsions and poor suck

17. CNS complications

•Management/monitoring: monitor systemic blood pressure, intracranial pressure (by feel of fontanel), and structural changes/damage (usually MRI)

•Pharmacologically management: anticonvulsants (phenobarbitone, phenytoin); sedation, especially if ventilated and cooled (morphine, midazolam)

•Prevent fluid overloading

18. Cardiovascular & Renal complications•Hypovolaemia, hypotension, shock and renal

failure are the most serious sequelae of HIE•Need to monitor: urine output (weigh

nappies or measure hrly if a catheter is insitu), monitor electolytes, urea & creatinine

•Have to find the balance between adequate hydration for renal function but not fluid overloading (somewhere between 60 – 150mLs/kg/day)

19. Cardiovascular & Renal complications•Hypovolaemia & hypotension may require

management with volume expanders, blood transfusion and/or inotropes (improve cardiac contractility and cardiac output; therefore good for improving renal function as well)

• If there is hypovoleamia/hypotension the bodies response is to vasoconstrict (peripheral and splanchnic), hence, there is poor perfusion to gut and kidneys. Shock response/maintain function of vital organs

20. Pulmonary complications

•Provide respiratory support if required (CPAP or ventilation)

•Monitor respiratory status by observation and blood gases

•Treat underlying pathology, ie. Sepsis (antibiotics), meconium aspiration/PPHN (ventilation/nitric oxide), poor or no respiratory drive due to CNS complications (ventilation)

21. Metabolic & Haemological complications

Monitor and manage sequelae such as: • Metabolic acidosis (ventilate and use sodium

bicarbonate corrections)• Hypoglycaemia (initial infusion of 10% dextrose, but

more concentrated solutions may be required if fluid restriction is required)

• Hypocalcaemia (calcium corrections)• Hyponatraemia: dilutional or actual? (Fluid restrict

for dilutional or replace Na if losing it through the kidneys)

• Monitor blood pressure, iatrogenic blood loss (from mulitiple tests) and haematocrit level (will give you an indication of degree of haemodilution or concentration)

22. Reperfusion Injury• Reperfusion injury is the tissue damage caused

when blood supply returns to the tissue after a period of ischaemia

• The absence of O2 and nutrients from blood during the ischaemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than the restoration of normal function

• The inflammatory response is partially responsible for the damage of reperfusion injury

• Restored blood flow reintroduces O2 within cells that damages cellular proteins, DNA and the plasma membrane

23. ICE (infant cooling evaluation) trial• Conducted throughout 28 centres in Australia,

New Zealand, Canada and the USA (2001 - 2007)• Cooling is started within 6 hrs of birth• Cooling can be started at the hospital of birth

and continued throughout transport, by using simple equipment (gel ice packs)

• The aim is to lower the brain temperature to protect it from damage

• This treatment could prevent as many as 1 in 7 from dying or surviving with a significant disability

24. Management - Hypothermia•Aim for body temperature 33 – 34 degrees•Treatment continues for 72hrs•Babies are rewarmed gradually over a 12 –

24hr period after this time•Supportive management continues

throughout treatment•EEG monitoring is performed continuously•Blood tests are performed to monitor

electrolytes, liver function, renal function etc

25. Hypothermia - Mechanism of Action• Reduces cerebral metabolism, prevents edema• Decreases energy utilization• Reduces/suppresses cytotoxic amino acid

accumulation and nitric oxide• Inhibits platelet-activating factor,

inflammatory cascade• Suppresses free radical activity• Attenuates secondary neuronal damage• Inhibits cell death• Reduces extent of brain damage

▫ DEATH OR SEVERE DISABILITY AT 18 MONTHS OF AGE SIGNIFICANTLY REDUCED!!

26. Criteria for Hypothermia• Generally only used on term infants• Must be commenced within 6 hrs• Infants must meet at least 2 of following

criteria:1.Apgar score of 5 or less at 10 minutes2.Mechanical ventilation or resuscitation still required at

10 mins3.Cord or arterial pH of <7, or base deficit of 12 or more

within 60 minutes of birth• Core goal temperature of 33 – 34 degrees C for

72 hrs

27. Outcomes•The location and extent of damage, and the

immediate medical management, will determine the short and long term outcomes

•It is possible to have no long term complications as a result of a brain injury at birth

•But complications that can occur are delayed, or failure to reach, milestones (as determined by developmental assessments); cerebral palsy; death

28. Nursing Management• Initial resuscitation• Transfer to SCN/NICU for ongoing management &

observation• Baseline observations• Consider need for cooling (discuss with

paediatricians/NETS)• Observe for seizure activity• Intravenous access & bloods to be taken• Medications & fluids as ordered• Measure urine output (mLs/kg/hr): weigh nappy,

divide weight of urine by weight of baby and no. of hrs since last measured. Eg: 20mLs/3.3kgs/4hrs = 1.5mLs/kg/hr

Questions1. The mother of a baby with suspected HIE

inquires about the possibility of a brain insult in her infant. Of the following, the single most useful predictor of brain insult in this infant is the evidence of:

A. Abnormal neurologic exam findingsB. Cerebral edema on cranial USC. Elevated creatinine phosphokinaseD. Hemodynamic and pulmonary imbalanceE. Multisystem organ dysfunction

Questions2. The severity of HIE can be graded as

mild, moderate, or severe, using a classification proposed by Sarnat and Sarnat. Of the following, the criterion most consistent with the diagnosis of mild HIE is:

A. Absence of seizuresB. Low Apgar scoresC. Need for assisted ventilationD. Proximal muscle weaknessE. Obtunded state of consciousness

Questions3. Several ancillary tests have been

proposed to improve the prediction of long-term outcome of infants who have suffered from HIE. Of the following, the most useful and practical test for determining the prognosis of HIE is:

A. Cranial ultrasoundB. MRIC. EEGD. Near-infrared spectroscopy

E. Somatosensory evoked potentials

References• Allan WC. The clinical spectrum and prediction of outcome in

hypoxic-ischemic encephalopathy. Neoreviews 2002; 3; e108-e115• Delivoria-Papadopoulos M, et al. Biochemical basis of hypoxic-

ischemic encephalopathy. Neoreviews 2010; 11; e184-e193• Casey, D.M., Tella,N., Turesky,R. & Labrecque,M. Therapeutic

Hypothermia: Treatment for Hypoxic-Ischaemic Encephalopathy in the NICU. Neonatal Network. Nov/Dec 2011, Vol. 30, No. 6 pp 370-380.

• Fanaroff and Martin’s Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, 9th edition. 2011, p 952-976

• Marro, PJ, et al. Pharmacology review: Neuroprotective treatments for hypoxic-ischemic injury. Neoreviews 2010; 11; e311-e315

• Shankaran S. Neonatal encephalopathy: Treatment with hypothermia. Neoreviews 2010; 11; e85-e92

• Fomufod,A.K.,White,P.L Perinatal asphyxia II: Clinical management of multisystemic sequelae. Journal of the National Medical Association (1979), Vol. 71, No. 11 pg 1065-1066

KH18th September

•Transferred to Ballarat to establish bottle feeding•Captopril and frusemide

21st September•All bottle feeds, NG removed

24th September – day 39 of life•75g weight loss noted, lethargic•FBE WCC 20, n11.3, CRP 34

KH24th September – afternoon•Vomiting•Offensive diarrhoea +++, flecks of blood•Lethargic, pale, floppy, CRT 3-4s

•Difficult IV access•Lactate 3.6•10mL/kg NS bolus x 2•Triple antibiotics commenced, NBM, NG inserted•Apnoeas•Mild abdo distension, tender ++ → morphine infusion•NETS

KH24th September – evening

•Difficult intubation – laryngeal mask after 5 attempts at intubation•Third NS bolus – total 30mL/kg•Dobutamine and morphine infusions•Pancuronium•Persistently tachycardic on transfer•Loaded at left at 2240

RCH•Intubated, inotropes•No growth on faeces MCS, enterovirus PCR pending

Issues•When to intubate, when to wait for NETS

•Septic, unstable neonate with cardiac condition•When to use laryngeal mask•When to start inotropes

Intubation ? When to

Inotropes

Laryngeal masks

Baby Harry

HSV in neonates

case studies - neonates by: nicole stevens. case studies - neonates haemolytic disease of the...

Documents

case study

baby ericday

baby ericplan

baby eric175

baby ericsbr

case studies neonatesby

hrs blood group

baby ericinduction of