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 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 incompatability
Review 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.
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%
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. KH
G1P0
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. KH
Day 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?
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 Aorta
Repair:
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’s
Screening:
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’s
Prostaglandin 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 central
Eg. 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 facility
Fluids 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 & symptoms
Gastrointestinal dysfunction:
Abdominal distention
Vomitting
Bilious drainage from enteral feeding tubes
Blood in stool
Systemic
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 findings
Non 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: complications
Surgery requiring ileostomy results in long term issues:
Require supplemental Na even when well
High risk of rapid dehydration with gastroenteritis
Stricture:
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 pregnancy
Plan:
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
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!!
13. Xray interpretation (1/8/12 @ 2006hrs)
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
16. Xray interpretation (2/8/12 @ 0028hrs)
R) sided pleural catheter insitu
Air space opacity in both lungs unchanged
ET tube is seen with tip at the level of the clavicle
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!!
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
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
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
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:
Apgar score of 5 or less at 10 minutes
Mechanical ventilation or resuscitation still required at 10 mins
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
Questions
1. 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 findings
B. Cerebral edema on cranial US
C. Elevated creatinine phosphokinase
D. Hemodynamic and pulmonary imbalance
E. Multisystem organ dysfunction
Questions
2. 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 seizures
B. Low Apgar scores
C. Need for assisted ventilation
D. Proximal muscle weakness
E. Obtunded state of consciousness
Questions
3. 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 ultrasound
B. MRI
C. EEG
D. 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
KH
18th September
Transferred to Ballarat to establish bottle feeding
