Neonate essays a.) What are the clinical features of respiratory distress in a newborn? (5m)

Download 172.19 Kb.
Size172.19 Kb.
Neonate essays
a.) What are the clinical features of respiratory distress in a newborn? (5m)

  • tachypnoea >60

  • grunting – breathing against a closed glottis to prevent airway collapse

  • retractions – because the chest wall is more compliant

  • flaring of nostrils, open mouth – to reduce resistance

  • cyanosis – bluish discoloration best seen on tongue

  • apnoea – cessation of breathing more than 20s w/or without bradycardia

  • stridor – inspiratory sounds indicating upper airway obstruction

b) 4 important causes of respiratory distress in a TERM baby (4m)

- pulmonary causes: TTN, HMD, MAS, congenital pneumonia, pneumothorax

- cardiac: cong heart dz, PDA
- metabolic: acidosis

- persistent pulmonary hypertension of newborn

c) Mx of newborn born thru TMSL (10m)
The passage of meconium is a sign of Fetal Distress, n is a warning tt baby may be in poor condition at birth. Secondary problem is tt the baby may inhale meconium-stained liquor during delivery

This can cause MAS which results in severe ventilatory problems

To avoid this, as soon as the head appears, must thoroughly suck out the mouth and oropharynx. When the baby is completely delivered, take him quicing to the Resuscitaire for further suctioning. It is best to start suction when baby’s head is at perineum
If there is a large amt of meconium, need to directly visualize the vocal cords with the laryngoscope and suck away any meconium frm arnd the laryngeal inlet. May need to insert an ETT an suction meconium from the trachea.
Babies who are covered in meconum will have swallowed some as well. Aspirate the stomach contents with an NG tube otherwise they regurg mucus for days and feed poorly.

- To prevent MAS at birth:

- 1st: oral/ nasal suctioning by obstetrician at CROWNING

- then laryngo-tracheal suction with meconium aspirator by neonatologist b4 ventilating lungs (ventilating lungs only indx if meconium is thick like pea soup, and infant did not cry or is not vigorous i.e. depressed infant)

- nx: respiratory tx, antibiotics, supportive tx

- respi tx

1. stabilization/ resus at birth, transfer to NICU if indicated\

2. resp tx aims to maintain normal pH, pCO2, p02 and Sa02 thru

- oxygen hood

- oxygen cannula


- intubation and ventilation with IPPV

3. monitor of Pa02, PaCO2, SaO2 during resp tx achieved by

- intermittent sampling thru arterial catheters (thru umb or periph arteries)

- continous blood gas monitoring thru trancutaneous PaO2 & PaCO2 probes or oximetry for SaO2

- supportive tx

1. maintain neutral thermal environment (warmer, clear shield, incubator)

2. consider empirical IV ATBs (usually ampicillin/ penicillin and genta) wahile awaiting culture results to exclude infxn as a cause for RD

3. correct polycythaemia, hypoglycaemia, hypocalcemia if present

4. insert catheters for intra-arterial monitoring of bld gases and BP (umbilical arterial or peripheral arterial); correct metab acidosis if present

5. monitor BP; consider vol expanders (colloid, plasma) or ionotropic support (dobutamine, dopamine) if low BP

6. withhold enteral nutrition if in RD (avoid aspiration); give adequate fluid and e’lytes thru parenteral nutrition. Monitor input output strictly

7. consider chest physiotx in aspiration syndromes, avoid xs handling in RDS

8. provide counseling and emotional support for parents; consider referral to the medical social worker (MSW) if necc.

Evaluation of NN RD

  1. Hx – gestation, bw, apgar score

Mode of delivery, resus at birth

AN US – oligohydramnios

Intrapartum pyrexia, chorionamnionitis and other maternal infxns

Durature of ROM

Color of liqor (TMSL)

Placental appearance

  1. PE

  2. ABGs

    1. pH 7.35-.7.45

    2. paCO2 35-45 mmHg

    3. Pao2 >60mmHg

    4. SaO2 >90-92%

    5. Bircarb 16-24mEq/L

    6. Base xs =5 to +5 mEq/L

  3. CXR

  4. FBC – central Hct, TWC, differential, platelet

  5. serum glucose and calcium level

  6. cultures: blood, surface swabs, placental, maternal vaginal

Resp and Supportive Tx

What r the clinical signs of RD in newborn infant?

  • Tachypnoea (over 60 per min), grunting (grunt/ squeak heard at end of expiration), subcostal and intercostals retractions, sternal retraction, nasal flaring open mouth

  • cyanosis, period of apnea (>20s) and stridor

List 6 common causes of resp distress in a 36 weeker delivered by Caesarean

  • 36 = preterm. And caesarean. Hence..

    • 1 Hyaline membrane disease – surfactant deficiency

    • 2 Pneumonia especially due to GBS (commoner in premmies) – immature immune systems, thin skin, repeated exposures to invasive procedures e.g. iv and intra-arterial cannulae, central lines, ETTs

    • 3 Pneumothorax – most commonly occur during ventilation of premature babies

    • 4 Intra cranial hemorrhage – sudden collapse, pale hypotensive and apneic

    • 5 feeding difficulties causing poor sucking.. and also a poor cough reflex

    • 6 hypoglycaemia – due to lack of glycogen stores

    • 7 hypothermia causing increased energy and 02 requirement and metabolic rate  cold baby prone to acidosis, hypoxia and hypoglycaemia. Resp distress worsened to the deleterious effect of cold on surfactant function

    • note: MAS cannot becos its due to a full term fetus distressed before delivery

outline the clinical features, radiographic findings and mx of any one of the disorders
HMD (oh, but surfactant usually poorly produced before 34/52. this baby is 36/52.. how?!)

Commonest COD in babies born before a gestation of 36/52

Due to deficiency of pulmonary surfactant which is poorly produced b4 34/52 gestation

Without surfactant, the smaller alveoli tend to collapse at the end of expiration and a pressure greater than what the BB is able to generate is required to re-expand them

clinical features:

  • onset usually within 3-4 hrs, may be sooner in premature babies

  • tachypnoea, nasal flare, retractions grunt

  • on top of that, develop central cyanosis, apnoea and creps

  • poor chest expansion with reduced breath sounds and crepitations may be heard


  • often be normal in 1st few hrs

  • later lung fields show a fine reticular pattern and may then appear opaque with classic ‘ground glass appearance’

  • contrast between the air in the bronchi and the dense lung fields produce an air bronchogram


  • required nursing in neonatal unit

  • mild cases may only require O2 given in a headbox. Most case however require ventilatry support with regular arterial bld gas monitoring

  • artificial surfactant has recently been dev and is given by instillation down the ETT in infants with severe dz, sometimes with dramatic efx

  • babies shdnt be fed but given IV fluids

  • IV ATBs are necc as RDS cannot be different frm GBS pneumonia until bld culture results arek known, in addition, premat babies are susceptible to infxn and is possible a baby with HMD may also have pneumonia

  • Depending on degree of prematurity, most cases begin to improve within a week. This is indx by a decrease in ventilatory requirement. Unfortunartely some babies will dev chronic lung dz with long-term o2 requirement


  • Causative organisms: GBS esp if onset within 1st 24 h, and E coli are e most common

  • esp GBS can lead to early onset resp distress

  • other possibilities are Staphylococcus, pneumococcus, Listeria monocytogenes, Klebsiella, Pseudomonas

  • or following aspiration of milk due to poor cough reflex in premmies and also prone to gerd

  • means tt material such as regurg milk in the pharynx easily aspirated into lungs

Clincal presentation:

  • usually acc by septicaemia

  • baby has non specific symptoms e.g. poor feeding, persistent vomiting, lethargy, xsv sleepiness, xsv crying or abnormally quiet baby, apnoiec episode in a preterm baby, floppiness, irritability, tachypnea, cold mottled extremities, hypothermia or fever, hypoglycaemia, jaundice

  • resp: grunt, retractions, nasal flare, cyanosis and creps


  • usu unhelpful at first, revealing only non specific changes

  • later there may be an area of consolidation (a white patch) or collapse

  • occ, air or fluid filled spaces (pneumatoceles) are seen which indx staphylococcal infxns,


  • bld cultures and culture respi secretions

  • CXR usually unhelpful at first

  • ABGs may show respi acidiosis with degress of hypoxemia


  • IV atbs 7-10 ds

  • Early onset pneumonia best rx with benzylpenicillin and gentamicin. After 48 h of age, staphylococcus more likely than GBS so flucloxacillin shd replace the benzylpenicillin.

  • Severe cases may need to be ventilated

  • Mainstay of rx is to start early, hence rapid recognition of GBS essential..

a. Brief outline of neonatal bilirubin metabolism and describe y physiological jaundice develops in the newborn (6m)

BR is derived frm catabolism of proteins tt contain heme

Most impt source of BR is the brkdwn of Hb frm RBCs

In the reticuloendothelial system, heme oxidized to biliverdin which is then rapidly reduced to bilirubiin
Native BR is relatively insol in H20 at physiological pH, but v lipid sol.

In serum, BR circulates bound to albumin (as unconj BR) in equilibrium with its (small but variable amt, approx 0.1%) unbound or ‘free’ fraction

It is the UNBOUND fraction tt readily xes the BBB and results in NEUROTOXICITY
Unconj Br is processed by liver made more water-sol in liver – by conjugation with glucuronic acid to prduce ‘conjugated’ BR. (by the glucuronyl transferase enzymes)

Conj BR then excreted frm liver into gut  cleared thru bile into intestines and out into feces.

PhotoTx works by bypassing this hepatic system by producing photoisomers of BR tt are more water sol

Thus can be cleared directly into bile or urine without conjugating in the liver.

Jaundice is a yellow discol of skin due to deposition of BR pigment. Occurs when serum BR is raised.
Physiological jaundice – due to a functional immaturity of the liver and its enzymes, particulary common amongst preterm infants. Also occurs freq in term babies.

A temporary deficiency of glucuronyl transferases reduces the rate of conjugation of BR with consequent rise in unconj BR.

In addition, there is a rapid hemolysis of fetal red cells tt takes place after birth
Hence reasons y Newborn is prone to jaundice:

  1. physio immat of the conjugation mechanism in the liver

    1. uptake mech of unconj BR frm e bld

    2. Intracellular transport of BR

    3. Its conjugation by glucuronyl transferases

    4. And its transport out of the cell into the bile duct

Are all delayed in newborn in comparision w older infant

This results in unconj BR circulating in bld

  1. excessive brkdwn of RBCs.

    1. Hb levels fall gradually after birth frm mean of 15g/L at birth to 11g/L at 3 months of age.

    2. Fetal RC has a mean lifespan of only 80days cf to tt of infant which is 120 days

    3. Birth trauma, esp if there is hematoma formation, results in large load of Hb to be broken down

  1. Lack of bacteria in e gut

    1. Gut is sterile at birth. Becomes colonized with bact over the 1st days

    2. BR present in the meconium in the gut is avaible to be reabsorbed

    3. Delay in passage of meconium is assoc with increased risk of jaundice

  • In full term infants, jaundice appears after 24 hr following birth, reaches peak on 4th/ 5th day. Changes in serum BR precede the visible jaundice so tt serum levels peak on the 3rd day, drops rapidly by day 6 and r normal by 11-14 days.

In preterm bbs, jaundice usu begins within 48hrs of birth and may last up to 2 weeks.

b. A newborn Chinese baby is noted to be jaundiced on Day 2 of life. What are the most likely causes of jaundice. (4m)

- physiological (full term after 1st 24 h following birth, preterm babies jaundice usu begins within 48 h of birth, may last up to 2 weeks)

- breast feeding jaundice

- 2 separate types of breast milk jaundice:

1. early type (breast feeding Jaundice)

- in 1st 5 days.

- Exaggerated form of physiological jaundice

- often attributed to both caloric deprivation and poor fluid intake in the early stages of breast feeding (during the 1st few days of life)

2. late type (breast milk Jaundice)

- recognized towards end of 1st week. Usually cont for 3-6 weeks, even 2-3 months

- diagx of exclusion, by definition, babies are otherwise healthy

- if breastfeeding stopped and formula milk given for 48h, rapid fall in BR level. Meanwhile mother shd express her milk otherwise lactation may cease. When breast milk is restarted, BR rises a little (usu 20-60umol/l) but never to prev high level

- Red cell incompat

- usually of rapid onset, noted within 1st 24 h after birth. Incompatibility leads to hemolysis of RBCs causing an unconj hyperBRnaemia. There are different types

1. Rh incompat

2. ABO incompat (mom is O, baby A or B.) cf to rhesus, this can affect 1st baby. Dz less severe with rhesus

3. other bld groups e.g. C, c, E, e, kell and duffy can also cause hemolytic jaundice

  • Increased RC brkdwn

    • Traumatic deliv tt leads to extensive bruising will inevitably produce jaundice and preterm babies are particularly susceptible to this

    • A cephalohematoma always causes jaudnce when the bld clot is broken down

    • If the bb is polycythaemic and appears v red on 1st day, mother can be warned tt he will soon turn yellow as the extra red cell load is broken down

  • G6PD deficiency

    • X linked condition, deficiency of enzyme responsilble for maintaing stability of RBC membrane. Usu p/w in NN with severe unconj jaundice

c. How wld u mx this baby (10m)

- Carefully review FH and clinical Hx, and Phys findings:

- History:

- FH of sigf hemolytic dz

- ethinic bkgrnd suggestive of inherited dz e.g G6PD defcy etc

- birth trauma  cephalhematoma

- polycythaemic at birth

- GDM mother’s infant (IDM)

- gestation less than 37 weeks (preterm)

- Phys findings:

- pallor, heptatosplenomegaly (haemo jaund)

- cephalhematoma, ecchymosis (incr RBC brkdwn)

- SS of other dzs causing jaundice: vomiting, lethargy, poor feeding, tachypnea, hi pitched cry, apnea.

  • ixs

    • >7-8mg/dl in 1st24 hrs of life  furter lab workup, close observation and evaluation, possibly tx is warranted:

      • Maternal ABO and Rh typing, maternal serum screen for unusual isoimmune Abs if not already done.

      • Baby’s bld grp, Rh type. Direct’s coombs test

      • FBc and differential, reticulocyte count and bld smear

      • Repeat msmt of BR in 4 to 6 hrs

  • mx:

    • rapidly rising BR (>0.5mg/dl/h)  phtx indicated

    • shd be and remain hospitalized under phtx til BR levels stablise at a safe level based on infant;s age and whether infant was full or preterm

    • Phototx:

      • Bluelight fluorescent lamps, ideally wave length 450-460 nm

      • 45 cm above infant, Plexiglas cover or shield + eyepatch

      • 2 hr turning

      • monitoring serum BR, T, urine outpt, weight

      • dehydration a/w with incr serum BR conc, may be exacerbated by phto tx

      • brestfeding not CI

    • presence of documented hemolytiz dz due to coomb’s +ve ABO incompat or other etiologies req aggressive evaluation and tx, and probably use of phtx at lower levels.

    • True hemolysis: xchange transfusion indx if BR levels reach levels btwen 18-23 mg/Dl in full terms and 15-18 in preterms.

    • Exchange transfusions:

      • If phototx fails to control rising BR levels. Healthy termies 400-430umol/L. Those w RFs  340 umol/L

      • To rmoeve BR, and sensitive RBC b4 hemolysis and correction of anemia

      • Double vol exchange

      • Fresh whole bld (less than 72 h old)

    • G6PD: preventable kernicterus by mass newborn screening and early detection of babies with disorder. Exposure to oxidative challenge  agents include mothballs, dyes, viral or bact infxns, drugs and fava beans.

Male infant weighing 4.3 kg delivered at 35/52 amenorrhea. Mother did not have any antenatal checkup

  1. List 5 problems tt this infant may encounter in 1st week of life

      1. 4.3 kg = macrosomia

        1. birth trauma (brachial plexus injurym clav #s, intracranial hrrhage) and perinatal asphyxia are associated with shoulder dystocia

        2. macrosmic infants of diabetic mothers can develop hypoglycaemia, hyperbilirubinaemia, polycythamia and hypocalcaemia

        3. Higher incidence of congenital malformations

      2. 35 weeks

        1. poor thermal control

        2. Resp problems

          1. HMD

          2. Apnoeic attacks

          3. Aspiration pneumonia

        3. neurological problems e.g. immat of sucking and swallowing, immat ctrl of respi

        4. PDA

        5. GI problems – NEC

        6. jaundice

        7. anemia

        8. infections

        9. renal problems

        10. metab problems

          1. hypoglycaemia becos lack of glycogen rserves as these are primarily laid down in last 4/52 of preg

  1. discuss diagnosis and mx of 3 of these problems:

    1. Hypoglycaemia

1) Diagnosis:

- s ymptoms of hypoglyacemia are non specific

        • Irritability, lethargy, apathy, hypotonia, recurrent apnoea, seizures (convulsions), coma, poor feeding, vomiting, jittery, irritability and cyanosis

      • Often asympt, and may only then be detectged by performing a BM stix test for blood glucose

      • 2.5mmol/L or less in any infant who show clinical manif compat w signif low bld glucose is an indx for clinical interventions

      • term babies sigf hypogly said to occur with <1.9mmol/L in 1st 72 h and <2.6mmol/L after thie period

      • in premat and small-for-dates babies, the cut-off is set at 1.4mmol/L

2) Mx:

- primarily aimed at prevention. Identify high risk groups and have their blood glucose monitored regularly at first

- can be done with heel prick capillary sample using BM stix test. If reads <1.4mmol/L  a venous blood sample should be taken to measure the true plasma control

- early feeding is the key to prevention

- start milk feed within 2 hr of birth, fed 3 hrly for 1st 24 h. if got problem with feeding, NG tube give milk via it.

- regular BM stix can be discont once they are consistently >2mmol/L for 24 h as long a feeding well

- if premat and hence likely will dev respi problems due to their GA, dun give enteral fits initially. IV line, 10% glucose infusion with maintenance sodium

- IDM babies should also start early feeds within 1-2 h using NG tube if necc. Shd be fed 3 hrly for 24 hours. If bottle fed, shd be given 60ml/kg/day. Breastfed bb should be put to the breast but may need complementary formula milk if glucose falls below 1.5mmol/l

- Rx asympt hypoglycaemia

- as soon as low BM stix noted, baby shd be given nx fee tt is due. If he will not take the milk, must be given down NG tube

- Repeat BM stix 1 h after feed. If still low, venous bld sample shd be taken which can be done at e same time as inserting iv cannula

- bolus 10% IV glucose shd then be given. Abt 0.5g/kg

- after bolus given, infusion of 10% glucose shd start at 60ml/kg/d in all cases. Ensure baby not overloaded by checking fluid vlumes..

    1. HyperBR

      1. Diagnosis

      • clinical assessment as a rough guide.

        • Cephalopedal (100umol/L in face, 150 if trunk to umb, 200 if umb to knee. 250 if from mid upper arm to wrist or knee to ankle, >270 if hands and feet)

        • point of most distal progression assessed by pressing on skin with thumb to make it blanch, see whether appears yellow

        • at serum BR levels <70umol not noticeable

        • clinical assessment of baby’s health shd be made -> attention to lethargy, floppiness and feeding well or not. Chk color of urine and stools.

      • Bld tests:

        • Serum BR is key to assess severity; all tt is needed is a small capillary bld sample taken frm a heel-prick. This is centrifuged for a few min and eaily read in a Bilirubinometer (which most paeds dept possess). Shdnt leave samples in light if got delay in process and BR can be degrade and u will get a falsely low result. Machine gives total BR but is enuf for initial assessment of severity and monitoring of rx

        • Alternatively, venous sample (0.5 ml in orange lithium heparin bottle) can be sent to lab. In this case, both conj and unconj fractions will be obtained

        • Level of serum BR tt is acceptable depends on the age of child and wheter full term or pretrm. Phototx charts give guidance of necessity of treatment

      1. Mx

        • ix the cause:

          • <24 h whatever the level  prob bld group incompt so carry out following

            • serum Br (both conj, unconj)

            • FBC, bld film

            • Bld grp ----------- both require 0.5

            • Coombs test ------- ml of clotted bld

          • Onset after 24h but serum BR >300umol/L

            • Mild jaundice babies are perfectly well, need only serum BR monitoring, assumed to have physio jaundcice

            • However if the result is hight enuf to suggest tt the baby require phtotx, even if bb isi asympt, causes of jaundice shd be inx as follows:

              • Serum BR – conj and uncon

              • Fbc and White count differential

              • Bld grp

              • Coomb’s test

              • Blod culture (for latent infxn)

              • Urine culture (for asympt infxn)

              • G6pD levels in appropriate racial groups  0,5 ml bld in pink EDTA bottle)

          • Prolonged Jaudnice >14 days

            • Serum BR – conj and uncon

            • FBC and differential

            • TFTs

            • Liver enzy

            • G6pd if appropriate

            • Urine cluture

            • Urine for reducing substances (for galactosaemia)

            • Urine for presence of BR which reflects a high conj BR (on labstix)

In all cases of conj BR, or obstructive jaundice, biliery atresisa must be excluded

      • treatment

        • phototx  plot serum BR result on phototx chart

        • chart indx levels above wich phtx is necc

        • if below line, no further action nec, but reassess child e nx day

        • FULLTERM: after d 5, serum B 320umol/L is cut-off for phtx

        • In preterms: cut off level for rx is reduced: e.g 34-37/52s old babies will have rx at 270umol/L

        • Phtx is ineffective at levels < 100umol/L

        • Exchange transfusion

          • Cos occasionally phtx isn’t sufficient to combat an everincreasing BR level. Rarely happens now due to low incidence of severe Rh incompat resulting from the preventive measures undertaken with RH-ve mothers

          • Main indx are in cases of severe jaundice due to haemolytic dz or newborn. In addition to lowering serum BR, removes some of the haemolytic antibodies and corrects anaemia

          • Acts quickly so tt it is useful in babies who are showing early signs of BR encephalopathy

          • Principal is to completely exchange the bb’s blod with donor bld. Can not be done to one stage so a small amt of withdrawn followed by transfusion of equal amt

          • Cycle then repeated many times until enuf bld has been exchanged

          • For a complete exchange, twice the bb’s bld vol is used i.e. 170ml/kg BW

    1. Infections

1.) Diagnosis

  • non specific signs usually unless site of infxn obvious.

  • Often the case with more serious and systemic infxns such as septicaemia or meningitis. Non specific SS of infxns may include:

    • Poor feeding, persistent vom, lethargy, apathy, exsv sleepiness, poor cry or irritable, apnoiec episode in preterms, poor urine o/p, floppiness, tachypnea, cold mottled extremeties, hypothermia or fever, hypoglycaemia, jaundice

2) Mx

  • Septic screenL

    • If there is any suggestion tt a baby may have an infxn then early intervention is necc. After taking Hx, and performing thorough PE, full septic screen must be carried out:

      • Full bld count with white cell differential

        • Baby may be anemic (N = 15-18g/dl in a NN)

        • White count may nt be v helpful. Normal total WCC is up to 30x10^9/l in 1st 48 h, during this period, more neutrophils and polymorphs, but after 48h, lymphocytes comprise abt 60% of the TWCC. Infxn may be assoc with lymphocytic or neutrophil leucocytosis but often the WCC is Normal

        • However after e 2nd day, a neutrophil count >10x10^9/L suggests infxn

        • Infxn may cause low platelet count (thrombocytopenia) tho sometimes the count is raise as a non-specific response to inflmmn. The Normal Platelet count is 100-300 x 10^9/L in e 1st week

      • Bld culture from peripheral vein

        • Clean the skin properly else skin commensals will contaminate culture. Min of 0.5ml bld necc, tho more bld obtained, more chance of growing organisms

      • Swabs

        • Umbilicus, ear, throat and rectum

        • Skin swabs frm any suspicious areas

      • Gastric aspirate shd be sent in the 1st few hrs of life but only if the bb has not yet been given any milk

      • Urine microscopy and culture

        • Clean catch urine or suprapubic aspirate performed. Abnormal microscopy result signified by >100 white cells per ml and the presence of organisms on Gram-staining.

        • A positive culture is pure growth of >10^5 organism per mL

      • Lumbar Puncture

        • Normal CSF in NN shd be clear colorless and up to 3 WC per mL, predom polymorphs

        • Infxn is indx by cloudy CSF w raised WCC and ther’ll be organisms seen on gram staining

        • CSF protein N 0.1-2.0g/L though may be up to 3.0g/L in preterms. Raised in bacterial infxns

        • CSF glucose: 2-4mmol/L, usu abt 80% of bld glucose level. Assuming baby not hypoglycaemic, CSF glucose is <1mmol/L or less than 80% of blod glucose. Bact infxn is thus indicated.

      • CXR: if baby is v sick shld be done in ward rather than XR dept

      • Others: latex antigen tests or counter current immunophoresis e.g. menigococcus, H,influenzae, pneumococcus, E coli

      • Following shd be checked in a sick baby:

        • Serum Na K Cr and Ca

        • Bld glucose (done at same time as an LP)

        • Arterial pH, o2, co2, base xs

  • initial Rx

    • if baby is v sick, cannot wait for all microb results b4 starting rx

    • iv cannula inserted and maintenance fluids given

    • shd not be given any oral feeds

    • Iv atbs shd be started immed

      • E.g. benzylpen + genta

      • Flucloxacillin plus genta

      • Ampicillin plus genta

      • Cefotaxime or 3rd G cephosporin + benzy

      • Whenever genta is used, bld levels must be chkd b4 3rd dose as high bld levels are a/w deafness and renal tox. Trough levels taken b4 dose given (shd be <2mg/L) and peak levels 20-30 min after IV does (shd be 6-10mg/L) : 0.5 ml clotted bld needed

    • Once full culture and ATB sensitives are known, atbs may be adjusted accordingly

    • Attn paid to fluid and elytes balance as well as any acidosis or hypotension tt oft accompanies severe infxn

    1. HMD

      1. Diagnosis

  • onset of RD usually within 3-4 hrs

  • tachypnea grunting recession and may dev central cyanosis

  • poor chest expansion with reduced breath sounds

  • CXR normal in first few hrs, later lung fields show fine reticular pattern then may appear opaque with classic ground glass appearance

  • Contrast between air in bronchi and dense lung fields produces an air bronchogram

      1. Management

  • nursed in neonatal unit

  • mild cases required o2 in headbox

  • most cases however req ventilatory support w regular ABG monitoring

  • artificial surfactant given down ETT in infants with severe dz

  • NBM, iv fluids

  • IV ATBs

  • Most cases will improve within a week

    1. Polycythaemia

      1. Diagnosis

      • too many RBCs in circ. Hct >65% in a venous bld sample or 70% in a heel-prick cap sample

      • cap sample tt is high must always be confirmed with a venous/ arterial sample

      • Hct Is calc by centrifuging the sample in cap tube for at least 10 min then measuring the proportion of RCs to plasma. Gives slightly different result from PCV (packed cell vol). use either Hct or PCV to monitor progress but they shdnt be interchanged

      • Causes:

        • Delayed clamping of cord at deliv

        • Recipient of TTTS

        • IDMs

        • IUGR bbs

      1. Rx

      • plethoric baby, problems lie in the fact tt there is increased bld viscosity with high PCv which increasese exponentially above 65%. This afx bld flow thru the capillaries wich may become rather sluggish

      • main risk is of cerebral venous thrombosis which can cause convulsions and damage to the brain. CVS may be afxd, CCF or pulm HPT can occur. Increased incidence of RD and TTNB. Jaundice always follows due to large RC load. Polycythemia also a/w hypogly and hypocalc. Finally due to the poor capillary flow, there is an assoc with NEC and renal vein thrombosis

      • When to rx is controversial some only rx symptomatic bbs or those w v high pCV

      • Some rx babies as long as PCV >70%

      • Since cerebral venous thrombosis can be devastating, and rx not difficult, we favor the cautious approach

        • Partial exchange transfusion using 20-30ml/kg plasma which dilutes thickened blood.

  1. what advice shd u give mother regarding future pregnancies:

  • Pre pregnancy care

    • Gd AN care begins b4 pregnancy

    • See a doc for counseling regarding gen health, med and fam Hx

    • Advice on lifestyle

      • 400 mcg FA perday b4 trying to conceive and for 1st 12/52 of preg to reduce NTDs

      • Adverse efx of smoking shd be highlighted esp wrt IUGR

      • Discont of hormonal contraception to allow return of reg ovulation and menstruation thus facilitating proper calc of GA

      • Baseline observations of mat wt, BO and rubella and HIV status

      • Dm, gd glycaemic control. Anemic – take folate

  • AN followup v important e.g booking, 1st trimester USS (NT..), regular BP and urine, bld tests for anaemia, 20/52 FA scan, growth scans. Etc

  • Esp since her this baby is > 4kg

  • Post partum – breast feeding. 6 weeks FU

  • later FU

An infant delivered at 42/52 gestation with BW 3.2kg was found to be tachypneic and cyanosed after 1st feed 2 hrs after delivery

Mother had prolonged ROM with foul smelly liquor and fever

Discuss possible diagnoses and Mx
MAS? - baby is full term. Hence problems a/w premmies not applicable MAS happens in full terms more than premmies.

  • mother had ROM with foul smelly liquor and fever

    • ROM >24 h, risk of bb becoming infxted from contaminated liquor

    • Risk tt baby has been infxd can be assessed at birth by performing a gastric aspirate

    • Shd be done immed after deliv and must be performed b4 1st feed

  • This baby has been fed already, 2 hr post deliv 

    • NG tube shd have been passed and stomach contacts apirated into sterile syringe

  • Infxn calc from a points scheme

    • GA <37/52 – 1 point

    • Mat temp during lab >38deg C - 1 point

    • PROM >24h - 2 points

    • Apgar score <7 at 1 min - 2 points

  • <2 ie. No RF apart from PROM, min risk of infxn even if gastric aspirate positive

  • 3-4: 5% risk

    • take bld cultures, observe child in ward

    • if aspirate positive, 10% risk hence shd receive IV atbs

  • 5-6 points: 30% risk if aspirate negative, but 40% if positive

    • bld cultures taken and immed start IV atbs

  • Most common pathogen is GBS infxn which can cause rapidly progressive septicaemia or pneumonia. If the blod cultures are negative after 48h and child remains well, atbs can be discontinued

  • All times, clinical evidence of infxn paramount and shd overrule the above scheme

  • Pointers are pyrexia, tachypnoea, hypoglyc, irritab or poor feeding

  • do septic screen after taking hx and thorough PE: FBC, bld culture, swabs, gastric aspirate only if no milk has been given, urine microscopy and culture, LP, CXR, latex antigen test, counter current immunophoresis

  • also chk serum Na Cr K and Ca, bld glucose, aterial ph O2 CO2 and Base xs

  • initial rx b4 cultures and sensitivity come back  antibiotics, benzylpen and genta

  • cld be septicaemia  IV atbs 10-14 days

    • use benzypen 60mg/kg/dose 12hrly if less than 7d old or 8 hrly if >7d old

    • and gentamycin 2.5mg/kg/dose 12hrly if less than 7d old or 8hrly if >7d old

  • meningitis

  • pneumonia : IV atb 7-10 days.

  • MAS: meconium deliveries causing inhalation resulting in severe ventilatory problems

    • Clear mouth and oropharynx to prevent aspiration

    • May cause bronchial obstruction and air trapping

Prematurity and problems as well as Mx
HMD – due to surfactant deficiency in immature lung

Can cause RD.

If mild only req oxygen in headbox but often ventilatory support is needed

Apnoea – rpeated episodes of absent resp mvmt >20s or short episodes a/w bradycardia and/or color


immature resp centre

weak resp mucles

compliant thoracic cage

Aspiration pneumonia

Regurg easily

Weak cardiac sphincter

Strong pyloric sphincter

Immature pharyngeal co-ordination and protective reflexes

Intracranial hemorrhage

Common in preterm babies and is a major COD and neurological handicap

May be intraventricular, sAH, Intracerebral (into brain subst itself)

Unless severe the h’rrhage not usually accompanied by symptoms and only detectable by a cranial US examination directed thru the anterior fontanelle

Baby may however present with a suddenly collapse, becoming pale, hypotensive and apneic.

This may be followed by fall in Hb level

Other sympts are irritability or sometimes undue lethargy, poor or increased muscle tone and convulsions


Particularly high in infants VLBW, <34 weeks

GBS, E coil, staph epidermis, pseudomonas

Increased susceptibility cos of poor resistance

Weak skin, inefficient granulocytes, decrease in complement acitivty, decrased Igs

Increased opportunity for infxn

Natural defense bypassed, indiscriminate use of ATBs

V susceptible becos immature immune system, thin skin easily damaged and repeated xposure to invasive procedures e.g IV, IA cannulae, central lines ETTs

Cross infxn

Barrier nursing


Greater BR prodt due to shorter RBC lifespan

Decrease excretion due to hepatic immaturity leading to decreased uptake and conjugation

Decreased BR binding capacity

Immature BBB hence increase risk of kernicterus at lower serum BR levels than in term infants

And increased susceptibility to long-term efx of basal ganglia (kernicterus)

Phtx is req at lower serum br levels cf to full term babies


Indq rate of prodtn

Decr Fe stores

<12g/dl in 1st week

or <10g/dl after 1st week


Poor temp control, immature heat reg centre

Limited ability to increase heat production

Lack of brown fat

Poor oxygen consumption

Poor muscular activity

Limited ability to decrease heat loss

Lack of SQ fat

Greater SA

Fluid and E’lyte imbal

Thin skin leads to marked evaporative fluid loss esp if under radiant warmer

In turn can lead to marked hypernatraeima

Alternately, the immat kidney fails to conserve Na resulting in hypoNatremia

Lower GFR

Poor tubular fn

E’lyte balance needs daily monitoring and in a sick infant, may have to do even more often

Feeding difficulties

Under 34/52 GA do not suck properly

Poor cough reflex  aspiration into lungs

Heart problems

PDA (large lt to rt shunt, LV activity not well dev)




Artificial feed



Cardiac catherisation

Early feeding in assoc w above

        1. Mx body temperature

          1. Incubator care

          2. LBW infant’s scalp  large SA so use a hat

        2. feeding

          1. hi protein

          2. hi CHO

          3. breast milk best

          4. parenteral nutrition

            1. feed increment slow

        3. protection against infxn

          1. strict handwash

          2. incubators

          3. aseptic conditions e.g administering drugs or prep milk

        4. prevent vit and Fe defcy

Baby A born at 40 weeks GA with BW 2.0kg

5 common problems A would have after birth and briefly describe how u wld diagnose these problems
Small for dates baby

  1. genetic background

  2. placental insufficiency esp becos of maternal hpt

  3. maternal hpt esp if assoc if proteinuria

  4. other maternal illness such as renal dz, sickle cell dz, cyanotic heart dz

  5. maj congenital abnormalities and chromosome abn often result in small babies

    1. trisomy 21

    2. potter’s syndrome

    3. anencephaly

  6. congenital infxns e.g. rubella, CMV and toxoplasma

  7. drugs given for maternal illness such as carbamazpeine, phenytoin, sodium valproate]

  8. xsv alcohol intake

  9. smoking during preg retards growth in 3rd Trimester


  1. hypoglycemia

    1. lack of glycogen stores

    2. preventable by early feeding w milk which shd be continuous or every 3h for 1st day

    3. asympt hypoglycaemia must be detected by performing BM stix test every 3h for the 1st 24h

    4. if baby feeding well and BM stix consistently above 2 mmol/L then testing can stop after 24 h

  1. hypothermia

    1. can start v quickly in small infants

    2. heat loss may be considerable becos they have Large SA in reln to BW

    3. also deficieint in SQ fat which acts as insulation

    4. hypotherm a/w incr metab rate and incre energy and 02 reqmt. A cold baby is prone to acidosis hypoxia and hypoglycaemia. RD is worsened due to the deleterious effect of cold on surfactant function.

    5. Prevention of hypothermia starts in delivery rm

    6. Keep the rm warm, dry baby quickly, wrap in warm bklankets, put on a hat

    7. Radiant heater

    8. Take to NN unit without delay in portable transport incubator

  1. polycythaemia

    1. venous Packed Cell Vol >65% is sometimes seen

    2. neonatal partial exchange transfuision

  1. hypocalcemia

    1. serum ca <1.75 mmol/L may occur in SFD babies

    2. usu asympt but may be jittery or even have convulsions

    3. rx w oral ca supplements if child asympt (5-10ml/day 10% calcium gluconate divided into the feeds)

  1. perinatal asphysxia

    1. acute fetal hypoxia superimposed on chr fetal hypoxia, acidosis

    2. or plc insuff, inadq glycogen reserves

    3. mxL antepartum and itrapartum monitoring, efficient neonatal resuscitation

Term baby vacuum extraction 20 min ago cos of abN ctg trace

Review baby cos he looked pale

a)if Hb 17g/dL, what other pathophysiological mechanisms might cause pallor in baby

b) if Hb was 11g/dL, describe ur mx of this child in the 1st 24h
a) what other mech cause pallor in baby?
Dy/dx of pale newborn

  • asphyxia

    • neurological

      • abnormal transition period, hypotonic, decreased arousal state

    • respiratory

      • RD, O2 requirement

    • Cardiovascular

      • Normal to bradycardia

    • Haematolgoical

      • Hb stable, may dev thrombocytopenia or DIVC from hypoxic injury to marrow

    • Course: Fluid restriction, Cardioresp support, may need rx of seizures

  • acute h’rrhage

    • Neuro:

      • Normal or hyperalert or hyper irritable “catecholamine response”

    • Resp

      • Tachypnea, O2 requirement rarely needed

    • Cardiovasc

      • Tachycardia, hypotension

    • Haematological

      • Hb nay be Normal, followed by drop in Hb: normocytic, normochrmic

    • Course: Promptly rx hypovolemia, may need rapid vol expansion

b) Hb 11g/dL  mx of child in 1st 24h

  • Hemolysis

    • Haemato:

      • Low hb, HSmegaly, jaundice, +ve coomb’s test, microcytic hypochromic

    • Course:

      • May need rx for Congestive Heart Failure and hydrops

      • May need rx for severe jaundice

  • Mx:

    • Hx:

      • Mom’s bld group, rhesus factor, antibody and serology results

      • Was pregnancy complicated

    • PE

      • Hc wt length

      • Vitals, 4 extremeties BP

      • Pallor, jandice

      • Hypotonic, alert n active

      • Sl nasal flaring, no grunting, tachypnea, cyanosis

      • Pulse oximeter saturation

      • Cephalohematoma

      • Anterior fontanellesn

      • Cong abn? Ears nose oropharynx

      • Respiration symm? Chest clear to auscultation?

      • Abdo soft and non distended

      • Um cord stump – no of vessels

      • No abn of back genitalia extremities

      • Skin perfusion fine or not

      • Neurologic examination – tone, moro grasp suck reflexes

    • Possible sepsis so do bld culture and FBC

    • Blood glucose test

    • Give ampi and genta

  • reticulocyte count, low – congenital hypoplastic anemia

  • normal or high = coombs test

    • Positive: immuno hemolytic anemia

    • ABO, Rh, Minor Blod group e.g Kell incompat

    • negative do MCV

      • MCV low = chr intrauterine bld loss or a-thalassemia syndrome

      • Mcv normal or high

        • Periph bld smear

          • Normal = blod loss or infxn

          • Abnormal = hereditary spherocytosis

              • Hered elliptocytosis

              • Pyruvate kinase defcy

              • G6PD defcy

              • DIVC

  • Dyldx: anaemia usually due to hemolysis or blood loss

    • alloimmune hemolytic dz – coombs and rhesus

    • congenital infxn – cmv, toxoplasmosis, syphilis even bact sepsis can trigger off massive hemolysis (chk bb’s appearance)

    • hereditary RBC defect e.g spherocytosis, elliptocytosis, even thalassemias or enzymatic defect e,g, G6PD can result in hemolytic dz of newborn

      • order test of con and unconj br

    • underprdt of RBCs??

      • Blackfan and Diamond – congenital disorders tt can cause low Hb

      • Human parvo-virus B19 suppressing marrow

        • Periph bld smear: elevated reticulocyte count or incr no of nucleated RBCs effectively rules out hypoplastic anaemia

    • Blood loss: evidence of blood loss at birth, hx of APH – placenta previa, abruption placenta or umb cord rupture. No cephalohemtoma or CNS or abdo bleed

    • Chr hemorrhage frm fetus into mother

      • Kleihauer Betke test for fetomaternal hemorrhage

        • Elute hemoglobin A from maternal RBCs with acid, whererus fetal RBCs, tt contain hbF are resistant. Take up eosin stain

Download 172.19 Kb.

Share with your friends:

The database is protected by copyright © 2023
send message

    Main page