NB: it \200\231s possible that looking for soluble immunological mediators may help: ideal ones may be interleukin-1 receptor antago- nist (IL-1ra), and interleukin-6 (IL-6). Speci \201 c- ity: 92% and 83%, respectively. Circulating intercellular adhesion molecule-1 (ciCA M-1) is less reliable.107 lated7 \200 Respiratory rate \211 603 \200 Lethargy3 \200 Grunting3 \200 T \211 37.5 3 A rule requiring any one sign has high sensitivity (87%) and speci- \201 city (7 4%). The number in blue refers to the odds ratio.108 s c i r t a i d e a P De \201 nitive cultures of bloodet al take 48 \200\22372h. Normal values are often hard t o de \201 ne, eg a CSF WCC of up to 10/mm3 with 60% polymorphs may be normal in neonates. Changing patterns of antibiotic resistance Ampicillin/amoxicillin and gentamicin is a safe combination for most neonates. This duo may reduce over-use of vancomycin.109 \200\223112 D rug pharmacokinetic problems These are only partly obviated by doing plasma levels. Creatin ine, sex, and birthweight in \202 uence what is an accept- able level in complex ways. Wit h aminoglycosides, adjust dose as indicated in the Data sheet if renal function is poor. If doing levels is problematic, ce- fotaxime is a good alternative (p202).113 Gentamicin: see p175. Subtle manifestations of neonatal seizures Unless you have a high index of suspicion, you m ay miss seizures referable to the brainstem, eg nystagmus, conjugate eye movements, posturi ng, sucking movements, lip smacking, etc. Grand mal is rare. EEGs are helpful in diagnos- i ng when unsure. Always look for metabolic abnormalities (these are treated with metabolic a pproaches; don \200\231t rely on conventional anticonvulsants). 114 Examination of the neonate1 The aim is to screen for abnormality, and to see if the mother has any ques- tions or diffi culties. The following is a recommended routine before the bab y leaves hospital \200\224or during the 1st week of life for home deliveries. Before the ex amination \201 nd out if the birthweight was normal. Was the birth and preg- nancy normal ? Is mother Rh \200\223ve? Find a quiet, warm, well-lit room. Enlist the mother \200\231s h elp. Explain your aims. Does she look angry or depressed? Listen if she talks. Examine syst ematically, eg head-to-toe. Wash your hands meticu- lously. Note observations (eg T ; rect al is more reliable than tympanic). 115,166 Head Circumference (50th centile=35cm, p224), s hape (odd shapes from a diffi - cult labor soon resolve), fontanelles (tense if crying or i ntracranial pressure \200\200; sunken if dehydrated). Eyes: Red re \202 ex (absent in cata ract & retinoblastoma); corneal opacities; conjunctivitis. Ears: Shape; position. Are they low set (ie below eyes)? The tip of the nose, when pressed, shows jaundice in white ba- bie s. Breathing out of the nose (shut the mouth) tests for choanal atresia. En- sure oto-acous tic screening is done (p548). Are follow-up brainstem evoked responses needed? 117 Complexi on: Cyanosed, pale, jaundiced, or ruddy (poly- cythaemia)? Mouth: Look inside; insert a \201 nger: is the palate intact? Is suck good? Does the baby \200\231s face look normal? Dy smorphism can be diffi cult to de- tect soon after birth as the baby may have some puffi ne ss in the face. Arms & hands Single palmar creases (normal or Down \200\231s). Waiter \200 \231s (porter \200\231s) tip sign of Erb \200\231s palsy of C5 & 6 trunks (p77; p766). Numb er of \201 ngers. Clinodac- tyly (5th \201 nger is curved towards the ring \201 nger, eg in Down \200\231s). Thorax Watch respirations; note grunting and intercostal recession (respira- tory distress). Palpate the precordium and apex beat. Listen to the heart and lun gs. Inspect the vertebral column for neural tube defects. Abdomen Expect to feel the liver. Any other masses? Inspect the umbilicus. Is it healthy? Flare suggests sepsis. Next, lift the skin to assess skin turgor. In- spect genitalia and anus. Are the ori \201 ces patent? Ensure in the 1st 24 hours the baby passes urine (consider posterior urethral valves in bo ys if not) and stool (consider Hirschprung \200\231s, cystic \201 brosis, hypothyroidism) . Is the urinary mea- tus misplaced (hypospadias), and are both testes descended? The neona tal clitoris often looks rather large, but if very large, consider CAH, p134. Bleeding PV m ay be a normal variant following maternal estrogen withdrawal. Legs Test for congenital dis location of the hip (p684). Avoid repeated tests as it hurts, and may induce dislocation. C an you feel femoral pulses (to \200\230exclude \200\231 coarctation)? Note talipes (p684). Toes: too many, too few, or too blue? Buttocks/sacrum Is there an anus? Are there \200 \230mongolian spots \200\231? (blue \200\224and harmless). Tufts of hair dimples suggest bi \201 da occulta? Any pilonidal sinus? CNS Assess posture and handle the baby. Intuitio n can be most helpful in decid- ing if the baby is ill or well. Is he jittery (hypoxia/isch aemia, encephalopathy, hypoglycaemia, infection, hypocalcaemia)? There should be some contr ol of the head. Do limbs move normally. Is the tone \202 oppy2 or spastic? Are responses absent on one side (hemiplegia)? The Moro re \202 ex rarely adds important infor- mation ( and is uncomfortable for the baby). It is done by sitting the baby at 45 , supporting the head. On momentarily removing the support the arms will ab- duct, the hands open and then t he arms adduct. Stroke the palm to elicit a grasp re \202 ex. Is the baby post-mature, lig ht-for-dates, or premature (p128)? \200\207Discuss any abnormality with the parents after liaising with a senior doctor. 114 \200 \200 s c i r t a d e a P i 1 The neonatal period is the 1st 28 days of life; if prem, 44 completed weeks of the infant \200\231s conceptional age (=the chronological age plus gestational age at birth).118 2 Ca uses of \202 oppiness: Sepsis; hypoglycaemia; dehydration; hypothermia; trauma/abuse; myo pathy; poor nutrition; botulism (may look like near sudden infant death syndrome)119; mater nal drugs (loraze- pam; clozapine); alcohol withdrawal; rickets; Down \200\231s, Ehlers \200\223Danlos, or Prader \200\223Willi syndromes; cerebral palsy; CNS syndromes \200\224eg muscular dystrophy, myasthenia, Zellweger leukodystrophy, Guillain \200\223Barr \200\224 or myotonic dystrophy (shake hands with the mother: she may have delayed release of grip). 120 Neonatal jaundice \200 121 Neonatal jaundice is common, occurring in 60% of neonates. \200 121 Most do not need any treatment. Jaundice is caused by raised bilirubin levels. Whe n severe, or not properly managed, kernicterus, a permanent form of brain damage, may occur . Transcutaneous bilirubin levels measured by midwives in homes may prevent kernicterus in babies discharged early by allowing early detec- tion of jaundice. In non-Caucasians, the d evice needs recalibration: don \200\231t rely on tests such as pressing the nose. 122 Manag ement of severe neonatal jaundice typically involves phototherapy, and exchange transfusion if very severe. The threshold levels for these treatments varies with gestational age, and post- natal age. (see NICE GUIDELINES at www.nice.org.uk/cg98) Hyperbilirubinaemia (<200 mol/L) after 24h is usually \200\230physiological \200\231: 1 Increased bilirubin producti on in neonates due to shorter RBC lifespan. 2 Decreased bilirubin conjugation due to hepati c immaturity. 3 Absence of gut \202 ora impedes elimination of bile pigment. 115 \200 s c i r t a i d e a P Exclusive breastfeeding (esp. if there are feeding diffi culties \200\203 \200\201intake \200\203 dehydration \200\203 \200\201bilirubin elimination + \200\200enterohepatic circul ation of biliru- bin \200\224not usually a reason to stop 123). Visible jaundice within 24h of birth is always abnormal. Causes: \200\207Sepsis or: \200 Rhesus haemolytic disease: +ve direct Coombs test (DCT, p117). \200 ABO incompatibility: (mother O; baby A or B, or mother A and baby B, or vise versa) DCT +ve in 4%; indirect Coo mbs +ve in 8%. Maternal IgG anti-A or anti- B haemolysin is \200\230always \200\231 presen t. 124 \200 Red cell anomalies: congenital spherocytosis (fragility tests/EMA binding, p1 96); glucose-6-phosphate dehydrogenase de \201 ciency (do enzyme test). 125 Tests: FBC; \201 lm; blood groups (eg rare group incompatibility.); Coombs test; urine for reducing age nts; syphilis/TORCHet al screen, p34. 126 Prolonged jaundice (not fading after 14 days) Cau ses: breastfeeding; sepsis (UTI & TORCH, p34); hypothyroidism; cystic \201 brosis; biliar y atresia if conjugated and pale stools. Galactosaemia: urine tests for reducing agents (eg Clinitest ) are +ve, but speci \201 c tests (Clinistix ) for glycosuria are \200\223ve (an insensitive test; galactose-1-phosphate uradyl transferase levels diagnostic). Kernict erus refers to the clinical features of acute bilirubin encephalopathy (ABE): lethargy/poor feeding/hypertonicity/opisthotonus/shrill cry \200\224and chron- ic bilirubin encephalopat hy, as well as the yellow staining in the brain associ- ated with ABE. Risk is increased wi th extremely high bilirubin levels (360 mol/L (lower in prems)). Long-term sequelae includ e athetoid movements, deafness, and \200\201IQ. It is prevented by phototherapy (below) exchange transfusion. 127 Phototherapy uses light energy to convert bilirubin to soluble p roducts (lu- mirubin and other isomers) that can be excreted without conjugation. This oc- curs most effi ciently when blue light with a wavelength of 460nm is used. 128 Effi cacy d epends on irradiance (measured in W/cm2) \200\224so exposing baby will lead to more rapid reduction in serum bilirubin, as will using light from above and below. SE: T \200\200 \200\201; eye damage (baby will need eye protection); diarrhea; separation from mother; \202 uid loss. Intense phototherapy is an adjunct to exchange transfusion. 129,130 To decid e when to start phototherapy/exchange transfusion use NICE guidelines(www.nice.org.uk/cg98) , or your unit \200\231s protocol. Exchange transfusion Uses warmed blood (37 C), 160ml/kg (double volume), given ideally via umbilical vein IVI, with removal via umbilical artery. Monitor ECG, U&E, Ca2+, bilirubin, clotting, FBC, and glucose. Consider more exchanges if b ilirubin goes on rising. Stop if the pulse rate \202 uctuates by >20 beats/min. \200\207 Ensure the volumes exchanged always balance. If anemic, consider a sim- ple fresh blood tra nsfusion (20mL/kg). Complications (may be fatal): Pulse \200\201, apnoea, platelets \200 \201, glucose \200\201, Na+ \200\201, 131 O2 Hb saturation \200\201 (as fetal Hb \200\201). 132 Rhesus haemolytic disease Physiology When a RhD \200\223ve mother delivers a RhD+ve baby a leak of fetal red cells into her circulation may stimulate her to produce anti-D IgG antibo dies (isoimmunization). In later pregnancies these can cross the placenta, caus- ing worsen ing rhesus haemolytic disease (erythroblastosis fetalis) with each successive Rh+ve pregnan cy. First pregnancies may be aff ected due to leaks, eg: \200 Threatened miscarriage \200 APH \200 Mild trauma \200 Amniocentesis \200 Chorionic villous sampling \200 External cephalic version. An aff ected oedematous fetus (with stiff , oedematous lungs) is called a hy- drops fetalis. Anemia-associated CCF causes oedema, as does hypoalbumi- naemi a (the liver is preoccupied by producing new RBCs). \201\231 \201\231 : Thalassaemia; infe ction (eg toxoplasmosis, CMV, p34); maternal diabetes. Clinical Rh disease \200\207Test fo r D antibodies in all Rh \200\223ve mothers, at booking, 28 & 34 weeks \200\231 gesta- tion . Anti-D titres <4U/mL (<1 : 16) are very unlikely to cause serious disease; it is wise to check mater- nal blood every 2 weeks. If >10U/mL, get the advice of a referral center: feta l blood sampling intra- peritoneal (or, with fetoscopy, intravascular via the cord) tran sfusion may be needed. 116 \200 Signs \200 Jaundice \200\224eg on day 1 \200 Yellow vernix \200 CCF (oedema, ascites) \200 Hepatosplenomegaly \200 Progressive anemia \200 Bleeding \200 CNS signs \200 Kernicterus (p115) s c i r t a d e a P Expect fetal Hb to be <7g/dL in 10% of those with i titres of 10 \200\223100U/mL (75% if titres >100U/mL). Do regular ultrasound (+amniocentesis if anti-D titre >4U/mL). Timing is vital. Do it 10 we eks before a Rh-related event in the last pregnancy (eg if last baby needed delivery at 36 weeks, expect to do amniocentesis at 26 weeks). Fetuses tolerating high bilirubins may be s aved risky transfusions (fatality 2 \200\22330%) if monitored by serial measurements of fet al Hb (by fetoscopy or non-invasive middle cerebral artery peak velocity) and daily ultraso und to detect oedema, cardiomegaly, pericardial eff usion, hepatosplenomegaly, or ascites. 133 Anti-D is the chief antibody. Others: Rh C, E, c, e, Kell, Kidd, Duff y (all are IgG). Low concentrations sometimes produce severe disease. Prognosis is improving. Mortality is <20% even for hydropic babies. Note that maternal anti bodies persist for some months, and continue to cause hae- molysis during early life. 134 E xchange transfusion Indications/technique: If Hb <7g/dL, give 1st volume of the exchange tr ansfusion (80mL/kg) as packed cells, and subsequent exact exchanges according to response. \200\207Keep the baby warm. Ultraviolet photodegradation of bilirubin (with phototherapy l amp) may be all that is needed in less than severe disease. Give extra water (30mL/kg/24h P O). Avoid heat loss. Protect the eyes. Keep the baby naked. Giving Rh \200\223ve mothers an ti-D immunoglobulin (p9) This strategy has mark- edly reduced need for exchange transfusion (cost per QALY \211\210 11,000 \200\22352,000, see OHCM p12). 135,136 ABO incompatibili ty 1 in 45 of group A or B babies born to group O mothers will have haemolysis from materna l antibodies. Exchange transfusion may be needed, even in \201 rst-borns. 117 Hydrops fetalis: management \200 Get expert help. \200 At birth, take cord blood for Hb , PCV, bilirubin (conjugated and unconju- gated), blood group, Coombs test,1 serum protein, LFT, and infection screen (p112) to \201 nd the cause \200\224eg isoimmunization; thalas saemia; infection (eg toxoplasmosis, syphilis, parvoviruses, CMV p34); maternal diabetes; t win \200\223 twin transfusion; hypoproteinaemia. Expect to need to ventilate with high inspiratory peak pressure and posi- tive end pressure. HFOV may have a role, p110. Monitor plasma glucose 2 \200\2234-hourly, treating any hypoglycaemia. \200 Drain ascites and pleural eff usions if severe. \200 Correct anemia. \200 Vitamin K 1mg IM, to reduc e risk of hemorrhage. \200 If CCF is present, furosemide may be needed, eg 1 \200\2232mg/ kg/12h IV. \200 Limit IV \202 uids to 60mL/kg/24h (crystalloid); if exchange transfusin g, aim s c i r t a i d e a P for a de \201 cit of 10 \200\22320mL/kg. Monitor urine output. Prognosis: 90% of those with non-immune hydrops die in utero; 50% die postnatally. Babies w ith non-immune hydrops not secondary to infection have a good neurological outcome. 137 Biliary atresia Incidence 1 : 17,000. This is rare but serious. Apparently healthy term bab ies have jaundice, yellow urine and pale stools due to biliary tree occlusion by angiopathy at around week 3 of life. The spleen becomes palpable after the 3rd or 4th week \200\224th e liver may become hard and enlarged. Early surgery ( Kasai procedure = hepatoportoenterost omy \200\224the extrahepatic biliary tree is identi \201 ed, a cholangiogram performed to check diagnosis, and an intestinal limb (Roux-en-Y) is attached to drain bile from the port a hepatis) has a good chance of restoring \202 ow of bile to bowel eg in 60%, but if pres enting for op- eration late (eg at 100 days) Kasai procedure is unlikely to be successful d ue to advanced liver damage and cirrhosis; and the baby will likely need liver transplant i n 1st year of life. It can occur in premature babies. 20% have as- sociated cardiac malform ations: polysplenia and situs inversus. Babies may be excessively hungry. Refer all term ba bies jaundiced at 1 week (preterm at 3) for conjugated/unconjugated bilirubia. Breast milk jaundice has \200\200 uncon- jugated bilirubin. Conjugated bilirubin >25 may re \202 ect serious liver disease (<20 mol is normal). Ultrasound may help with diagnosis. Percutaneo us liver biopsy may show bile duct proliferation and bile plugs. Babies suspected of biliar y atresia should be assessed in a liver unit. 1 The direct Coombs test (DCT) identi \201 es red cells coated with antibody or complement and a positive result usually indicates an immune cause of haemolysis (OHCM p330). Respiratory distress syndrome (RDS) RDS is due to a de \201 ciency of alveolar surfactant, which is mainly con \201 ned to premature babies. Insuffi cient surfactant leads to alveo lar collapse; re-in \202 a- tion with each breath exhausts the baby, and respiratory failu re follows. Hy- poxia leads to \200\201 cardiac output, hypotension, acidosis and renal fa ilure. It is the major cause of death from prematurity. Infants at risk: 91% if 23 \200\223 25 weeks; 52% if 30 \200\22331 weeks. 132 Also: maternal diabetes, males, 2nd twin, cesarea ns. Signs Respiratory distress shortly after birth (1st 4h) \200\224tachypnoea (>60/min), g runting, nasal \202 aring, intercostal recession and cyanosis. CXR: diff use granu- lar p atterns (ground glass appearance) air bronchograms. Diff erential diagnosis Transient ta chypnoea of the newborn (TTN) is due to excess lung \202 uid. It usually resolves after 2 4h. Meconium aspiration (p120); congenital pneumonia (group B strep); tracheo-oesophageal \201 stula (suspect if respiratory problems after feeds); congenital lung abnormality; sep sis. Prevention Betamethasone or dexamethasone should be off ered to all wom- en at risk of preterm delivery from 23 \200\22335 weeks (p51); mothers at high risk should be transferre d to perinatal centers with experience in managing RDS. Treatment 132 Learn at the cot side . Delay clamping of cord by 3 min (p51) to promote placento \200\223fetal transfusion. Give oxygen via an oxygen \200\223air blender, using lowest concentration of O2 possible provid ed there is an adequate heart rate response. If spontaneously breathing stabilize with CPAP (5 \200\2236cm H2O). Babies at high risk of RDS should get natural surfactant (reduces mor tality and air leaks). If gestation \200\20526wks, intubate and give prophylactic surfacta nt via ET tube 2 further doses if ongoing O2 demand/ventilation requirement. Rock gently to aid spread in the bronchial tree. Monitor O2, as needs may suddenly \200\201. 139 Aim f or sats between 85 \200\22393% to reduce risk of retinopathy of pre- maturity and bronchopu lmonary dysplasia. 132 Some centers give a dose of sur- factant then extubate pending devel opments; others keep the baby intubated and extubate as tolerated. \200 Wrap up warmly an d take to NICU/SCBU incubator. \200 If blood gasses worsen, intubate and support ventilat ion (p110), before fa- tigue sets in. \200\200PaCO2 suggests that the minute volume is too low. \200 Traditional ventilator settings: (p110) On connecting the endotracheal tube, c heck chest movement is adequate and symmetrical. Listen for breath sounds. PaO2 is increase d by \200\200mean pressure (not too high). PaCO2 is decreased by \200\200minute volume ( \200\200 breath frequency) by lessening expiratory time. One option is high-frequency oscil latory ventilation (HFOV). Ask a sen- ior colleague for advice. 140,141 \200 \200\207If any deterioration, consider: blocked or dislodged tube (a common occur- rence), infection, faulty ventilator, or pneumothorax. 118 \200 s c i r t a d e a P i Fluids: Give 10% glucose IVI (p123). Nutrition: Get help. Inositol is an essential nutrient promoting surfactant maturation and plays a vital role in neonatal life. Supplementing nut rition of prems with inositol reduces complications (IVH, p108; bronchopulmonary dysplasia, p119). 142 Full parenteral nutrition can be started on day 1. Minimal enteral feeding can also be started on day 1. 132 Signs of a poor prognosis Persistent pulmonary hypertension, large right to left shunt via the ductus; \200\200dead-space fraction in lungs. 143 \201 \201If, despite everything, hypoxia worsens, the baby is dying. Confer with your senior. Ex plain what is happening to the parents, and that the baby will feel no pain. Encourage chri stening, or what is congruent with parents \200\231 beliefs. Relieve pain (p172); keep the baby comfortable. In the light of dialog with parents and nurses it may be appropriate to d isconnect the tubes, so allowing the parents to hold the baby, and, in so doing, to aid the ir grief. NB: contact your Trust \200\231s head and defense organization if legal issues be ckon. 144 119 Communicating with parents Take time to explain to parents exactly what is happening to the ir baby \200\224 not just for the respiratory distress syndrome, but for any serious diseas es. Structured, tested interviews yield these guidelines: 145 \200 Ask both parents to be present (plus a nurse whom they trust). \200 Hand your bleep to a colleague. Allow time. Call the parents by name. \200 Look at the parents (mutual gaze promotes trust). \200 Name the illness concerned with its complications. Write it down. \200 Give support group details: www.cafamily.org.uk tel: 020 7240 0671 for a list. \200 Elicit what the parents now know. Clarify or repeat as needed. \200 Answer any questions. Arrange follow-up (<50 % may be remembered). Doctors \200\231 decisions are increasingly being questioned by paren ts. If you and your team are sure your actions are in the child \200\231s best interests, a nd the parents take a diff erent view, take any steps you can to resolve the issue in a non -confrontational way. Violent \201 ghts between doctors and parents endanger other childr en (some UK units have had to be evacuated while po- lice are called). You should know emer gency procedures for contacting the High Court to settle the issue (go through the on-call manager: your Trust can make applications day or night). Failure to get Court approval will leave you open to criticism from the European Court of Human Rights, which is likely to ta ke the view that \200\230do not resuscitate \200\231 notices fail to guarantee re- spect f or the child \200\231s \200\230physical and moral integrity \200\231 \200\224guaranteed by Article 8 of the Convention on Human rights \200\224see Glass vs United Kingdom, 2004 (618 27/00). 146 Bronchopulmonary dysplasia (BPD) This complicates ventilation for RDS in 40% of babies of <1kg birthweight. 147 There is persistent hypoxia diffi cult ventilator weani ng \200\224eg still requiring ventilation at 36 weeks postmenstrual age (eg SaO2 \211 88% in air). Classically, BPD is mainly from barotrauma and oxygen toxicity, whereas surfactant - related BPD is multifactorial with airway infections triggering in \202 ammatory cascade s. (Without surfactant, many would not survive to get BPD.) 148 Oxida- tive processes may a lso play a key role, but antioxidants are unproven. 149 Tests: CXR: hyperin \202 ation, ro unded, radiolucent areas, alternating with thin denser lines. Histology: necrotizing bronch iolitis with alveolar \201 brosis. Mortality: Variable, \200\223 complex interaction wit h surfactant use. 150 Early sequelae: \200\201IQ ; cerebral palsy; feeding problems. O2 de saturation during feeds is not uncommon. Visuospatial abilities at age 5 yrs are only redu ced in those with the severest forms of chronic lung disease. 151 Late sequelae: By adolesc ence/early adulthood the main changes remaining are airways obstruction, airways hyper-reac tivity, and hyperin \202 ation. Prevention: Steroids (antenatal & postnatal); surfactant a nd \200\230suitably high \200\231 calorie feeding. 152 Pulmonary hypoplasia Suspect this i n all infants with persisting neonatal tachypnoea feeding dif- \201 culties, particula rly if prenatal oligohydramnios. Hypoplasia may be a con- sequence of oligohydramnios, eg i n Potter \200\231s syndrome or premature rupture of the membranes. In diaphragmatic hernia it is a consequence of the \200\230space- occupying lesion \200\231. Cystic adenomatoid ma lformations are another cause. CXR is likely to be misleadingly reported as normal. The con dition need not be fatal: postnatal catch-up growth occurs. Differential: RDS, meconium asp iration, sepsis, or primary pulmonary hyper- tension. 153 Some degree of pulmonary hypoplas ia is the price of adopting an expectant plan for early spontaneous rupture of the membrane s, but despite this, expectant management leads to fewer deaths. 154 s c i r t a i d e a P Other neonatal problems Necrotizing enterocolitis (NEC) is an in \202 ammatory bowel necro sis. Pre- maturity is the chief risk factor: if weight <1500g, 5 \200\22310% develop NEC. O ther risk factors: enteral feeds, bacterial colonization, mucosal injury, rapid weight gain . 155 Signs: If mild, just some abdominal distension. A little blood/mucus may be passed PR . If severe, there is sudden abdominal distension, tenderness ( perforation), shock, DIC & mucosal sloughing. Pneumatosis intestinalis (gas in the gut wall seen on x-ray) is pathog nomonic for NEC. \201\227: Stop oral feeding 156 (except oral probiotics, eg Bi \201 doba cteria infantis, which can help); 157 barrier nurse; culture feces; crossmatch (may get ane mic); give antibiotics: eg ce- fotaxime + vancomycin. 158 Liaise early with surgeon; repeat ed imaging and girth measurement. Platelets mirror disease activity; <100 \211\210109/L is \200\230severe \200\231. 159 Laparotomy indications: Progressive distension, perforation ( up to 50% die). Prophylaxis: Expressed breast milk; probiotics; 160 oral antibiotics. 16 NN T \211\210 10. Meconium aspiration syndrome (MAS) occurs in the term/near term in- fant wh en meconium, the fecal material that accumulates in the fetal colon during gestation, is pa ssed in utero, leading to meconium stained amniotic \202 uid (MSAF). MSAF occurs in 8 \200\22325% of births, usually due to fetal distress or advance fetal age. MAS occurs in on ly 5% of these infants; 162 it is de \201 ned as respiratory distress in the infant born t hrough MSAF which cannot otherwise be explained. Aspiration of meconium mostly occurs pre-b irth. 163 It may lead to airway obstruction, surfactant dysfunction, pulmonary vasoconstric tion, infection and chemical pneumonitis. Intrapartum suctioning of the oro/naso- pharynx i s not recommended. 164 Endotracheal suctioning is only needed for those infants who aren \200\231t vigorous at birth. 164 Cricoid and/or chest compression at birth to prevent aspir ation have not been shown to be useful. 165 Surfactant, ventilation, inhaled nitric oxide a nd antibiotics are all used. 166 Vitamin K de \201 ciency bleeding (VKDB=haemorrhagic dise ase of the newborn) occurs from days 2 \200\2237 postpartum. Cause: No enteric bacteria to make vit K. The baby is usually well, apart from bruising/bleeding. Prothrombin & partial t hrom- boplastin times (PT & PTT) \200\200; platelets \200\211. Prevention: (Many regimens) vit K 1mg (0.4mg/kg if prem) IM (if at \200\200risk1) \200\224or 2 doses of oral colloida l (mixed micelle) phytomenadione 2mg at birth, repeated in \211 7d; if breastfed, give a 3 rd dose at 1 month old; not needed if bottle-fed (already forti \201 ed). NB: a weak corre lation 167 with cancers caused a scare, but there is no hard evidence. \201\227: Plasma, 1 0mL/ kg IV & vit K ( \200\2051mg slow IV) for active bleeding (monitor coagulation). 168 Di sseminated intravascular coagulation (DIC) Signs: Septic signs (ill); pete- chiae; venepunc ture oozings; GI bleeding. Tests: Platelets \200\201; schistocytes (frag- mented RBCs); INR \200\200; \201 brinogen \200\201; partial thromboplastin time \200\200; D-dimer \200\200 (hard to interpret if birthweight low). 169,170 Treatment: Get help; treat cause (eg NEC, sepsis etc); give vit. K \200\2051mg slow IV platelet transfusion (aim for >30 \211\210 109/L). \200 Fresh plasma cryoprecipitate,[1] 10mL/kg IVI heparin IV protein C. 171,172 \200 If bleeding still continues, consider exchange transfusion. Autoimmune throm bocytopenia (ITP) <10% of babies of women with ITP are thrombocytopenic (p88). Alloimmune t hrombocytopenia (1 : 2000 births; via fetomaternal incompatibility of platelet antigens). I t develops in utero. 50% are 1st born (it recurs in 80% of later pregnancies with same or \200\200severity). If aff ected in utero 25% have CNS problems. Platelets fall for 48h pos t-delivery. Treat severe thrombocytopenia with compatible platelets or irradiated ma- terna l platelets. IV Ig 400mg/kg/day[6] for 48h and steroids may help. Platelet transfusion via cordocentesis from 24wks may be needed in later pregnan- cies. Diagnose by detecting matern al platelet allo-antibody against father \200\231s platelets. Do neuroimaging on all patien ts. 173 120 \200 s c i r t a d e a P i 1 Asphyxia, bleeding problems, cholestasis \200\224or mother with liver disease or on carba mazepine, pheno- barbital, phenytoin, rifampicin, or warfarin. 121 Minor neonatal problems Most neonates have a few minor lesions; the more you examine neonat es the better you will become at reassuring mothers. 174 Strawberry naevus: Typically disap pear by age 2. Milia: 1 \200\2232mm pearly white/cream papules caused by retention of kerat in in dermis. Found on fore- head, nose, cheeks. Will resolve spontaneously. Erythema toxic um (neonatal urticaria): These are harmless red blotches, often with a central white pustul e which come and go in crops. Described as \200\230 \202 ea bitten \200\231 in appearance . They last 24h, in contrast to septic spots which are smaller and not mobile. Miliaria cr ystallina (a prickly-heat like-rash) develops due to transient sweat-pore disruption 175 or immaturity 176 \200\224hence its charac- teristic 1 \200\2232mm retention vesicle. 177 Pre valence: \200\205 8%. 178 In miliaria rubra there is a surrounding \202 ush. Stork mark: These are areas of capillary dilatation on the eyelids, central fore- head and back of the neck \200\224where the baby is deemed to have been held in the stork \200\231s beak. They blanch on pressure and fade with time. Harlequin color change: Transient, episodic, demarca ted erythema on left or right, with simultanous contralateral blanching \200\224occasionall y related to use of systemic prostaglandin E1 (no need to stop: the condition is self-limit ing). 179 Peeling skin/desquamation: Common in postmature babies, it does not de- note futu re skin problems. Olive oil prevents skin folds from cracking. Petechial hemorrhages, facia l cyanosis, subconjunctival hemorrhages: These temporary features generally re \202 ect su ff usion of the face during deliv- ery (sometimes inaccurately referred to as \200\230trau matic asphyxia \200\231). Swollen breasts: These occur in both sexes and occasionally lacta te (witch \200\231s milk). They are due to maternal hormones and gradually subside if left alone, but if infected need antibiotics. Milk may persist until 2 months old. 180 The umbil icus: It dries and separates through a moist base at about day 7. Signs of infection: odor, pus, periumbilical red \202 are, malaise. Isolate the baby, take swabs and blood culture s, give antibiotics. Granuloma: exclude a patent urachus and cauterize with a silver nitrat e stick. Sticky eye: (commonly from an unopened tear duct, p418.) Swab to exclude ophthalmi a neonatorum (p36)/chlamydia (special swab). When vertically transmitted sexual infections occur, liaise with your microbiologist and local genitourinary medicine (GUM) clinic. 181 F eeding anxieties: Healthy term babies require little milk for the \201 rst few days and e arly poor feeding is not an indication for investigation or bottle top- ups. The exceptions are babies of diabetic mothers, and light-for-dates babies, because of their risk of hypog lycaemia. Fig 1. Strawberry naevus. s c i r t a i d e a P New babies may have diffi culty co-ordinating feeding and breathing, and brie \202 y choke , gag, or turn blue. Exclude disease, check feeding technique (too much? too fast?) and rea ssure. Regurgitation is often due to over \201 lling a tiny stomach with milk and air. Check feed ing technique; if bottle fed, is the teat too big for the mouth or the hole too small or th e amount too great? Winding during feeds may help but is not essential to health. Red-stained nappy: This is usually due to urinary urates but may be blood from the cord or baby \200\231s vagina (estrogen withdrawal bleed). Neonatal sneezing clears nasal amniotic \202 uid. If jittery T \200\200/ muscle hyperto- nia, suspect \202 uoxetine or opi ate withdrawal. 182,183 RSV (p160) is another cause. Enteral and parenteral nutrition Breastfeeding ( expressed breast milk, p124 \200\2236) i s the ideal way to feed term babies; if <2kg, powder sachets of breast milk forti \201 ers (eg Cow & Gate) have a role. In prems, extrauterine growth restriction and neurodevelopmen tal delay from under-feeding is only partly preventable by oral/tube feeding \200\224owing to fear of necrotizing enterocolitis.1 Parenteral nutrition can meet many of their nutritio nal needs, but has signi \201 cant side eff ects \200\224intestinal atrophy, sepsis, incre ased susceptibility to in \202 ammatory stimuli, and systemic in \202 ammatory responses. 184 Nasogastric tube feeding Indications: Any sick infant who is too ill or too young to f eed normally (eg respiratory distress syndrome). Expressed breast milk or formula milk is f ed via a naso- or orogastric tube either as a bolus or as a continuous infusion. If gastro- oesophageal re \202 ux or aspiration is a prob- lem, then a silastic naso-jejunal tube can be used. After entering the stomach, the tube enters the jejunum by peristalsis: con \201 rm its position on x-ray. When the baby improves, start giving some feeds by mouth (PO), e g by increasing the ratio of oral to nasogastric feeds, either in whole feeds, or by fracti ons of each feed. If during oral feeds, cyanosis, bradycardia, or vomiting supervene, you m ay be trying too soon. Trophic feeding Synonyms: Minimal enteral or hypocaloric feeding; gu t priming. Rationale: If prems go for weeks with no oral nutrition, normal GI structure and function are lost despite an anabolic body state. Villi shorten, mucosal DNA is lost, and enzyme activity is less. Early initiation of subnutritional en- teral feeding may help by p romoting gut motility and bile secretion, inducing lactase activity, and by reducing sepsis and cholestatic jaundice. 185 Technique: Typically, milk volumes of 1mL/kg/h are given by tube starting on day 2 \200\2233. Use expressed breast milk (or a preterm formula, eg Nutr iprem ). Effects: Studies show that weight gain and head growth is better, and that there are fewer episodes of neonatal sepsis, fewer days of parenteral nutrition are needed, and t ime to full oral feeding is less. If too much is given, NEC (p120) may ensue. 186 Eligibili ty: Experience shows that almost all prems with non-surgical illness tolerate at least some milk as trophic feeds. 187 Parenteral nutrition (PN, via a central vein). Indications: pos t-op; trauma; burns; if oral nutrition is poor (eg in ill, low-birthweight babies) and necr otiz- ing enterocolitis (when the gut must be \200\230rested \200\231). Day-by-day guide: see BOX. \200\207Sterility is vital; prepare using laminar \202 ow units. Monitoring mus t be me- ticulous.2 Daily checks: Weight; \202 uid balance; U&E; blood glucose; Ca2+. Tes t for glyco- suria. Change IVI sets/ \201 lters; culture \201 lters, Vamin , and Intral ipid samples. Weekly: Length; head circumference; skinfold thickness. LFT; Mg2+; PO4 phos ; ammonia; triglycerides; FBC; ESR/CRP (helps determine if there is sepsis). Complications: Infection; acidosis; metabolic imbalances; thrombophlebitis; 3 \200\223 \200\201, consider hepatobiliary stenosis; cholelithiasis; osteopenia. 188 If plasma PO4 3 \200\223 (1mmol/kg /day for neonates, 0.7mg/kg/day if 1 \200\22324 months old) as giving PO4 the potassium sal t. Mix with glucose, but not Vamin or trace element mix- tures. PN is complex: get expert help. In addition, some precipitation errors are preventable by using computer-based decis ion support. 189 Stopping IV nutrition Do in stages to prevent hypoglycaemia. 122 s c i r t a d e a P i 3 \200\223; alk 1 What is it about NEC which makes oral feeding problematic? Relevant factors: \200 Ischae mia \200 Intro- duction of novel metabolic substrate into the gut \200 Gut maturation \200 In \202 ammation \200\224proin \202 ammatory cytokines (tumor necrosis factor- \200 , interleukin (IL)-6, IL-18, and platelet-activating factor) \200 Paucity of protective Gr am +ve organisms. \200\207The best way of providing protective bacteria with feeds is unkn own.190 2 See British Association for Parenteral and Enteral Nutrition Guidelines, ISBN 1-8 99-467 \200\223408 Fig 1. \200\230Gavage \200\231 (from an old French word meaning \200\230to gorge \200\231 ) denotes a controver- sial farming and gastronomic method entailing insertion of a long fu nnel into a goose \200\231s throat. Down this funnel is pumped a slurry of ground corn and water, to pro- duce obesity \200\224and, to some palates, a delicious (if unnaturally fatty ) p t \200\224p t de foie gras). On the neonatal unit, gavage feeding should not be q uite so enthusiastic. But French farmers were right about one thing: bolus gavage feeding i s better than continuous tube feeds, at least with regard to trophic feeding.191 123 s c i r t a i d e a P Parenteral nutrition: day-by-day guide. \200\207All values are per kg/day PROTEIN CARBO- HYDRATE Glucose 10%; mL IONS (mmol) FLUID FAT Type of baby Day of PN Age days Vamin- olact \210\217; mL 14 20 26 \211 35 12 18 24 Ca PO4 PN vol. Intra- lipidy \210\217 20%; mL 2.5 5 10 15 Na K mL1 97.5 115 115 100 Neonates & low- birth- weight babies Infants >1 month1 & <10kg 10 \200\22330kg 1&2 1 2 3 3 4 5 >5 3 3 3 3 3 3 3 3 1 1 1 1 0.4 \200\2231 120 0.4 \200\2231 150 0.4 \200\2231 165 0.4 \200\2231 165 M 95 \200\223125 80 \200\223110 65 \200\223125 5 10 15 2.5 2.5 2.5 1 2 2.5 2.5 2.5 0.6 0.4 0.6 0.4 0.6 0.4 120 \200\223150* 120 \200\223150* 120 \200\223150* M 8 16 \200\22318 14 \200\22310 14.5 45 \200\223100* 45 \200\223100* 45 \200\22375* 45 \200\22375* Note: M=maintenance. *See p23 4 for 24h \202 uid requirement. \200\207See datasheets/ SPC data Trace elements: Peditra ce eg 1mL/kg (max 10mL) if renal function OK \200\224caution if prolonged treatment, eg > 1 month, or if \200\201biliary excretion (stop if cholestasis); checking Mn+ may be needed . Vitamins: Solivito N : add 1mL/kg/day (max 10mL) to Vaminolact (protect from light). C ater for A, D, & K with Vitalip N 1 \200\2234mL/kg/ day (max 10mL/kg/day) to Intralipid . \200\207These values are a guide only. Individual needs vary greatly. Supplementing very preterm infants with selenium is con- troversial. It may help reduce sepsis; data are domi nated by one large trial from areas with low selenium levels and may not be readily transla ted elsewhere. 192 Get expert help. 23.5 \200\22378.5 7.5 7 \200\22357 26 \200\22356 14 \200\22351.5 0.2 0.1 2 2 0.2 0.1 1.5 \200\2232 1.5 \200\2232 0.2 0.1 1.5 \200\2232 1.5 \200\2232 0.2 0.1 2 2