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1
Q

Hypoglycemia in newborns

A

Higher brain to body weight ratio , higher glucose demand, %90 cerebral usage

If feeding delayed 3-6 hours: hypoglycemia
Preterm, IDM, sga, lga.: hypoglycemia risk

Fetal glucose: 2/3 of maternal (doğunca daha düşük oluyor)

Hypoglycemia: <47

Glycogen storage made last month of 3rd trimester

Either:
Inadequate glycogen
Increased glucose utilization
Excessive insulin

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2
Q

High risk infants for hypoglycemia

A

IDM
SGA
LGA
<37 weeks
Stressed/ill infant
Exposure to medications ( preterm labor, htn, diabetes tretment, diuretic , antidepressant)

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3
Q

At risk groups for hypoglycemia

A
  1. Increased insulin:
    Intrapartum glucose
    Asphyxia
    SGA
    Insulinoma
    IDM
    Hyperinsulinemia
  2. Decreased storage:
    Placental abnormality
    Preterm, low birth weight
    Discordant twins small one
    3.ıncreased need:
    SGA
    İll( Septic, RDS)
    Hypoxia, ischemia, hemorrhage,meningits
    Cyanotic heart disease
    Hypothermia
    4.ınadequate production or substrate delivery:
    Galactosemia
    Glycogen storage disease
    Fructose intolerance
    Maple syrup urine disease
    Lipid metabolism disease
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4
Q

Persistent hypoglycemia

A

> 7 days or higher amount needed to preserve

Causes:
1.Hyperinsulinism( congenital, adenoma,syndrome)
2.Endocrine disorder( gh def, hypopituitarism)
3. Inborn error of metabolism( Galactosemia, GSD, lipid/ protein metabolism)

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5
Q

IDM

A

Birth injury, stillbirth, congenital anomalies, cesarean risk, NICU admission increased

(Oxygen radicals damage mitochondria, this oxidative stress disrupts vascularization of tissues)

Hyperglycemia causes fetal anomalies like:
RDS, VSD, transposition of greater vessels, polycythemia, asymetric septal hypertrophy!!!
Renal agenesis, hydronephrosis, cystic kidneys, micropenis, anencephaly, spina bifida. Caudal dysplasi, cns damage

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6
Q

Monitoring for hypoglycemia

A

Glucose monitoring within 1 hour
1-2 saat aralıklarla ilk 6 saat monitor

For İDM maternal glucose control is the determinant

Screening at risk babies:
1.symptomatic: immediatly
2.asymptomatşc high risk: 30-60 min of life
3. Asymptomatic but at risk: 3-4 hours

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7
Q

Tratment of hypoglycemia

A

Asymptomatic:
<25: iv glucose infusion
>25: enteral feeding

Symptomatic: iv glucose infusion
+glucagon, glucocorticoid, somatostatine

Prevention: early screening, feeding, awareness, temperature

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8
Q

Signs of hypoglycemia

A

Cyanosis, cardiac arrest
Hypotonia, irritability, tremor
+seizures, high pitched cry, lethargy, tachypnea, apnea, poor suck

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9
Q

Hypocalcemia

A

Term infants: <8
Preterm infants: <7
Ionized Ca: <2.5

Tetany, muscle cramps,fatigue, irritability
Severe hypocalcemia: bronchospasm, seizures
Chronic: rickets,deminerilazation, apnea, elevated ALP
Acute: irritable, tremor,seizure,apnea, cardiac dysfunction

Early hypocalcemia: first 3 days
Immature parathyroid gland/ kidneys,
Premature,lbw,idm, ihm, asphyxia

Late hypocalcemia: >3 days
Due to excessive phosphate
Congenital defects in pth metabolism (digeorge,isolated hypoparathyroidism, pseudohypoparathyroidism)
Magnesium deficiency
Vit D deficiency

Treatment: %10 calcium gluconate: 2 ml/kg slow infusion 1ml/min, check for bradycardia
+calcium chloride(high Ca), Mg, bolus levels will fall in 30 mins, 3-4 times a day

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10
Q

Risk factors for hypocalcemia

A

Preterm and ill infants, first 3 days
Blood transfusion(citrate sebepli)
Insufficent feeding
IDM
Asphyxia
Diuretics
Alkalosis
Exscess phosphate
Mg deficiency
Confemital hypoparathyroid

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11
Q

Hyponatremia

A

<130
Seizures, lethargy
Early: 1st week
SIADH( most common) (pneuomina, meningitis,RDS, sepsis)
Increased maternal water intake
Renal impairment

Late: CAH, diuretics, preterm, hypotonic iv

Treatment: urgent : <125
Hypertonic saline 6ml/kg over one hour to 125. Further correction one to two days. Treat the cause

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12
Q

Hypernatremia

A

> 150
Water loss from weight loss, diarrhea, polyuria
Excess na intake from NaHco3 or medications

Severe hypernatremia fixed 48-72 hours or brain edema and IC bleeding

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13
Q

Clinical Na level questions

A

Dehydrated
Ongoing loss
Urinary output
Medication containing na

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14
Q

Hypokalemia

A

K is intracellular, 0.1 ph change= 0.6 K change
<3.5
Lethargy, ileus, arythmia, u wave?

Causes: diuretics, renal tubular defects, ileostomy, nasogastric tube

Trx: daily k intake 1-2 mg/kg
Severe: KCl infusion with ecg monitoring

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15
Q

Hyperkalemia

A

> 6
T genişliği

Causes:
Increased K release from cells( IVH,asphyxia,trauma, hemolysis)
Decreased k excretion with renal failure
Medication error, excess adminis.

Trx: Glucose-insulin combination, dialysis
+exchange transfusion, calcium gluconate, sodium bicarbonate, beta agonists,lasix

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16
Q

Early onset sepsis

A

First 5-7 days
Multi system fulminant ilness
Respiratory symptoms
Pneumonia mostly
Source: intrapartum period from maternal genital tract

Chorioamnionitis :
Rupture of membranes, vaginal flora, bacteria reached amniotic fkuid and fetus

Aspiratiom of infected amniotic fluid: resp symptoms

Primary sites of colonization:
Nasopharynx, oropjarynx, conjunctiva, umbilical cord

Clinical: respiratory distress

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17
Q

Late onset sepsis

A

> 5 days
Usually focused, meningitis +sepsis

Nosocomial sepsis:
İn high risk infants:underlying ilness, NICU flora, invasive methods

Clinical: alteration in established feeding behaviour

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18
Q

Causative organism of sepsis

A

Primary sepsis:
(From vaginal flora usually)
Group B strep
Entero, Staph, e. Coli, l. Monocytogenes, h.influenza, anaerobs

Nosocomial sepsis:
Staph( s. Epidermidis)
Gram - rods( pseudomonas, klebsiella, fungal)

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19
Q

Risk factors of sepsis

A

> males
Prematurity, low birth weight
Rupture of membranes
Amniotic fluid problems
Maternal fever( infection, chorioamnionitis,uti, vaginal E.coli
Invasive procedures
Resuscitation
Galactosemia, immune defects
Iron therapy
Multiple gestation

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20
Q

Clinical manifestations of sepsis

A

Tachypnea, chest retractions, apnea, inactivity, poor feeding, gasping, grunt, cyanosis

Fever, seizures bulging fontanelle, irritable,high pitched cry, neck retraction, blank look

Refusal to suckle, hypothermia,lethargy, poor cry, comatosed, shock, abd. Distention, diarhhea, vomiting
Sclerema, poor perfusion, cyanosis

21
Q

Differential dgx for sepsis

A

RDS
metabolic/ genetic, Hematologic, neurologic diseases
Congenital heart diseases
Other infections( TORCH)

22
Q

Diagnostic tests for sepsis

A

Blood, CSF, urine culture
Tracheal aspirates
PCR
WBC, platelet, CRP, ESR, Procalcitonin!!!, IL-6, bilirubin, glucose, Na

WBC: leucopenia(<5000), neutropenia(<1750), i/t neutrophil>0.2

Chest X-ray, urinary tract imaging, lumbar puncture (>72h), examination of placenta and fetal membrane for chorioamnionitis

23
Q

Treatment of sepsis

A

Primary:
penicillin(ampicillin)
Aminoglycoside(gentamycin, netilmisin)

Nosocomial:
Vancomycin
Aminoglycoside/ 3rd gen cephalosporin

Normalize temperature, correct hypoglycemia, prevent bleeding,stabilize cardiopulmanory status , NO ivig in neonatal sepsis

O2, ventilation support, support BP and perfusion to prevent shock: pressors: dopamine, dobutamine, monitor fluid intake and output
Observe for DIC: bleeding, thrombocytopenia, PT, a PTT, vit K, platelet infusion, neutropenia: G-CSF
Convulsions: fenobarbital
SIADH
Metabolic: glycemic levels, acidosis

GBS prophylaxis, hand washing

Respiratory, cardiovascular,hematologic, CNS, metabolic

24
Q

Intrauterine Infections manifesting at birth

A

Rubella
Varicella zoster
CMV
Hepatit b/c
Hiv
toxoplasma gondii
Syphilis

25
Intrauterine Infections acquired at birth, symptomatic later
HSV Hepatit B/C HIV CMV Group B strep Chlamydia trachomatis N. Gonorrhea E. Coli L. Monocytogenes
26
TORCH syndome
Toxoplasma gondii Other(varicella, tr. Pallidum, P. B19) Rubella CMV HSV Rubella only one that can only be congenital
27
Congenital Rubella(measles)
Rna togavirus, opthalmologist discovered, live vaccine Rubella sundrome: PDA Cataracts, pigmentary retinopathy,micropthalmia, glaucoma Hearing loss (diagnoses by 2 of these or 1 of there plus one of: encephalitis,microcephaly,purpura, splenomegaly, jaundice in 24h,development delay, radiolucenct bone + pneumonia,sensory abnormalities, Expanded Rubella syndrome: SGA, microcephaly,PDA, pulmanory stenosis, hepatosplenomegaly/ lymphadenopathy - meningoencephalitis, microcephaly, mental retardation -glaucoma, cataracts,pigmentory retinopathy( salt/pepper retinopathy) -hearing loss -PDA - hepatosplenomegaly, jaundice - purpura, thrombocytopenia -radiolucent bone - low birth weight Routine immunization: MMR: 15m, 4 y Routine screening in pregnancy Non immune women offered vaccibe postnatally Precomceptual/ marital screen
28
Congenital Cytomegalovirus
Most common congenital inf Mostly asymptomatic at birth NON HEREDİTARY SENSORİNEURAL HEARİNG LOSS(SNHL) Double strand DNA virus Humans only host Latency and reactivation common Incubation period 8 weeks Vertical transmission: ante(transplacental)/ intra( blood,genital secretions)/post( breast milk) partum Symptomatic neonate: petechiae, hepatosplenomegaly, jaundice at birth, SGA, microcephaly/ hydrocephal/ calcifation, hearing loss, hypotonia, chorioretinitis SNHL , most common trait, may be present or delayed Chorioretinitis most common ocular abnormality in symptomatic infants Cmv retinit: hemorrhage,white fluffy areas Life threatinimg disease: severe pneumonitis, myocarditis, hepatitis, enterocolitis, thrombocytopenia, retinit, neurologic disease %10, severe end organ involvement, many infants with fulminant disease die within days weeks Clinical: microcephaly, SGA, hepatosplenomegaly, jaundice, thrombocytopenia, Abnormal neuroimaging!!!( white matter disease, ventriculomegaly), mother with infection, SNHL!!! Dgx: viral culture, PCR, antibodies(m and g positive at congenital) Prevention: blood transfusion, breast mişk treatment, personal protectivity fpr mothers, no kissing sharimg food Treatment: in first 30 days of life Gangiciclovir Valganciclovir Alternative: foscarnet, cidofovir Do not treat in utero or asymptomatic, only symptomatic, immunodeficent or isolated hearing loss ones
29
Congenital toxoplasmosis
Toxoplasma gondii, cat is the host, infected meat or cat litter, soil, mostly not symptomatic at birth Triad: hydrocephalus, IC calcification, !!!!chorioretinit: retinal scar w/ pigment surrounding, most common Hepatodplenomegaly, jaundice, thrombocytopenia, rash, growth retardation, deafness, low iq Treatment: postnatal dgx and treatment: entire first year of life
30
Congenital syphilis
T. Pallidum Fetal death, miscarriage, stillbirth Asymptomatic at birth, manifest later If mother has primary infection, but risk decreases with next pregnancies Discrete macular lesions, rash, interstitial keratitis Positive trepenoma serology: treat mother, repeat serology monthly, infant xray, CSF exam, !Treat infant one dose , 10/ 14 days
31
Comgenital parvovirus B19
Common febrile examthematous infection, %50 women immune Slapped cheek syndrome/ 5th disease Lacy rash, influenza like synptoms, arthropathy !!!severe Anemia, myocardit, cardiomyopathy, hepatic dysfunction, hydrops fetalis, fetal death Dgx: specific IgM Treatment: Exhange transfusion in utero
32
Congenital VZV
Result of first 20 weeks infection 2 days before 5 days after birth is severe disseminated varicella in newborn, in this case give VZig to infant, if lesions develop iv aciclovir Specific ig in 96 hours, up to 9 days to mother, in case it helps the baby, but usually mothers infection does not pass to baby
33
Congenital HSV
From primary maternal infection, if recurrent herpes risk lower, may be confined to cervix Type 2 inf more severe Prevention: cesarean at term or <4 hours after membrane rupture
34
HBV infection
Chronic hbv with persisten hbsag Infected vertically, some 1-5 years old Carrier state after vertical transmission increases risk of chronic liver disease and hepatoma For perinatal transmission: baby receieve hep B vaccine, administer hbig Prevention: routine antenatal hbv testing, to give prophylaxis to baby
35
HCV
Most transmission at birth May become chronic İdentify mothers at risk
36
To prevent neonatal infections
Standard precautions Screening bacteriuria Serologix screenimg GBS carriage screening
37
Biochemical changes with seizures
Abnormal depolarization Disruption of Na/K atp pump Excessive aa release: glutamate Lack of inhibitory: GABA Decreased: ATP brain glucose Phosphocreatine GABA Adp to pyruvate to lactate Increased: Pyruvate Lactate Glutamate
38
Respiratory distress symptoms
Tachypnea Flaring of nostrils Grunting Chest retraction Cyanosis
39
Primary Causes of respiratory distress
Transient tachypnea of newborn RDS due to surfactan deficiency(preterm) Aspiration syndromes Pulmanory air leaks Pneumonia Pulmanory hemorrhage Pulmanory hypoplasia Chronic neonatal lung disease
40
Secondary Causes of respiratory distress
Congenital heart diseases Asphyxia Infections(sepsis) Surgical conditions( choanal atresi diaphragmatic hernia, fistula tracheeso) Persistence of fetal circulation(pulmanory htn) Anemia, polyctemia Metabolic diseases
41
Non respiratory Causes of respiratory distress (tachypnea)
Hypo/hyperthermia Hypovolemia Hypotension Hypoglycemia Anemia Polyctemia
42
Infant at risk for respiratory distress
Preterm Asphyxia IDM C-section Meconium in amniotic fluid Foul smelling amniotic fluid Mother with fever
43
Respiratory distress not normal if
Persist for >1 hour, worsens or causes cyanosis
44
RDS/ hyaline membrane disease
First 6 hours Resolution in a week Surfactan deficiency, high surface tension, prematurity The more preterm, the lower weight: the more risk SURFACTANT: phospholipid+protein Week 20: start, viability limit 28-32: max levels 26 altına surfactan veriyoruz Stimulator: glucocorticoids(bethamethasone) Inhibitor: insulin, pulmanory edema Causes atelectasis, decreased lung compliance
45
Etiology of comvulsions
HIE !!! (1-2days) ICH. !!!! (1-7 days) Intracranial infection(bacterial meningitis, TORCH) !! Infarction ! Metabolic disorders (Hypo glycemia (1-2 days)/ calcemia/ magnesemia/ natremia,Hypernatremia) Inborn errors Pyridoxine dependency Benign neonatal seizures Epileptic syndrome (3-10 days) Malformation
46
Subtle seizures
Most common, prematures, no EEG correlation, subcortical 1.Ocular, oral-facial-lingual, limb movements: eye deviation, flutter,fixation, chewing, lip-smacking, cycling, paddling 2.autonomic phenomona: tacy/bradycardi 3.apnea
47
Clonic seizures
Term, focal cerebral injury, EEG seizure Rhytmic movements with slow return 1-3 jerks per second Best prognosis
48
Tonic seizure
Preterm, sustained flexion/extension of extremity or body, Severe ICH in preterm, poor prognosis neocortical damage EEG may or may not
49
Myoclonic seizure
Mostly upper, fast contractions without slow return, jerks Serious brain injury May be normal Worst prognosis in neurodevelopmental outcome, seizure recurrence Rare

Pediatrics (10 decks)

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