1. Diagnostic criteria of asphyxia of newborn.

A25
American Academy of Pediatrics –
Essential criteria
● metabolic acidosis (ph <7.0) on umbilical blood
● APGAR score of 0-3 for longer than 5min
● Neurologic manifestations in the immediate neonatal period
to induce seizures, hypotonia, coma or stupor(Hypoxic ischemic
encephalopathy)
● Evidence of multi organ system dysfunction in the immediate neonatal
blood
American College of Obstetrics and Gynecology
The essential criteria:
- Metabolic acidosis in early neonatal blood sample (<7.0 and base
deficit >12mmol/l)
-Moderate or severe encephalopathy
-Cerebral palsy of spastic quadriplegia
The 5 additional criteria
● Sentinel events
● Severe changes in fetal heart rate
● Apgar score <3 beyond 5mins
● Multi system involvement
● Early imaging evidence

Cerebral dysfunction
● Mild asphyxia: hyperalertness, depressed. Slightly increased
musce tone, brisk deep tendon reflex. Poor feeding, excessive crying
or sleeping
● Moderate asphyxia: infant is lethargic with hypotonia and
hyporeflexia of deep tendon reflexes. Absent or sluggish grasp, moro
and sucking reflex. Occasional periods of apnea.
● Severe asphyxia: stupor or coma. Breathing may be irregular.
Generalized hypotonia, depressed deep tendon reflexes. Absent
neonatal reflexes. Bulging fontanelle, increased cerebral oedema,
Seizures (absentia, baby stares at one place for long time) Heart and
BP irregularities. Disturbances of eye movements: nystagmus, loss
of conjugate eye movements, skewed deviation of eyes.
 2. Severe asphyxia of newborn, outcomes. A26
● Severe metabolic acidosis pH ≤ 7.00 in arterial blood of
umbilical vessels;
● Assessment by Apgar is 0-3 during more than 5 minutes;
● Neurological symptoms such as general hypotonia, lethargy,
coma, seizures, brainstem, autonomic dysfunction;
● Evidence of multiorgan system dysfunction in the immediate neonatal
period - damage of vital organs (lungs, heart and others) in newborn
● Severe asphyxia is associated with coma, intractable seizures
activity, cerebral oedema, intracranial haemorrhage.
● The infant often becomes progressively more depressed over the
first 1 to 3 days, as a cerebral oedema develops, and death may
occur during this period.
Outcomes:
● hypoxic-ischemic encephalopathy (HIE)
o Mild HIE: hyperalertness, irritable, decreased suck
reflex, mydriasis, tachycardia, normal EEG
o Moderate HIE: lethargic or obtunded, decreased spontaneous
movement, mid hypotonia, weak reflexes, miosis, occasional
apnea bradycardia, seizures, EEG abnormalities
o Severe HIE: stupor or coma, absent reflexes, flaccid
muscle tone, poor light reflex, anizokoria, periodic apnea,
EEG abnormalities
● persistent pulmonary hypertension
● hypoxic cardiomyopathy
● necrotizing enterocolitis
● acute tubular necrosis
● adrenal hemorrhage and necrosis
● disseminated intravascular coagulation
● Hypoglycemia, polycythemia
● hypotension
● seizures
●
Short term Outcomes
● HIE
● Seizures
● Death
Long term
● Motor cerebral palsy
 ● Sensory hearing loss, visual impairment
● Cognitive episodic and working memory attention
● Educational increased support requirement,
lower test scores ● Behavioral-attention,
irritability, explosiveness

3. Neonatal seizures: etiology, diagnosis and treatment.

A27 Etiology:
● Hypoxic Ischemic Encephalopathy most common, presents 12-
24hours after birth.
● Hemorrhage (intracranial, subdural, subarachnoid, germinal
matrix)occurs about 1-7days after birth. Associated with preterm
● Metabolic disorders (Infant of diabetic mother;hypoglycemia), inborn
errors of metabolism ,
● Blood chemical abnormalities:hypocalcemia, hypomagnesemia,
Genetic disorders.
● Intracranial infections. ; TORCH, maternal Fever,
sepsis/meningitis
● Malformation syndromes,
● Drug withdrawal
Diagnosis:
● Clinical features:
subtle seizures include chewing, pedaling, or ocular movements. Can also
be tonic clonic(clonic rhythmic contraction alternating with relaxation
of all muscle groups,tongue biting,eyes roll back,apnea,loss of
consciousness)or myoclonic seizures(brief,symmetric muscle
contraction and loss of body tone with falling forward)
● Instrumental:
 ElectroEncephaloGram, cranial ultrasound in preterm to diagnose
bleeding, cranial CT scan in term, Cranial MRI
● Lab: Serum glucose and electrolytes, TORCH infections, urine
organic acids, CSF analysis
Treatment:
Phenobarbital 20mg/kg IV
Phenytoin 20mg/kg IV
Diazepam 0.5mg/kg IV
Lorazepam 0.05-0.1mg/kg IV
Persistent seizures may require the use of an intravenous
benzodiazepine, such as lorazepam or midazolam. Vitamin B6

Resuscitation of the newborn with asphyxia.IF U’RE ASKED)

 ● The initial steps of resuscitation are to provide warmth by
placing the baby under a radiant heat source, position the head in
a “sniffing” position (place towel under baby’s neck) to open the
airway, clear the airway with a bulb syringe or suction catheter,
and dry the baby and stimulate breathing.
● Aspiration of meconium before delivery, during birth, or during
resuscitation can cause severe aspiration pneumonia. One obstetrical
technique to try to decrease aspiration has been to suction meconium
from the infant’s airway after delivery of the head but before delivery
of the shoulders (intrapartum suctioning).

4. Classification of birth trauma. A28

Causes of birth trauma;

I. Soft-tissue injuries
● caput succedaneum
● subcutaneous and retinal hemorrhage, petechiae
● ecchymoses and subcutaneous fat necrosis
II. Cranial injuries
● cephalohematoma
● fractures of the skull
III. Intracranial hemorrhage
● subdural hemorrhage
● subarachnoid hemorrhage
● intra- and periventricular hemorrhage
● parenchyma hemorrhage
IV. Spine and spinal cord
● fractures of vertebra
● Erb-Duchenne paralysis
● Klumpke paralyses
● Phrenic nerve paralyses
V. Peripheral nerve injuries
● Facial nerves palsy
VI. Viscera (rupture of liver, spleen and
adrenal hemorrhage)
VII. Fractures of bones.
 Differential diagnosis of caput succedaneum and cephalohematoma. (IF
YOU’RE ASKED!!!!!)
criterions
Situation on the head
skin in this region
fluctuation symptom
peripheral roller
dynamic
Cephalhematoma Caput succedaneum
Limited by one bone,
Situated along few
does not cross suture
bones, crosses suture
lines
lines
Without changes
Cyanotic with petechiae
+ ––
+ ––
disappears in the month
disappears in 3-4 days
period

prolonged jaundice + ––

Cephalohematoma is subperiosteal collection of blood resulting from

rupture of blood vessels between the skull and periosteum.
Capput Succadeneum is serosanguinous, subcutaneous
extraperiosteal fluid collection with poorly defined margins.

5. A29 Differential diagnosis of intracranial injury and neonatal meningitis.

Criterions Intracranial Injury Neonatal Meningitis
Anamnesis injury during child birth as a result of infection

Loss of Present absent

conscious
Leading General Cerebral no meningeal syndrome in neonate
syndrome Meningeal syndrome (positive
 syndrome
brudzinski, kernig, nuchal rigidity
CSF analysis protein-cell
Cell-protein dissociation, bacteria or
dissociation, increased
virus present
ICP
Blood May be normal or
analysis May show leukocytosis or leukopenia
anemia
CT scan may show injured areas subarachnoid hemorrhage

6. Spine and spinal cord injuries in newborns. Clinical signs of Erb

palsy, Klumpke palsy. A30
Erb palsy:
upper trunk plexopathy. Injury to C5-C6
* Elbow extended and forearm pronated
● Wrist is flexed, “waiter's tip” position
● Moro, biceps and radial reflexes absent
● Arm falls limply to side of body when passively adducted
● Affected arm is adducted and internally rotates
● +/- Horner syndrome
Klumpke palsy:
lower trunk plexopathy. Injury to C8-T1
● Absent or poor grasp reflex “total claw hand”
● Absence of movements of the wrist
● Horner syndrome: ipsilateral ptosis, anhydrosis and miosis

7. Differential diagnosis of hemolytic and parenchymal

jaundice in newborns. A1
Hemolytic Jaundice(prehepatic) Parenchymal Jaundice

Occurs on first day of life Occurs later

 increased Unconjugated increase in conj &unconjugated

Hepatosplenomegaly Hepatosplenomegaly

Normal liver enzymes Increased liver enzymes

Urine and stool not changed dark urine, light stool

Anemia with reticulocytosis Anemia without reticulocytosis

Absent intoxication or hemorrhagic

Present intoxication and hemorrhagic
syndrome
syndrome
Positive Direct Coombs test Negative direct coombs test
Hemolytic occurs in:
● Hemolytic disease of Newborn
● Hereditary spherocytosis, elliptocytosis
● G6PD deficiency, alpha pyruvate kinase deficiency
● Alpha and beta thalassemia
Parenchymal jaundice occurs in:
● Congenital hepatitis (CMV, herpes,etc)
● Hep. B, C
● Sepsis
● Galactosemia, Tyrosinemia, glycogen storage disease
● Drugs
● Long parenteral
Obstructive jaundice(blockage of the bile in the liver) occurs in:
● Congenital obstruction and malformation of biliary system:
- Extrahepatic biliary atresia
- Bile duct stenosis
- Paucity of bile duct “Alagille’s syndrome”
- Choledochal cyst
- Bile plug syndrome
Diagnostic criteria of physiological jaundice.
 ● appearance of jaundice after 36 hours of age, usually on 3rd – 4th
day of life;
● lasts up to 10-14th days of life
● jaundice is present in the face and torso
● no hepato- and splenomegaly
● no anemia
● Total serum bilirubin concentration doesn’t exceed 205
mcmol/L (12 mg/dL).
● Rate of bilirubin rise <5mg/dl/d

Diagnostic criteria of Pathological Jaundice

● Jaundice appears in the first 24hours or the 2nd week
● Jaundice persists after 4weeks of life
● Total serum bilirubin level more than 239mcmol/l for term
infants,>205,2 mcmol/l for preterm infants
● Cord bilirubin levels >60mcmol
● Level of direct bilirubin >34mcmol
● Bilirubin rising faster than 85,5mcmol in 24hours
Severe hyperbilirubinemia:Total serum bilirubin >340mcmol// at
any time during first 28days

Critical hyperbilirubinemia: TSB >425mcmol during first 28days of life

8. Differential diagnosis of hemolytic and obstructive

jaundice in newborns. A2
Hemolytic Jaundice Obstructive Jaundice

Occurs on first day of life Occurs on 3-5th day of life, Jaundice with greenish tinge

Increased Unconjugated bilirubin Increased conjugated bilirubin

Hepatosplenomegaly Hepatosplenomegaly

Urine and stool not changed Very dark urine with very light or acholic stool

Anemia with reticulocytosis Anemia absent

 Positive Direct Coombs test Negative coombs test

9. Differential diagnosis of parenchymal and obstructive

jaundice in newborns. A3
Parenchymal Jaundice Obstructive Jaundice

Occurs later in life Occurs on 3-5th day of life, Jaundice

with greenish tinge
Increased conjugated and unconjugated
Increased conjugated bilirubin
bilirubin
Hepatosplenomegaly Hepatosplenomegaly

Increased liver enzymes Normal liver enzymes

dark urine, light stool Very dark urine with very light or acholic
stool
Anemia without reticulocytosis Anemia absent

Present intoxication and hemorrhagic syndrome

Absent intoxication and hemorrhagic syndrome

(IF YOU’RE ASKED)Differential diagnosis of physiological

and parenchymal jaundice in newborns.
Physiological Jaundice Parenchymal Jaundice

Jaundice after 36 hours of age or on 3-4th

Jaundice from first days of life
day of life
Jaundice lasts up to 10-14 days of life,
Jaundice lasts until treatment and
mainly on face and torso
present on whole body
No hepatosplenomegaly Hepatosplenomegaly

No anemia Anemia

Urine and stool not changed dark urine, light stool

Total serum bilirubin doesn’t exceed

Increased conjugated and
12mg/dl
unconjugated bilirubin
Normal liver enzymes increased activity of liver enzymes

Absent intoxication or hemorrhagic

Present intoxication and hemorrhagic
syndrome
syndrome

Diagnostic criteria and causes of hemolytic jaundices in

newborns
Causes of hemolytic jaundice in new borns
● Hemolytic disease of the newborn (Rh incompatibility, blood group
A and B incompatibility);
● Red cell membrane defects (hereditary
spherocytosis, elliptocytosis,stomatocytosis);
● Red cell enzyme deficiencies (glucose-6-phosphate
dehydrogenase deficiency, a pyruvate kinase
deficiency);
● Hemoglobinopathies (alpha thalassemia, beta thalassemia);
● Others types of hemolytic anemias.
Diagnostic criteria
● jaundice appears on the 1st day of life
● increased level of unconjugated bilirubin;
● hepato- and splenomegaly;
● signs of intensive anemia, level of reticulocytes is
increased; ● direct Coomb’s test (+)
● urine and stool not changed

Differential diagnosis of physiological and hemolytic jaundice in newborns.

Physiological Jaundice Hemolytic Jaundice

Jaundice after 36 hours of age or on 3-4th

Jaundice from first days of life
day of life
Jaundice lasts up to 10-14 days of life,
Jaundice lasts until treatment and
mainly on face and torso
present on whole body
No hepatosplenomegaly Hepatosplenomegaly

No anemia Anemia with reticulocytosis

Urine and stool not changed Urine and stool not changed

Total serum bilirubin doesn’t exceed

increased unconjugated bilirubin
12mg/dl
Negative Direct coombs test Positive direct coombs test

Differential diagnosis of physiological and obstructive jaundice in

newborns.
Physiological Jaundice Obstructive Jaundice

Jaundice after 36 hours of age or on 3-4th

Appears on 3-5 day of life
day of life
Jaundice lasts up to 10-14 days of life,
Jaundice with greenish tinge on
mainly on face and torso
whole body
No hepatosplenomegaly Hepatosplenomegaly
 No anemia No anemia

Urine and stool not changed Very dark urine with very light or acholic
stool
Total serum bilirubin doesn’t exceed
Increased conjugated bilirubin
12mg/dl

10. Hemolytic disease of the newborn, criteria, complications. A4

Hemolytic disease of the newborn and fetus (HDN) coursed by the

destruction of the RBCs of the fetus and neonate by antibodies
produced by mother because of immunological conflict.

The fetal red blood cells (RBCs), has an antigen that the mother
lacks, crosses the placenta into the maternal circulation, where they
stimulate antibody production. The antibodies return to the fetal
circulation and result in RBC destruction.
Etiology:
Rh (mother is Rh- and baby is Rh+) and ABO incompatibility (in type O
mothers)
Icteric type
● early appearance of jaundice;
● the intensity increases during the first 3-4 days of life;
● stages of appearance of jaundice - head, trunk, limbs, palms, soles
(severe course);
● enlargement of the spleen and liver;
● anemia with reticulocytosis;
● signs of bilirubin encephalopathy
Anemic type
● paleness of skin, mucous membranes;
● jaundice is moderate;
● moderate enlargement of the spleen and liver;
● neurological status without disabilities;
● anemia (HB level <120 g/L) with reticulocytosis;
● benign course
Hydropic type
● Burdened obstetric history of miscarriage, still birth,
premature birth, children with HDN, severe gestosis,
preeclampsia
● Pallor, respiratory distress syndrome
● Swelling of genitals, face, extremities
● Ascites, pleural and pericardial effusions, anasarca
● Hemorrhagic syndrome
● Cardiopulmonary insufficiency
● Hypoproteinemia, anemia, thrombocytopenia
Laboratory diagnostic of Hemolytic disease of newborn
● Anemia
● Reticulocytosis (6 to 40%)
● Hyperbilirubinemia
● + Direct Antiglobulin Test;
● Rh negative blood type
● Leucopenia
● Thrombocytopenia
● Smear: polychromasia, anisocytosis, no spherocytes
● Hypoalbuminemia
● Positive coombs test
Laboratory findings in ABO different from Rh disease
● Smear:microspherocytosis
● MCV<95,microcytic for newborn
● Direct Coombs test is often weakly +
Complications
● Cholestasis syndrome (bile flow from the liver is blocked)
● Acute bilirubin encephalopathy: clinical manifestation of
bilirubin toxicity seen in first few weeks after birth.
● Chronic bilirubin encephalopathy: Pathogenic diagnosis of
persistent brain dysfunction arising from hyperbilirubinemia
● Kernicterus: Pathological finding of deep-yellow straining of
neurons and neuronal necrosis of basal ganglia and brainstem
nuclei.
11. Hemolytic disease of the newborn, criteria, treatment.
A5 Mild HDN
● the level of Hb in cord blood - more than 150 g / L;
● the level of indirect bilirubin in cord blood - less than 60
mmol / l;
● hourly increase of indirect bilirubin less than 5 mmol / h
 ● conservative treatment with Intravenous
Immunoglobulin
Moderate HDN
● jaundice appears after 5-11 hours after birth;
● the level of Hb in cord blood -100-150 g/l;
● the level of indirect bilirubin in cord blood - to 85
mmol / l; ● 3 or more risk factors for bilirubin
encephalopathy; (seizure, confusion)
● no signs of bilirubin encephalopathy
● Phototherapy treatment
Severe HDN
● jaundice at birth;
● the level of Hb in cord blood - less than 100g/l;
● the level of indirect bilirubin in cord blood - more than 85
mmol / l;
● signs of bilirubin encephalopathy;
● often requires exchange transfusion

Treatment
● Phototherapy ;temperature, eye patches, hydration
● Intravenous immunoglobulin;500mg/kg or 1g/kg
over 4hours
● Exchange transfusion
- Blood should be as fresh as possible
- In the case of Rh blood group incompatibility can be used Rh
negative blood of the same group(with baby) or Rh negative packed
red cells O(I) in the plasma of AB(IV)
- In the case of ABO blood group incompatibility can be used the Rh
same (with baby) packed red cells O(I) in the plasma of AB (IV)
- In the case of both ABO and Rh incompatibility can be used Rh
negative packed red cells O(I) in the plasma of AB(IV)

12. Kernicterus: pathogenesis, clinical presentation and

preventive measures. Hemorrhagic disease in newborns;
classification,clinical signs and lab,treatment A6
Pathogenesis: the pathological finding of deep-yellow staining of neurons
and neuronal necrosis of the basal ganglia and brainstem nuclei.
Occurs when bilirubin passes the BBB and stains neurons (indirect
bilirubin)
 Clinical presentation
● Drowsiness or lack of energy
● Uncontrollable or very high-pitched/shrill crying
● Fever
● Trouble feeding
● Limpness or stiffness of the whole body
● Unusual eye movements
● Muscle spasms or reduced muscle tone
● Seizures or convulsions
● Unusual motor development and movement
● Muscle spasms and/or writhing
● Hearing and other sensory problems
● Inability to gaze upward
Preventive measures: Early detection and treatment Hemolytic
disease of new borns. Effective treatment of HDN ie. Photothreapy,
exchange transfusion, intravenous immunoglobulin

*Hemorrhagic Disease of newborn

It is caused by deficiency of vitamin K
They are 3 types ( early onset, classic , late onset)
Laboratory diagnosis:-
Prothrombin time -increased
Blood coagulation-increased
Partial prothrombin- increased
Factors VII, IX, X and are decreased
Treatment:- Oral and IM vit k

Clinical signs of acute and chronic bilirubin encephalopathy in

newborns. Acute bilirubin encephalopathy
Initial Phase
● Slight stupor (“lethargic,” “sleepy”)
● Slight hypotonia, paucity of movement
● Poor sucking, slightly high-pitched cry
Intermediate Phase
● Moderate stupor—irritable
● Tone variable, usually increased; retrocollis-opisthotonos
 ● Minimal feeding, high-pitched cry
Advanced Phase
● Deep stupor to coma
● Tone usually increased; some have retrocollis-opisthotonos
● No feeding, shrill cry
Chronic bilirubin encephalopathy
● Athetoid cerebral palsy with or without seizures
● Developmental delay
● Auditory disturbance, especially sensorineural hearing loss
● Oculomotor disturbances including paralysis
of upward gaze ● Dental dysplasia
● Intellectual deficits, but minority in mentally retarded range

13. Prematurity. Classification. Clinical signs. A7

Prematurity is a term for neonates born at less than 37 weeks' gestation.
Classification
Based on gestational age
● moderate to late preterm (34-37weeks),
● very preterm (28-31 weeks)
● extremely preterm (<28 weeks)
Based on birth weight
● Low birth weight (LBW);is btw 1500-2500g
● Very low birth weight (VLBW);less than 1500g
● Extremely low birth weight(ELBW); less than 1000g

PHYSICAL CHARACTERISTICS
● thin, smooth, shiny, almost translucent skin :
● veins are easily seen through the skin (transparent skin)
● wrinkled features
● soft, flexible ear cartilage
● lack of subcutaneous fat
● body hair called lanugo ;covering forehead, shoulder,
and arms
● Vernix caseosa abundant
● Extremities appear short
● weak cry
● usually inactive, may be unusually active
immediately after birth
● ineffective suck and swallow (poor feeding)
 ● enlarged clitoris (female infant)
● small scrotum, smooth without ridges (male infant)

14. RDS-syndrome: causes, clinical signs, prevention.

A8 Neonatal Respiratory Distress Syndrome or surfactant
deficiency is lung disease in infant caused by a deficiency of
pulmonary surfactant .
Surfactant deficiency causes the alveoli to collapse, resulting in
impaired gas exchange.
Causes
● Premature birth
● Genetic predisposition
● Scheduled CS
● Maternal diabetes Mellitus
● Hydrops fetalis
● Multifetal pregnancy
● Rarely hereditary
Clinical signs
● Onset can occur 6hours after birth
● Signs of increased breathing effort
● Tachypnea >60 per minute
● Expiratory “grunting” (from partial closure of glottis)
● Nasal flaring
● Subcostal/intercostal and jugular retractions
● Cyanosis
● Extremely immature infants may develop apnea and/or
hypothermia.
● Auscultation:decreased breath sounds
● SpO2 <95%
Prenatal prevention and prediction of RDS:
● Obstetricians with experience in fetal medicine should care for mothers
whose infants are at an increased risk for developing RDS.
Strategies to prevent premature birth (eg, bed rest, tocolytics, and
appropriate antibiotics)
● Antenatal corticosteroids(help to stimulate surfactant in the
lung) from 24-34 at risk of giving birth within days. - Given
48hiurs before delivery
- 2 doses of IM betamethasone 24hours apart or 4doses of IM
dexamethasone 12 hours apart.
Treatment
● Surfactant replacement therapy : initiated as soon as possible in hours
after birth. Repeated dose via endotracheal tube after 6-12hours for a
total of 2-4doses.
● Survanta 4ml(100mg phospholipid)/kg
● Infasurf 3ml/kg
● Curosurf 2.5ml/kg
“INtubation, SURfactant,Extubate”

15. RDS-syndrome: differential diagnosis with pneumonia. A9

Respiratory distress
Pneumonia
syndrome
Lung auscultation Reduced breath sounds Crackles or rales

Lung volume Decreased Normal

Pulmonary opacity Uniform inhomogeneous

Heart Enlarged Normal

Similarities
● Tachypnea
● Grunting
Differences
● Anamnesis in pneumonia
- History of chorioamnionitis; >18hours PROM
● Clinical features
- crackles or rales
- Fever
- Dull sound on percussion
- No retractions
● Additional examination
- positive culture of amniotic fluid
 - Increased inflammatory markers;CRP, procalcitonin,
leukocytosis
-Chest X-ray;infiltrate in lung tissue
RDS: ground glass densities, low lung volumes and air bronchograms

16. RDS-syndrome: differential diagnosis with congenital

heart disease. A10

Similarities
● Cyanosis
● Tachypnea
● Dyspnea
Differences
● Anamnesis for Congenitl HD
• Genetic syndromes
- • Trisomy 21 • Turner syndrome
• Maternal factors
- • Obesity • Diabetes• Epilepsy • Hypertension • Preeclamps
• Medications
- • NSAIDs • ACE inhibitors
• In utero infections
- • Rubella • Coxsackie virus
● Clinical features for CHD
- Tachycardia, Excessive irritability,sweating, sleeping
- Poor weight gain
- Loud systolic murmur
- Cyanosis;when crying or feeding
- Abnormal femoral pulses
● Additional examination
A. Chest x-rays ;• Heart size and shape
• Dextrocardia
• Enlarged heart size
• Boot shaped heart
● Pulmonary vascular markings
• Decreased markings
• ↓ pulmonary blood flow
• Asymmetric markings
17. Bronchopulmonary dysplasia: clinical manifestations and treatment.
A11 Bronchopulmonary dysplasia is a result of lung injury in infants
requiring mechanical ventilation and supplemental oxygen.

Bronchopulmonary dysplasia is a form of chronic lung disease

that develops in preterm neonates treated with oxygen and
positive-pressure ventilation.

The new BPD is a disease primarily of infants with birth weight <1000g
born at less than 28week gestation some of whom have little or no lung
disease at birth but experience progressive respiratory failure over the
first few weeks of life.

Risk factors
- presence of interstitial emphysema
- Male sex
- Low PaCO2 during the treatment of RDS, PDA
- high peak inspiratory pressure
- Family history of atrophy or asthma
- Overhydration during the 1st days of life
Clinical manifestation
● tachypnea
● tachycardia
● increased work of breathing (with retractions, nasal flaring,
and grunting)
● Cyanosis due to hypoxia
● frequent desaturations
● significant weight loss during the first 10 days of life
● Arterial blood gas shows hypoxemia and hypercarbia
with eventual metabolic compensation for the respiratory
acidosis.
● Chest X-ray-pulmonary interstitial emphysema, wandering
atelectasis with concomitant hyperinflation and cyst formation.
●
Treatment:
● Nutritional supplementation
● Supplemental oxygen. Maintain PaCO2 >55mmHg;
SpO2 88-93%
 ● Pulmonary fluid retention is treated with diuretics.
Furosemide 0.5-1mg/kg/dose IV BID or 2mg/kg/dose daily
orally BID
● Postnatal corticosteroids;Dexamethasone 0.25mg/kg/day for
5-7days ● Vitamin A; 5000IU 3 times weekly for 1st 28days
of age

18. RDS-syndrome: clinical signs, assessment of respiratory

disorders severity and treatment. A12

Clinical signs
● Onset can occur 6hours after birth
● Signs of increased breathing effort
● Tachypnea >60 per minute
● Expiratory “grunting” (from partial closure of glottis)
● Nasal flaring
● Subcostal/intercostal and jugular retractions
● Cyanosis
● Extremely immature infants may develop apnea and/or
hypothermia.
● Auscultation:decreased breath sounds
● SpO2 <95%

Severity

Treatment
● Surfactant replacement therapy : initiated as soon as possible in hours
after birth. Repeated dose via endotracheal tube after 6-12hours for a
total of 2-4doses.
● Survanta 4ml(100mg phospholipid)/kg
● Infasurf 3ml/kg
● Curosurf 2.5ml/kg
“INtubation, SURfactant,Extubate”
● Continuous positive airway pressure
● Assisted Ventilation: mechanical ventilation
● Supportive Therapy: temperature regulation,

19.Neonatal osteomyelitis: diagnostic criteria, treatment. A13

Acute osteomyelitis is a rare disease affecting bones and joint in
neonates, Due to their immature immune response neonates are more
susceptible to osteomyelitis than are older children.
Preterm infants are at high risk for osteomyelitis because of frequent
blood drawing bacteria (secondary to heel or venipuncture, umbilical
catheterization, infected cephalohematoma, etc.)
, invasive monitoring/procedures and intravenous drug
administration

Diagnostic criteria
● Children often present with a sudden onset of fever and bony
tenderness or a limp. The pain can be throbbing and quite
severe; however, presentation in neonates can be quite subtle.
● Infants can appear well except for failure to move an extremity or
pain on movement. Redness or swelling indicates that infection has
spread into the subperiosteal space. Rupture of a focus of
osteomyelitis into a joint space can result in septic arthritis. This is
often observed in neonates.
● septic arthritis. This is often observed in neonates..
● Children with vertebral osteomyelitis present with back pain, and
those younger than 3 years present with refusal to walk or with a
limp. Occasionally, children with vertebral osteomyelitis may have
incontinence as a presenting symptom. Children with discitis tend to
present with less fever and often appear less ill than those children
with vertebral osteomyelitis.
Laboratory studies:
- Blood cultures are positive only in 50% of pediatric patients.
 -Cultures of bone aspirate are useful in obtaining the organism and
planning for long-term therapy.
In addition, C-reactive protein or erythrocyte sedimentation rate are
generally elevated in acute disease.
● Plain radiography can show soft tissue swelling and destroyed
fascial planes within days after onset of infection,
● Computed tomography, magnetic resonance imaging,
ultrasound, radiography and bone scintigraphy scanning have
been reported to be useful in detecting osteomyelitis
● Magnetic resonance imaging (MRI) has high specificity (94%) and
sensitivity (97%) for the diagnosis of acute osteomyelitis, showing
changes as early as day 3 to 5 after the onset of infection.
Treatment
● Starting a semisynthetic penicillin, such as oxacillin (150
mg/kg/d), empirically is a good choice for most cases of
community-acquired osteomyelitis.
Nafcillin, clindamycin. In patients with allergy to penicillin, a first-
generation cephalosporin and lincomycin (40 mg/kg/d) are both
excellent alternatives. Cefuroxime (150 mg/kg/d)
● Surgical Care: Surgery is usually indicated to drain
purulent material from the subperiosteal space or if infected
foreign material is present.

20. Differential diagnosis of neonatal osteomyelitis and Erb palsy. A14

Signs; Osteomyelitis(inflammation of the bone due Dushen
to infection) Erb
paralysis

history: mother infecions during pregnancy, Birth

delivery(infection) trauma
Time of appearing: On the 3-5 day after birth From the birth

Changes of the movements: + +

Intoxication ; fever + –
 Local infiltration: + –

Active movements in the arm;

absent absent
Passive movements in the arm; very painful painless

Blood count (leucocytosis, formula left shift)

Positive negative

Roentgenologic signes + –
21. Classification and diagnostic criteria of necrotizing
enterocolitis in newborns. A15
Necrotizing enterocolitis (NEC) is an inflammation in the
intestines and usually occurs in premature babies
Necrosis of the bowel wall may complicate bowel ischaemia after
asphyxia, infection or shock in newborn infants.

Ukrainian classification
Stage Clinical signs X-ray
І - Incidence Bad thermoregulation, poor sucking, loss of
bowel wall
appetite, vomiting; Local signs: meteorism,
thickening and
defecation up to 10 per day with large amount
bubbles of air in
of mucus.
Bowel
ІІ - height General status is hard, often apneas,
Enlargement
bradicardia, hypotonia, lethargy; blood in
bubbles of air in
stools; Local signs: vomiting is often, edema
bowel, levels of
of the anterior abdominal wall, sex organs.
the fluid, bubbles
 Abdomen is enlarged, lustering, peristalsis is
of air in bowel
depressed or absent
wall

ІІІ - The same + increasing of the brease and

progressive Fluid
cardiac defficiency, hypothermia, jaundice,
sequestration in
DIC-syndrome; peritonitis, bowel inpassage,
the abdominal
ascitis
cavity, bowel wall
necrosis
ІV - Perforation, peritonitis, anuria, DIC-syndrom,
complication s The same +
septic shock.
pneumoperitoneu
m

Bells classification
Stage I Suspected NEC Lethargy, distended and shiny abdomen,
gastric retention, vomiting, diarrhea, rectal bleeding
Stage II Proven NEC Stage I symptoms + abdominal tenderness,
visible intestinal loops lacking peristalsis
Stage III Advanced NEC Intestinal perforation, symptoms of
sepsis, flank redness If left untreated: rapid progression to
disseminated intravascular coagulation (DIC) and shock
 22. NEC: diagnostic criteria, treatment. A16

Necrotizing enterocolitis (NEC) is an inflammation in the intestines and

usually occurs in premature babies..
● The clinical presentation of necrotizing enterocolitis (NEC) includes;
nonspecific aspects of the history, such as vomiting, diarrhea, feeding
intolerance and high gastric residuals following feedings.
More specific GI tract symptoms include abdominal distention and
frank or occult blood in the stools.
classic clinical triad consists of abdominal distension, bloody stools,
and pneumatosis intestinalis.
● With disease progression, abdominal tenderness, abdominal wall
edema, erythema, crepitans, or palpable bowel loops indicating a
fixed and dilated loop of bowel may develop.
Systemic signs, such as apnea, bradycardia, lethargy, labile body
temperature, hypoglycemia, and shock, are indicators of
physiologic instability.
● NEC most commonly affects the terminal ileum and the proximal
ascending colon. However, varying degrees of NEC can affect any
segment of the small intestine or colon. The entire bowel may be
involved and may be irreversibly damaged.
● NEC typically occurs in the second to third week of life in the
infant who is premature and has been formula fedOccasionally, signs and
symptoms include temperature instability, lethargy, or other nonspecific
findings of sepsis.
Abdominal radiography
- Pneumatosis intestinalis: Bubbles of gas within the wall of the
intestine - Portal venous gas (pneumatosis hepatis) Increased
intestinal wall thickness - Dilated intestinal loops
- Air-fluid levels
- Pneumoperitoneum as a result of intestinal perforation (stage 3)
Abdominal ultrasound:
Indication: Ultrasound may be helpful for diagnosing NEC when
abdominal radiography is inconclusive.
Findings
- Pneumatosis intestinalis
- Portal venous gas
- Increased intestinal wall thickness
- Decreased intestinal wall perfusion
Lab:
leukopenia or leukocytosis with neutropenia, decreased hematocrit and
hemoglobin (anemia). Thrombocytopenia. Hyponatremia, metabolic
acidosis sodium bicarb<20.
● Neutrophil counts < 1500/μL are associated with a poor
prognosis.
TREATMENT:
● stop the feeding
● parenteral antibiotics: ampicillin, gentamicin, and clindamycin or
metronidazole) ; gentamicin 4-5mg/kg/dose or amikacin
15mg/kg/dose IV every 24hours and amoxicillin 50-100mg/kg/dose
IV every 12hours.
● nasogastric decompression
● parenteral nutrition
 ● fluid replacement
● insure adequate oxygen delivery
● cardiovascular support ( dopamine or dobutamine)
Treatment according to stages
● Bell stages IA and IB: The patient is kept on an Nothing Per
Oral(NPO) diet with antibiotics for 3 days. IV fluids are provided,
including total parenteral nutrition (TPN).
● Bell stages IIA and IIB: Treatment includes support for respiratory
and cardiovascular failure, including fluid resuscitation, NPO, and
antibiotics for 14 days. Surgical consultation should be considered.
After stabilization, TPN should be provided during the period that the
infant is NPO.
● Bell stage IIIA: Treatment involves NPO for 14 days, fluid
resuscitation, inotropic support, and ventilator support. Surgical
consultation should be obtained. TPN should be provided during
the period of NPO.
● Bell stage IIIB: Surgical intervention

Indications
The principle indication for operative intervention in necrotizing
enterocolitis (NEC) is perforated or necrotic intestine. Infants with
necrotic intestine are identified based on various clinical, laboratory, and
radiologic findings. The most compelling predictor of intestinal necrosis
indicating a need for operative intervention is pneumoperitoneum (see
the image below). Other relative indications for operative intervention are
erythema in the abdominal wall, gas in the portal vein, and positive
paracentesis.

23. Diagnostic criteria of neonatal meningitis, treatment. A17

Diagnostic criteria are based on .
● Early onset:
Symptoms appearing in the first 48 hours of life are referable
primarily to systemic illness rather than to meningitis. Such symptoms
include temperature instability, episodes of apnea or bradycardia,
hypotension, feeding difficulty, hepatic dysfunction, and irritability
alternating with lethargy.
Respiratory symptoms can become prominent within hours of birth in
group B streptococcal (GBS) infection; however, the symptom
complexc also is seen with infection by E coli or Listeria species.
● Late-onset bacterial meningitis (ie, symptom onset after 48 hours
of life) is more likely to be associated with neurological
symptoms. Most commonly seen are stupor and irritability.
Neurological signs:
- Seizures,
- Bulging anterior fontanel,
- Extensor posturing or opisthotonos.
- Focal cerebral signs including gaze deviation and
hemiparesis.
- Cranial nerve palsies.
- Nuchal rigidity is the least common sign in neonatal bacterial
meningitis, occurring in fewer than 25% of affected neonates.
Laboratory:
Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF)
by culture and/or visualization by Gram stain
● Increased CSF white blood cell (WBC) count (typically >1000
WBC/mL, but may be lower, especially with gram-positive
organisms) with a predominance of neutrophils
● Elevated CSF protein concentration (>150 mg/dL in preterm
(premature birth) and >100 mg/dL in term (on time) infants)
● Decreased CSF glucose concentration (<20 mg/dL [1.1 mmol/L]
in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on
time) infants)
Treatment
● combination of ampicillin and gentamicin is a common
regimen. Penicillin.
● In treating meningitis, many centers administer cefotaxime
in addition to or instead of gentamicin
● Acyclovir in HSV

24. Differential diagnosis of neonatal meningitis and

asphyxia. A18

Similarities
- irritability
- Lethargy
- Hepatic dysfunction
- Feeding difficulty
- Seizures
Differences
● Anamnesis
- Risk factors for the development of meningitis include
low birth weight (< 2500 g), preterm birth (< 37 weeks’ gestation),
premature rupture of membranes, traumatic delivery, fetal hypoxia,
and maternal peripartum infection (including chorioamnionitis).
- Risk factors of asphyxia:
● Diseases of mother:
- Anemia, leukemia
- Pulmonary and cardiovascular diseases
- Smoking, drug abuse
- Influence of toxins and chemical substances, some
medicine - Hemorrhages
● Uterine-placental hemo circulation
disturbances Pathology of placenta and its’
presentation
Damage of placenta by infection
Cord abnormalities
● Diseases of the fetus
Isoimmune incompatibility of mother and
fetus TORCH-infections
Fetal abnormalities
● Intranatal
meconium in the amniotic fluid,changes of the cardiac rhythm and breathing
muscular hypotonia, hyporeflexia, pallor or cyanosis of the skin, changes of the
blood gases

Clinical differences
- Meningitis has neurological signs: Seizures, Bulging anterior
fontanel, Extensor posturing or opisthotonos, Focal cerebral signs
including gaze deviation and hemiparesis
- Asphyxia: generalized hypotonia, suppressed reflexes, generalized
seizures, decerebrate posture. Apgar score <3 beyond 5min,
● Additional examination
- CSF analysis Elevated CSF protein concentration (>150 mg/dL in
preterm (premature birth).
- Decreased CSF glucose concentration (<20 mg/dL [1.1 mmol/L] in
preterm (premature birth)
Pleocytosis and culture.
- In asphyxia: metabolic acidosis. No CSF changes.
 25. SIRS-syndrome: criteria, causes. A19
Systemic Inflammatory Response Syndrome is defined as 2 or more of these
criteria;
● Fever of more than 38°C (100.4°F) or less than 36°C
(96.8°F)
● Tachycardia;Heart rate of more than 90 beats per
minute
● Tachypnea; Respiratory rate of more than 20 breaths per minute or
arterial carbon dioxide tension (PaCO2) of less than 32 mm Hg
● Abnormal white blood cell count (>12,000/µL or <4,000/µL or
>10% immature [band] forms)
SIRS in neonates
● Temperature instability <36C or >38.5C
● Respiratory dysfunction;tachypnea >2SD above the mean
for age, hypoxemia (PaO2<70mmHg or room air)
● Cardiac dysfunction;tachycardia >2SD above the mean for
age, delayed capillary refill >3secs, hypotension >2SD below the
mean for age
● Perfusion abnormalities
- oliguria urine output<0.5ml/kg/hr
- Lactic acidosis elevated plasma lactate and or arterial
ph <7.25 -Altered mental status
SIRS caused by:
● perinatal asphyxia
● respiratory tract disease(meconium
aspiration pneumonia)
● cardiac disease(congenital,acquired)
● metabolic disease (hypoglycemia, congenital adrenal
hyperplasia, organic acidosis, urea cycle disorders)
● neurologic disease(intracranial hemorrhage)
● hematologic disease(methemoglobinemia, congenital leukemia)

26. Neonatal sepsis - diagnostic criteria, treatment. A20

Neonatal sepsis refers to an infection involving bloodstream in newborn infants less than 28
days old i
CLASSIFICATION:
A. Early onset <0-72hours of age: Early-onset sepsis syndrome is
associated with acquisition of microorganisms from the mother.
Transplacental infection or an ascending infection from the cervix
 may be caused by organisms that colonize in the mother's
genitourinary tract. The infant may acquire the microbe by passage
through a colonized birth canal at delivery.
The microorganisms most commonly associated with early-onset
infection include group B Streptococcus (GBS), Escherichia coli,
Haemophilus influenzae, and Listeria monocytogenes.
B. late onset >72-90days of age: acquired from the caregiving
environment. Organisms that have been implicated in causing late-
onset sepsis syndrome include coagulase-negative staphylococci,
Staphylococcus aureus, E coli, Klebsiella, Pseudomonas,
Enterobacter, Candida, GBS, Serratia, Acinetobacter, and
anaerobes.
C. nosocomial : Risk factors for nosocomial
- prematurity, LBW, Prolonged hospital stay
- Invasive procedures, indwelling vascular catheter
- Parenteral nutrition - Endotracheal tube, ventricular shunt
- Frequent use of broad spectrum antibiotics - Alterations in skin and
mucous membranes
Diagnostic criteria for sepsis
● General variables
- Fever, hypothermia - Tachycardia,bradycardia
- Tachypnea - Altered mental status - Significant edema
● Inflammatory variables
- leukocytosis - Leucopenia
- >10% immature forms - CRP - Procalcitonin
● Hemodynamic variables
- Hypotension
● Tissue perfusion variables
- Hyperlactatemia
- Decreased capillary refill
● Organ dysfunction variables
- Hypoxemia - Oliguria
- Increased creatinine - Coagulation abnormalities
- Thrombocytopenia - Hyperbilirubinemia
Laboratory signs of neonatal sepsis
● Leukopenia <5000*10^9/l
● Leukocytosis
o Up to 4 days of life > 30000*10^9/l
o After 4 days >20000*10^9/l
 ● Absolute number of stab neutrophils
o Up to 4 days of life >500/mm3
o After 4 days of life> 1000/mm3
● Leukocyte index intoxication >0,2
● C-reactive protein increased >20mg/l
● Thrombocytopenia <150 000*10^9/l
● Procalcitonin after 4 days of life increased > 0,5ng/ml
● Blood, CSF, Urine culture or gram staining
● Serology: detection of bacterial
antigens Evidence of inflammation:
● CRP, procalcitonin, ESR, serum amyloid,
Multisystem Organ Dysfunction Syndrome:
(MODS
Treatment
● IV nutrition
● An infant with temperature instability needs thermoregulatory
support with a radiant warmer or incubator.
● IV aminoglycoside (gentamycin 4-5mg/kg/dose) or amikacin
15mg/kg/dose IV every 24hours and amoxicillin 50-100mg/kg/dose
IV every 12hours
● EOS: ampicillin 150mg/kg/dose IV every 12hours and an
aminoglycoside(gentamicin 4mg/kg/dose IV every
24hours).
● LOS from community: ampicillin 75mg/kg/dose IV every
6hours and gentamicin 4mg/kg/dose IV every 24hours.
● LOS hospitalized: vancomycin 10-20mg/kg every 24hours
according to creatinine and gentamicin 4mg/kg/dose IV every
24hours.

27. Herpes infection: clinical forms, diagnosticis, treatment in

newborns. A21

Infants are asymptomatic at birth but later in neonatal period 3 forms

occur

● SEM form(5-14days): Skin Eyes and Mouth lesions maculopapular

vesicular rash
● Herpes encephalitis(3-4weeks): bulging fontanelles, apnea, seizures,
CSF pleocytosis, and elevated protein concentration
● Disseminated disease(5-7days): multi organ failure, septic
presentation. Hepatitis, pneumonitis, disseminated
intravascular
 coagulation, or a combination, with or without encephalitis or
skin disease.
● Other signs, which can occur singly or in combination, include
temperature instability, lethargy, hypotonia, respiratory distress,
apnea, and seizures.
Diagnosis
● Best diagnosis:PCR, antibody fluid
● Skin vesicles;swab for viral culture and HSV PCR
● Rapid diagnosis by viral culture or HSV PCR is essential.
● If no diagnostic virology facilities are available, a Tzanck test of the
lesion base may show characteristic multinucleated giant cells and
intranuclear inclusions
Treatment
● High dose parenteral acyclovir 30mg/kg/dose q8h 14-21d.
Premature infants 20mg/kg/d PO/IV divided q12h for14-21d
● In case of disseminated disease. Treat for 21 days
o Encephalitis and SEM form treat for 14 days
o Ocular involvement requires topical therapy
● Desintoxication: glucose or ringers solution
● Seizures: Phenobarbital

28. CMV-infection: diagnosis, treatment in newborns. A22

● Signs at birth, if present, are intrauterine growth restriction,
prematurity, microcephaly, jaundice, petechiae,
hepatosplenomegaly, periventricular
calcifications, chorioretinitis, pneumonitis, hepatitis, and
sensorineural hearing loss.
● If acquired later in infancy, signs may include pneumonia,
hepatosplenomegaly, hepatitis, thrombocytopenia, sepsis-like
syndrome, and atypical lymphocytosis.
Most severe form of CMV is Cytomegalic Inclusion disease.
Characterized by:
● IUGR
● Hepatosplenomegaly
● Thrombocytopenia
● Petechiae and purpura; blueberry muffin baby
● Microcephaly
● Ventriculomegaly
● Cerebral atrophy
 ● Chorioretinitis
● Sensorineural hearing loss
Diagnosis
● CT scan :intracerebral calcifications
● Urine culture for CMV(in first 2weks of life confirms
congenital infection)
● Cord or infant blood for CMV PCR

Treatment is mainly supportive.

● Parenteral ganciclovir 5mg/kg IV BID 2-6weeks or oral
valganciclovir 90mg/kg IV q12h infused over a minimum of 1h
for 14-21days in symptomatic infants

(IF YOU’RE ASKED) Listeriosis: diagnostic criteria, treatment in

newborns.
● In utero infection with Listeria monocytogenes can result in fetal
dissemination with granuloma formation (eg, in the skin, liver,
adrenal glands, lymphatic tissue, lungs, and brain). If a rash is
present, it is referred to as granulomatosis infantisepticum.
● Aspiration or swallowing of amniotic fluid or vaginal secretions
can lead to in utero or perinatal infection of the lungs, manifesting in
the first several days of life with respiratory distress, shock, and a
fulminant course.
● Abortion, premature delivery with amnionitis (with a
characteristic brown, murky amniotic fluid), stillbirth, or neonatal
sepsis
Treatment:
● Ampicillin and gentamicin for 14 days.
● Other possible drugs include ampicillin or penicillin with
rifampin or trimethoprim/sulfamethoxazole,
trimethoprim/sulfamethoxazole alone
29. Congenital lues: diagnostics, treatment in newborns. A23
Also known as syphilis
Symptoms and Signs
● Many patients are asymptomatic, and the infection may
remain clinically silent throughout their life.
● Early congenital syphilis commonly manifests during birth-2years
Manifestations include characteristic vesiculobullous eruptions or a
macular, copper-colored rash on the palms and soles and papular
 lesions around the nose and mouth and in the diaper area, as well as
petechial lesions.
● Condylomatas lesions in mucosal membrane
● Generalized lymphadenopathy and hepatosplenomegaly often occur.
The infant may fail to thrive and have a characteristic mucopurulent
or blood-stained nasal discharge causing snuffles. A few infants
develop meningitis, choroiditis, hydrocephalus, or seizures, and others
may be intellectually disabled. Within the first 8 mo of life,
osteochondritis (chondro epiphysitis), especially of the long bones and
ribs, may cause
pseudoparalysis of the limbs with characteristic radiologic
changes in the bones.
● Late congenital syphilis typically manifests after 2 yr of life and causes
gummatous ulcers that tend to involve the nose, septum, and hard
palate and periosteal lesions that result in saber shins and bossing of
the frontal and parietal bones. Neurosyphilis is usually asymptomatic,
but juvenile paresis and tabes may develop. Optic atrophy,
sometimes leading to blindness, may occur. Interstitial keratitis, the
most common eye lesion, frequently recurs, often resulting in corneal
scarring. Sensorineural deafness, which is often progressive, may
appear at any age.
● Hutchinson's triad:1. Interstitial keratitis 2. Hutchinson incisors
and mulberry molars 3. Eight nerve deafness
● perioral fissures (rhagades), and maldevelopment of
the maxilla resulting in “bulldog” facies are characteristic,
if infrequent, sequelae.
Diagnosis
● Early congenital syphilis: Clinical evaluation; darkfield microscopy
of lesions, placenta, or umbilical cord; serologic testing of mother
and neonate; possibly CSF analysis
● Late congenital syphilis: Clinical evaluation, serologic testing
of mother and child
Treatment:
Crystalline penicillin(200000-300000U/kg/d) IV q6h 10-14d
Neurosyphilis: aqueous crystalline penicillin G 200000-300000U/kg/d IM q4-
6h
10-14d, followed by single dose benzathine penicillin 50000U/kg/dose in 3
weekly dose.
 (IF YOU’RE ASKED)Clinical manifestations, diagnosis of congenital rubella.
Gregg’s triad.
The classic Gregg triad for congenital rubella syndrome is;
● Sensorineural deafness
● Eye abnormalities—especially retinopathy, cataract, and microphthalmia
● Congenital heart disease—especially pulmonary artery stenosis and
patent ductus arteriosus
In the fetus, there may be no effects, death in utero, or multiple anomalies referred
to as congenital rubella syndrome (CRS). The most frequent abnormalities include
● Intrauterine growth restriction
● Microcephaly
● Meningoencephalitis
● Cataracts
● Retinopathy
● Hearing loss
● Cardiac defects (patent ductus arteriosus and pulmonary artery stenosis)
● Hepatosplenomegaly
● Bone radiolucencies
● Less common manifestations include thrombocytopenia with
purpura, dermal erythropoiesis resulting in bluish red skin lesions,
adenopathy, hemolytic anemia, and interstitial pneumonia.
Diagnosis
● Maternal serum rubella titers
● Viral detection in the mother via culture and/or reverse transcriptase–PCR
(RT-PCR) of amniotic fluid, nose, throat (preferred), urine, CSF, or blood
specimens
● Infant antibody titers (measured serially) and viral detection as above
Treatment: effectively treat mother with immune globulin. Prevented by
vaccine.

30. Congenital toxoplasmosis: forms, diagnosticis, treatment A24

Infection with T. gondii occurs primarily from ingestion of inadequately cooked
meat containing cysts or from ingestion of oocysts derived from food or water
contaminated with cat feces.
Similarly, infected neonates are usually asymptomatic at birth, but manifestations
may include
 - Prematurity, Intrauterine growth restriction

● Jaundice, Hepatosplenomegaly

● Microcephaly, Chorioretinitis

● Seizures, Myocarditis

● Pneumonitis

● Various rashes

● Neurologic involvement, often prominent,

includes chorioretinitis, hydrocephalus,

intracranial calcifications, microcephaly,

and seizures

. The classic triad of findings consists of

chorioretinitis, hydrocephalus, and

intracranial calcifications. Neurologic and

ophthalmologic sequelae may be delayed for

years or decades.

Diagnosis

● Serial IgG measurement (for maternal infection)

● Amniotic fluid PCR (for fetal infection)

● Serologic testing, brain imaging, CSF analysis,

ophthalmologic evaluation (for neonatal

infection), and PCR testing of various body

 fluids or tissues

Treatment

● Sometimes spiramycin 50-100mg/kg/d PO

bid/wide 3-4weeks for pregnant women

Pyrimethamine 2mg/kg/d PO divided q12h for 2-4days, sulfadiazine

100mg/