MedicoNotebook: February 2013

0 Not enhance on CECT

MCQ 112

Which of the following does not enhance or shows minimal enhancement on CECT ?
a. Meningioma
b. Area Postrema
c. Median eminence
d. Cavernous Angioma

ANSWER:

0 Circumventricular organs (CVOs)

Circumventricular organs (CVOs) are structures in the brain that are characterized by their extensive vasculature and lack of a normal blood brain barrier (BBB).

Area postrema
Organum vasculosum of the lamina terminalis (OVLT)
Subfornical organ (SFO)
Posterior pituitary
Median eminence
Pineal gland

Note:

Inclusion of Choroid Plexus in CVOs is debatable , but it is also outside BBB. Thus enhance on CECT.

0 Normal Cerebral blood volume

MCQ 111 (All MN FB Page MCQs)

What is the normal range of cerebral blood volume ?

a. 4-5 ml/100g
b. 6-7 ml/100g
c. 40 - 50 ml/100g
d. 50 - 60 ml/100g

ANSWER:

0 Arlt

ARLT

"Arlt's line": Linear scar present in sulcus subtarsalis during Chlamydia trachomatis infection.

"Arlt's operation": Transplantation of eyelashes back from the edge of the eyelid for treatment of distichiasis.

"Arlt's syndrome": A contagious eye infection caused by Chlamydia trachomatis.

"Arlt's triangle": keratic precipitates distributed in a wedge-shaped area on the inferior corneal endothelium.

Source : http://en.wikipedia.org/wiki/Carl_Ferdinand_von_Arlt

1. Can be Still birth

2. Can be Preterm , IUGR

3. Macrosomia

4. HMD

5. Neonatal Jaundice

6. Hypo Glycemia/Calcemia/Magnesemia

7. Polycythemia - Renal vein thrombosis

8. Lazy left colon syndrome (pseudo-obstruction of intestine - hypoperistaltic)

9. Heart diseases -

MC - TGA (also MC congenital anomaly in Infant of diabetic mother)
Asymmetrical Septal Hypertrophy
Cardiomyopathy
Persistent pulmonary HTN

Important points :

MC congenital anomaly in Still borns of diabetic mother - Neural tube defects

MC congenital anomaly in Infants of diabetic mother - TGA

Most Specific anomaly in Infants of diabetic mother - Sacral Agenesis

Other Points to remember :

MC sign of Acute Hypoxia in Neonates : Bradycardia

IOC to look for cerebral perfusion in birth asphyxiated newborn : ( NIRS ) Near-infrared spectroscopy.

Earliest and Most Common organ affected in Birth Asphyxia : Kidneys (ATN-Acute tubular necrosis) , later Brain (HIE - Hypoxic ischemic encephalopathy).

MC cause of Renal failure in Newborn - Birth Asphyxia.

0 Hypocalcemia in Infants

Hypocalcemia in Infants

Normal Serum Calcium : 9 - 11mg/dl

Hypocalcemia - S. Calcium <7mg/dl ( ionized Ca - <4mg/dl or < 1 mmol/l )

Early Onset ( <72hrs)	Late Onset ( >72hrs)
Cause : Prematurity Birth Asphyxia Infant of diabetic mother	Feeding with phosphate rich milk (cow milk)

100ml Cow milk
Phosphate – 100mg
Calcium – 118mg

Good Ca/Po4 ratio is 2:1

100ml Breast Milk
Phosphate - 15mg
Calcium - 35 mg

Therefore Breast milk is good Calcium supplement and so no late onset hypocalcemia

Cerelac (Docosahexanoic acid , Omega 3 EFA - for brain and eye )
has Ca/Po4 >2

Clinical Features :

Tremors
Jitteriness (Can be stopped by passive limb restriction)
Seizures
No Tetany

Treatment : IV calcium

0 Hypoglycemia in Infants

Hypoglycemia in Infants

Blood sugar : <40mg/dl

Causes

Inadequate feeding
Inadequate stores (Preterm , IUGR)
Sepsis
Galactosemia
Polycythemia
HyperInsulin (Infant of diabetic mother)

Pedersen Hypothesis :

In Maternal diabetes - high glucose passes to fetus - Thus fetus' Beta cell undergo hyperplasia and increases Insulin.

Thus tell mother to do frequent feeding and we have to do frequent monitoring.

Treatment :
IV dextrose - Start with glucose infusion 3-5mg/kg/min
or
IM Glucagon (short term measure to tide over hypoglycemia)

Note:

Peripheral Vein : till 12.5% glucose can be given.
Central Vein (Umblical vein) : if >12.5% glucose to be given.

0 Medical One Liners 111 - 120

111. Breast Milk is Contraindicated in Galactosemia

112. If Mother Sputum +ve TB - Still give breast milk to baby ( with 6months course of 5mg/kg INH )

113. Mother with HIV - Never mix feed i.e give exclusive trophic feed or give expressed milk of other women )

114. Mother to Child transmission of HbsAg - Prevent by

HBIG within 12 hr of life
Vaccine on day 1 of life.

115. Anti HbsAb Protective Titre - > 10 mIU / ml

116. Liver biopsy in Alpha 1 anti-tripsin deficiency : PAS +ve and Diastase resistant granules

117. CMV : Intranuclear Owl eye inclusion bodies.

118. Nystagmus induced by Valsalva maneuver :

Chiari Malformation
Perilymph fistula
Superior Canal dehiscence syndrome

119. GABA is formed from Pyridoxine.

120. If pregnant lady shows Rubella antibody +ve : It means she is immune to rubella during her pregnancy and need not worry for rubella infection.

0 Cytomegalovirus (CMV)

Cytomegalovirus (CMV)

Periventricular Calcifications
Chorioretinitis
Convulsions

Asymptomatic CMV is leading cause of Sensoryneural hearing loss ( 7% cases of CMV infection )

Diagnosis :
CMV is in all body secretions
Thus can be isolated - Urine and Saliva are best specimens for CMV culture

Antigen PP65 - PCR against this is used.

Typical "owl eye" inclusion indicating CMV infection of a lung pneumocyte

Treatment :
IV - Gancyclovir (Side effect - Bone marrow depression)
if resistant - Foscarnet

Image Source : http://en.wikipedia.org/wiki/File:Cytomegalovirus_01.jpg

0 Congenital rubella syndrome

Congenital rubella syndrome

Triad :

Sensorineural deafness (58% of patients)
Eye abnormalities—especially "Salt-and-pepper" retinopathy, cataract and microphthalmia (43% of patients)
Congenital heart disease—especially patent ductus arteriosus (50% of patients)

Other heart defects :

Peripheral pulmonary stenosis
VSD
ASD is rare

Congenital Cataracts (white pupils) due to congenital rubella syndrome

Other abnormalities to remember :
Microcephaly (Mental Retardation)

Image Source : http://en.wikipedia.org/wiki/File:Cataracts_due_to_Congenital_Rubella_Syndrome_(CRS)_PHIL_4284_lores.jpg

0 Congenital Syphilis

Congenital Syphilis

Early ( <2yr )

Late ( >2yr )

Mucocutaneous Rash or rhinitis (Snuffles)

Similar to Secondary Syphilis in adults

Triad

Hutchinson Teeth (1^st lower molors)
Deafness (8^th Nerve)
Interstitial Keratitis

Lymphadenopahy
Autoimmune Haemolytic anemia
Osteochondritis and Metaphysitis
Glaucoma
Pseudoparalysis of parrot (Painful limbs)

Saddle Nose
Frontal bossing
Olympian’s Brow
Higoumenakis sign (Prominence of Sternoclavicular joint )
Rhagades (rash at shin area)
Clutton’s joints

Treatment : Crystalline Penicillin G for 10-14 days

Other causes of Pseudoparalysis of parrot :

Scurvey
Osteomyelitis
Hypokalemia

0 Mother to Child Toxoplasma

Toxoplasma (protozoa)

Definitive Host : Cat
Incidental host : Human

Prevention : Spiramycin to Mother to prevent vertical transmission to child.

If not prevented :

a. Hydrocephalus
b. Convulsions
c. 24 - 50% cases show Calcifications in

Caudate Nucleus
Choroid Plexus
SubEpendyma

Note : In CMV - Calcifications are Periventricular.

0 TORCH infections

TORCH infections

Toxoplasma

Others

Syphilis
HIV
Hep B
Varicella

Rubella
CMV
Herpes

If Mother gets Rubella after 16wks - Nothing to fetus
But if 10-11 wks - Increased chances of fetal abnormalities

Common points :
1. 50 - 60 % are asymptomatic
2. If symptomatic :

IUGR
Failure to thrive
Anaemia
HepatoSpleenomegaly
Thrombocytopenia
Rash
Cholestasis

Infectivity
1. All of them - at time of delivery.
2. Rubella - 2 peaks -

10-11 wks
At time of delivery

If HIV to mother -

Zidovudine after 14 wks pregnancy
then For delivery - do elective LSCS
If in labor - intrapartum Nevirapine
Neverapine to child (oral) x 4-6wks

Diagnosis is based on Serology :

1. IgM - is made by the child itself

2. IgG - is transmitted from mother

Considered marker only if :

IgG persists 6-9 months
or increases in titre

Note : in HIV cases -

No IgM in child
IgG persisting >18months is taken as marker. (not 6-9 months)

Thus for 1st 18 months : (as Child of HIV mother will be having +ve ELISA)

p24 assay
PCR (best but difficult)
Viral Culture

1 Cytotoxic vs Vasogenic edema (MCQ)

Which of the following imaging modality will best differentiate Cytotoxic from Vasogenic edema ?

a. Diffusion Weighted MRI
b. FLAIR sequence
c. Contrast enhanced CT
d. T2 weighted MRI

ANSWER:

0 Neonatal Seizures

Neonatal Seizures

Most Common cause : HIE ( Hypoxic Ischemic Encephalopathy )

Many neonatal seizures are Metabolic.

Day 1 :

Hypo-Glycemia
Hypo-Calcemia
Hypo-Magnesemia
IVH
Rarely - Pyridoxine dependent seizures.

Day 3 - 7 :

Late Onset sepsis
Late Onset Hypo-Calcemia
Tetanus Neonatorum
Kernicterus

Most Common type : Subte Seizures

Vacant Stare
Paddling movements

Because :

Myelination is not completed in NewBorn
Arborization of neurons is not completed

DOC : Phenobarbitone (But 1st check Glucose , Calcium , Magnesium )

Not Diazepam - it has Benzyl Alconium Chloride (preservative) which binds to albumin and displaces bilirubin - therefore can precipitate Kernicterus.

Pyridoxine dependent seizures : (AR)

Diagnosis of exclusion

Previously diagnosed by response of IV or Oral Pyridoxine ( Used in India Now also )

Diagnosed Now by : CSF or Plasma - Pyridoxine-5-phosphate.

GABA is formed from Pyridoxine
Therefore if decreased Pyridoxine - decreased GABA - Therefore decrease Inhibitory stimulus.

0 Neonatal Cholestasis ( Conjugated Jaundice )

Neonatal Cholestasis ( Conjugated Jaundice )

Direct bilirubin > 2 mg/dl
or
>15 % of Total bilirubin

=> Jaundice + Clay Coloured Stools + Dark yellow urine.

Causes :

1. Medical -

MC cause - Neonatal Hepatitis (because of TORCH)
Sepsis
Galactosemia
Alpha 1 Antitripsin deficiency
Neonatal Hemochromatosis

2. Surgical -

Extra Hepatic biliary atresia (should be operated in 1st 8 wks - Kasai Operation - else 80% die)

In Biliary Atresia

1. USG :

GB Absent
Triangular Cord

2. HIDA scan - IV dye

Not excreted into gut in biliary atresia

3. Gold Standard - PerOperative Cholangiography

MRCP is as good as PerOp Cholangiography

Galacosemia

Galactose 1-phosphate uridyltransferase is deficient.

Therefore Galactose 1 Phosphate Increase - Hepatotoxic

Triad :

Jaundice
Hypoglycemia
Cataract (because of Galactitol - from Galactose 1 phosphate)

0 Breast Milk vs Feeding Jaundice

Breast Milk Jaundice	Breast Feeding Jaundice
Because of pigment in breast milk which inhibits conjugation.	Because of decrease feeding and increased enterohepatic circulation.
At day 14 , approx. 20-30 mg/dl	At around Day 3 of life
Can also occur in next pregnancy
Treatment : Temporary interruption of breast feeding for 48 – 72 hrs	Ensuring breast milk.

2 Neonatal Jaundice

Neonatal Jaundice

Jaundice is visible in newborn skin when bilirubin > 5 mg/dl
Progression - CephaloCaudal

Kramer's Rule/Zones :

Zone Bilirubin
1 ----- 5 mg/dl
2 ----- 10
3 ----- 12
4 ----- 15
5 ----- >15

1g Hb = 34 mg Bilirubin = 1.34 ml O2

1g/dl of Albumin binds 8mg Bilirubin

The bilirubin gets conjugated in Liver (via UDP Glucuronyl Transferase).

Unconjugated Unbound bilirubin causes Kernicterus.

Physiological Jaundice of Newborn

Reasons :

Hematocrit of Newborn is more
Life span of fetal RBC = 90days {Adult is 120}
Y Ligandin - Low
UDP - GT - Low
Excretion - Less
Enterohepatic circulation More

In Term babies - Peaks on day 3 and normal in 7 days (Peak upto 12 mg/dl)

In Pre-term babies - Peaks on Day 5 , normal in 14 days (Peak upto 15mg/dl)

i.e >15mg/dl is Pathological { Palms and Soles - Yellow (see Kramer zones above) }

Pathological Jaundice

1. Jaundice on Day 1

2. If

Mother Rh - , Child Rh +
Cord Blood Hb <10 g %
Corl Blood Bilirubin > 5 mg %
Direct Coomb's +ve

This is an Indication for Exchange transfusion.

3. if Bilirubin increase rate > 0.5 mg/dl/hr

4. If Jaundice persists

>7days in term
>14days in preterm

5. Jaundice which require therapy.

Most important cause - Rh incompatibility.

Other causes:

Minor blood group incompatibility
ABO incompatibility
Spherocytosis , Elliptocytosis
RBC enzyme deficiency - G6PD def , Pyruvate Kinase def.

T/t -

Phototherapy
Exchange transfusion

Phototherapy ( 425 - 475 nm ) - Blue White Light

Water insoluble bilirubin ------> Water Soluble -----> Excreted

Mechanism:

Structural Isomerization (Bilirubin to Lumirubin) (Irreversible)
Photoisomerization
Photo-Oxidation

Child 40 cm away from tube.
4 - 6 mg/day fall of bilirubin.

Side effects :

Fever , dehydration ( therefore do frequent feeding or increase IV fluids by 20%)
Retinal Damage (so cover eyes)
Mutations in Gonads (so cover gonads too)
Hypocalcemia
Diarrhoea (watery) - because of bile pigments in gut.
Contraindicated in Conjugated Jaundice (Hepatitis) - else Bronze baby syndrome.

Persistence / Exaggeration of Physiological Jaundice :

Congenital Hypothyroidism
IVH , Cephalhematoma
Battered baby syndrome
Crigler Najjar Type II / partial deficiency of UDP-GT (Needs life long phototherapy)
Breast Milk Jaundice

Note : In Crigler Najjar Type I - UDP - GT is absent - so all have kernicterus and die.

0 Necrotizing enterocolitis (NEC)

Necrotizing enterocolitis (NEC)

Necrosis of immature gut.

Risk factors :

Prematurity
Ischemia to intestinal mucosa because of RDS/HIE/Hypothermia
Artificial feed
Maternal Cocaine

Clinical Features :

of Sepsis
Abdominal distention
Blood in stools

BELL'S Staging :

I - Suspected NEC -

Abdominal distention
Paralytic Ileus
Occult blood in stool

II - Definite

IIa - Gross blood in stools , Hyponatremia , Metabolic acidosis , Thrombocytopenia.
IIb - Pneumatosis Intestinalis (Air in Gut wall)

III - Advanced - Air perforated gut - Shock , Pneumoperitoneum.

Prevention:
Trophic feeds -
Minimal breast milk through NGT (nasogastric tube) {20-30 ml / kg / day}

It is for local effect on gut
Not for nutrition - for nutrition give IV fluids

Treatment :

Stop all oral feeds
Put on TPN (Total parenteral nutrition)
Ceftriaxone
Metronidazole
Stage III - May require Surgery -Resection

Probiotics : Commensals - Prevent NEC ( Not for Treatment )

Lactobacillus acidophilus
Bifidobacterium infantis

to Very Low birth weight infant.

Also always Think of NEC in infant when :

Gas under diaphragm
Newborn with Right hypochondrial air in portal tract

0 Medical One Liners 101 - 110

101. Maple syrup urine disease (MSUD) is caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex , leading to a buildup of the branched-chain amino acids (leucine, isoleucine, and valine)

102. The SMA lies to the left of the SMV as it crosses over the third portion of the duodenum. ( Clinical Importance : to check malrotation )

103. Meta-analysis is best for Probiotics' Trial.

104. Vertical crest in fundus of internal auditory canal is - Bill's Bar.

105. Sphincter of oddi has 3 sphincters.

106. Sheath surrounding the neurovascular bundle in axilla is derived from - Prevertebral fascia.

107. 1st part of duodenum has duodenal cap/bulb.

108. Spleen projects into Greater sac.

109. Axillary abscess is drained safely through Floor.

110. The primary direct stimulus for excitation of central chemoreceptors - H+ increase.

0 X linked Dominant disorders

X linked Dominant disorders

Rett Syndrome (Only seen in female - as it is lethal in males)

Urea cycle disorder (OTC deficiency )

Familial hypophosphatemic Rickets

Incontinentia Pigmenti

Alport Syndrome (can be AR and AD also but MC it is X-D)

0 Chromosome 22

CHROMOSOME 22 :

Meningioma

Neurofibromatosis 2 ( merlin )

Acoustic Neuroma

Di George syndrome

Velocardiofacial syndrome

Note:

NF1 - Chromosome 17

NF2 - Chromosome 22

0 Chromosome 21

CHROMOSOME 21 :

Down syndrome (Trisomy)

Amyloidosis

Reduced folate carrier ( SLC19A1 ) ( Folate Transporter )

Homocystinuria

Note :

Folate Receptor genes (FOLR 1 adult , FOLR 2 fetal , FOLR 3 ) are mapped on Chromosome 11

Reduced folate carrier (SLC19A1) (Folate Transporter) - Chromosome 21.

0 Chromosome 20

CHROMOSOME 20 :

Severe combined immunodeficiencydisease (SCID) - (characterized by a deficiency of the enzyme adenosine deaminase )

Type 1 MODY

Note:

SCID - Most common form is X-Linked recessive (so k/a - X linked SCID )
Type 2 MODY - Chromosome 7

0 Chromosome 19

CHROMOSOME 19 :

Myotonia dystrophica

Insulin receptor gene

NPHS 1 (Nephrin) - Congenital FINNISH type of Nephrotic Syndrome (AR)

Note :

NPHS 1 - Chromosome 19

NPHS 2 - Chromosome 1

Human Insulin gene - Chromosome 11
Insulin Receptor gene - Chromosome 19

0 Chromosome 18

CHROMOSOME 18 :

Edwards syndrome ( Trisomy )( MC syndrome linked to Chromosome 18)

de Grouchy Syndrome (distal 18p - ) (2nd MC)

Pitt-Hopkins syndrome

Bipolar disorder

0 Chromosome 17

CHROMOSOME 17 :

p53 gene

Neurofibromatosis 1 (neurofibromin gene - NF1 )

Medulloblastoma

BRCA 1

Canavan disease

Small Patella Syndrome.

Note :

BRCA 1 - Chromosome 17

BRCA 2 - Chromosome 13

NF1 - Chromosome 17

NF2 - Chromosome 22

0 Bilateral Choanal Atresia

Bilateral Choanal Atresia

{ Newborns are mouth breathers till 4 months. }

Therefore Pink when Cries , Blue when feeding.
To operate - 1st Do CT scan

if Unilateral - Asymptomatic.

0 Transient tachypnea of the newborn ( TTNB )

Transient tachypnea of the newborn ( TTNB )

Wet Lungs - full of fluid.
Resolves in 48-72 hrs

Risk Factors :

LSCS - as the lungs are not squeezed.
Precipitous labor.
Delayed cord clamping.
Macrosomia.
Excessive milking of cord.
Maternal sedation.

Clinical Features :

Tachypnoea - resolves in 48-72 hrs.

X-Ray : Prominent horizontal fissure (Most specific and earliest sign)

0 Meconium Aspiration Syndrome (MAS)

Meconium Aspiration Syndrome (MAS)

- > MC in post term babies , Rare in Preterms.

- > Because of Perinatal hypoxia

Glottis open
Peristalsis Stimulated
Anal Sphincter relax - thus pass Meconium (and as glottis is open - so aspiration)

Meconium effects :

1. Physically -

Block bronchus - thereore cause collapse
Ball Valve mechanism - Air leaks - Pneumothorax , Pneumomediastinum.

2. Chemically - irritant

3. Biologically - Good culture medium - therefore risk of sepsis.

Prevention : By Obstetric care

Previously Management (if Meconium stain) - IntraPartum Suction (as head is born) - 1st Mouth , then Nose. {Not done now}

Now Management :

Do TABC ( Thermoneutral environment and ensure Airway, Breathing and Circulation )
Check if Vigorous or Not : if Not - then Do ET suction.

Vigorous baby :

1. Respiratory effort - Good - cry

2. Muscle tone - Good

3. Heart rate > 100 bpm

0 Retinopathy of prematurity (ROP)

Retinopathy of prematurity (ROP), previously known as retrolental fibroplasia (RLF)

If 100% O2 given to Preterm.
Proliferation dilatation and tortuous vessels in Vitreous.
100% babies are blind.

Severe ROP - tractional retinal detachment.

Stages:
I - Hypoxic demarcation line
II - Ridge formation
III - Neovascularization
IV - SubTotal Retinal detachment
V - Total RD

In a preterm - protocol to follow -

Look for peripheral retina (Indirect ophthalmoscopy at regular intervals) - Do Cryosurgery if Vascular proliferation.
1st Ophthalmoscopy at 32-34 wks or 4-6wks after birth (preterm baby) , whichever is early.
Then at every 2wks , till Retina looks like that of term baby.

ROP + (ROP PLUS ) : Posterior retinal vessels are also involved.

Treatment : Cryotherapy , Laser Photocoagulation , Vit. E therapy.
Severe - may require Retinal Reattachment Surgery.

Risk is HIGH with LBW and ELBW ( <1kg birth weight -> 60-70% have ROP)

0 Total anomalous pulmonary venous connection (TAPVC)

Total anomalous pulmonary venous connection (TAPVC), is a rare cyanotic congenital heart defect (CHD) in which all four pulmonary veins are malpositioned and make anomalous connections to the systemic venous circulation.
Types :

1. SupraCardiac

Most Common
Pulm. Veins join Superior Vena Cava

2. Cardiac

Pulm. Veins join Coronary sinus

3. InfraCardiac

Pulm. Veins join Portal Vein
Most severe - because of Obstructive pulmonary venous hypertension.
Newborn with cyanosis.

All patients have ASD - Very important.
Without ASD there will be pulmonary circuit with no blood for systemic circuit.

MCQ point : O2 Saturation in Pulmonary artery is more than Aorta.

X-Ray features:
1. SupraCardiac - Snowman Shaped Heart
2. InfraCardiac - Ground Glass appearance with Kerly B lines.

0 Neonatal Pulmonary Alveolar Proteinosis

Neonatal Pulmonary Alveolar Proteinosis

Autosomal Recessive

Mutation in gene which coats for Protein B or C or GM-CSF (granulocyte macrophage colony stimulating factor).

No response to Surfactant.

All will die or Do Lung Transplant.

0 Hyaline Membrane Disease - HMD

Hyaline Membrane Disease - HMD

Exclusively in Preterm (Never in IUGR baby - as they are in stress so release steroids)
> 30% Neonatal Mortality
Preterm with respiratory distress.

Normally : Type 2 Pneumocytes produce Pulmonary Surfactant in Alveoli - reduces the surface tension and prevents it from collapsing during expiration.

Surfactant Components :

Phosphatidyl Choline
Phosphatidyl Glycerol
Phosphatidyl ethanolamine
Phosphatidyl inositol
Protein A,B,C,D

Term Baby with HMD - if Infant of diabetic mother.

Prenatal Diagnosis : L/S ratio in Amniotic fluid. ( Lecithin / Sphingomyelin )
Normally - L/S >2
but in an Infant of Diabetic Mother , Good L/S is > 3.5

Management Prenatal - IM Betamethasone to mother.
Not Dexa - Because it increases risk of PVL (Periventricular Leuckomalacia)

Benefit occurs only after 24hrs to 7days

PostNatal Diagnosis :

1. Shake Test -
Amniotic fluid or gastric aspirate + Alcohol (equal amount) , shaken for 20 sec.
Then kept in stand for 20 min

Term : Layer of bubbles at top of test tube.
Preterm : Bubbles Absent

2. X-Ray - Ground Glass Appearance / White out lungs.

Baby <28wks - 60 - 80% have HMD

Treatment -
1. CPAP - Nasal/PEEP - to keep alveoli distended.
2. Definitive treatment - Surfactant - Prophylactic to preterm , Therapeutic /Rescue

Route : IntraTracheal
Most commonly used - Survanta (Bovine)
Others - Curosurf (Porcine) , Infasurf ( Calf )

0 Respiratory Distress in Newborn

Respiratory Distress in Newborn

1. Tachypnoea - >60

2. Respiratory distress - Tachypnoea + Increase work of breathing
- Dilation of Ala Nasi
- Intercostal & Subcostal retractions
- Grunting

Causes

1. Preterm : HMD (=RDS) - Most Common in preterm

2. Term :

TTNB (Transient tachypnoea of newborn)
MAS (Meconium aspiration syndrome)

3. Congenital : Diaphragmatic Hernia , Tracheo-oesophageal fistula

Diaphragmatic hernia - (Surgical Emergency)

Scaphoid Abdomen
Barrel shaped chest
Mediastinal shift to right (in Bochdalek)
Apparent Dextrocardia (in Bochdalek)
Peristaltic sounds on left side (in Bochdalek)

Develops from ( for a related MCQ - Click here )
a. Septum transversum
b. Pleuroperitoneal Membrane
c. Dorsal Oesophageal mesentry
d. Body wall
e. Cervical Myotome

Types : Read More

Bochdalek (90% cases) - Left Posterior ( Mnemonic : BPL )
Morgagni - Right Anterior ( Mnemonic : ARM)

There is Pulmonary hypoplasia due to this and it causes distress.

Bag and Mask ventilation is Contraindicated in diaph. hernia.
Because some air goes to stomach and distends it - thus press diaph. even more.

So Intubate.

Tracheo-oesophageal Fistula : Not Emergency

MC - Upper end blind and lower end communicate with trachea.
Sign - Nasogastric tube coils in upper end of oesophagus.

Dribbling saliva from mouth
Aspiration of gastric juice (Aspiration Pneumonia - This is Emergency)

Do Continuous Suction and prop the child up.

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The Online medical study zone.

Making medical study easy.

0 Neonatal Sepsis

Neonatal Sepsis :

Clinical features of Sepsis and bacteremia.

Lethargic
Feeding difficulty
Seizures

Early ( <72hrs )	Late ( >72 hrs )
Pneumonia more common	Septecemia , Meningitis is common , Pneumonia. Therefore LP is done
Maternal Risk factors Maternal fever <2wks Maternal foul smelling liquor Premature rupture of membrane Maternal Pain abdomen Chorioamnitis Multiple Vaginal examinations in mother	Nosocomial
Organisms : E.Coli , Group B Sterptococcus	Klebsiella , Listeria , E.Coli
Treatment : Ampicillin + Gentamycin	3^rd Generation cephalosporins Cefotaxime + Amikacin

Overall MC organism - Klebsiella
2nd MC - Staphylococcus Aureus

Sepsis Screen for early diagnosis :
1. TLC : < 5000 /cumm (More Suggestive)
> 5000 /cumm

2. Absolute Neutrophil count : <1500 / cumm

3. Peripheral Smear for band cells (immature neutrophil) & toxic granules : >20% of total neutrophils

Thus I / T : >0.2 (Immature / Total Neutrophil )

4. Micro ESR : >15 mm fall in 1st hour

5. CRP : +ve

6. LP : in Late onset sepsis

7. CxR

Antibiotics Course duration
Bacteremia : 10-14 days
Meningitis : 3wks
Arthritis ; Osteomyelitis : 4-6wks

0 Hypothermia in Newborn

Hypothermia in Newborn :

Grading based on Core Temperature (i.e temperature of Middle ear or Oesophagus)
Normal Core body temp. - 36.5 - 37.5 degree C
Rectal Temperature is close to it.

36 - 36.5 -- Cold Stress (Abdomen warm , Soles Cold ) -- Do Kangaroo Mother Tech.
32 - 36 ---- Moderate Hypothermia
< 32 ------- Severe Hypothermia

In Hypothermia < 36 - Admit NICU

Normal Baby - Abdomen Warm , Sole Warm and Pink.

All Newborns have NON-Shivering Thermogenesis -- Brown fat

Brown Fat - ( Fatty Acid Oxidation - Generate heat - distributed by Blood Vessels)

Nape of Neck
InterScapular area
Around Kidneys and adrenals

Q. Mechanism of Heat transfer in Over head Radiant Warmer ?

ANSWER:

0 Normal Neonatal Phenomenons

Normal Neonatal Phenomenons

1. Milia - (distended sebaceous glands) white spots on face , nose

2. Erythema Toxicum - (day 2 - 3 life ) erythematous macules on face and trunk

3. Stork Bites - (Capillary Hemangiomas) Pinkish greyish

4. Epstein pearl - (epithelial inclusion cyst) - Palat and perpuce , white spots

5. Natal teeth - (predeciduous teeth - lower incisor position)

if interfere in feeding - remove them
are loose therefore risk of aspiration

6. Withdrawal vaginal bleed - (on 5 - 7 day) Because of withdrawal of maternal hormones.

7. All newborns loose weight

Term - can loose 10% Birth weight and regain BW by 7-10 days
PreTerm - can loose 15% , take 2wks to regain

No Phase of Weight Loss in IUGR babies.

0 Neonatal Reflexes

1. Moro Reflex

(A response to a sudden loss of support, when the infant feels as if it is falling.)

Appears - 28 - 32 wks
Fully developed - 37 wks
Disappear at around 3 months
Abnormal If persists >6months

1st Phase
Abduction at shoulder , Extension at elbow , Opening of fingers

2nd Phase (37 wks)
Adduction at shoulder , Flexion at elbow

Prolonged in Cerebral Palsy

Exaggerated in Birth asphyxia

Asymmetric in-
a. # humerus , clavicles
b. Erb's Palsy
c. Spastic hemiplegia

2. Grasp Reflex
Followed by Shoulder traction

Onset - 28 wks
Fully developed - 32 wks
Disappear at 12wks(3months) of age.

3. Sucking and Rooting reflex

Appear at 32wks
Co-ordinated at 34 wks

Therefore child >34 wks or >1.8 Kg Birth weight can breastfeed.

<32 wks -> Nasogastric expressed breast milk
32 - 34 wks -> Catori , spoon , Paladay

4. Asymmetric Tonic Neck Reflex (ATNR)

Occiput side - flexed
Side facing - extended

Appears - 35 wks
Fully developed - 1 month life

Stays for 6-7 months

Thus rolling of child - approx. 6 months (when ATNR disappears)

5. Symmetrical TNR

If extend head of a newborn -
Tone increases in UL and decreases in LL

If Flex head of newborn
Tone decrease in all 4 limbs

It is the Most difficult Neonatal reflex to elicit

Disappears at 6-7 months

0 Apnea at birth

Apnea at birth :

Causes : MC cause in Preterm is MIXED

Central	Obstructive
Preterm babies	(Normally - All Newborns are Nose breathers till 4 months.)
Asphyxia	Secretions in Nose
Sepsis	Preterm
Hypoglycemia

Apnea of Prematurity (rare cause of Apnea) :

<28 wks --> 100% have apnea
28-34 wks --> 25%

Onset - Usually 1st 2 days of life (Never after 1st week of life)

T/t -

CPAP
MethylXanthines (Theophyline , Aminophyline)
Caffeine Citrate (DOC for Apnea of Prematurity)

Aminophyline :
Used in

Status asthamaticus
Apnea of Prematurity

Loading Dose : 5 - 6 mg/kg
Maintenance dose : 1-2 mg/kg (every 6-8 hrs)

0 Contraindications of Indomethacin

Q. Contraindications of Indomethacin include all except ?

a. Large IVH
b. Renal Failure
c. Hepatic Failure
d. NEC

ANSWER:

0 Complications of Preterm

Complications of Preterm

1. HMD (Hyaline membrane disease) = RDS Respiratory Distress syndrome (>30% of neonatal mortality)

2. Apnea ( >20sec , or Any period if associated with central cyanosis and bradycardia )

3. Chronic lung disease (= Bronchopulmonary dysplasia) - Oxygen dependence even after >4wks life - Therefore give Home O2 Therapy.

4. CNS Depression (Birth asphyxia) , IVH (Intraventricular haemorrhage) , PVL (Periventricular Leucomalacia)

IVH - because capillaries in germinal matrix are fragile

Sudden death ,
Sudden shock ,
Bulging out Anterior fontanale (Therefore do Transfontanale USG)
Seizure

(Note : Term babies IVH - because of breech presentation.)

Birth Asphyxia

In Preterm - PVL --> Commando Crawling (UL strong , LL weak) -- Spastic Diplegia --> Cerebral Palsy

In Term - Parasagital --> Prolonged asphyxia --> Diffuse neuronal loss --> Status Marmoratus --> When child grows -- Spastic Quadriplegia --> Cerebral palsy

Cerebral Palsy Complications :

Global developmental delay
Microcephaly & Mental Retardation
Seizures
Feeding difficulties

5. CVS - Hypotension , PDA ( because of prostaglandins due to asphyxia ) (Treatment of PDA here - NSAIDS - Brufen , Indomethacin )

Brufen is preferred over Indomethacin because of less renal side effects , i.e both decrease GFR but its less with brufen.

In Term

6. Blood - Anaemia , Jaundice of Prematurity

7. Hypothermia , Hypoglycemia , Hypocalcemia

8. Gut - NEC

9. Infections (because of decreased immunity)

10. ROP (Retinopathy of prematurity = Retrolental fibroplasia - if 100% oxygen given) - Proliferated, dilated and tortuous vessels in Vitreous.

0 IUGR Types

Intra Uterine Growth Retardation Types :

Symmetrical MC in west	Asymmetrical MC in India
Cause : Chromosome Abnormality	Maternal Complication
Decreased Cell Number Cell size decreased/normal Brain size decreased	Cell number Normal Cell size decreased Head size normal (Head Sparing = Brain sparing) Therefore HC > CC by >3cm
Ponderal Index (PI) = { Weight (g) / Length³ (cm) } x 100 Here PI > 2 (also in Normal babies)	PI < 2