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FACULTY OF CLINICAL MEDICINE AND SURGERY

Unit 1: Topic 1 Introduction to Paediatrics and Child Health 1

—UNIT 1 LESSON 1
Learning outcomes

  1. —By the end of this lesson, the learner should be able to:
  2. —Define Paediatrics and child health  terminologies
  3. —Explain concepts and principles in Paediatrics and Child health
  4. —Take a comprehensive paediatric history
  5. Pediatrics is a •Is a medical speciality that is concerned with the health of infants, children, and adolescents;
    •their growth and development; &
    •their opportunity to achieve full potential as adults.

—

Neonatology:
 is a medical specialty of care of newborn babies, sick babies and premature babies
Neo-new   natal—birth
ology---science of

Preterm:- baby born before 37 weeks gestation
A preterm can be an
(AGA)- appropriate for gestational age
 small for gestational age(SGA)
or LGA –Large for gestational age

Very low birth weight (VLBW) –Is a baby weighing 1.5kgs 0r less
Extremely low birth weight– is a baby weighing 1kg or less
Incredibly low birth weight-- 750g or less.
LGA=Birth wt > 90th centile for gestational age.
SGA– Birth wt < 10th centile for gestational age

Infant mortality rate:- number of deaths in the 1st 12months per a 1000 live births
Neonatal mortality rate:-no. of deaths in the 1st 28 days per a thousand live births
Perinatal mortality rate:- still births and neonatal deaths up to 7 days per 1000 total births

Perinatal mortality =includes all stillbirths &neonatal deaths in the 1st wk of life. It is any death or abortion > 500g or death at 24 wks and more
still birth – a baby born after 24 weeks gestation of pregnancy and does not show at any time signs of life (cardiopulmonary activity
Neonatal mortality accounts for 50% of infant mortality in developing countries

A normal newborn
is a baby born between 37—41wks
weighs 2.5kgs—4kgs
head circumference 33—37cm
APGAR score 7—10
length 50cm, no abnormalities & does not require resuscitation at birth

UNIT 1: Topic 2 Paediatric History

Topic two:

Topic name

PAEDIATRIC HISTORY

  Introduction

  1. —  History taking is the corner stone of clinical practice
  2. —  One needs to have the ability to distill the important information from history
  3. —  This builds up clinical skills, attitude towards patients knowledge about diseases and disorders
  4. —  Parents are acutely interested in and anxious about their children
  5. —  Parents usually can recognize clinicians who are empathic, demonstrate interest and concern
  6. —  Parents seek out clinicians who possess appropriate skills and attitudes towards their children

Child age is always a key feature, it determines

The nature and presentation of illness, development or behavioral problems

The way in which the history taking and examination are conducted

The way in which any subsequent management is organized

—  Never ignore parents, these are astute observers of their children

—  Make sure you have read any referral letter and scanned the notes before start of the interview

—  Welcome child and parents and address them by name

—  Introduce yourself

—  Determine relationship of adult to child

—  Establish eye contact and rapport with the family. Infants and toddlers are most secure in a parents arms or lap.

—  Young children may need some time to know you, don’t rush them

—  Ensure that the interview room is as welcoming and unthreatening as possible

—  Have toys available. Observe how the child separates, plays and interacts with other sibling available

—  Do not forget to address questions to the child when appropriate

—  Some occasions the parents would not like to be with the child or when the child should be seen alone

—  This is to avoid any embarrassment to the child e.g. teenage children

—  It is important to note that

—  Pediatrics is a specialty governed by age, the illnesses and the problems children encounter are highly age dependent.  The child’s age will determine the questions to be asked on history taking, how to conduct the examination, the diagnosis and ddx and the management plan

—  Start with the patients identification data: name, age, occupation/ level of education residence, address, next of kin, inpatient number, ward, date of admission

—  Complains and duration (what brought the patient to hospital

History of presenting illness. History must be adapted to the age e.g. the age when a

—  Make sure you have read any referral letter and scanned the notes before start of the interview

—  Welcome child and parents and address them by name

—  Introduce yourself

—  Determine relationship of adult to child

—  Establish eye contact and rapport with the family. Infants and toddlers are most secure in a parents arms or lap.

—  Young children may need some time to know you, don’t rush them

—  Ensure that the interview room is as welcoming and unthreatening as possible

—  Have toys available. Observe how the child separates, plays and interacts with other sibling available

—  Do not forget to address questions to the child when appropriate

—  Some occasions the parents would not like to be with the child or when the child should be seen alone

—  This is to avoid any embarrassment to the child e.g. teenage children

—  It is important to note that

—  Pediatrics is a specialty governed by age, the illnesses and the problems children encounter are highly age dependent.  The child’s age will determine the questions to be asked on history taking, how to conduct the examination, the diagnosis and ddx and the management plan

—  Start with the patients identification data: name, age, occupation/ level of education residence, address, next of kin, inpatient number, ward, date of admission

—  Complains and duration (what brought the patient to hospital

—  History of presenting illness. History must be adapted to the age e.g. the age when a child first walks is relevant when taking history of a toddler but irrelevant to a teenager with headaches. Full details of presenting problems are required. Let the parent and child recount the presenting problems in their own words and at their own pace. Note the parents words verbatim about the presenting complaint. Ensure that you ask about:  

—  Onset of the complaints

—  Duration and previous episodes

—  What relieves/aggravates symptoms

—  What is the time course of the problem

—  Is the problem getting worse and are there any associated symptoms

—  Has the child’s or family lifestyle been affected? If so what has the family done

—  Find out: What prompted referral to a doctor

—  What is the fear that the parents have, this is an important factor

 

Past medical and surgical history

—  What past illnesses has the child suffered from

—  Any hospitalizations and operations (what was the reason, what age, what was the nature and were there any complications)

—  Are there any allergies

—  Are there any bleeding tendencies

—  Any history of accidents and injuries

—  Any past and present medications

 

Antenatal history

—  How was the health of the mother during the pregnancy of this child

—  Any relevant genetic history of parents

—  Any history of infection during pregnancy

—  Any abnormality detected in antenatal u/s

—  History of amniocentesis

—  Antenatal profile and results (HIV, VDRL, Urinalysis, BS for MPS, HB), ITN, SP, Folate, ferrous sulphate

—  Any immunization e.g. TT

 

Natal history

—  What was the kind of labour

—  Type of delivery

—  Birth weight

—  Duration of labour

—  How was first cry

—  State of infant at birth

—  Neonatal: APGAR score, color, respiratory distress, excessive salivation, abdominal distension, meconium passed or not.

 

Nutrition history

—  Exclusive breast feeding

—  Eating patterns

—  History of vomiting after feeds

—  Difficulty in swallowing

Developmental Milestones (key developmental milestones)

—  Neck support, sitting, standing, walking, speaking, schooling,

—  Urinary continence

—  Control of defeacation

—  Unusual growth

—  School grade

—  Current milestone and whether upto date

Immunization history

—  KEPI schedule

—  Comment on either up to date; fully immunized or defaulter

Personal Social economic History

—  Check

—  Relevant information about the family and the community-parental occupation, economic status, housing, refuse disposal, water treatment, relationships, parental smoking, marital stresses, habits and hobbies.

—  Is the child happy at home, Is the child happy at school

—  many childhood illnesses or conditions are permeated by adult problems e.g.

—  Alcohol and drug abuse

—  Long term unemployment/poverty

—  Poor, damp and crammed housing

—  Parental psychiatric disorders

—  Unstable partnership

Family history

—  Position of the patient in the family

—  Should include information about illnesses in the family e.g. parents, siblings and grandparents

—  Cause of death of close relatives (parents and siblings)

—  Presence of any serious illnesses in the family (chronic familial disease (diabetes, asthma heart disease, hypertension, sickle cell).

Systemic review

—  Selected as appropriate

—  Respiratory system – cough wheeze, breathing problems, throat infections, stridor (noisy breathing), snoring

—  CVS – oedema , cyanosis, exercise intolerance, orthopnoea, dyspnoea

—  GIT – vomitting, diarrhea/constipation, abdominal pain

—  GUT – dysuria, frequency, wetting, toilet trained

—  CNS – seizures, headaches, abnormal movements, paralysis

Examination

Approach

—  Obtain child’s cooperation

—  Make friends with the child, Be confident but gentle, Avoid dominating the child

—  Do short mock examinations e.g. on the mother or teddy bear – this may allay a young child’s fears, Start examination from non-threatening areas e.g. hand or knee

—  Explain to the child what you are about to do, what you want him/her to do, in a language they can understand.

—  A smiling talking doctor appears less threatening, but this should not be overdone as it can interfere with ones relationship with the parents

—  Leave unpleasant procedures until last

—  Babies in the first few months are best examined on the couch with the parent next to them

—  A toddler is best examined initially on the mother’s lap, or occasionally on the parents shoulder. Parents are reassuring to the child and can facilitate good examination if guided on what to do

 

—  Preschool children can in the beginning be examined as they play

—  Older teenagers are often concerned of their privacy. A teenage girl should be examined in the presence of their mother, nurse or chaperone. Be aware of cultural sensitivities from different ethnic groups

Undressing Children

—  Be sensitive on children’s modesty

—  It is easiest and kind to ask the parent to do the undressing

—  The area to be examined should be inspected fully, but done in stages, redressing the child when each stage has been completed

—  Warm clean hands:  hands must be washed before and after examining a child. Warm smile, warm hands and warm stethoscope all help

—  Requirements

A well-lit room, Chair, Examination coach, Stethoscope, Touch, Sterile gloves, Tongue depressant

 

General examination

Initial survey or Observations

—  Careful observation is key to success in examining children. Look before touching the child

Inspection will provide

—  Severity of illness, Growth and nutrition, Behaviour and social responsiveness, Level of hygiene

—  Is the child sick or well?

—  If sick, how sick. For the acutely ill infant or child, perform the 60 sec rapid assessment

Airway and breathing – respiration rate and effort, presence of stridor, wheeze, cyanosis etc

Circulation – heart rate, pulse volume, peripheral temperature, pallor

Disability – level of consciousness

—  general state of health

—  Dressing, grooming and personal hygiene

—  height, weight, build, motor activity, facial expression,

—  state of awareness or level of consciousness.

—  The general morphological appearance may suggest chromosomal or dysmorphic syndrome

—  In infants palpate the fontanelles and sutures

Check the skin, head, face, eyes, nose and

Check for clinical signs: Pallor, Jaundice, Cyanosis, Finger clubbing, Oedema, Dehydration, Lymphadenopathy

Systemic examination

Respiratory System Examination

—  Inspection

—  Nose: is there any discharge, abnormality of the nose, flaring of alae nasae

—  Mouth: cyanosis (central cyanosis)

—  Harrison sulcus (indrawing of lower ribs, Rachitic rosary (rickets), Barrel chest/ pigeon chest  (COAD), count the Respiratory rate, Chest movements .

—  Signs of respiratory distress (nasal flaring, subcostal and intercostal recession, head nodding cyanosis, grunting) noisy breathing wheeze. Tachypnea: rate of respiration is usually age related

—  Dyspnea: labored breathing. This is judged by nasal flaring, expiratory granting,  use of accessory muscles of respiration, retraction of the chest wall from use of suprasternal, intercostal, and subcostal muscles

Harrison sulcus (from diaphragmatic tug), this occurs from poorly controlled asthma

Asymmetry of chest movements

Respiratory Rates in Children

Age                  normal       Tarchypnea

Neonate          30-50               >60

Infant               20-30               >50

Young child     20-30               >50

Older child      15-20               >40

—  Difficulty in speaking or feeding

—  Chest shape, hyper-extension or barrel shape e.g. in asthma

—  Pectus excavatum (hollow chest) or pectus carinatum (pegion shaped)

Palpation – tracheal deviation, tenderness, swelling, chest expansion.

Percussion Note any localized dullness – dullness suggests lung collapse,  consolidation or fluid

Auscultation (use ears and stethoscope)Note the quality and symmetry of breath sounds and added soundsHarsh breath sounds from the upper airway are transmitted to the upper chest in infants

·         Note hoarse void – refers to abnormality of the vocal cords Auscultation  --normal vesicular sounds, bronchial breathing, ronchi, crepitations, air entry)

·         Stridor – is a harsh, low pitched, mainly inspiratory sound from upper airways obstruction

·         Note the breath sounds – normal breath sounds are vesicular,

·         Bronchial breathing is high pitched and the lengths of inspiration and expiration are equal

·         Wheeze is high pitched, expiratory sound from distal airway obstruction

·         Crackles – discontinuous moist sounds from the opening of bronchial

·         Chest abnormalities in children

·         Bronchiolitis – labored breathing,  hyperinflated chest, chest reccession, hyper-resonant, fine crackles in all zones, wheeze may or may not be present

·         Pneumonia – reduced breath sounds on the affected side on chest movement, rapid, shallow breaths, bronchial breathing on auscultation, crackles

 

Cardiovascular system

—  Use the inverted J

Hand- pallor, cyanosis, oslers nodes, finger clubbing, splinter haemorhages, janeways lesions, Radial pulse, (Pulse- check for the rate, rhythm – sinus arrhythmia (variation of pulse rate with respiration) is normal. Check volume of pulse – is feeble in circulatory failure/insufficiency or aortic stenosis. It is increased in high output states e.g. stress, anemia. It is collapsing in patent ductus arteriosus

—   Blood pressure , Jugular Venous Pressure

Palpate the precordium- apex beat (4th ics) thrills, heaves

—  Auscultation –  S1, S2, aortic area, pulmonary area, mitral area, tricuspid area. Heart rate and rhythm,  Added Heart sounds, Murmurs, Additional sounds – pericardial rub

Murmurs check for

—  Site, Timing, Intensity, Character /pitch, Radiation, Relation to respiration, posture and exercises

—  Fixed splitting of second heart sound is heard in atrial septal defect

—  Third heart sound in mitral area is normal in young children

—  Murmurs – when you ausculate a murmur, check for

—  Timing – is it systolic, diastolic or continuous

—  What is the duration – mid systolic (ejection), pansystolic

—  How loud is it – systolic murmurs are graded as:

—           Grade 1 – 2: soft, difficult to hear

—            Grade 3: audible, no thrill

—             Grade 4-6: loud with thrill

—  Check for the area of maximum intensity – mitral, pulmonary, aortic or tricuspid area

—  Check where the murmur radiates to – to neck (aortic stenosis), to the back (coarctation of the aorta or pulmonary stenosis)

—  Hepatomegally -- It’s a sign of heart failure in infants. An infants liver is palpable 1-2cm below the costal margin.

—  Femoral pulses - In coarctation of the aorta, there will be decreased volume or may be impalpable in infants, there will be brachiafemoral delay in older children

—  NB: heart diseases are common in children with other congenital abnormalities or syndromes e.g. downs syndrome or turners syndrome

—  Femoral pulses

—  In coarctation of the aorta, there will be decreased volume or may be impalpable in infants, there will be brachiafemoral delay in older children

—  NB: heart diseases are common in children with other congenital abnormalities or syndromes e.g. downs syndrome or turners syndrome

—  Normal resting pulse rate in children

—  Age                                                        beats/min

—  <1 year                                                 110-160

—  2-5 years                                              95-140

—  5-12 years                                           80-120

—  <12 years                                             60-100

—  Pulse rate increases in children when there is stress, fever, arrhythmia, exercise

—  Features suggesting a murmur is significant

—  It is conducted all over the precordium

—  Is loud

—  There is a thrill (grade 4-6)

—  Any diastolic murmur

—  Is accompanied by other cardiac signs

—  Features of heart failure in infants

—  Poor feeding, failure to thrive

—  Sweating

—   

Features of heart failure in infants..

—  Tarchypnoea

—  Tarchycardia

—  Gallop rhythm

—  Cardiomegally

—  Hepatomegally

 

 

Practical quiz:

 Explain the difference on auscultation of the following abnormal respiratory Conditions

1.       Consolidation

2.       Lung Collapse (atelectasis)

3.       Pleural effusion

4.       Pneumothorax

 

 

 

Per abdominal examination

—  This is performed in 3 major clinical setting

◦      During routine examination

◦      When there is an acute abdomen

◦      When there is abdominal distension or mass

—  Associated signs in abdominal examinations

◦      Examine eyes for jaundice

◦      Examine tongue for coating and color

◦      Examine fingers for finger clubbing

 

Inspection

—  Abdomen is protuberant in normal toddlers and young children

—  Generalized abdominal distension is explained by the five f’s

◦      Fat

◦      Fluid (ascites – uncommon in children, commonly nephrotic syndrome)

◦      Faeces (constipation)

◦      Flatus (malabsorption, intestinal obstruction)

◦      Fetus (remember this when female child is in puberty)

 

Occasionally abdominal distension is caused by a grossly enlarged liver and or spleen or muscle hypotonia)

Causes of localized abdominal distension are

·         Upper abdomen: gastric dilatation from pyloric stenosis, hepatosplenomegaly

·         Lower abdomen: distended bladder or masses

·         Other signs to be inspected are dilated veins and abdominal striae

—  Inspect for operative scars

—  Inspect for peristalsis – from pyloric stenosis, intestinal obstruction

—  Inspect buttocks if well rounded or wasted as in malabsorption as in coeliac disease or malnutrition

Palpation

—  Use warm hands, explain, relax the child and keep the parent close at hand. Ask if it hurts

—  Palpate in systematic fashion – liver, spleen, kidneys, bladder through the four abdominal quadrants

 

—  Ask about any tenderness. Watch the child’s face for any grimacing as you palpate

—  NB: a young child may be cooperative if you first start palpating with his hand or putting your hand on top of his

Tenderness

—  Is localized in appendicitis, hepatitis, pyelonephritis, generalized mesenteric adenitis, peritonitis

—  Guarding: often not impressive on direct palpation in children. However pain on coughing, on moving about, on walking, bumps during a car journey suggests peritoneal irritation.

—  Back bent on walking maybe be from psoas inflammation in appendicitis

—  Hepatomegally

—  Palpate from right illiac fossa

—  Locate edge with tips or side of finger

—  Edge maybe soft or firm

—  One is unable to get above it

Hepatomegally…

—  Moves with respiration

—  Measure (in cm) extension below costal margin in mid clavicular line. Liver tenderness is likely to be inflammation from hepatitis

Spleenomegally

—  Palpate from left illiac fossa

—  Edge is usually soft

—  Unable to get above it

—  Spleenomegally..

—  It moves with respiration

—  Measure size below costal margin (in cm) in mid clavicular line

—  If uncertain whether it palpable or not

—  Use bimanual approach

—  Turn child onto right side

—  A palpable spleen is at least twice its normal size

—  A hyperextended chest in bronchiolitis or asthma may displace liver and spleen downwards mimicking hepatosplenomegaly

Causes of Spleenomegally

—  Congenital Infections, Infectious mononucleosis

—  Hepatitis, Malaria, Parasitic infections, Haematological, -Sickle cell anemia, Thallasemia

Causes of Hepatomegally

—  Liver disease, Chronic active hepatitis, Portal hypertension, Polycystic disease, Malignancy-  Leukemia Lymphoma, Neuroblastoma, Wilms tumor, Hepatocellular carcinoma

—  Metabolic - Glycogen and lipid storage disorders, Mucopolysaccharidosis

—  Cardiovascular- Heart failure

 

Kidneys

—  Not usually palpable beyond neonatal period unless enlarged or the abdominal muscles are hypotonic

—  On exam

◦      Palapate by balloting bimanually

◦      They move on respiration

◦      One can get above them

—  Tenderness implies inflammation

Abdominal masses – these could be:

—  Wilms tumor – these are renal masses, sometimes are visible and does not cross the midline

—  Neuroblastoma – these are irregular firm masses, may cross the midline, the child is usually very unwell

—  Faecal mass – these are mobile, non tender, indentable

—  Intussusception – child becomes acutely unwell, mass may be palpable and most often in the right quandrant.

Percussion

—  Liver – dullness delineate upper and lower border, record the span

—  Spleen – dullness delineate the lower border

—  Ascites – shifting dullness. Percus from most resonant spot to most dull point

Auscultation

—  Not very useful in routine examination, but important in acute abdomen

Auscultation..

—  Increased bowel sounds – intestinal obstruction, acute diarrhea

—  Reduced or absent bowel sounds – paralytic ileus, peritonitis

 

 

 

 

 

Genital examination

—  Check for inguinal hernia or perineal rash

—  In males check for:

◦      The size of the penis

◦      Development of scrotum

◦      Are the testes palpable? Place one hand on the inguinal area, palpate with the other hand. Record if the testes is descended, retractile or impalpable

In males…

◦      Is there any scrotal swelling (it could either be hernia or hydrocele)

In females:

—  Examine the external genitalia, comment whether it looks normal. Does the anus look normal? Any evidence of fissure?

 

 

 

Rectal examination

—  This is not part of routine exam

—  It is unpleasant and disliked by children

—  It’s usefulness in acute abdomen (e.g. appendicitis) is debatable in children as they have a thin abdominal wall and so tenderness and masses can be identified on palpation of the abdomen

—  If intussusception is suspected, the mass maybe palpable and stools looking like redcurrent jam maybe revealed on rectal exam

 

CNS - Neurological screen

—  Conduct a quick neurological and development overview

—  Avoid unnecessary examination

—  Adapt it to the child’s age

—  Take into account the parents account of the developmental milestones

—  Watch child draw or write, assess manipulative skills, language, speech, social interactions as appropriate, vision and hearing (are they normal)

In infants

—  Assess first by observation…what does one assess?

◦      Posture and movement of limbs

◦      When picking child note the muscle tone. The body or limbs may feel normal or floppy or stiff. Head control maybe poor, with abnormal head lag on pulling to sitting

—  NB: Most children are neurologically intact and do not require formal neurological examination of reflexes, tone etc.

—  Detailed neurological exam is performed only if indicated

Detailed Neurological Exam

  1. Patterns of movement

—  Observe walking or running

Normal walking heel – toe: a toe – heal walking suggests pyramidal tracts (cortico-spinal) dysfunction particularly hemiplagia or diplagia

A foot drop – suggests superficial peroneal nerve lesion

A tight tendo achilles as in muscular disorder

A broad based gait – immature gait or secondary to cerebellar disorder

Patterns of Movement…

Standing from lying down supine – observe children from 36 months of age will turn prone in order to stand because of poor pelvic muscle fixation. But if beyond this age it suggests neuromuscular weakness (duchennes muscular dystrophy)

2. Coordination

—  Assess this by

Asking child to build one brick upon another

 

Coordination…

Ask child to stretch his arms out straight, close their eyes and observe for tremors or drift

Finger nose testing (use teddy’s nose to reach out and touch if necessary)

Rapid alternating movements of hands and fingers

Touching tip of each finger in turn with thumb

Ask the child to walk heel-toe, jump and hop

 

Inspection of Limbs

—  Muscle bulk

—  Wasting maybe secondary to cerebral palsy, meningomyelocele, or a muscle disorder or from previous poliomyelitis

—  Increased bulk of calf muscles may indicate duchennes muscular dystrophy

4. Muscle Tone

—  Best assessed by taking the weight of a whole limb and then bending and extending it around a single joint

◦      Testing is easiest at the knee and ankle joints. Assess for the range of movement as well as the general feel of it

—  Increased tone at adductors and internal rotators of the hips, clonus at the ankles or increased tone on pronation of forearms at rest is due to pyramidal dysfunction

—  Scissors of legs in posture of limbs with pronated forearms result from increased tone

5.  Truncal Tone

—  In pyramidal tract disorders, the trunk and head tend to arch backwards (extensor posturing)

—  In muscle disease and some central brain disorders, trunk maybe hypotonic. Child feels floppy to handle and cannot support the trunk

—  Head lag: best tested by pulling the child up by the arms from a supine position

6. Power

—  Difficult to test in babies

—  Watch for anti-gravity movements and note motor function

—  From 6 months onwards; watch pattern of mobility and gait

—  From age 4 years, power can be tested formally

6. Reflexes

—  Test with the child in a relaxed position

—  Brisk reflexes may reflect anxiety in the child or due to pyramidal disorder

—  Absent reflexes may be due to neuromuscular lesion or within spinal cord or may be due to poor technique

—  Plantar responses: equivocal. With over reaction. Its unpopular in children as it is unpleasant

◦      Its unreliable in children under 1 year, however upgoing plantar responses provides additional evidence of pyramidal dysfunction

8. Sensation

—  You test the ability to tickle

—  Loss of sensation is likely in meningomyelocele. In this instance do a more detailed sensory testing

—  Cranial Nerves

—  CN 1-These can usually be tested formally from 4 years of age

—  No need to test during routine practice. Can be done by recognizing smell of a hidden mint sweet

—  CN 2- Visual acuity: determined according to age. It refers to clarity of vision, determine smallest letter they can read. Direct and consensual pupillary response tested to light and accommodation

—  CN 3,4,5 – full eye movement through horizontal and vertical planes.

—  Check the presence of squint

—  Check presence of nystagmus – avoid extreme lateral gaze as it can induce nystagmus in normal children

—  CN 6 – clench teeth and waggle jaw from side to side against resistance

—  CN 7 – close eyes tight, smile and show teeth

—  CN 8 – hearing: ask parents, although unilateral deafness may be missed this way

—  CN 9 – levator palate…let them say aagh

—  CN 10 – Recurrent laryngeal nerve – listen for hoarseness or stridor

—  CN 11 – Trapezius and sternomastoid muscles are responsible for power – shrug shoulders and turn head against resistance

—  CN 12 – let them put out tongue and waggle it from side to side

 

Bones and Joints

—  Presentation of bone and joint disorders include

—  Limb pain, Unwillingness to use limb, Limb, joint or muscle pain

—  Joint swelling, Muscle wasting

Inspection

—  Swelling could be due to joint effusion (there will be loss of joint outline)

—  Inspection…

—  Swelling may also be due to synovial thickening (there will be redness, pain on movement)

Palpation

—  Palpate for heat, comparing both joints, tenderness, fluctuation or effusion

Movements – passive before active in order not to hurt the child. Explain movements in child friendly words. If necessary show with your own limbs the movements you want to test. Record joint movement in degrees

—  Scoliosis – inspect spine especially in older children/adolescents. Ask them to stand straight as a soldier and note the shape of spine

—  Neck Examination

—  Thyroid

—  Inspect for swelling, it is uncommon in childhood, occasionally at puberty

—  Palpate behind and front for swelling, nodule or thrill

—  Auscultate if enlarged

—  Look for sign of hypo/hyper thyroidism

 

Examination of Lymphnode

—  Examine symmetrically – check the occiput, cervical, inguinal, axillary. Note the size, number and consistency of the nodes felt

—  Nodes can be small, discrete, pea sized, mobile in the neck, groin and axilla. This is common in normal children especially if thin

—  Nodes can be small, multiple nodes in the neck. This is common in URTI which is either viral/bacterial

—  Multiple lymph nodes of variable size in child with extensive eczema

—  Lymph nodes can be large, hot, tender sometimes fluctuant usually on the neck. This can be due to infection or abscess

—  Nodes can be of variable size and shape

—  Nodes can be caused by

—  Infections e.g. viral (infectious mononucleosis), or bacterial (TB)

—  Rare causes e.g. malignancy (usually non tender), kawaski disease, cat scratch

 

 

Indications for taking a blood pressure

—  Critically ill child, Child with renal or cardiac disease, Diabetes mellitus, If receiving drugs such as cortico-steroids causing hypertension

Technique

—  Measured by use of sphygmomanometer

—  Show child the ballon in the cuff and demonstrate how it is blown up

—  Use a cuff that fits comfortably, covering atleast 2/3rds of the upper arm

—  The child must be calm, relaxed and not crying

—  Systolic pressure is easiest to determine in young children and clinically the most useful

—  Diastolic pressure is when the sounds become muffled

—  Normal: use the available charts related to age. An abnormally high reading must be repeated, with the child relaxed

 

Examination of the eye

—  Inspect eyes, pupil, iris and sclera

—  Are eye movements full and symmetrical? Is nystagmus detectable? If present, may have cerebellar or occular cause

—  Are pupils equal and central? Is there a squint?

Ophthalmoscopy

—  In infants the red reflex is seen from a distance of 20-30cm, absence of red reflex occurs in corneal clouding, cataract or retinoblastoma

Fundoscopy

—  Is difficult to conduct, it requires experience and cooperation from the child. Myriadrics are needed in young children

—  Check for the condition of fundi of the eye

—  Retinopathy of prematurity

—  Retinopathy of congenital infections

—  Choriodo-retinal haemorrhages

—  Retinal haemorrhages maybe seen in the shaken baby syndrome (non accidental injury)

—  Exam usually left till last, as it can be unpleasant

Explain the procedure

—  Show the parent how to hold and gently restrain a younger child to ensure success and avoid possible injury

—  Throat:

—  Look at the uvula, tonsils, pharynx, and posterior palate

—  Older children, 5 years plus will open their mouths wide open as possible to avoid spatula

—  Look for redness, swelling pus or palatal petechiae, teeth, dental caries and gross abnormality

—  Ear

—  Examine the ear canals and drums gently, trying not to hurt the child

—  Look for anatomical landmarks on the ear drum and for swelling, redness, perforation, dullness and fluid.

 

Topic summary

By the end of this topic you should be able to take a comprehensive paediatric history and perform general and systemic examination. A good history  helps establish relevant facts,  it is a source of diagnostic information

·         It helps elicit all relevant clinical findings,

·         It helps collate the findings from the history and examination. It helps formulate a working diagnosis or differential diagnosis on the basis of logical deduction

·         It helps to assemble a problem list and management

·         At the end of history and examination: Summarize the key problems (in physical, emotional, social and family terms if relevant).

·         List the diagnosis and differential diagnoses

—  Draw up a management plan to address the problem, both short and long term. This could be reassurance, period of observation, performing investigations or therapeutic interventions

—  Provide explanation to the parent and child, if old enough provide further written information

—  Ensure your notes are well written, dated and signed.

 

Quiz

In summary you should be able to answer the following questions.

·         Outline the schema for history taking in children

·         Why is biodata important

·         Why should we always weigh the children

·         What is contained in the following:-

·         Complains and duration

·         History of presenting illness

·         Past medical and surgical history

·         Birth history.(antenatal, natal, post -natal)

·         Diet history

·         Immunization history

·         Developmental milestones

 

 

Unit 1: Topic 3 Neonatal conditions

Topic name

RESUSCITATION OF THE NEWBORN

 Topic outcome

By the end of this lesson the learner should be able to assess and resuscitate a newborn

Topic objectives

Define neonatal resuscitation

Explain the steps in neonatal resuscitation

3. Define birth asphyxia

4. Outline the causes

5. Manage birth asphyxia

6. Interpret an APGAR score

What is neonatal resuscitationResuscitation of the new born infant is the intervention after birth, to help the baby breathe and to help its heart beat.(Lorr R.Frankel et al 2007).  Transition from placental gas exchange in a liquid-filled intrauterine environment to spontaneous breathing of air requires dramatic physiological changes in the infant within the first minutes to hours after birth. Passage through the birth canal is a hypoxic experience for the fetus, since significant respiratory exchange at the placenta is prevented for the 50-75 s duration of the average contraction. Though most babies tolerate this well, the few that do not may require help to establish normal breathing at delivery. Newborn resuscitation is intended to provide  this help which  comprises the following elements:

·         Drying and covering the newborn baby to conserve heat;

·         Assessing the need for any intervention;

·         Opening the airway;

·         aerating the lung;

·         rescue breathing;

·         chest compression;

Administration of drugs (rarely)

Common causes of neonatal deaths

18 %

Other causes

09 %

Malformation

29 %

Perinatal hypoxia

17 %

Infection

27 %

Prematurity

Deaths

(n = 1800)

Cause

Perinatal asphyxia

Definition

·         A range of disorders that occur subsequent to oxygen deprivation of a fetus/newborn during the two weeks surrounding delivery

·         The main syndrome usually involves the brain but many other organs can be involved.

Pathophysiology –molecular Accumulation of intracellular calcium

·         Increase of excitatory amino acids in the damaged cells

·         Elaboration and increased liberation of reactive oxygen species (free radicals)

 

Etiology

·         Prenatal: Placental insufficiency syndromes

·         Labor/Delivery: Prolonged / obstructed labor

·         Cord accidents/ Ante partum hemorrhage

·         Post Natal: Ineffective resuscitation at birth

·         Severe respiratory diseases

Pathophysiology –Gross

·         Reduction of oxygen supply to the body organs (hypoxia)

·         progressive reduction of systemic blood flow (ischemia)

·         eventual decrease of cerebral & coronary blood flow (loss of autoregulation).

·         Hypoxic/Ischaemic cell death

·         Clinical Diagnosis

APGAR scoring

·         This signifies presence of Central Nervous system depression

·         Presence of encephalopathy: Suggesting actual neurological damage

·         APGAR SCORING  

§  0                                  1                      2

·         Appearance    Pale/blue    peripheral cyanosis    pink

·         PULSE              0                      <100            >100

·         Grimace           None            Weak                     Strong

·         Activity            None            Weak                     Strong

·         Respiration     None             Shallow             Lusty

 

Performed at 1&5 minutes.  If abnormal repeated at 10 & 20 minutes

APGAR Interpretation

·         1 minute score identifies those needing resuscitation

·         5 minute score defines asphyxia as:

·         Mild                     6&7

·         Moderate            4&5

·         Severe                 0-3

·         Extended scores estimate or predict later outcomes

 

Hypoxic Ischaemic Encephalopathy (complication of severe birth asphyxia)

·         Grade 1; MILD

·         Hyperactive and jittery, no convulsions 

·         Grade 2; MODERATE

·         Dull and lethargic but awake or arousable

·         Convulsions frequent 

·         Grade 3;  SEVERE

·         Stuporous/comatose with intractable fits

·         Other organ involvement, decorticate or decerebrate posture

                                                                                                

Laboratory evaluation

·         Cerebral ultra sound

·         Electro encephalography

·         CT Scan

·         MRI

 

Principles of management

·         Effective resuscitation at birth

·         Active maintenance of normal homeostasis during the acute phase

·         Appropriate management of convulsions and other complications

 

NORMAL NEWBORN

Outcomes

1. Describe a normal newborn

2. Perform a systematic examination of the newborn

A normal newborn

A normal new born infant  is any baby with all of the following:-

·         Is a baby born between 37—41weeks gestation,

·         Weighs 2.5kgs—4kgs,

·         Head circumference 33—37cm,

·         APGAR score 7—10,

·         length 50cm,

·         no abnormalities & does not require resuscitation at birth.

Note:  A complete physical examination is an important part of newborn care. Each body system is carefully examined for signs of health and normal function. Look for any signs of illness or birth defects. Physical examination of a newborn often includes assessment of the following:

·         Vital signs:

o    Temperature. Able to maintain stable body temperature 98.6 degrees F (36.50 c to 37.40c) in normal room environment

o    Pulse. Normally 100 to 140 beats per minute for infants,  80—120 older child.

o    Breathing rate. Normally 30 to 60 breaths per minute

o    Blood pressure:  80/50 to 115/80   (100-140 systolic /60—90 diastolic

·         General appearance. Physical activity, tone, posture, and level of consciousness

·         Skin. Color, texture, nails, presence of rash

Systematic 'Head-to-Toe' Examination

·         This should be done carefully after washing and rubbing hands, in good light and warmth (under a radiant warmer/Resuscitaire) to detect abnormalities and prevent hypothermia.

·         Head:

·         Shape, presence of fontanelle and whether normal, sunken or bulging

·         Measure and record head circumference on growth chart

·         Assess facial appearance and eye position

·         Look for any asymmetry or abnormality of facial form

·         Eyes:

·         Normal shape and appearance?

·         Check for presence of red reflex

·         Look for obvious cataracts or signs of ophthalmic infection

·         Ears:

·         Shape and size

·         Are they set at the normal level or 'low set'?

·         Check patency of external auditory meatus

·         Mouth:

·         Colour of mucous membrane, observe the palate

·         Check sucking reflex by inserting a clean little finger gently inside baby's mouth

·         Arms and hands:

·         Are they of normal shape and moving normally?

·         Look for evidence of traction birth injury (eg Erb's palsy) by checking neck, shoulders and clavicles

·         Count fingers and observe their shape – is there any evidence of Clinodactyly (incurving of fingers) or polydactyly

·         Check palmar creases – are they multiple or single? A single palmar crease may be normal, but can also be a sign of Down's syndrome, look for other signs (low set ears, thick epicanthic fold, flat facies, and flat nasal bridge.

·         Peripheral pulses:

·         Check brachial, radial and femoral pulses for rate, rhythm and volume

·         A hyperdynamic pulse may suggest persistent ductus arteriosus

·         A weak pulse may occur with a congenital cardiac anomaly (impairing cardiac output and in conjunction with other signs from the examination)

·         Check for radio-femoral delay (aortic Coarctation)

·         Heart:

·         Check cardiac position by palpation and feel for any thrill or heave

·         Listen to the heart sounds carefully and for any added sounds or murmurs, Suspected abnormalities require further examination and often more expert opinion and investigation

·         Lungs:

·         Observe respiratory pattern, rate and depth for a few seconds

·         Look for any evidence of intercostal recession

·         Listen for stridor

·         Auscultate lung fields for added sounds

·         Abdomen:

Look at abdominal girth and shape

Carefully check the umbilical stump for infection or surrounding hernia

Palpate gently for organs, masses or hernia

It is common to be able to feel a tip of the liver and/or spleen in healthy new-borns.

Check the external genitalia carefully R/O Ambiguous Genitalia

Palpate for testicles in boys (Undescended testis (cryptorchidism) is common in premature boys).

Inspect the anus (has meconium been passed?)

·         Back:

Look carefully at skin over back and at spinal curvature/symmetry

Is there any evidence of spina bifida occulta or pilonidal sinus hidden by flesh creases or dimples?

Palpate the spine gently

·         Hips:

Specifically test for congenital dislocation of the hip (a.k.a. congenital hip dysplasia) using combination of Barlow and Ortolani manoeuvres

·         Legs:

Watch movements at each joint

Check for any evidence of tallipes equinovarus

Count toes and check shape

·         CNS:

Observe tone, behaviour, movements and posture

Elicit newborn reflexes (Rooting, sucking, Moro, stepping grasping

 

Record findings of your examintion

Common abnormalities detected in the newborn screening examination

·         Capillary or macular haemangioma: also known as stork mark/bites, or salmon patch; found around eyes and nape of neck in 30–50% babies. Those around eyes normally disappear in first year, commonly persist if on nape of neck

·         Blue-black pigmented area: Mongolian blue spots; seen at base of back and on buttocks. These are common in dark-skinned parents but can occur in Caucasian infants. They normally disappear over first year

 

 



Unit 1: Topic 3 Neonatal conditions

Topic name

RESUSCITATION OF THE NEWBORN

 Topic outcome

By the end of this lesson the learner should be able to assess and resuscitate a newborn

Topic objectives

Define neonatal resuscitation

Explain the steps in neonatal resuscitation

3. Define birth asphyxia

4. Outline the causes

5. Manage birth asphyxia

6. Interpret an APGAR score

What is neonatal resuscitationResuscitation of the new born infant is the intervention after birth, to help the baby breathe and to help its heart beat.(Lorr R.Frankel et al 2007).  Transition from placental gas exchange in a liquid-filled intrauterine environment to spontaneous breathing of air requires dramatic physiological changes in the infant within the first minutes to hours after birth. Passage through the birth canal is a hypoxic experience for the fetus, since significant respiratory exchange at the placenta is prevented for the 50-75 s duration of the average contraction. Though most babies tolerate this well, the few that do not may require help to establish normal breathing at delivery. Newborn resuscitation is intended to provide  this help which  comprises the following elements:

·         Drying and covering the newborn baby to conserve heat;

·         Assessing the need for any intervention;

·         Opening the airway;

·         aerating the lung;

·         rescue breathing;

·         chest compression;

Administration of drugs (rarely)

Common causes of neonatal deaths

18 %

Other causes

09 %

Malformation

29 %

Perinatal hypoxia

17 %

Infection

27 %

Prematurity

Deaths

(n = 1800)

Cause

Perinatal asphyxia

Definition

·         A range of disorders that occur subsequent to oxygen deprivation of a fetus/newborn during the two weeks surrounding delivery

·         The main syndrome usually involves the brain but many other organs can be involved.

Pathophysiology –molecular Accumulation of intracellular calcium

·         Increase of excitatory amino acids in the damaged cells

·         Elaboration and increased liberation of reactive oxygen species (free radicals)

 

Etiology

·         Prenatal: Placental insufficiency syndromes

·         Labor/Delivery: Prolonged / obstructed labor

·         Cord accidents/ Ante partum hemorrhage

·         Post Natal: Ineffective resuscitation at birth

·         Severe respiratory diseases

Pathophysiology –Gross

·         Reduction of oxygen supply to the body organs (hypoxia)

·         progressive reduction of systemic blood flow (ischemia)

·         eventual decrease of cerebral & coronary blood flow (loss of autoregulation).

·         Hypoxic/Ischaemic cell death

·         Clinical Diagnosis

APGAR scoring

·         This signifies presence of Central Nervous system depression

·         Presence of encephalopathy: Suggesting actual neurological damage

·         APGAR SCORING  

§  0                                  1                      2

·         Appearance    Pale/blue    peripheral cyanosis    pink

·         PULSE              0                      <100            >100

·         Grimace           None            Weak                     Strong

·         Activity            None            Weak                     Strong

·         Respiration     None             Shallow             Lusty

 

Performed at 1&5 minutes.  If abnormal repeated at 10 & 20 minutes

APGAR Interpretation

·         1 minute score identifies those needing resuscitation

·         5 minute score defines asphyxia as:

·         Mild                     6&7

·         Moderate            4&5

·         Severe                 0-3

·         Extended scores estimate or predict later outcomes

 

Hypoxic Ischaemic Encephalopathy (complication of severe birth asphyxia)

·         Grade 1; MILD

·         Hyperactive and jittery, no convulsions 

·         Grade 2; MODERATE

·         Dull and lethargic but awake or arousable

·         Convulsions frequent 

·         Grade 3;  SEVERE

·         Stuporous/comatose with intractable fits

·         Other organ involvement, decorticate or decerebrate posture

                                                                                                

Laboratory evaluation

·         Cerebral ultra sound

·         Electro encephalography

·         CT Scan

·         MRI

 

Principles of management

·         Effective resuscitation at birth

·         Active maintenance of normal homeostasis during the acute phase

·         Appropriate management of convulsions and other complications

 

Congratulations - end of lesson reached

Well done!

Return to PCH 216:Paediatrics and Child Health IView grades

NEONATAL CONDITIONS - BIRTH INJURIES

Learning outcome

By the end of the lesson the learn should be able to diagnose and manage common birth injuries 

Topic objectives

1.      Define birth injury

2.      Explain the causes

3.      Outline common birth injuries

4.      Manage specific birth injuries

 

What is a birth injury?

Injuries to the infant resulting from mechanical forces during birth (compression, traction) or Physical injury sustained during the birth process. Can coexist with hypoxemic-ischemic insult - may predispose to each other. This is sometimes called birth trauma or birth injury.

Predisposing factors

—  Primigravida

—  Cephalopelvic disproportion

—  Small maternal stature

—  maternal pelvic anomalies

—  Prolonged or rapid labor

—  Arrest of descent of presenting fetal part

—   Oligohydramnios

—  Fetal anomalies

—  Fetal neuromuscular disease

—  HIE

—  Resuscitation with CPR

—  Abnormal presentation (breech/face)

—  Use of forceps or vacuum extraction

—  Versions

—  VLBW infant or extreme prematurity

—  Macrosomia

—  Large fetal head

 

Common birth injuries

 Common birth injuries include: Caput succedaneum, Cephalohematoma, bruising/forceps marks, Subconjunctival hemorrhage, Facial paralysis, Brachial palsy, Fracture, Facial Nerve Paralysis

Intracranial Hemorrhage
This is when blood vessels are broken inside the baby's skull. This bleeding can occur in many locations depending on what caused the bleeding. It is much more common in premature infants. Signs are poor feeding and seizures. If your baby is at high risk for bleeding, screenings will be done

Injuries may be caused by a combination of mechanical trauma and hypoxia. Birth injuries may be minor and transient but they can produce serious and permanent effect as well as being fatal.

Skull injuries

Cephalohaematoma

  • Bleeding between the periosteum and skull causes a haematoma, usually in the parietal region and sometimes the occipital region. Spread is restricted by suture lines that are adherent.
  • Blood loss can cause anaemia and even hypotension.
  • As the haematoma resolves, breakdown of haemoglobin can cause hyperbilirubinaemia that may need treatment. An underlying skull fracture is found in up to 20% cases. If it is thought to be depressed, CT or MRI imaging is required. Spontaneous remission may take weeks and there is sometimes residual calcification.
  • A haematoma may rarely become infected.
  • Consider the possibility of a coagulation defect.

Subgaleal haematoma

  • Bleeding between the periosteum and scalp is usually associated with use of ventouse extraction.
  • 77% follow instrumental delivery and 40-50% overlie a skull fracture or brain haemorrhage.[9]
  • It usually appears within 12-72 hours of birth as a soft, fluctuant mass within the scalp, especially over the back of the head.
  • It can spread slowly and be unnoticed and present as hypotension.
  • The spread is not restricted by suture lines.
  • As with cephalohaematoma, management is conservative but check for anaemia.

Caput succedaneum

  • This is a poorly defined, subcutaneous collection of serosanguinous fluid that spreads over suture lines and the midline.
  • It is very common after prolonged labour.
  • It does not cause significant problems and needs only to be monitored.

Cuts and abrasions

  • These may result from operative delivery, including cutting the baby with the scalpel blade at LSCS. Great care is needed in cutting the last layer of the uterus, even in an emergency.
  • Cuts need closing and dressing. Topical antibiotic may be indicated.

Subcutaneous fat necrosis

  • This is not usually apparent at birth.
  • Sometime later, irregular, hard, subcutaneous plaques appear with overlying dusky red-purple discoloration.
  • They occur on the extremities, face, trunk or buttocks, having been caused by pressure during delivery.
  • There is no treatment and they should resolve but sometimes there is calcification.

Brachial plexus injury

The majority of these are Erb's palsy involving the upper part of the brachial plexus. The underlying problem is usually injudicious traction when the anterior shoulder is trapped (shoulder dystocia).[10][11] Only 10% involve the whole brachial plexus.[12] Associated injuries include:

  • Fractured clavicle.
  • Fractured humerus.
  • Subluxation of cervical spine.
  • Cervical cord injury.
  • Facial palsy.
  • Occasionally, phrenic nerve paresis.

Erb's palsy

  • There is damage to the C5, C6 segments of the brachial plexus.
  • It produces loss of motion of the shoulder with a limp arm, adducted and internally rotated. The elbow is pronated and extended with wrist flexed.
  • The grasp reflex is normally maintained but Moro, biceps and radial reflexes are lost.

The position of the hand is said to be reminiscent of a porter who is turning away but is holding out his hand behind him for a tip.

Klumpke's paralysis

This is much less common than  Erb's palsy in infants.

  • It is due to damage of the nerves of segmental origin C7, C8, T1 in the brachial plexus.
  • It causes paralysis with weakness of the hand and loss of grasp reflex.
  • Horner's syndrome may be seen if there is T1 damage

Management

  • Most cases of brachial plexus injury resolve spontaneously within four months, but it can take up to two years.
  • X-rays to exclude fractures and examination for phrenic nerve paresis are required. Further investigations include MRI scan, electromyography, nerve conduction studies and CT myography.
  • To prevent contractures, immobilise the arm across the upper abdomen for seven days, then start physiotherapy using wrist splints.
  • Consider surgery if movement is not returning after three months and electrophysiology results suggest a poor prognosis.[13]

Cranial nerve injury

Cranial nerve and spinal cord injuries result from hyperextension, traction and overstretching with simultaneous rotation. Neurapraxia will resolve swiftly but complete nerve or cord transection is a much more serious matter.

  • Central damage to the facial and vagus nerves causes an asymmetrical face on crying, with swelling and smoothness of the affected side and drooping of the side of the mouth.
  • Peripheral damage causes paralysis to the eye, forehead or mouth only.
  • Most cases soon start to recover but full recovery may take months.
  • The eye must be protected with a covering and synthetic tears.
  • If there is no improvement after 7-10 days, investigation is required.
  • Phrenic nerve damage can cause paralysis of half of the diaphragm, leading to breathing difficulties with significant mortality. Ultrasound or X-ray shows an elevated hemidiaphragm but this may be absent in the early stages. Screening may show immobility.

Laryngeal nerve injury

  • Unilateral paralysis often presents with a hoarse cry or stridor and may affect swallowing.
  • Bilateral damage causes severe respiratory problems.
  • Diagnosis is by laryngoscopy to exclude other causes of the symptoms.
  • Recovery usually occurs after 4-6 weeks but can take up to a year.

Spinal cord injury

  • Damage to the spinal cord often results in stillbirth or babies who die soon after delivery due to an inability to breathe.
  • Ventilation may be life-saving but, if the lesion is not a temporary neuropraxia, there will be later agonising decisions about turning off the ventilator.
  • Those who survive are weak and often develop spasticity.
  • Diagnosis is by MRI or CT myelography.
  • Treatment is supportive.

Fractures

Clavicle

  • Fractured clavicle is common and presents with apparent paralysis.
  • Palpation may show crepitus, uneven bone and muscle spasm.
  • It  heals within 7-10 days with the arm immobilised.
  • Confirm the diagnosis by X-ray.
  • Look for other damage.

Arm and leg bones

  • Fracture may be heard during delivery.
  • It presents with absence of normal movement of the limb, with swelling becoming apparent later.
  • Confirm with X-ray.
  • Treat with 8-10 days of splinting or reduction and casting if displaced.
  • Check for radial nerve damage in arm fractures.

Abdominal bleeding

  • This presents with shock, pallor and a distended abdomen, possibly bluish in colour.
  • Check for anaemia.
  • Diagnose with paracentesis.
  • Causes include hepatic laceration and rupture of spleen, so this is serious.

Hypoxia

Factors within labour are complex, but processes such as uteroplacental vascular disease, reduced uterine perfusion, fetal sepsis, reduced fetal reserves and cord compression can be involved alone or in combination producing fetal distress. Gestational and antepartum factors modify the fetal response to them.
Cerebral palsy is strongly associated with a low Apgar score 5 minutes after birth, The majority of cases are now thought to be a consequence of postpartum insults to the fetus.

UNIT 1: Topic 5: CONGENITAL ABNORMALITIES


CONGENITAL ABNORMALITIES

b) Learning  outcome

By the end of this lesson the learner should be able to diagnose and manage congenital abnormalities

 Topic objectives

Define congenital abnormalities
state the signicance
outline common life threatening congenital abnormalities

 

c) Topic Content

Definition

Congenital malformations are anatomical defects present at birth. Defects of the CNS and  heart account for more than  half  of  the  total

Significance

 1—2% of all babies are born with serious congenital malformations.

·         Are  major  causes  of  Perinatal  and infant death  to the  extent  of  increase in infant  mortality rate

·         The incidence of serious  defects and chromosomal  anomalies amongst   spontaneous  abortions is very  high.

·         Some  of  them  are  predisposing  factors  to  diseases e.g   UTI in congenital  obstruction  of the  urinary  tract

 

Life threatening abnormalities

CHOANAL ATRESIA;

Presents with;- respiratory distress in the delivery room.  Apnoea, inability to pass a nasogastric tube through the nares

 Suspect CHARGE Syndrome 

·         C—Coloboma of the eyes

·         H—Heart anormaly

·         A—Atresia of the choana

·         R—Retardation         

·         G—Genital  anomaly

·         E—Ear anomaly

2. PIERRE ROBIN SYNDROME;-- Micrognathia, cleft palate, air way obstruction

3. DIAPHRAGMATIC HERNIA Scaphoid abdomen, bowel sounds present in the chest   Respiratory distress

4. TRACHEOESOPHAGEAL FISTULA.  Polyhydramnious , aspiration pneumonia, excessive salivation, Inability to pass a NGT in to the stomach

 Suspect VATER Syndrome

·         V=Vertebral defects

·         A=anal may be imperforate

·         T-E= Tracheo -Esophageal fistula

·         R=Radial and Renal dysplasia

Intestinal obstruction;-  Polyhydramnious , bile stained emesis, abdominal distension

-Volvulus, duodenal atresia  ileal  atresia;-- suspect trisomy 21

cystic  fibrosis

Gastroschisis, omphalocele;-- Polyhydramnious, intestinal obstruction

Renal  agenesis, potter syndrome—oligohydromnious, anuria , pulmonary hypoplasia                       

PneumothoraxNeural tube defects;-- Encephalocele,  meningomyelocele=

  • polyhydramnious , alpha feto- protein, Decreased fetal activity

 

Ductal- dependant congenital heart disease;- present with cyanosis, hypotension,  murmurs

Aetiology 

§  Environmental  and  genetic  factors

§  -Idiopathic  accounts  for  50%

§  -single  gene  defects 

§  -Chromosomal   anomalies  e.g  Down syndrome

§  Infections  e.g  rubella  syndrome [ consist  of  cataract , deafness ,cardiac  abnormalities]

§  Teratogenic   drugs  e.g  thalidomide   causes  phocomelia

§  Social  economic  factors  e.g  an  ence phaly,  and  spina  bifida  is  high  in  low  socio-economic  status. 

§  Parental  age   e.g 

§  Maternal  age  dependant  trisomy  21 > 35yrs

§  Paternal  age  dependant  -  achondroplasia

§  Seasonal:-  some  are  more  common  in  winter   than   summer

§  Regional  incidence:—an  encephaly  is  highest  in  highlands  e.g  Liverpool  in  England

§  Congenital  dislocation  of the  hip is  high  in  Finland

§  Sex : Congenital  pyloric  stenosis 

§  M : F ratio  is  5  : 1.

§  Dislocation  of the hip :- F: M ratio  is 6:1.

§  Birth  order    -first  borns  have  high  incidences  of  malformation

§  Ionizing   radiation

§  Mechanical  factors  e.g  tallipes  equino varus, CDH,

§  Parity  of  the  mother

§  Multiple   factors

 

DIAGNOSIS, Is  by  history, Physical  examination, Relevant  investigations

SPINA  BIFIDA

Is  the  most  common  neural- tube  defect, most  frequently  occurring  Permanent  disabling   birth  defect. Results  from  failure  of  the  spine to  close  during  the  first  month  of  pregnancy. May  cause  paralysis  leading  to bowel  and  bladder  complications A  large  percentage also  has  hydrocephalus It  can  cause  profound  defects  on  the  childs  motional  and  social  development

LOW   FOLIC  ACID  Status  before  conception  and  during  the  first  week  of  pregnancy increases  the  risk

TYPES

1. Spina -  bifida  occulta;  Features;-  a dimple,   Tuft  of  hair,  Lipoma

2. Spina  bifida  cystica: Observe  a  cyst  or  sarc  on  the   back,  May  be  covered  with  a  thin  layer  of  skin,  May be  a  Meningocoele, Contains   meninges   and  CSF or a  Meningomyelocele; Contains   tissue,  CSF,  nerves, and  part  of  spinal  cord.

3. Encephalocele  [cranial   bifida);  The  bones  of   the  skull  fail  to  develop  properly.  May  contain  brain  tissue,  CSF  with  or  without  part  of  the  brain. Examine   lower   limbs   for  paralysis and   head  circumference  to rule out hydrocephalus.

4. An – encephaly:  Complete absence of peripheral   hemisphere  and   overlying  skull. 90%   are female,   common in   first borns. High incidence in low  socio  economic   class. Is associated with  hydramnious   due  to  inability  of  the  fetus   to  swallow.

5. Umbilical  hernia  Two   types :- True  umbilical  hernia and Supra  umbilical  hernia. Natural  cure  is  expected.  Spontaneous  closure  at  one  year. Surgery   if  there  are  symptoms   or  at  5years   if  it persists. 

CONGENITAL   URETHRAL VALVES:

May cause  recurrent  UTI , Reflux  hydronephrosis,  obstructive  uropathy

Micturating  cysto  urethrogram  (M C U)  is  a must

Treatment is  surgery.

 

HYPOSPADIA

The  urethral  opening  is  on  the  ventral  surface  of  the  gland  or  shaft  Epispadia,  hypospadia  with  chordate,  penile,  or  coronal. Avoid  circumcision - skin is  used  to  repair. Repair  is  advised   at  the  age  of  4—5yrs

UNDESCENDED TESTIS [CRYPTORCHIDISM]

33% of   premature male develop cryptorchidism. 3% of term infants. May descend   in the first few months   after birth. Surgical  correction  is  best  at  2years  BUT    MUST   be  done   by  7-9yrs. Infertility  results  if  bilaterally  undescended   past  puberty.  May be cancerous if remains for a long time. Treatment is   orchidopexy.

Congenital  dislocation   of  the  hip

It is Common  in  girls, Girl : boy  ratio  is  6: 1;  Ortolani,s  test  is  positive.   Treatment is   Reduction and immobilize  in  POP  for  3 months.

CONGENITAL  HYPERTROPHIC  PYLORIC  STENOSIS

Features include   projectile  vomiting  from  the  second  to  third  week of  life,  never  bile  stained, Common  in  first  borns. More common in males than females. There is marked weight loss and dehydration. There  is  visible  peristalsis   left  to  right  after  feeds  and  before  vomiting.

Investigations 

Blood for urea and electrolytes - reduced sodium (Na+) Potassium (k+), chloride (Cl) Increased   PH. It leads to Hypochloraemic alkalosis.  Barium   meal    is mandatory.

Treatment

 Correct the electrolyte    imbalance   and   dehydration with  IV  fluid. Definitive treatment is by surgery   [pyloromyotomy].

 

CONGENITAL   TALLIPES   EQUINO  VARUS    [CTEV]  / CLUB  FOOT]

Common  in  boys, Majority  are  mechanical   in  origin

Defects.  Equinus- plantar flexion.  Varus  -- displacement   towards  the  midline  together  with  medial  rotation  of  tibia.    And   fore   feet   adduction

Treatment:  Starts   from first day of  life. Dennis   brown   splint   is   applied    for   3 months 33 %   are fully corrected.

 

 

DOWNS SYNDROME /MONGOLISM /TRYSOMY  21

Is  the  commonest  form  of  mental  retardation   with  a  prevalence  of  1: 700 live birth. The frequency is   related  to  maternal  age i.e  >35 years

Chromosomal  anomalies  associated   with Downs syndrome

1. Full  trysomy  21  - 95%   of  cases    [non  dysfunction]

  • 2. T 21  Mosaicism = 2.4 %  of  the  cases
  • 3.  T 21 translocation  = 3.3%  of  cases
  • Males  are  affected  more  than  females 

Clinical  features

Slanting  palpebral  fissures, Marked  epicanthic  folds

Small  mouth  with  a protruding  tongue, Hypotonia, Poor  moro  reflex, Hyperflexibility  of joints  

Excess  nuchal  skin, Flat  facial  profile, Delayed  dentition, Delayed  closure  of  fontanels, Single  palmar   crease  [simian  crease]

Dysplasia  of  the  pelvis, Wide  gap  between  first    and  second  finger  and  toes, Low  set  ears. Have  a  good  temperament   -  are  quiet  most  of  the  time  with  a lot  of  interest in  music, Are  short  statured

Complications

·         40%  have  a congenital  heart  defect   [ AVSD , PDA , VSD]

·         IQ  range  =25—50

·         Hypothyroidism    5%

·         Leukaemia   1: 95

·         Atlanto  axial  instability  12—20 %   usually  asymptomatic

·         Mean  age  for  survival  =65 years

 

Diagnosis:   Chromosomal analysis

 

ACHONDROPLASIA

  • It  is  inherited  through  autosomal  dominant
  • Are  dwaft   <  4 ft, Have  a  large  head,  Depressed   nasal   bridge
  • Short   extremities, The  trunk  is  of  normal  size,
  • They are   intelligent
  • Have  a  protruded  upper  mandible  and  deformed  pelvis
  • Paternal   age   is a  possible  factor

 

Discussion

A 3weeks old baby is brought to you with a 1/52 history of vomiting after feeds. the reports that the child does not look sick at all. He feels hungry after feeding and wants to breastfeed again. On examination you observe projectile non -bilious vomiting, dehydrated babay.  You suspect a congenital anomaly. What is your impression

How will you confirm your diagnosis

Manage this baby.

Topic 7: PREMATURITY


PREMATURITY

 Learning outcome

By the end of this topic the learner should be able to diagnose and manage prematurity

 Topic Outcomes

Define premature newborn

Outline the causes

State the features

Explain LBW, SGA,LGA

Discuss the complications

Describe the management

 a)      Topic Content


 

POST MATURE BABY

They have marked loss of s/c fat

The skin is dry, cracked, ringled, peeling &  may be meconium stained  with absence of vernix caseosa, Are hungry & they feed well, Unusual alertness, Wide eyed look

Common complications of an SGA

Hypoglycaemia

Hypothermia

Massive pulmonary haemorhage

Skin infections

Meconium aspiration is evident in post mature

 

b)     Topic Summary

 

Neontal Tetanus

NEONATAL TETANUS

Neonatal Tetanus is a bacterial infection of the neonate caused by Clostridium Tetani. It begins in the neonatal period – 3—10 days after birth. Follows contamination of umbilical stamp during delivery, associated with high mortality.

HISTORY

History of a newborn who was able to breast feed normally but suddenly develops inability to breast feed, lock jaw, spasms, seizures & death.

¢  Usually there is a history of un sterile cutting of the cord or treatment  of stamp with cow dung.

Management

·         Sedate baby by Phenobarbitone  15mg/ kg start

·         Diazepam 0.2mg/kg over 3 minutes. Repeat every 30 min x 3 doses to stop spasms

Do not exceed 2mg/kg/24hrs

·         Clean cord thoroughly

·         Pass a NGT for feeding

Subsequent  care

·         Nurse the baby in a quiet dark room

·         Avoid too much handling

·         Keep umbilical cord clean & dry

·         Paint cord with povidine iodine or spirit

·         Feed  Exressed Breast Milk (EBM)  through NGT

·         Phenobarbitone 5mg/ kg/ day in 2 doses

·         Chlorpromazine 2mg / kg /day

·         Antibiotics iv crystalline penicillin 100 000u/kg/day in 2 doses

·         Monitor v/s – watch respiration

·         Counsel the mother.

·         Refer to ICU

·         Immunize baby after recovery.

Prevention

·         Tetanus toxoid to  all pregnant women

·         Education on hygiene

·         Appropriate cord care

Neontal Tetanus

NEONATAL TETANUS

Neonatal Tetanus is a bacterial infection of the neonate caused by Clostridium Tetani. It begins in the neonatal period – 3—10 days after birth. Follows contamination of umbilical stamp during delivery, associated with high mortality.

HISTORY

History of a newborn who was able to breast feed normally but suddenly develops inability to breast feed, lock jaw, spasms, seizures & death.

¢  Usually there is a history of un sterile cutting of the cord or treatment  of stamp with cow dung.

Management

·         Sedate baby by Phenobarbitone  15mg/ kg start

·         Diazepam 0.2mg/kg over 3 minutes. Repeat every 30 min x 3 doses to stop spasms

Do not exceed 2mg/kg/24hrs

·         Clean cord thoroughly

·         Pass a NGT for feeding

Subsequent  care

·         Nurse the baby in a quiet dark room

·         Avoid too much handling

·         Keep umbilical cord clean & dry

·         Paint cord with povidine iodine or spirit

·         Feed  Exressed Breast Milk (EBM)  through NGT

·         Phenobarbitone 5mg/ kg/ day in 2 doses

·         Chlorpromazine 2mg / kg /day

·         Antibiotics iv crystalline penicillin 100 000u/kg/day in 2 doses

·         Monitor v/s – watch respiration

·         Counsel the mother.

·         Refer to ICU

·         Immunize baby after recovery.

Prevention

·         Tetanus toxoid to  all pregnant women

·         Education on hygiene

·         Appropriate cord care

Neonatal Jaundice

Topic objectives

Prematurity  is not synonymous with LBW

It can be assessed by gestational dates, and physical features at birth

Management and care depends on the birth weight and the level of prematurity

Important to note in the care is

·         Thermoregulation

·         Fluid electrolyte balance

·         Feeding

Define neonatal jaundice

Explain bilirubin metabolism

Outline the causes according to age of onset

State the predisposing factors

Outline the diagnosis

Explain the modes of Rx

List complications

Define kernicterus

 

 

Topic Content

DEFINITION

Increased neonatal serum bilirubin levels sufficient enough to result in jaundice.

        This can be physiological or

         pathological.

BILIRUBIN METABOLISM

Bilirubin is made from breakdown of RBCs. Myoglobin,and other heame containing substances in the body.The heame is metabolised to bilirubin:-

HEAME→BILIVERDIN→BILIRUBIN

                 ↑                       ↑

             heame               biliverdin

             oxygenase.        Reductase.

Uncojugated       energy depen    conjugat

Bilirubin          →    liver metab    →bilirubin

                           transferase enz

   In serum, unconjugated bilirubin is bound to albumin.↓serum albumin leads to ↑free bilirubin.This is fat soluble and crosses the blood / brain barrier to cause kernicterus if the levels are high.

Some factors displace bilirubin from the albumin binding sites.

   Acidosis, drugs esp. sulphonamides

METABOLISM contd

Conjugated        water            excreted via

  Bilirubin      →     soluble   →   urine/stool

Conjugation is an energy dependant activity that can be disrupted by various factors

 

Causes according to age of onset

First 24—48  hours

ABO & Rhesus incompatibility

3rd –4th day

Physiological jaundice  ( it does not mean its harmless; it depends on the level)

It is due to fetal RBC break down

They lack bacterial flora

The liver conjugation system is immature

7th day onset

It is due to infections  (acquired or congenital)

Prolonged jaundice (>1/52)

Caused by;

Congenital billiary atresia,

Neonatal hepatitis – hepatitis B, syphilis, CMV

Hypothyroidism – thyroid hormone enhances the efficiency of conjugation system

Congenital hemolytic anemias

G6PD deficiency

Congenital spherocytosis

Pyruvate kinase deficiency

Hereditary spherocytosis

Others

Haematoma - cephalohaematoma

Breast milk jaundice- 4th –10th day- pregnanediol substance in milk inhibit the fxn of glucuronil transferase in some newborns

PHYSIOLOGICAL  JAUNDICE

Serum bili increases after birth to a peak at around day 3-4 of life.

This is due to breakdown of fetal RBCs in the face of inadequate liver metabolism.

The level starts to reduce around day 6.

The peak may result in jaundice.

6-7% of full term infants are affected.

physiological jaundice

Is that jaundice that occurs in a full term infant around day 3-4 of life and no pathological cause can be found.

A diagnosis  of exclusion

 JAUNDICE OF PREMATURITY

Jaundice occurring in a preterm infant.

Usually caused by;- ↑RBC mass.

                                    immature liver metabolism

                                    prone to hypo-glycemia, anoxia acidosis.

p/s premature infants can also have pathological jaundice described ahead

PATHOLOGICAL JAUNDICE

DUE TO:- (a) Overproduction of bilirubin  Such as increased RBC destruction.

                    (b) Reduced metab/excretion Such as enzymatic defficiencies

                      c) Overproduction of bilirubin

HEMOLYTIC DISEASE OF THE NEWBORN (HDN);-

   ABO incompatibility…..mother O+ve baby is either A,B or AB.

   Can occur with 1st baby

   Can be very severe.

    common in our country.

HDN

Rhesus incompatibility..

     mother rh-ve while baby is rh+ve

     occurs in subsequent deliveries after the 1st because the mother has to be sensitised by prior exposure to rh+ve stimuli.

   Less common than ABO in our setup but is frequent.

HDN

Minor blood group incompatibilities.

        Not routinely tested for e.g Kell, Duffy and others that may be restricted to regions

RBC membrane defects e.g congenital spherocytosis

RBC enzymatic defects e.g G6PD defficiency

OVERPRODUCTION

POLYCYTHEMIA…infants of diabetic mothers, intra-uterine growth retardation(SGA),etc

Collections of free blood e.g cephalohematoma.

Traumatic birth that destroys myoglobin and injures the cytochrome system

REDUCED EXCRETION

Either by interfering with metabolism, excretion or both.

Asphyxia,hypoglycemia,infections….all interfere with liver cell function hence its ability to metabolize bilirubin.

Enzyme deffeciencies….lack of the transeferase enzyme---Criggler Najar type 1 and 2, …..lack of ligand proteins x and y---roto syndrome.

REDUCED EXCRETION

Biliary atresia…..intra or extra hepatic. Conjugated bilirubin cant be excreted via bile as the ducts are atretic within or outside the liver.

Intestinal obstruction….conjugated bilirubin gets to the gut but due to obstruction,there is stasis allowing the enzyme –glucuronidase--to deconjugate it with re-absorbtion of unconjugated bilirubin (enterohepatic circulation)

BREASTMILK JAUNDICE

Juandice associated with breastfeeding.

For some mothers ,their breastmilk contains factors that interfere with bilirubin metabolism.(glucuronidase)

   Exclusively breastfed infants have a higher peak of bilirubin that results in jaundice. May be due to dehydration resulting from initial low milk output.=breastfeeding jaundice.

RX  stoppage of breastfeeding for 24hrs resolves the jaundice!

HYPERBILI clinical features

Jaundice on the skin,sclera of eyes,under the tongue , and palms and soles of feet.

Generally jaundice occurring on 1st or 2nd day of life is pathological.

Jaundice on the 3rd or 4th  day may be physiological and if physiological it should last less than 2 weeks.

Jaundice appearing after day 4 is also most likely pathological.

CLINICAL FEATURES

HISTORY----any history of previously affected sibling.

                    --mothers blood group if known.

                    --suggestive pre-desposing

                       factors to sepsis.

         

CLINICAL FEATURES

EXAMINATION…jaundice,pallor

,hepatomegally,vomiting,lethargy,

poor feeding.

    With onset of kernicterus,there is high pitched cry,hypertonicity,jitteriness

   convulsions, bulging fontanelles,

   opisthotonus posturing.

DIAGNOSTIC EVALUATION

HISTORY and CLINICAL FINDINGS

LABORATORY WORKUP

      (a)Total bili and differential..serially to

           monitor effectiveness of treatment.

      (b) Heamogram…HB and reticulocyte  count.

      (c) Blood group….mother and baby

LABORATORY INV

(d) Coombs test to identify case of HDN that may not involve ABO or RH factors.

(e) Peripheral blood film….may show features of infection or hemolysis.

(f) Total protein and albumin to determine albumin binding capacity.

MANAGEMENT

PREVENTION:-

    use of anti-d to prevent maternal rhesus sensitisation if she is rh-ve and has:-

                        (a) blood tx of inco. Blood

                        (b) fetal loss i.e abortion

                        (c) delivers rh+ve baby

MANAGEMENT

SUPPORTIVE:-

(a) maintain hydration                          

(b) ensure nutrition or

adequate caloric  intake to avoid hypoglycemia.

(c) correct acidosis and  hypoxia.

MANAGEMENT

SPECIFIC:-(1) Phototherapy

  Works by a process of photo-isomerization so that isomers are produced  which are water soluble and do not require liver  for excretion.

PHOTOTHERAPY

Light of 420-470 nm wavelength is most effective. Blue light is most appropriate.

Distance from light source to the baby should be not more than 15-20 cm

Turn baby frequently or use photo-optic blanket.

May cause loose stools,

skin rashes, dehydration,retinal damage,overheating.

MANAGEMENT

EXCHANGE TRANSFUSION.(EX TX)

              (a) removes xs bilirubin.

              (b) removes sensitized RBCs.

              (c) improves HB level.

EXCHANGE TRANSFUSION

INDICATIONS:

 (1) Very rapid rise of bilirubin 8-17 umol/dl/hr.

  (2) Rapid fall in HB.(hemolysis)

  (3) ill child—sepsis/meningitis

  (4) Prematurity

  (5) Previously severe dx in sibs

  (6) Reticulocyte count > 15 %

EXCHANGE TRANSFUSION

PROCEDURE:

·         Use fresh blood preferably heparinized. Blood group O-ve most suitable.  Can use babies ABO type but RH-ve cross matched against mothers serum.

·         Warm blood to 35-37°c

·         Continuously mix the blood to avoid sedimentation.

·         Empty infants stomach with NGT and leave it in situ.

·         Aseptically cannulate infants umbilical vein (up to 7cm for full term baby)

·         Take pre exchange sample for HB and Bilirubin baseline.

·         Exchange over 45-60 minutes using 5-20ml aliquotes depending on baby size and condition.

Monitor HR, RR by a continuous monitor if possible otherwise use observation and stethoscope strapped on infants precordium.

Take post exchange sample for HB and Bilirubin at end of procedure.

Continue phototherapy and serial bilirubin monitoring at end of procedure.

In exchange transfusion , use double volume transfusion

Assumes baby blood vol. of 85 mls /kg body weight.

(2 x 85) wt in kg= vol of blood required.

HYPERBILIRUBINEMIA

COMPLICATIONS

1. KERNICTERUS

 Unconjugated bilirubin crosses the blood/brain barrier and if very high can lead to kernicterus.

High unconjugated bilirubin crosses the blood brian barrier and interferes with oxygen uptake of the brain cells.

It is deposited in the basal ganglia giving them a yellow colouration.

Some pre-desposing factors increase the chance of kernicterus

Pre-disposing factors:

            (a) Low serum albumin.

            (b) Prematurity.

            (c) Sepsis esp. with meningitis.

            (d) Asphyxia.

            (e) Acidosis.

            (f) Intra-ventricular hemorrhage

Features of Kernicterus

Lethargy, poor suck, loss of Moro response, reduced tendon reflexes.

Respiratory distress, bulging fontanels, shrill high pitched cry, convulsions and spasms eventually develops opisthotonic posturing.

75% mortality while survivors have various degrees of brain injury including athetotic cerebral palsy.

Topic Summary

 

Summary Quiz

·         Discuss neonatal jaundice under the following subheadings

A) Definition

B) Causes

C) Management

D) Kernicterus

·         What are the indications for exchange transfusion

·         What are the side effects of phototherapy

 

NEONATAL SEIZURES

NEONATAL ANAEMIA

Learning outcome

By the end of this lesson the learner should be able to diagnose and manage anaemia in children

 Topic objectives

·         Define anaemia

·         Classify anaemia according to the causes

·         State the investigations

·         Outline the management

Topic Content

Definitions

Anemia is when the Central venous hemoglobin < 13 g/dL or capillary hemoglobin < 14.5 g/dL in infant > 34 weeks and 0-28 days old

Average value for central venous hemoglobin at birth for > 34 weeks GA is 17 g/dL

Reticulocyte count in cord blood 3-7%

Average mean corpuscular volume 107 fL

Physiological anemia of infancy

In healthy term infants, hemoglobin levels begin to decline around the third week of life

Reach 11 g/dL at 8-12 weeks

Differences in premature infants

At birth they have slightly lower hemoglobin levels, and higher MCV and retic counts

Average level  is 7-9 g/dL and is reached at 4-8 weeks of age. Related to a combination of decreased RBC mass at birth, increased iatrogenic losses from lab draws, shorter RBC life span, inadequate erythropoietin production, and rapid body growth

Pathophysiology

Anemia in the newborn results from three processes

•      Loss of RBCs: hemorrhagic anemia (Most common cause)

•      Increased destruction: hemolytic anemia

•      Underproduction of RBCs: hypoplastic anemia

Hemorrhagic anemia

Antepartum period (1/1000 live births)

•      Loss of placental integrity

•      Abruption, previa,

•      traumatic amniocentesis

•      Anomalies of the umbilical cord or placental vessels

•      abnormal insertion of the cord in twins, communicating vessels,

•      cord hematoma, entanglement of the cord

•      Twin-twin transfusion syndrome

•      Only in monozygotic multiple births

•      13-33% of twin pregnancies have TTTS

•      Difference in hemoglobin usually > 5 g/dL

•      Congestive heart disease common in anemic twin and hyperviscosity common in plethoric twin

Hemorrhagic anemia

Intrapartum period

•      Feto-maternal hemorrhage (30-50% of pregnancies)

•      Increased risk with preeclampsia-eclampsia, need for instrumentation, and c-section

•      C-section: anemia increased in emergency c-section

•      Traumatic rupture of the cord

•      Failure of placental transfusion due to cord occlusion (nuchal or prolapsed cord)

•      Obstetric trauma causing occult visceral or intracranial hemorrhage

 

Hemorrhagic anemia

Neonatal period

·         Enclosed hemorrhage: suggests obstetric trauma or severe perinatal distress, cephalohematoma,  

·         Intracranial hemorrhage, visceral hemorrhage, Defects in hemostasis, Congenital coagulation factor deficiency, Consumption coagulopathy: DIC, sepsis, Vitamin K dependent factor deficiency.

·         Failure to give vit K causes bleeding at 3-4 days of age

·         Thrombocytopenia: immune, or congenital

·         Iatrogenic blood loss due to blood draws

 

Hemolytic anemia

·         Immune hemolysis: Rh incompatibility or autoimmune hemolysis

·         Nonimmune: sepsis, TORCH infection

·         Congenital erythrocyte defect: G6PD, thalassemia, unstable hemoglobins, membrane defects (hereditary spherocytosis, elliptocytosis)

·         Systemic diseases: galactosemia, osteopetrosis

Nutritional deficiency: vitamin E presents later

 

Hypoplastic anemia

Congenital causes

•      Diamond-Blackfan syndrome,

•      congenital leukemia,

•      sideroblastic anemia

Acquired

•      Infection: Rubella and syphilis are the most common

•      Aplastic crisis,

•      aplastic anemia

Clinical presentation

Determine the following factors

•      Age at presentation

•      Associated clinical features

•      Hemodynamic status of the infant

•      Presence or absence of compensatory reticulocytosis

Presentation of hemorrhagic anemia

Acute hemorrhagic anemia,

·         Pallor without jaundice or cyanosis and unrelieved by oxygen,

·         Tachypnea or gasping respirations

·         Decreased perfusion progressing to hypovolemic shock

·         Decreased central venous pressure

·         Normocytic or normochromic RBC

·         Reticulocytosis within 2-3 days of event

 

Presentation of hemorrhagic anemia

Chronic haemorhagic anaemia

•      Pallor without jaundice or cyanosis and unrelieved by oxygen

•      Minimal signs of respiratory distress

•      Central venous pressure normal

•      Microcytic or hypochromic RBC indices

•      Compensatory reticulocytosis

•      Enlarge liver d/t extramedullary erythropoiesis

•      Hydrops fetalis or stillbirth may occur

 

Presentation of hemolytic anemia

•      Jaundice is usually the first symptom, Compensatory reticulocytosis

•      Pallor presents after 48 hours of age

•      Unconjugated hyperbilirubinemia of > 10-12 mg/dL

•      Tachypnea and hepatosplenomegaly may be present

Presentation of hypoplastic anemia

•      Uncommon

•      Presents after 48 hours of age

•      Absence of jaundice

•      Reticulocytopenia

Presentation of other forms

Twin-twin transfusion

•      Growth failure in the anemic twin, often > 20%

Occult internal hemorrhage

•      Intracranial: bulging anterior fontanelle and neurologic signs (altered mental status, apnea, seizures)

•      Visceral hemorrhage: most often liver is damaged and leads to abdominal mass. Pulmonary hemorrhage: radiographic opacification of a hemithorax with bloody tracheal secretions

Diagnosis

Initial studies

•      Hemoglobin

•      RBC indices

•      Microcytic or hypochromic suggest feto-maternal or twin-twin hemorrhage, or a-thalassemia

•      Normocytic or normochromic suggest acute hemorrhage, systemic disease, intrinsic RBC defect, or hypoplastic anemia

•      Reticulocyte count

elevation suggests antecedent hemorrhage or hemolytic anemia while low count is seen with hypoplastic anemia

Diagnosis

Initial studies continued

•      Blood smear looking for

•      spherocytes (ABO incompatibility or hereditary spherocytosis)

•      elliptocytes (hereditary elliptocytosis)

•      pyknocytes (G6PD)

•      schistocytes (consumption coagulopathy). Direct Coombs test: positive in isoimmune or autoimmune hemolysis

Other diagnostic studies

Blood type and Rh in isoimmune hemolysis

Kleihauer-Betke test on maternal blood looking for fetomaternal hemorrhage

CXR for pulmonary hemorrhage

Bone marrow aspiration for congenital hypoplastic or aplastic anemia

TORCH: bone films, IgM levels, serologies, urine for CMV

DIC panel,

platelets count

Occult hemorrhage: placental exam, cranial or abdominal ultrasound

Intrinsic RBC defects: enzyme studies, globin chain ratios, membrane studies

Management

Simple replacement transfusion

Indications:

acute hemorrhage

Use 10-15 ml/kg O, RH- packed RBCs or blood cross-matched to mom and adjust hct to 50%

Give via low UVC or central UVC if time permits

Draw diagnostic studies before transfusion

ongoing deficit replacement

maintenance of effective oxygen-carrying capacity

Haematocrit  < 35% in severe cardiopulmonary disease

Haematocrit < 30% in mild-moderate cardiopulmonary disease, apnea, symptomatic anemia, need for surgery

Haematocrit < 21%

Management

Exchange transfusion

•      Indications

•      Chronic hemolytic anemia or hemorrhagic anemia with increased central venous pressure

•      Severe isoimmune hemolytic anemia

•      Consumption coagulopathy

Nutritional replacement: iron, folate, vitamin E

Prophylactic management

Erythropoietin

•      Increased erythropoiesis without significant side effects

•      Decreases need for late transfusions

•      Will not compensate for anemia due to labs

•      Need to have restrictive policy for blood sampling and micro methods in the lab

Nutritional supplementation: iron, folate, vitamin E


NEONATAL ANAEMIA


NEONATAL ANAEMIA

Learning outcome

By the end of this lesson the learner should be able to diagnose and manage anaemia in children

 Topic objectives

·         Define anaemia

·         Classify anaemia according to the causes

·         State the investigations

·         Outline the management

Topic Content

Definitions

Anemia is when the Central venous hemoglobin < 13 g/dL or capillary hemoglobin < 14.5 g/dL in infant > 34 weeks and 0-28 days old

Average value for central venous hemoglobin at birth for > 34 weeks GA is 17 g/dL

Reticulocyte count in cord blood 3-7%

Average mean corpuscular volume 107 fL

Physiological anemia of infancy

In healthy term infants, hemoglobin levels begin to decline around the third week of life

Reach 11 g/dL at 8-12 weeks

Differences in premature infants

At birth they have slightly lower hemoglobin levels, and higher MCV and retic counts

Average level  is 7-9 g/dL and is reached at 4-8 weeks of age. Related to a combination of decreased RBC mass at birth, increased iatrogenic losses from lab draws, shorter RBC life span, inadequate erythropoietin production, and rapid body growth

Pathophysiology

Anemia in the newborn results from three processes

•      Loss of RBCs: hemorrhagic anemia (Most common cause)

•      Increased destruction: hemolytic anemia

•      Underproduction of RBCs: hypoplastic anemia

Hemorrhagic anemia

Antepartum period (1/1000 live births)

•      Loss of placental integrity

•      Abruption, previa,

•      traumatic amniocentesis

•      Anomalies of the umbilical cord or placental vessels

•      abnormal insertion of the cord in twins, communicating vessels,

•      cord hematoma, entanglement of the cord

•      Twin-twin transfusion syndrome

•      Only in monozygotic multiple births

•      13-33% of twin pregnancies have TTTS

•      Difference in hemoglobin usually > 5 g/dL

•      Congestive heart disease common in anemic twin and hyperviscosity common in plethoric twin

Hemorrhagic anemia

Intrapartum period

•      Feto-maternal hemorrhage (30-50% of pregnancies)

•      Increased risk with preeclampsia-eclampsia, need for instrumentation, and c-section

•      C-section: anemia increased in emergency c-section

•      Traumatic rupture of the cord

•      Failure of placental transfusion due to cord occlusion (nuchal or prolapsed cord)

•      Obstetric trauma causing occult visceral or intracranial hemorrhage

 

Hemorrhagic anemia

Neonatal period

·         Enclosed hemorrhage: suggests obstetric trauma or severe perinatal distress, cephalohematoma,  

·         Intracranial hemorrhage, visceral hemorrhage, Defects in hemostasis, Congenital coagulation factor deficiency, Consumption coagulopathy: DIC, sepsis, Vitamin K dependent factor deficiency.

·         Failure to give vit K causes bleeding at 3-4 days of age

·         Thrombocytopenia: immune, or congenital

·         Iatrogenic blood loss due to blood draws

 

Hemolytic anemia

·         Immune hemolysis: Rh incompatibility or autoimmune hemolysis

·         Nonimmune: sepsis, TORCH infection

·         Congenital erythrocyte defect: G6PD, thalassemia, unstable hemoglobins, membrane defects (hereditary spherocytosis, elliptocytosis)

·         Systemic diseases: galactosemia, osteopetrosis

Nutritional deficiency: vitamin E presents later

 

Hypoplastic anemia

Congenital causes

•      Diamond-Blackfan syndrome,

•      congenital leukemia,

•      sideroblastic anemia

Acquired

•      Infection: Rubella and syphilis are the most common

•      Aplastic crisis,

•      aplastic anemia

Clinical presentation

Determine the following factors

•      Age at presentation

•      Associated clinical features

•      Hemodynamic status of the infant

•      Presence or absence of compensatory reticulocytosis

Presentation of hemorrhagic anemia

Acute hemorrhagic anemia,

·         Pallor without jaundice or cyanosis and unrelieved by oxygen,

·         Tachypnea or gasping respirations

·         Decreased perfusion progressing to hypovolemic shock

·         Decreased central venous pressure

·         Normocytic or normochromic RBC

·         Reticulocytosis within 2-3 days of event

 

Presentation of hemorrhagic anemia

Chronic haemorhagic anaemia

•      Pallor without jaundice or cyanosis and unrelieved by oxygen

•      Minimal signs of respiratory distress

•      Central venous pressure normal

•      Microcytic or hypochromic RBC indices

•      Compensatory reticulocytosis

•      Enlarge liver d/t extramedullary erythropoiesis

•      Hydrops fetalis or stillbirth may occur

 

Presentation of hemolytic anemia

•      Jaundice is usually the first symptom, Compensatory reticulocytosis

•      Pallor presents after 48 hours of age

•      Unconjugated hyperbilirubinemia of > 10-12 mg/dL

•      Tachypnea and hepatosplenomegaly may be present

Presentation of hypoplastic anemia

•      Uncommon

•      Presents after 48 hours of age

•      Absence of jaundice

•      Reticulocytopenia

Presentation of other forms

Twin-twin transfusion

•      Growth failure in the anemic twin, often > 20%

Occult internal hemorrhage

•      Intracranial: bulging anterior fontanelle and neurologic signs (altered mental status, apnea, seizures)

•      Visceral hemorrhage: most often liver is damaged and leads to abdominal mass. Pulmonary hemorrhage: radiographic opacification of a hemithorax with bloody tracheal secretions

Diagnosis

Initial studies

•      Hemoglobin

•      RBC indices

•      Microcytic or hypochromic suggest feto-maternal or twin-twin hemorrhage, or a-thalassemia

•      Normocytic or normochromic suggest acute hemorrhage, systemic disease, intrinsic RBC defect, or hypoplastic anemia

•      Reticulocyte count

elevation suggests antecedent hemorrhage or hemolytic anemia while low count is seen with hypoplastic anemia

Diagnosis

Initial studies continued

•      Blood smear looking for

•      spherocytes (ABO incompatibility or hereditary spherocytosis)

•      elliptocytes (hereditary elliptocytosis)

•      pyknocytes (G6PD)

•      schistocytes (consumption coagulopathy). Direct Coombs test: positive in isoimmune or autoimmune hemolysis

Other diagnostic studies

Blood type and Rh in isoimmune hemolysis

Kleihauer-Betke test on maternal blood looking for fetomaternal hemorrhage

CXR for pulmonary hemorrhage

Bone marrow aspiration for congenital hypoplastic or aplastic anemia

TORCH: bone films, IgM levels, serologies, urine for CMV

DIC panel,

platelets count

Occult hemorrhage: placental exam, cranial or abdominal ultrasound

Intrinsic RBC defects: enzyme studies, globin chain ratios, membrane studies

Management

Simple replacement transfusion

Indications:

acute hemorrhage

Use 10-15 ml/kg O, RH- packed RBCs or blood cross-matched to mom and adjust hct to 50%

Give via low UVC or central UVC if time permits

Draw diagnostic studies before transfusion

ongoing deficit replacement

maintenance of effective oxygen-carrying capacity

Haematocrit  < 35% in severe cardiopulmonary disease

Haematocrit < 30% in mild-moderate cardiopulmonary disease, apnea, symptomatic anemia, need for surgery

Haematocrit < 21%

Management

Exchange transfusion

•      Indications

•      Chronic hemolytic anemia or hemorrhagic anemia with increased central venous pressure

•      Severe isoimmune hemolytic anemia

•      Consumption coagulopathy

Nutritional replacement: iron, folate, vitamin E

Prophylactic management

Erythropoietin

•      Increased erythropoiesis without significant side effects

•      Decreases need for late transfusions

•      Will not compensate for anemia due to labs

•      Need to have restrictive policy for blood sampling and micro methods in the lab

Nutritional supplementation: iron, folate, vitamin E