Jaundice Flashcards
Jaundice
Yellow discolouration of skin and sclera cause by raised levels of bilirubin in the blood
Causes of physiological jaundice
Normal breakdown of excessive RBC needed by newborn in extra uterine life. Fetus has greater need for RBC than newborn
Physiological jaundice
Normally never appears before first 24 hrs of age
Fades between 7-10days
Bilirubin levels rise to
200mmol/l term
250 premi
Pathological jaundice
Occurs before 24 hrs
Rapid increase in bilirubin levels
Persists beyond 10 days
Midwife role in jaundice
Educate symptoms
Who to contact
What to look for
Causes of pathological jaundice
Anything that increases the production of bilirubin or inhibits the transport, metabolism or excretion of it. Eg blood group incompatibility, sepsis, hypothermia, abs, dehydration
The normal breakdown of bilirubin process / conjugation
Into haem and gloving
Haem- is catabolised into bilirubin
It is lipid or fat soluble- unconjugated bilirubin
Body transports to liver to bind with albumin
If it’s not bound to albumin it can go to Brian or skin
Once at liver, conjugation occurs with aid of liver enzymes
Once conjugated, able to excrete
Moves via Villary system into small bowel excreted in faeces and some urine via kidneys
If conjugation occurs, why do they develop jaundice
Level of bilirubin they need to transport, convert and excrete exceeds ability to do so
Lower albumin conc- less transport
Liver immature
Lack bacteria in bowel
How does the lack of bacteria in bowel contribute to bilirubin
It ensures conjugated bilirubin is excreted properly, if not reconversion to unconjugated (lipid or fat soluble) which is reabsorbed by body
Supportive jaundice care
Early feeding
Freq feeing
How does early / freq feeding aid in jaundice care
Hydration and Glucpse for energy Encourages bowel flora and morality Glucose assists anymore process in liver Motility- dec time billirubin in bowel, dec amount it is reabsorbed Maintains warmth
Jaundice ax
Every 8-12 hrs Is visible at 80-90mms/L Alert/ drowsy Feeding Output Kramer rule OR transcutaneous billirubinometer
Kramer rule
Blanching of skin with finger a different zones and observing colour
K1
Head and neck
K2
Chest an shoulders
K3
Umbi lower abdo and knees
K4
Lower arms and lower legs
K5
Whole of baby
Hands feet fingers and toes
Trancutaneous billirubinometer
Screens jaundice level to determine need for serum billirubin test (SBR)
Older than 24 hrs
Photo therapy
When level needs to be supported more than early and freq feeds
Blue lights to enhance billirubinn conjugation and therefore ability to excrete
Photo therapy rules
Intermittent or continuous Exposure to entire skin Control temp 40-50cm from baby Eyes protected
Cons of phototherapy
Fluid loss increase, dehydration
Separation
Skin ax unreliable when exposed
When ceased - (rebound)
Importance of newborn ax
Monitor health / wellbeing Responses to physiological changes Check growth Behaviour Affects I birth Detect congenital malformation Sick baby Baseline
Principles of newborn ax
Communicates Quiet and alert Systematic approach Heart and lungs first Symmetry
Sequence of new born ax
History Heart lungs Skin Head neck Chest abdomen Spine Limbs and joints Neurological
History before nba
Genetic factors Maternal blood group Apgar Birth weight Mode of del
Average length
45- 50cm
Average weight
3500g -4500g
Normal to lose 10% normal physiological diuresis
Regain birth weight by day
10-14
Head circ average
34.5-35.5cm
Head circ measurement taken from
Occipitofrontal diameter
Normal auxilla temp
36.5-37.5
NBA heart lungs
RR effort rise and fall abdomen simultaneous
30-60 RR
HR 110-160 regular
When listening to heart in NBA
Reg
Diaphragm high pitch
Bell low pitch
S1 and s2
Skin NBA
Lanugo Millia Mottling Colour Pallor Acrocyanosis Plethora Jaundice Mongolian blue spot Vernix
Head and neck NBA
Symmetry shape Injury Sutures Fontanelles Plagiocephally Face Hair Moulding Caput succedaneum Cephalhamltoma
Sutures
Frontal
Coronial
Sagital
Lanbdoidal
Fontanelles
Anterior- hard on palp
Posterior -flat not sunken or bulging
If post Frontanelle is bulging
Intracranial haemorrhage
If posterior Frontanelle is sunken
Dehydration
Cephalhaematoma
Bleeding eternal periostium and none of fetul skull
Most common site for Cephalhaematoma
Parietal bones
Can have more than one
How does Cephalhaematoma happen
Occurs from forceps, friction of fetal scull on pelvic bones
Because periostrium separating from skull bone and haemorrhaging between them
In Cephalhaematoma the swelling is confined to
One single bone per haematoma- won’t cross suture line
When does Cephalhaematoma occur
12-72hrs
Cephalhaematoma pit on pressure?
No
True false Cephalhaematoma may be bilateral
True
Cephalhaematoma enlarge or reduce after birth
Enlarges
Cephalhaematoma can contribute to
Jaundice
Anaemia
Caput succedaneum
Oedemous swelling of superficial tissues inside scalp
In unsupported part of head
Causes of caput succedaneum
Pressure on fetal head during contractions
Can caput succedaneum cross suture line
Yes
Caput succ reduces or enlarges afterwards
Reduces
Does caput succ pit on palp
Yes
Soft swelling
Tx for caput vs Cephalhaematoma
Caput no tx
Cephalhaematoma gentle handling and vita k
Face NBA
Eyes -discharge moving ocular organs gaze epicantal fold red reflex othalmascope
Nose- patent
Mouth- symmetrical, rooting reflex, asses lips gums palette complete, tongue tie, candida
Chest and abdo NBA
Round and soft Nipples symmetrical Exclude hernia with palp of groins Genetalia Excited undescended testes
Spine NBA
Palp Lumps Swelling Dimpling Butt creases Anus patent
Limbs and joints
Check auxilla for skin tags Open hands Webbing Equal ROM joints Flexion Tone
Neurological NBA
Alert
Reflexes
Grasp
Babinski reflex
Stimulus sole of foot
Response big toe bends back toward top of foot and other toes fan
Startle (mono) reflex
Stim- loud sound or movement
Red- head thrown back, extends arms and legs, pulls them back in
Root reflex
Stim- corner of mouth stroked
Re- head turns to touch
Suck reflex
Roof of mouth touched
Res sucking
Truncal incuration / galant reflex
Tap side of spine
Red- twitch hips towards touch
Tonic neck reflex
Stim - head turned to one side
Res- extremities on same side straighten Opp side flexed
Grasp reflex
Touch palms or fingers
Res- close fingers in grasp
Meconium stained liquor risk
Aspirate- infection
Common disorders of neonate
Oral thrush Sucking blister Septic spots Breast engorgement Vom mucous
True false urates normal in nappy first 24 hrs
Yes
Stool changes
Meconium- black green tenacious
Transitional- 3-5 brownish yellow
Feeding established- loose yellow offensive
Newborn physiological adaptations
Resp Haematological Thermal GIT Metabolic
Primary functional change of lungs
Lungs change from fluid excretion function to gas exchange
Fluid needs to be removed for this
Expelled- through oral an nasal pharynx
Reabsorbed- remainder with inflation
The first few breaths encourage
Remaining intra alveolar fluid to move peri bronchial and peri vascular spaces to be absorbed into local vascular system
Establish resp
RR is irreg
Apnoea 5-15 secs norm
Effort is diaphormatic
Resp adaptations
Primary functional change of lungs
Establish resp
Increase expansion of terminal sacs
Expansion of terminal sacs
Complet inflation - complete inflation I terminal alveolar sacs- efficient gas exchange
Lung vol per kg
25ml
Haematological adap
Fetal haemoglobin - at birth 17g per decilitre of blood
Fetal type has high affinity of oxygen to compensate for prev hypoxic uterine enviro
After, hb no longer req, hemolysis will occur = jaundice
Why vita K
Newborn doesn’t have adequate supply of vita k to be able to synthesis thrombin and other Clotting factors
What stimulates synthesis of vita k
Feeding,’colonisations of bowel
End of First week
Thermal adaptation
Need to adapt to cooler enviro Uterine temp 37.7 Dry and wrap Thermoregulation Risk of heat loss
Why are babies at risk of heat loss
Less subcutaneous fat
Large surface area to mass ratio
Thin epidermal layer
Blood vessels superficial decrease ability to shiver
Loss of heat from baby
Convection to moving air
Conduction to cold surface
Evaporation to air through wet skin
Radiation to cold structures
How do babies gain heat
Brown adipose tissue- provided heat through chemic thermogenesis
Withdrawal of prostaglandin and adenosine which prevents shivering
Decrease ability to sweat Flexed posture Chemical thermogenesis- metabolic activity Limb movement Sucking
To use brown fat
SNS stimulates release of adrenaline, TSH, & catecholamines which increase metabolism of brown fat, enhance production of bfat and make extra glucose to fuel this conversion
Rapidly metabolised and produces heat- transfers through vascular system by strategic placement around bodies with high circulation (kidneys adrenal glands head and neck)
GIT adaptations
Sucking and swallowing- reflexes present at birth
Stomach capacity- 6mL/kg meaning 3.5kg=21 ml normal increases rapidly
Cardiac sphincter immature at birth- causes positing so this plus size of stomach and competition of ingested air in stomach = regurgitation of milk
Digestion adaptations
Milk feeding stimulates production of enzymes within the git tract and stimulates rapid proliferation of cells lining the tract
At term has the ability to digest simple carbs, protein and fat
Glucose adaptations
Maternal glucose withdrawn
In 3rd try feotus lays down stores of glycogen to ensure enough in first few days
More efficient in synthesis rather than using it- need for ketones and ffa as immediate source of energy - gluconeogenesis
Decrease in serum insulin- NB ability for fat metabolism (lipolysis) increases- supports while gluconeogenesis occurs
The release of ffa and ketones relies on lipolysis
Metabolic adaptations
Fat metabolism
Protein metabolism
Protein metabolism
Learns to digest milk proteins to provide source of amino acids to so in remodelling urging rapid cell differentiation to Feed rapid cell growth
Adult hb
180
Fetal hb
220
Fetal circulation
Structures of fetal circ enable efficient transport of gases to and from placenta
Aimed at quick transport of O2 and nutrients to vital organs
Why is there a greater need for 02 to be transported quickly in fetal
Gas exchange not as effective in placenta than lungs
Why do fetid have different hb
Fetal hb allows 20-30% greater 02 carrying capacity than adult and O2 disengages easily from this - supplies tissues more effectively
Why is fetal circ a temporary thing
Minimises circ to I rgans that are less improtant in fetal life like lungs and git- must be temporary to allow for rapid transition
When does cvs develop
En of 3rd week (5wks gestation)
Fetal placental villi forming along with fetal placental vessels. A rudimentary umbi cord can be seen.
Fetal vessels are made of mesoderm- one of the basic layers of the tri laminae embryo
At week four (6wks gest) CVS
Rudimentary two chambered heart begins to beat
Critical time for cardiac Dev is
20-50 days after fertilisation
6wks (8g)
Umbi cord developed
Carries 02 rich blood to embryo
2 umbi arteries carry deox to placenta
8 was (10g)
Structures making up fetal circ in place
Whartons jelly protects vessels in cord
Feto-placental circ
Deox to placenta via 2 umbi arteries away from fetal heart.
Umbi arteries divide and subdivide entering into villi of placenta for gas exchange
Return circ through umbi vein 02 blood fetus toward fetal heart
Temporary structures of fetal circ
Umbilical vein Ductus venosus Foramen ovale Ductus arteriosus Umbilical arteries
Umbilical vein
From the umbi cord to underside of the liver. Has branch that joins portal vein. Half the blood supplies from
Vein enters this branch- other half shunted through temp structure ductus venosus
Ductus venosus
Connects umbilical win to inferior vena cava high in 02 directed toward the heart
Foramen ovale
Opening between r and L atria of heart
Allows blood entering heart to bypass pulmonary circ
Has flap which can open or close with changing pressures of heart
Ductus arteriosus
Connection between pulmonary artery and the aorta
Allows like entering pulmonary circ to be diverted before entering lungs
Umbilical arteries
From hypo gastric arteries to the umbilical cord
Carries 02 rich blood back to placenta via hypo gastric artery which are branches of the internal illiacs
Pic
Foramen ovale at birth
Functional closure 1-2 hrs after permanent within 6 months know as fossa ovalis
Ductus arteriosus changes a birth
Functional closure in 15 hrs- fibroses takes within 3 weeks becoming known as ligamentum arteriosum
Ductus venosus changes a birth
Functional closure soon after birth
Fibroses takes within 2 months belong known as ligamentum venosum
Umbilical vein & arteries (intra abdominal) changes
Constricts and fibrose to become the ligamentum teres and the medial umbilical ligaments and superior vesicular artery (supplying the bladder)
Signs functional structures changing
Take a breath Crying Peaks up Umbi cord apps pulsating Pink Warm
What physiological factors can interfere with adaptations
Hypothermia- lowers bsl
Will revert back to fetal circ
Apgar score
1 activity (tone) 2 pulse (hr) 3 grimace (reflexes) 4 appearance (colour) 5 resps (rate and effort)
