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D: SGA: birth weight < 20th percentile for gestational age or < 2.5 kg.
LGA: birth weight > 90th percentile for gestational age or > 4 kg.
A: SGA: may be familial, constitutional, or due to IUGR.
IUGR is defined as either symmetrical or asymmetrical:Asymmetrical IUGR: relative sparing of head circumference in relation toweight and length:. Due to impaired uteroplacental function 28 to maternal pre-eclampsia, DM
or nutritional deficiency during the 3rd trimester.
. Occurs when foetal growth rate in 3rd trimester exceeds maximal supply
. There is preferential sparing of the cerebral perfusion at times of foetal
Symmetrical IUGR: head circumference, weight, and length are all propor-tionally affected to equivalent degrees:. Indicative of a prolonged period of poor intrauterine growth.
Caused by congenital intrauterine infections (TORCH) in the 1st trimester,genetic factors such as single gene deletions and chromosomal disorders,maternal smoking, drug and alcohol abuse, chronic medical conditions (e.g.
CRF), malnutrition, or multiple pregnancies.
LGA: macrosomia is a feature of infants of mothers with either gestational orpoorly controlled/undiagnosed DM.
A/R: IUGR: previous SGA infant, low pre-pregnancy weight and poor pregnancy
E: SGA: affects by definition 20% of the population and varies with ethnic back-
IUGR: 2/200 neonates; asymmetrical > symmetrical IUGR.
LGA: affects by definition 20% of live births; is more common in developedcountries where there is a higher prevalence of DM.
H& Antenatal: maternal examination and accurate dating aid diagnosis. Oligo-
E: hydramnios and poor foetal movements are indications of placental insuffi-
Perinatal monitoring: foetal tachycardia, loss of variability of the baseline inthe foetal heart trace, and late decelerations may indicate foetal distress onCTG.
Postnatal measurements: birth weight, length, and head circumference oncentile chart.
I: Radiology: USS is the 18 method of diagnosing IUGR or macrosomia ante-
Cordocentesis: percutaneous umbilical blood sampling may be used for de-tection of hypoxia, lactic acidosis, hypoglycaemia, chromosomal analysis, andDNA diagnosis of congenital intrauterine infections.
M: Antenatal: maternal bedrest and limitation of activity for severe IUGR.
Perinatal: maternal administration of O2, continuous assessment of foetalwell-being.
Delivery (IUGR): if foetus becomes hypoxic in utero, an emergencyCaesarean section is required.
Macrosomia: induce at 38/40 to prevent complications in a unit with goodneonatal facilities.
C: IUGR foetus: intrauterine hypoxia, birth asphyxia, and death.
IUGR infant: hypothermia (relatively large surface area), hypoglycaemia(poor fat and glycogen stores), hypocalcaemia, polycythaemia, and meconiumaspiration.
LGA: birth asphyxia due to prolonged/difficult delivery, birth trauma, espe-cially shoulder dystocia, hypoglycaemia in the neonatal period due to hyper-insulinism, and polycythaemia.
P: Depends on the cause of abnormal size at birth. Infants with asymmetrical
IUGR will rapidly put on weight in the postnatal period; symmetrical IUGRinfants are more likely to remain small permanently. Studies have shown thatIUGR infants are at "risk of developing "BP, Type II DM, and coronary heartdisease.
D: Inflammation of the pilosebaceous duct. Classified as mild, moderate, and
. "Sebum production: androgenic stimulation of hyper-responsive pilosebac-
. Impaired normal flow of sebum: obstruction of the pilosebaceous duct by
. Propioni acne bacteria: may play a role by producing cytokines and lipolytic
Infantile acne: < 3 months of life; transient and usually due to maternalandrogens.
A/R: Puberty, may " premenstrually, POS, excess cortisol (Cushing syndrome).
E: Developed world: affects 79–95% of the adolescent population, peaking at
14–18 years; tends to recede by early twenties.
Developing world: acne incidence is considerably lower; likely combination
of environmental and genetic factors.
H: Usually self-diagnosed, acute onset, greasy skin, may be painful.
E: Open comedones: whiteheads; flesh-coloured papules.
Closed comedones: blackheads; black colour is due to oxidation of the mel-anin pigment.
Other features: pustules, nodules, cysts, scarring, and seborrhoea.
Distribution: primarily affects the face, neck, chest, and back (where seba-ceous glands are most numerous).
P: Gross distension of the pilosebaceous follicle with neutrophil infiltration.
Closed comedones may contain serous fluid. Severe acne can create fistulaebetween inflamed glands.
I: Normally none required. Investigate for endocrine disorder if acne develops
during 2–10 years of age.
Bloods: FSH, LH (if female, suspect POS).
Urine: 24-h-urinary cortisol (if Cushing syndrome is suspected).
M: Many cases may not need treatment. Indication for treatment based on classi-
fication and degree of psychosocial impact. In severe acne, therapy should becommenced early to prevent scarring.
Topical preparations:(1) Benzoyl peroxide; keratolytic agent, encourages skin peeling, and # number
of P. acnes (S/E: irritation and bleaching of clothes).
(2) Vitamin A derivatives; tretinoin, may take 3–4 months to work.
(3) Azelaic acid.
Antibiotics:(1) Topical: clindamycin, erythromycin.
(2) Systemic: tetracycline only in > 16 years. (S/E: discolours teeth and may
A gradual " in P. acne resistance to many antibiotics has been documented;growing need to use either appropriate antibiotics or change the therapeuticstrategy in favour of other regimens.
Isotretinoin (Roaccutane P.O.): vitamin A derivative, 4–6-month course onlyby specialist prescription for severe acne (S/E: teratogenic; females require OCP,hyperlipidaemia).
Antiandrogens: in females only; OCP or cyproterone acetate.
UVB: adjunctive therapy, but rarely used.
Advice: improvement may not be seen for at least a couple of months, use non-greasy cosmetics, wash face daily, moderate exposure to sunshine is beneficial.
C: Physical: facial scarring (atrophic/keloid), hyperpigmentation of scars, 28 in-
fection and fistulae.
Psychosocial: lack of self-confidence.
P: Generally improves spontaneously over months/years. Persists into adulthood
D: Abnormalities of the female genital tract not present at birth.
A: Labial adhesions: adherence of the labia minora in the midline; may give the
appearance of absence of the vagina. A thin pale semi-translucent membranecovers the vaginal os. Trauma causes denudation of the epithelial layer of thelabia minora mucosa and leads to fibrous tissue formation; therefore sealingof the labia minora. Trauma can involve inflammatory conditions (vulvitis,vulvovaginitis), sexual abuse, or straddle injuries.
Vulvovaginitis: pruritus, vulval pain, vulval erythema, vaginal discharge orbleeding. Usually associated with poor perineal hygeine, constipation, and atopicdermatitis caused by local irritants (bubble bath, soaps, shampoo) or by occlusiveclothing causing irritation. May be caused by trauma 28 to abuse; therefore thisshould be considered if other concerns are present.
A/R: Vulvovaginitis is often misdiagnosed as a UTI due to its similar presentation.
E: Labial adhesions: peak age: 3 months to 6 years, incidence: 1–2%.
Vulvovaginitis: very common in < 5-year-olds.
H: Labial adhesions: usually asymptomatic and noted on routine examination.
Some patients may leak urine when they stand after voiding.
Vulvovaginitis: history should include toilet-training, type of nappy used,bad odour or dark discharge, scratching, history of eczema, allergic rhinitis, ordiarrhoea, tendency of child to insert objects, and any possible indication ofabuse.
E: General: should be by a skilled clinician, in a well-lit room with a relaxed and
distracted child (mother reading book).
Labial adhesions: the edges of the labia minora are sealed along the mid-line, beginning at the posterior fourchette and extending anteriorly towardsthe clitoris.
Vulvovaginitis: commonly, only vulvitis will be detected, although vaginaldischarge and bleeding may also be present.
I: Exclude other vaginal disorders such as imperforate hymen or septate vagina
prior to treatment.
Microbiology: vaginal swab if discharge present, MSU.
Radiology: indirect cystourethrogram may show urinary retention behindthe fused labia, bladder distention þ=À hydronephrosis in labial adhesions.
M: Labial adhesions: oestrogen cream dissolves the adhesions in 90% of cases.
Once adhesions have been lysed vasoline is used as prophylaxis for 1–2months.
Vulvovaginitis:. Treat any underlying infection with appropriate antibiotics.
. Education of adequate perineal hygiene and removal of potential irritants.
C: Labial adhesions: without adequate treatment 20–40% will develop UTI.
P: Labial adhesions: recurrence is common, therefore good follow-up is
Vulvovaginitis: outcome good with improved perineal hygiene.
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